DEPARTMENT OF AGRICULTURE
|ADVISORY COMMITTEE MEETING|
Pages: 293 through 516
Place: Washington, DC
Date: March 9, 1999
HERITAGE REPORTING CORPORATION
1220 L Street N.W., Suite 600
|IN THE MATTER OF:|
|ADVISORY COMMITTEE MEETING|
|Tuesday, March 9, 1999|
|1800 M Street N.W.|
The proceeding in the above-entitled matter was reconvened, pursuant to Notice, at 9:02 a.m.
P R O C E E D I N G S
(9:30 a.m.)CHAIRMAN GARZA: I have to congratulate this group. It is one of the most orderly ones I've ever had the pleasure of chairing. People start going to their chairs on the first notice.
Good morning. Very pleased to see so many of you return despite the weather forecast, which for Washington, I know, strikes terror and horror in everyone's heart. It reminds me a little bit of Houston where two snowflakes and people run for cover. So I've adjusted, you can tell, from after 10 years. Now, 12 inches and it looks normal to me.
Okay, we have the pleasure this morning of having Dr. Tim Byers, Professor of Preventive Medicine, University of Colorado School of Medicine. We've asked Professor Byers to come and review with us the links between fat fiber and carbohydrate intake. That was the original title. Then I called Tim back about a little bit over an week ago and said, "Tim, can you add alcohol to that, and help us look at the links between those four and the risk of cancer?" And he very graciously agreed.
And so with that very brief introduction, Professor Byers.DR. BYERS: Thank you. And you also said "add a little sugar."
So got a little added sugar to the presentation as well.
So this is my assignment really, to review findings just in the last four years relating cancer risk to these factors. It is snowing outside, I notice. I'll keep you all informed because I do have a little bit of a view of the outside from here.
And to comment as well, I was asked to comment as well on my views about food, the implications for food policy, which is what you all are about, and research approaches, so I'll try to do that.
My approach to looking at these four factors was sort of the usual thing, look at publications largely in the English literature in the past four years. My presentation, however, will not be intended to be comprehensive in the 20 minutes with these four topics, and I'm going to focus instead on two things: the larger pool studies, or read analyses, and focus on specific controversial areas. So we're sort of more of the same, I'll just say that, and focus really on what I think are the more cutting edge issues.
Prior to 1995, there were a few studies about dietary fat and prostate cancer. The emphasis was pretty, I think, weak and inconsistent, and I think since 1995, it's more of the same. I think the range of kinds of findings for prostate cancer is essentially unchanged; that is, that there is a lot of heterogen in either cross studies, there are some very good studies, including one published just a month or two ago indicating fats, in particular, saturated fats, are a risk factor, or a review written by Larry Colonel, published just this last month, I think, covers the topic well and makes a case that there are a range of findings. And if there are relationships with fats, there is probably more evidence for animal sources or saturated fats.
The other thing that I think is important is that there is continued to be evidence that there are effects of fats, especially saturated fats, on circulating androgens and perhaps androgen conversion in tissues, and I think that that's an important continuing development.
As far as colorectal cancer before '95, there were fairly consistent findings for associations with total and/or saturated fats. Most of the research at that point came from case control studies. Since 1995, the associations have generally been weaker from the larger prospective studies and it's pretty clear that various methods of caloric adjustment in epidemiology largely adjust away fat effects for colorectal cancer.
But this is problematic really because the kind of factors we adjust for are not only total calories but also relevant factors for colon cancer risk, including fruits and vegetables, physical activity and red meats, which are themselves associated with fat and saturated fat intake, really, I think, create problems with multi-variant adjustments such that it's really difficult given our current epidemiologic technique to be certain that we're not overly adjusting some of these models, and the new issues, I think, will be screening. In the past, there has been very little screening activity for colorectal cancer. In the future, as we increase screening in this country, it's likely that those people who are screened for colon cancer will also be on more hard, healthy diets, so that will be a new compounder in future studies, I think.
With regard to fats and breast cancer before 1995, the evidence was pretty inconsistent and really weak, and came from case control studies. In the last four years the evidence has been more consistent and more consistently now, and the larger cohort studies really are null for the dietary fats/ breast cancer hypothesis.
I think there is a new -- as we scramble to try to resurrect the hypothesis, there is a new area of confusion that I want to comment on, and that is some confusion about different types of fats.
These are the findings from the pooled analysis of seven large cohort studies conducted around the world, and these four were total, saturated, poly and mono, and I didn't label them because it doesn't matter. As you can see, they are all the same. And essentially across a fairly wide range of dietary fat intake findings are null for breast cancer risk.
And this range really does, I think, even accounting for measurement error, really does include the range from about between 25 or 30 percent of calories from fat, in the high thirties, 35 to 40 percent of calories from fat, so across the range of intakes that are typical in the diet, but probably not below 25 percent. We can conclude that there is not much for relationship between dietary fat and breast cancer. Of course, the women's health initiative is an experimental study to try to test the effect, possible effectiveness of lower levels.
I wanted to comment though on a new problem, which is an analytic problem, I think, and that is, as we try to separate out the effects of different kinds of fats using multi-variant models, there are particular problems that emerge. I think as an example here is a case control study within a cohort in Sweden published just last year in which these are the relationships between saturated, mono and polyunsaturated fats, and across, again, a fairly wide range of intakes, really not much evidence of a relationship. But in multi-variant models in which one type of fat is adjusted for the other, then these fats can separate, and I think that some of this separation of, in this case, mono fats came to be protective, and saturated and polies looking to be slightly risk factors is an unfortunate artifact of a statistical colonary. This is before adjustment, this is after, and the headlines from this were that olive oil or monofats protect against breast cancer.
I think, as we scramble and try hard to squeeze effects out of fats using multi-variant models, we're going to create some artifacts that I think are, unfortunately, probably not a reflection of true biology.DR. DWYER: All of those risks are below 1.4, right?
DR. BYERS: All of the risks are below 1.4.
Well, the model fat was a protective relationship that was marginally statistically significant.
The increase in risk for saturated and polies in that study was not statistically significant, and it was certainly below 1.4 as an observation.
Alcohol and breast cancer before '95, they were fairly consistent, but weak associations. There were a lot of questions though at that time about not only beverage specificity for the effect, but dose response relationship, biological mechanisms and latency. By latency, I mean at what point in life might alcohol really be relevant. Is it in later adulthood? Is it teenage years or whatever?
Subsequent to '95, the findings have really been more consistent, and I think we now have some good early answers to all the above questions that I want to comment on. But the new questions and the questions that policy panels such as you have to deal with are the trade-offs for heart disease. So I'll comment on all those things.
Here is a pooled analysis from the same seven large cohort studies showed before for dietary fats, indicating that above -- this would be 15 grams or so would be about a drink a day, and certainly above a drink or two a day you start to see a linear increase in risk for breast cancer.
The question of latency, I think, has been addressed nicely in three studies that have been published in the last two - three years, and they all agree that alcohol intake -- it appears that alcohol intake later in life is more relevant to breast cancer risk than alcohol intake early in life. One of the questions was, was maybe this weak, inconsistent relationship with alcohol might be sort of a residual effect of heavier drinking earlier in life, and it looks like that probably is not the case; that alcohol, in fact, does increase breast cancer risk -- because I believe it does -- then the effect appears to be more proximal to the breast cancer itself.
There are a couple of studies of alcohol and stage of breast cancer, and both studies agree really that alcohol drinkers, women who drink alcohol tend to present at later stages of breast cancer. The explanations for that aren't clear cause there is really two possibilities. One is that there is a biological effect of promotion by alcohol and breast cancer. I think that is plausible by affecting estrogens. The other possibility that needs to be teased out is that there may in fact be diagnostic delay, and that women who drink alcohol may be less attentive to breast cancer in terms of screening mammography. That should be fairly easy to answer pretty soon, I would think.
The real problem is, as you're well aware, is the trade-off. Here is data from two large prospective studies, the Nurses' Health Study and the American Cancer Society -- Cancer Prevention Study II. The solid lines from the two studies indicate this U-shape relationship with total mortality driven largely by benefits to cardiovascular health, of drinking one or two drinks a day in this range. The breast cancer risks shown in the dotted lines, and when you get up to one or certainly two drinks a day, then I think there are appreciable breast cancer risks.
The trade-off then, I think, has to be one, and the tough thing for you all to consider is that there is not only just gender-specific specificity for possible adverse effects of low drinking alcohol for cancer; that is, affecting women with regard to breast cancer, but also age-specificity as well.
Here are the U.S. mortality data showing the breast cancer relationship with age, showing the heart disease relationship with age, and a line that I've added, which is breast cancer mortality times two; two times breast cancer risk is something that a lot of women can fairly easily compute for themselves based on their family histories, other risk factors, previous biopsies or, in fact, previous breast cancer.
And for breast cancer, it's actually similar or maybe even a higher cause of death premenstaulpausily than is heart disease. For women at higher risk for breast cancer, the breast cancer times two curve, that cross-over really doesn't happen until about age 60. So the tough thing for you is that it's not only issues about gender-specificity, but also age-specificity as well.
Just a couple comment on fiber because I'm pretty much going to dismiss it in my conclusions, and a lot of studies have shown this kind of thing. This is a large study out of Italy of about 2,000 cases, 2,000 controls, showing that fiber from grain sources is unrelated or perhaps actually associated with increased risk, but I think most conservatively judged as unrelated to risk, whereas fruit, and especially vegetable fiber, associated with lower risk.
Now, a little sprinkling of sugar. Before '95, there were a few studies. After '95, there are still a few studies. Most of the interest in added sugar and cancer has been with regard to colorectal cancer, but I think really the findings are weak. Even as I look at the papers that ostensibly from their titles and their abstracts report a positive finding with sugar or sucrose and colon cancer, I think the findings are even weak within those analyses. I think there has been a tendency to feature on subgroup findings and the big picture is there's not much of a relationship there.
There is problems though with studying added sugars in cancer. The biological hypotheses are pretty compelling that either caloric load or maybe stimulation of insulin might help to drive the promotion of neoplasia, and it's biologically appealing. The problems, of course, in epidemiology is it's difficult to quantify many things in the diet, especially things like added sugar, and that sugar, choice of the sweet foods associated with other aspects of behavior and it may, in fact, be an indicator food. So if you ask somebody how often they eat candy, you can make a pretty good guess about some of their behaviors as well.
After reviewing about 100 studies on sugar in the diet, Burley actually published a pair of papers in The European Journal of Cancer Prevention, the most recent one last year, and concluded, after reviewing all of them, it's apparent that there is insufficient evidence to conclude whether sugar has a role in cancer at any site, and I would agree with that even though I didn't go through as many studies as Burley did.
So just to conclude my comments, first, with research recommendations. These are obviously in a nutshell. I think, with regard to alcohol, the main -- the effect of alcohol in upper elementary cancers is pretty clear, and those are higher doses. The only real cutting edge question is low dose alcohol and breast cancer, and there I think the research really needs to focus on estrogen effects as it has, but I think there needs to be more work on estrogen effects of alcohol.
With regard to fats, I think the only critical question now really is fats, especially saturated fats, in prostrate cancer, and there I think we need more studies on the effects of fats on androgens in men.
I think with regard to fiber, we just need to get over it and focus on foods and not fiber per se in cancer.
And with regard to sugar, I think studying insulin resistance syndrome as related to neoplasia, since that's really the primary method, mode that the hypothesis holds for sugar, is probably the way to go, to better understand insulin and missal-like growth factors as they relate to neoplasia, and then to back up from that and make inferences about sugars and starches.
So since 1995, there have been two important dietary guidelines issued apart from the ones that your predecessor panel did in 1995. The American Cancer Society a year later, in '96, and The World Cancer Research Fund, in conjunction with the American Institute for Cancer Research a year later, in 1997, issued dietary prevention, or cancer prevention guidelines, and they really overlapped substantially, and the substantial areas of agreement between these two guidelines are just summarized here: Eat more plants, eat less animals, avoid obesity, be physically active, drink little, if any, alcohol. Perhaps you just want to take this exact wording for your next guidelines.
Food policy implications of the finding in the last four years, I've summarized here. For alcohol, I think the policy challenge for you all is that I think the best evidence now is that there does need to be some gender and age specificity now in alcohol guidelines, how you translate that into words or how we translate it into bumper stickers or other messages for the U.S. population is indeed a challenge, but I think that science dictates this.
For fats, I think the types of fats to avoid to lower cancer risk, either for colon or prostate cancer, where I think there are still some questions especially about saturated fats are, fortunately, consistent with heart disease prevention recommendations. So I see no problem or no conflict here. I think cancer can take a back seat to heart disease when it comes to types of fats, so I think that's appropriate, just as in the past.
With regard to fiber, I think we should really avoid the term in recommendations and focus instead on the foods that contain fiber and, I think, other nutritional aspects of those foods that are more relevant for cancer anyhow.
And for sugar, I see really no need to add cancer to reasons to limit sugar intake.
So those are my comments. I'd be happy to take any questions or comments.CHAIRMAN GARZA: Any questions? Comments?
Dr. Meir?DR. STAMPFER: That was really great, Tim. I think that was the best 20-minute diet cancer summary I've ever heard. Just a comment and a question.
The comment is I agree with you on the fiber, but just to emphasize that this was for cancer and that there may be other health benefits for fiber besides cancer.
My question is, Tim, for the breast cancer what's your -- the current guideline is one drink per day for women. That's the current dietary guideline, and what's your take on the level of risk for breast cancer at that level of consumption?DR. BYERS: The med analysis indicates that at precisely one drink a day the risk is very small; maybe 10 percent range. But within that -- I said "med analysis" -- within that pool of analysis of seven studies, as you know since you're a co-author of it, is heterogeneter cross studies to where some studies indicate higher and some lower.
So at exactly one drink a day, I think, I think there is some elevation of breast cancer risk but it's probably of that order.CHAIRMAN GARZA: Dr. Grundy.
DR. GRUNDY: Obviously, there are people who believe very strongly about diet and cancer, and it was, you know, believed so strongly that they initiated that major study and millions of dollars are invested. What was the scientific data or has that changed?
DR. BYERS: Which study are you referring to?
DR. GRUNDY: Well, I'm taking about like the women's health study where they are going to have a low fat diet and obviously that was -- to mount a study like that there has to be a lot of presumptive evidence and cross-culture and all that.
DR. BYERS: Well, I think the best summary is -- Roy provided by the National Cancer Institute itself, the rationale for it. There has been repeated papers. Most recently, Peter Greenwall restated the rationale just a month or so ago. I think it's in JNCI or one of the national journals.
I think the rationale for that experiment is that you need to get to lower levels. There may be a threshold below which there is an effect, that's it hard to really measure that in observational studies. I wouldn't want to argue strongly for the rationale, but this is sort of water over the dam from a decade ago, and the trial is well underway, and the difficulty in interpretation of the trial is it is not just a low fat trial; it's sort of a total diet trial. But that's good enough for me.
I actually think the Women's Health Initiative Study is a reasonable thing to do.DR. GRUNDY: Why is that? I mean, from what you presented, it would have been hard to convince me to invest the money to do that?
DR. BYERS: I think if we would have had these data in hand 10 years ago when the debate -- I guess it was 10, it seems like 10 years ago when the debate was going on -- that trial may not have gone forward. But at the time I think there was uncertainly, certainly uncertainty in the extent to which we should believe observational epidemiology, uncertainty that there may have been a lower threshold.
My guess is that the trial is not going to be particularly positive, but nonetheless I think it's -- I thought when the decision was being made that it was a reasonable trial to do.DR. GRUNDY: The idea of thresholds and systems like this is very problematic, isn't it; a threshold concept is questionable?
CHAIRMAN GARZA: Dr. Lichtenstein.
DR. LICHTENSTEIN: A very informative presentation. You said that there had been some work done on the relationship between alcohol intake and breast cancer as a function of, I guess, age of women, age of diagnosis of the breast cancer.
I'm just wondering, has there any work been done on tumors that are estrogen-sensitive to estrogen-nonsensitive and any alcohol intake?DR. BYERS: Yeah, one would think that the alcohol effects would be more specific for the estrogen-receptive for positive tumors.
I'm sure somebody has looked at it. Meir, do you know the estrogen on that? I'm not sure what the literature -- what research has been done on that, to tell you the truth.DR. STAMPFER: There is no big distinction that's been noted so far.
DR. BYERS: You mean it hasn't been studied or there is no difference?
DR. STAMPFER: No, it has been studied in -- it has been studied, although not thoroughly, but the studies that have been done don't show a difference.
DR. LICHTENSTEIN: So then that would argue against the relationship between alcohol and estrogen or estrogen metabolism?
DR. STAMPFER: No, not necessarily, because estrogen sensitivity changes in the course of tumor progression.
DR. BYERS: So there may be effects on a tumor that as it becomes apparent looks to be estrogen receptive negative.
CHAIRMAN GARZA: Dr. Dwyer?
DR. DWYER: Just a quick question, Tim, on the alcohol breast cancer. Has anyone seen any relationships between hormone replacement therapy and the effect or lack of effect of alcohol?
DR. BYERS: I think that was included in the pooled analysis, HRT, and the report I'm understanding in general is that there was not much difference across a number of other risk factors.
Was HRT one of those?DR. STAMPFER: They're independent. They both raise risk, but there is no significant interaction. So women who drink and take HRT have a higher risk than women who drink and don't take HRT.
CHAIRMAN GARZA: Dr. Johnson.
DR. JOHNSON: Thanks, Tim.
I was curious about what you said about added sugar because I know in reading the World Cancer Research Fund and American Institute for Cancer Research, that book that came out, that they came to the conclusion in that section on colorectal cancer that sugar, particularly sucrose, was associated with colorectal cancer.DR. BYERS: I think they gave it some sort of guarded category.
DR. JOHNSON: Yeah. And, in fact, among the recommendations one of the -- in the end, when they give their recommendations, one of them is to limit consumption of refined sugar, and I'm going to show that in a minute. So I'm just curious if you could comment that you've clearly come to a different conclusion that that group did about sugar.
DR. BYERS: Yes. As I look at the studies, especially the bigger, stronger studies that ostensibly have themselves concluded that there is a relationship, it seems to be just within subgroups, so you get an effect in young men, but not older men, and no effect in women and so forth.
And so I think if there is a relationship, it's pretty weak.
Now, the weakness of that relationship may be a function of the difficulties I listed as how to measure sugar and analyze it and so forth, but that's my own take. I would be interested to hear yours.DR. JOHNSON: Well, do you think some of -- do you think it's possible that it's a displacement of the fact of fewer fruits and vegetables in the diets, or was that well controlled in those?
You know, I'm wondering is it the sugar or --DR. BYERS: It was controlled. It was well controlled. I don't know, to the extent which we can measure things, I don't know.
CHAIRMAN GARZA: Dr. Kumanyika.
DR. KUMANYIKA: Tim, do you know if there has been any dietary pattern analysis on any of these cancers? Because since obviously these are all related, has anyone done any of the scoring, index --
DR. BYERS: Yeah, there have been some, and some attempt at sort of cluster or factor analysis, and you can come up with clusters or factors, and you can attach names to them, but just what they mean, I mean, it takes somebody smarter than me to figure out what those clusters really represent.
There have also been some other analyses looking at patterns, but you get sort of a predicable thing like with fruits and vegetables especially. So I think that the food pattern approach and analysis that's been done to date has not really added to the field very much.CHAIRMAN GARZA: Dr. Weinsier.
DR. WEINSIER: I realize that you're charted to not include the relationship of physical activity, but you mentioned AICR's recommendation to be more physically active, and, in fact, it's part of our charge to consider in the weight guidelines.
Do you know of any evidence outside of the relationship of physical activity to obesity and then to cancer, particularly breast cancer, do you know of any direct evidence of physical activity and cancer?DR. BYERS: Yeah, I think there is pretty good evidence for colorectal cancer. Just what the mechanism -- presumably it's got something to do with gut mortality, but I think it's pretty clear that there is an independent protective effect of being physically active for colon cancer that's independent of body weight.
For breast and prostate cancer, the other two cancers where there has been thought to be a relationship, I think it's either not there or very much weaker that colon cancer.CHAIRMAN GARZA: Dr. Dwyer, did you have your hand up or not?
DR. DWYER: No.
CHAIRMAN GARZA: Any other questions?
Tim, there is one other one, and it wasn't in your charge either but perhaps you ran across the whole issue of selenium and prostate cancer.
How strong is that relationship, and obviously it has some implications then for how one balances between animal and non-animal food given the sources of selenium? Any observations you want to share with the group?DR. BYERS: Yeah, but let me stop with your implications first, because really the selenium in animal comes largely from the grain that it consumes, so that varies depending on grain sources. So the ultimate source really, or the source really is not the animal; it's just of the vehicle.
I think the possible effect of selenium on cancer is one of the most exciting things that's happened in the last decade in cancer research, but it still is possible and needs to be confirmed. I think if subsequent trials indicates even half the benefit of selenium, as Larry Clark's found in the secondary data points in his trial, then I think that's the biggest finding since tobacco and cancer.
So are we excited about it? I'm very much enthusiastic about new trials that are going to be underway, and I've got my fingers crossed.CHAIRMAN GARZA: All right. I just want to add a work on the selenium, a cautionary note, that in the Larry Clark trial, the benefit was almost instantaneous, which goes against what we think we know about how cancer works, and there is some suggesting that the rates may have been higher in the placebo group.
But another point of interest is that Finland, which is the lowest selenium country based on their early studies, decided to fortify and raise their selenium levels quite dramatically 10 years ago, and there hasn't been one iota of suggestion that their prostate cancer rates have decreased.
So, yeah, I'm hopeful too, and it would be great is the Larry Clark data were replicated, but I think we need to be cautious.DR. BYERS: Yeah, just a couple comments. One is that the adverse effects of beta carotene in the two large trials that indicated we could increase lung cancer risk by 20 percent or more with beta carotene also occurred much sooner than people would have believed. So it's quite possible that there are some late stage effects of nutrients on cancer that we don't yet understand the biology of.
The other aspect of Finland is very interesting, and that is that their lung cancer rates began to dip before the rest of Europe, and so I think the jury is out on selenium.CHAIRMAN GARZA: Okay. If there are no other questions or comments, thank you very much for an excellent presentation. I have to echo Dr. Meir. That was possibly the best 20-minute summary that I've heard. Thank you.
For those of you who missed the meeting yesterday, we did not get to grain products, vegetables and fruits despite heroic efforts on everybody's part, so we're going to go back to that portion of yesterday's agenda and take it up from there.DR. DECKELBAUM: Okay, I'm Richard Deckelbaum, and I guess what happened last night is that grain, fruits and vegetables got displaced by going out and figuring whether we should have one moderate or two moderate inputs.
So first slide, please. Can we lower that a bit because most titles will be missing then. That's fine.CHAIRMAN GARZA: While Dr. Deckelbaum is getting ready, I want to welcome Dr. Shirley Watkins, who has just joined us, under-secretary for the Food and Nutrition Service. Thank you so much for coming. We're trying to get her at the table and she refuses, but maybe publicly we can coerce her. I don't know.
DR. DECKELBAUM: So the grains, vegetable and fruits working group was consisted of myself, Alice Lichtenstein and Meir Stampfer, but we really had very substantial help and input from USDA and other staff, including Elta Salton, Shanthy Bowman, Andrea Lindsey, and Kathryn McMurry, Carol Davis, and they gave us a lot of materials and lot of substantive advice in formulating some of the things you are going to hear ago. And as well, I'd like to thank Carol Suitor and Suzanne Murphy and Burt Garza, who also took place in our meetings and had a role in what you're about to see.
Next slide, please.
So the 1995 guideline here is at the top of this slide, and the three major sections that were discussed in the previous guidelines are listed here underneath. Our charge was really to review the science base and add to it, focusing on literature since the previous report. If supported by new evidence, we were asked to make appropriate revisions, and as well, we looked at modalities to suggest approaches for better implementation of the content of the grain, fruits and vegetables guidelines.
So these are the options that we mainly focused on during our deliberations. We asked if there should be an increased emphasis on whole grains in the guideline itself and/or in the text. Should there be clearer definition of different types of carbohydrates?
Are carbohydrates in potatoes as good as carbohydrates in broccoli? And we also had discussions related to the potential role of the glycemic index in choosing carbohydrates, and Dr. Stampfer will be talking more on this in a few minutes.
Should there be more emphasis on quality versus the quantity of grains, vegetables and fruits ingested, and that's related to what I just said? But this could also include should we better point out grains, fruits and vegetables that are rich in certain macra nutrients, say fiber or micro nutrients, certain antioxidant vitamins?
Should we have an increased emphasis on not ingestion, and, again, Dr. Stampfer will be addressing that? And we also reviewed potential ways for clearer implementation guidance for grains, fruits and vegetables, and along these lines Dr. Lichtenstein will be giving a short talk as to the question should the grain guideline be separated from vegetable and fruits.
I'm not going to spend much time on this because the good news is that since 1995 there's an increasing body of literature showing beneficial effects of fruits and vegetables in decreasing cancer, cardiovascular disease, cataracts, diverticular disease and likely Type 2 diabetes, and the references for these will be provided in our updated report.
So I'd like to turn now to the question whether there should be increased emphasis on whole grain products and look at some evidence relating to coronary heart disease risk, cancer risk and Type 2 diabetes and insulin resistance.
Next slide. This is where slides didn't -- got messed up.
This is a meta-analysis study of Dr. Jacobs and his group, "Whole Grain Intake May Reduce the Risk of Ischemia Heart Disease, Death and Post-Menopausal Women," the Iowa Women's Health Study. So I will be focusing on the first few slide actually on coronary heart disease.
They studied almost 35,000 post-menopausal women. The relative risk was about .6 confidence integrals shown for the top versus lowest quintile of whole grain intake, and this was not explained when adjustments were made for fiber, Vitamin E and Folic, suggesting that whole grain intake is protective for ischemic heart disease.
The next two slides have been borrowed from Dr. Stampfer. This is unpublished data from the Nurses' Health Study, looking at whole grain foods and the risk of coronary heart disease in the Nurses' cohort, and looking at exposure of at least five to six servings per week. You can see that cereals, bran and brown rice, all markedly decrease the relative risk of coronary heart disease in women, but I don't know if this is good news or bad news, popcorn had no effect.
What about men? These are two studies that include men, Rimm paper published in JAMA is on the health professionals study; Pietinen study where it was the ATB study where the primary end point was cancer, but they looked at coronary heart disease and found that there was substantial decreases in risk associated with whole grain intake. Now, this is in addition to the effects that whole grains could have on improve lipoprotein profiles and separate, and along those lines I'd like to point out that the effects of carbohydrates, for example, and HDL cholesterol may not be -- may not be applicable to all types of carbohydrates.
We published a paper, Tom Stark and our group, last June in the American Journal of Clinical Nutrition, showing that in hypercholesterol anemic children when they went on to fat low, cholesterol lowering diets that HDL decreased only when simple sugar increased but not when complex carbohydrate intake was increased.
But, in general, the papers also seem to indicate that risk reduction is associated with higher levels of whole grain intake, and they cannot entirely be explained by adjustments for fiber intake.
This is another slide borrowed from Dr. Stampfer which shows that the relative risk for coronary heart disease is decreased in general across a number of studies looking at fiber consumption and relative risk for coronary heart disease. I think the important point here that it looks like whole grains do have an important effect, but we still can't dismiss fiber, as we just heard we might have to do in terms of cancer, in terms of coronary heart disease risk.
Now, what about whole grain intake and cancer, and I thought I was showing this slide earlier but it came up now? This is the study of -- another study of Jacobs, et al., looking at meta-analysis of 40 case controls studies between 1984 and 1997, looking at a variety of cancers, 20 in all, and colonic polyps, and, again, there is a lot of data in this paper and I'd be interested in Dr. Byers' comments on them.
But the pooled odds ratio, looking at the entire cohort, was about 0.66 for high versus low whole grain intake. And again, this was maintained in general through most cancers. Of interest, breast and prostate had lower correlations with whole grain intake in terms of reduced risk after -- this was maintained after adjustments for social-economic status, age, sex, BMI and other things listed here and not listed on the slide.
An interesting paper published by Chanteoud in the International Journal of Cancer looked at 10,000 cases and 8,000 control cases of hospitalized cases -- hospitalized patients, mainly in Italy, with different kinds of cancer, and they reported risk ratios, again, with high whole grain food intake reduced by substantial amounts for GI tract cancer, bladder and kidney, lymphomas and myelomas, but not for breast cancer. And again, these were maintained after adjustments for a number of potential other variables, other confounders.
Briefly, I'm just going to show an overhead. Here on whole grain intake in non-insulin dependent diabetes, two papers by Salmeron and Group. The top one, "Diabetes are," and the bottom one -- sorry, the top one is "Diabetes Care On Men." The bottom one is in JAMA on women, large cohorts again, the Nurses' Health Study and The Health Professional Study.
And the bottom line here is that glycemic index, they suggested foods that have a high glycemic index are associated with about a 1.4 to 1.5 increased risk of non-insulin dependent diabetes, and, again, whole grains are associated with a decreased risk, about .7 relative risk for non-insulin dependent diabetes.
So what are some of the issues that could be involved in considering adding whole to the guideline itself or increasing its emphasis in the text going with the guideline?
Well, there could be implications that grains that are not whole are not part of a healthy diet. That's actually related to something a little lower on the slide that we don't want to label necessary good versus bad food or should we.
Could there be a cost factor involved which might affect certain classes, lower SES classes who might not be able to afford some of the good whole grain products?
Will there be decreased intake of enriched and fortified foods and how would this affect, especially micro nutrient intake, and actually in some analysis we did we really didn't see any effect on this that we could sort of tease out relating to folate as well?
Would there be a decrease in food choices that could affect certain segments of the population?
Might certain important nutrients actually have decreased absorption? For example, might fitates in whole grains affect iron and zinc absorption? And again, there is really no evidence yet on this, but this is something that certainly would have to be looked at.
I mentioned good versus bad foods, and again, is the scientific evidence really strong enough to make these changes because as we've seen in a number of examples of where studies that came out, for example, in case control fashion a number of years ago are not supported by larger cohort studies or clinical intervention studies, so that we still have to consider whether the -- for example, even the papers I showed you are sufficient to allow us to make these substantial changes.
Next slide, please.
Just a couple of words on our plans, our thoughts towards better guidance provisions in the guidelines, and actually if we can just -- we have to actually raise the bottom of this slide. This is Box 9 from the current recommendations which sort of tells us how to go about getting the diet better with more grains, fruits and vegetables.
At the bottom of the box you've got to go to Box 2, page 7 for what counts as a serving. So, in other words, it's not a total user friendly, take one look, it's all there type of box.
So we're going to be looking at as a working group ways to improve the message, and this would be just one example for Box 9 where here would be some of the messages that we might want to include, and paralleling it right next to it would be a "how to" box with different kinds of messages. You know, pack X and X fruit in your purse or in your handbag for lunch or your afternoon snack, et cetera. So these are the kind of things we are considering.
I would like to ask Dr. Stampfer to come up and talk about glycemic index and different kinds of carbohydrates.DR. STAMPFER: Okay, thanks. I've been given the job to cover nuts and glycemic index in seven minutes. I'm going to try to stick to that.
Nuts are basically recommended against, if you take the dietary guidelines at their face value, because nuts are a high fat food and it says choose foods low in fat. And a lot of people have been doing that, and it's not a good thing I want to tell you about that. Although nuts are a very high fat food, most of the fatty acids are unsaturated and it's a good source of protein and some other good things.
Next slide, please.
Consequently, as you might expect, nuts have a favorable impact on the lipid profile because of their mostly unsaturated fat content, so with a high walnut diet the LDL/HDL ratio was substantially reduced. This is a very good predictor of risk of heart disease, diet supplement with almonds also lowered LDL substantially, and this is just what you'd expect from what we know about the impact of high unsaturated fats on the end -- monounsaturated fats on the LDL and HDL ratio.
Next slide, please.
Well, that's all well and good, but what about clinical end points, and I think this is something we need to keep coming back to and not just rely on the influence of diet on intermediate markers, but we need to look at actual disease outcomes, and there has been three published studies so far looking at nuts. All three find substantially reduced risks of coronary heart disease with nut consumption. We're not talking about mega doses here; just a handful of nuts a couple times a week was enough to reduce risk in the range of 30 or so percent, a very big decrease.
So I think nuts should not have this astigmia attached to them, but to the contrary. Their consumption should be promoted.
Next slide, please.
Okay, that's all I'm going to say about nuts. Now onto glycemic index. It's a complicated concept, and I don't know if I'm going to succeed in getting it across in the short time I have, but I'll try.
The basic idea is very simple. Different foods have a different propensity to raise blood sugar following their ingestion, and the glycemic index is a way of quantifying that. Typically, in the traditional sense nutritionists have divided carbohydrate into simple and complex. Simple being mono and diet sacarides, sugars, and complex being everything else. But this is not a physiologic distinction as the glycemic index is. The glycemic index is really based on what happens to real people who eat food, so that they're given various kinds of foods and blood sugar is actually measured, and it goes up sharply with foods that have a high glycemic index, and less so for foods that have a flow glycemic index.
So this shows, for example, what happens if you have the same caloric intake for three different kinds of carbohydrates, glucose, amylose pectin or amylose based on either the glycemic response -- let's see over here -- so you can see how glucose, blood sugar shoots up very fast with amylose pectin goes up but less so, and with amylose, which is less readily broken down, its much flatter, and consequently the same pattern emerges with insulin, and this has physiologic effects. It's not a good thing for the system to have your glucose and insulin shooting up and down very sharply that way.
Next slide, please.
There is -- in muscle, this is in animal studies, insulin sensitivity of muscle, glycogen synthesis is impaired in amylose pectin fat rats. That's a type of carbohydrate that has a higher glycemic index than amylose.
Next slide, please.
And post-meal lipogenesis, also another animal study looking at, again, the different kinds of carbohydrate here. The high glycemic index fed animals had a higher capacity for lipogenesis after a meal. So these are all adverse physiologic outcomes of high GI diet.
Next slide, please.
Now, it's important to distinguish between glycemic index and glycemic load. The glycemic index is the property of the food. It's the property of how the food can raise blood sugar. Glycemic load is what that food -- is basically taking into account the amount of carbohydrate that is in there, so it's not just the quality of the carbohydrate but the amount. So you can think of it as glycemic index is sort of the nutrient composition of the good whereas the glycemic load is the amount of that nutrient that you get from eating a normal portion size.
Now, everything is calculated in terms of percent of white bread. So you can see, for example, carrots have a high glycemic index, 131 percent compared to white bread is 100 percent, but there is very little carbohydrate per serving, so it only accounts in a typical diet to one percent of the glycemic load whereas potatoes are similar to white break, they have more carbohydrate, of course, and they account for eight percent of the glycemic load of a typical diet, and obviously it's going to change, but you can see those differences.
Next slide, please.
Well, again, what about clinical end points? Does this really matter for real people?
Well, these are data from the Nurses' Health Study looking at glycemic load and risk of coronary heart disease, unpublished data from Dr. Sima Lu in our group. And you can see that the high glycemic load in various statistical models, either adjusting for fat or adjusting -- without adjustment for fat, you can see in the best model, which adjusts for fat intake, the highest level of glycemic load is associated with about a doubling of risk of coronary disease, highly statistically significant, and this is taking into account all the other coronary risk factors.
Next slide, please.
Now, what is contributing to the glycemic load in the Nurses' Health Study diet? The number one contributor is potatoes. And so we looked specifically at potatoes and after adjusting for all the coronary risk factors what one finds in these data, again, is about a doubling in risk with high intake of potatoes. It's not -- the confidence intervals are broad and the trend is of borderline statistical significance, but it's clear that I don't think we can consider potatoes as a health food here.
Next slide, please.
Finally, you can ask why, if glycemic index and glycemic load is so important, why don't we have an epidemic of coronary disease in China, for example, where white rice makes up a big part of the diet? And that's a fair question.
And the answer is that the impact of a high glycemic load diet is mainly among people who are already marginally glucose intolerant; that is, overweight and inactive, and those qualities are uncommon in China, although they are getting more common, but in the U.S. they are very common.
So these are data showing the relation between glycemic load in relation to risk of coronary diseases by body mass index. So among people who are lean, glycemic load really doesn't matter very much. Unfortunately, most Americans don't fit into this lean category. Most Americans are here where high glycemic load will double the woman's risk of coronary heart disease.
I think I've gone over. I'll stop here.
Oh, let me just say one more thing on popcorn. Although it wasn't statistically significant, popcorn did have the same trend as all the other whole grains.DR. DECKELBAUM: Was that Cracker Jack?
(Laughter.)DR. STAMPFER: No brand name endorsement.
DR. DECKELBAUM: It has corn syrup, and Dr. Lichtenstein will now discuss the possibility or the question to splitting the guideline.
DR. LICHTENSTEIN: Okay. Well, as indicated, I would like to suggest that we consider splitting the grains from the fruits and vegetables and having two separate guidelines. One of the primary reasons I think we should consider this is I think we should really think a lot about what we are recommending people should do. We've spent a lot of time in the guidelines recommending what people should not do, and there's been word smiting over the years as far as, you know, consumer diet low in something while consider diet moderate in something, trying to make it sound more positive. But I really think what we need to go is give individuals more guidance on what they should do and what makes a healthy diet.
I think if you read the literature on the predictors of grain intake are different from the predictors of fruit and vegetable intake, so this is one reason for splitting them because people view them differently, and I also think the barriers to grain intake are different than the barriers to fruit and vegetable intake, and that's taking into consideration cost, storage, preparation, perishability so that -- and safety also, so that one needs to give different guidance and advice to individuals with respect to fruits and vegetables versus grains.
I tried to see if this issue had been addressed directly because we are supposed to propose changes on the basis of scientific -- a scientific basis for proposing changes, but the question has never really been addressed directly.
Now, there is an error. The first focus group that I'm going to mention was actually in 1995.
But what I did is I looked at the focus groups, and although that specific question had never been posed or considered, we can get certain nuggets of information about it, and when the fruit, vegetable and grain guideline were considered one of the comments was that the suggestion that increasing fruit and vegetables was challenging because of cost, and this speaks to the issue of different barriers to fruit and vegetable intake versus grain intake.
There was another focus group conducted in September of 1988, and one of the comments there, again since the question specifically was not posed, was "I like to eat more fresh fruit and vegetables but I can only shop once a week. In two or three days the stuff is no good. The rest of the week is going to have to be canned or frozen."
Well, clearly, we didn't get the message across because canned and frozen fruits and vegetables are quite acceptable, and it's not just that someone has to consume fresh fruits and vegetables to get the nutrient value.
Another very telling comment was in a focus group that was published in August of 1998, and in this case it had to do with the whole guideline, and the guideline has the word "You should consumer a diet that has plenty of grains, fruits and vegetables." One of the comment was, or on the term "plenty" because it was being equated actually with the "Five-a-Day Program," which is another federal program; that the comments were related to how much is "plenty." Well, it's five and that someone actually mentioned the Five-a-Day Program, so I think that there is a program specifically that focuses on fruits and vegetables. The "plenty" is not a quantitative term, although it's certainly quantitative in the food pyramid which, by the way, also distinguishes between grains, fruits and vegetables. So I think separating the two would be quite consistent with current programs that actually encourage increased consumption of fruit, vegetables, and then grains.
Again, just to reiterate, I think the message should really emphasize what people should be doing as opposed to what they shouldn't be doing, and that the message is if fruits and vegetables were separated from grains within each of those categories, I think we could be more focused and clearer in what guidance we're giving for grains, what guidance we're giving for fruits and vegetables.
Also, as mentioned, that Box 9 that's actually in the current guidelines is quite big. There is a lot of information, and I think that's where the difficulty lies in actually distinguishing between how to give advice for those different groups, so I think it's something that we should consider.CHAIRMAN GARZA: Thank you very much.
Are there any questions of any of the presenters?
Roland?DR. WEINSIER: First of all, compliment the group, all three of you, and all the assistance for doing such a great job.
Meir, help me with the glycemic index and trying to do something practice or make a practical, safe and reasonable recommendation to the public based upon these findings. If in fact the -- I don't know what you're calling it on the right side of the slide. What is it, "The relative glycemic impact of the diet which takes into account the glycemic index as well as the glycemic load." Potatoes are eight-fold greater impact on the diet than carrots. And I'm trying to envision populations in the world, whether it's China, or Papuans or other, you know, potato/rice eating populations that subsist in these foods, I guess, are healthy.
Their glycemic impact factor would be what, 100 percent? Ninety percent? You know, it would be extraordinary.
So we'd have to argue then, based upon the date you're representing, well, it doesn't have an impact on them because perhaps of their normal weight, and it's only with BMIs that are getting in the higher range with insulin resistance that's having an impact. And I don't know what the answer is, but I'm having trouble from a rational standpoint trying to separate that we would do something different from a dietary standpoint that prevents a disease, a chronic disease, than we do in people who have the chronic disease, i.e., if you're lean, we should have one diet prescription; if you're getting above a certain BMI, we have a different diet prescription.
Help me come up with a plan that would make sense.DR. STAMPFER: Okay.
DR. WEINSIER: A guideline that makes sense.
DR. STAMPFER: It will take a minute or two.
First, just let me explain that slide with the eight percent and the one percent. That slide represented different contributors to the total glycemic load in the Nurses' Health Study diet. So of the total glycemic load, eight percent was contributed by potatoes. That's what that eight percent means. It doesn't mean that potatoes are eight times as bad as carrots or something. It just means that the way the diet is distributed of the total glycemic load of the diet, eight percent was contributed by potatoes, which was the number one contributor.
Now, the question you raised about populations that seem to do fine, and certainly have very low rates of coronary disease despite a high glycemic load diet, I believe the reason for that is that they have -- do not have by and large the levels of insulin resistance that we have by virtue of physical activity, because muscle decreases insulin resistance and lean body mass, so that the adverse effects of the high glycemic load diet are manifest where there starts to -- starts to be insulin resistance.
Now, I wouldn't characterize that as a disease state because if we did, you know, three-quarters of the population in the U.S. would be characterized as diseased. Well, maybe they are. But to the extent that we as a country are fat and slothful in our physical activity patterns, there is a lot of insulin resistance and this is being exacerbated by the high glycemic load diet.
Now, how to implement that is another issue because it's kind of complicated to get across in a dietary guidelines, and also I think -- although I think this is an exciting area of research, I don't think the findings are completely proven or conclusive, so we need to decide, you know, if this is ready for prime time.
My take on it is that this lends strong support to what our group has been trying to get across, which is an emphasis on whole grains and minimally processed foods, and I think it also lends support to taking potatoes out of the vegetable group and maybe thinking of it as a starchy food group where it might be more appropriate. So those would be a couple ways to implement it.CHAIRMAN GARZA: Related to that, this has come up in previous committees, or at least in one previous committee that I was one, and we, the previous group felt that the concept was difficult to deal with because it was the total diet that contributed the glycemic load -- determined the glycemic load, and it was the diet glycemic index that we should be concerned with, and it was very difficult to sort out the dietary pattern from an imbalanced pattern, and the best analogy that I can recall were papers that were published about 10 years ago, warning us that, in fact, children that had very low fat diet were stunted, not realizing that in fact the way they were achieving the low fat intake were by having very low micro nutrient intakes because of the types of foods they were consuming was -- again, it was isolating one factor rather than looking at the total diet.
The ADA, the work of the Diabetes Association looked at the glycemic index and they found it difficult to deal with.
How in the studies that you've looked at do you look at pattern and say, well, maybe it's the pattern we have to be concerned about, to say, well, you know, you don't get to choose one guideline over another, you've got to take them all? And so that if you just take potatoes without variety or you just take this without the other, that in fact you can run into the sorts of problems that you've uncovered.
Is that something we need to be concerned about or do you really feel that, gee, we need to focus in on potatoes and other starchy vegetables because they are the culprit and not the pattern?DR. STAMPFER: No, I think -- I think you make a good point. And in terms of the pattern, obviously this is important, but in a sense our guidelines are supposed to be defining a pattern in a way, not just -- not just responding to a pattern.
I think the details of getting across the glycemic index concept may be too difficult, but in broad brush strokes I think it's actually not difficult, and that would be an emphasis on whole grain, minimally processed grains; get away from this concept that just because white bread is low fat that therefore it's healthy.
And I think the potato issue is just that right now, according to the guidelines, it's considered a vegetable, and if you have a large McDonald's french fries, you've got four out of your a day vegetables according to the guidelines, and I don't think this is right, and I think we ought to consider -- we oughtn't to consider potatoes along with broccoli and carrots and other things that we think of as vegetables.CHAIRMAN GARZA: Okay. Scott and then Johanna.
DR. GRUNDY: Ask a follow-up about the glycemic question. It seems like there might be two issues here.
One is the total carbohydrate load in the diet, which if you have a very high percentage of carbohydrate in the diet, then the problem, I think, with the American population that you point out, which tends to be sedentary, creates a metabolic stress on the insulin metabolism and so forth. And then the second is that the type of carbohydrate can accentuate that.
Is that what you're saying?DR. STAMPFER: Yes.
CHAIRMAN GARZA: Johanna.
DR. DWYER: Meir, I'm very much interested in the glycemic load concept, but I must admit to ignorance on much of it.
First of all, how many foods have glycemic indices experimentally determined? Are there a lot or a few?DR. STAMPFER: A lot. Yeah, there is --
DR. DWYER: How many is a lot?
DR. STAMPFER: Hundreds.
DR. DWYER: Hundreds.
And how does the glycemic index of an individual food affect the glycemic index of meals. I thought years ago that it changed depending on the total meal for example, if you mixed all the foods together in a meal.DR. STAMPFER: Yes, that's an important point, and it's one that's still somewhat controversial because some of the initial studies hadn't done the exact correct calculations for looking at the peak and area of glucose. But basically there have been about a dozen studies that have looked at that now. And what one finds is that the glycemic load of a mixed meal is the weighted average of the glycemic load of its -- of the component parts. And, in fact, the correlation between the glycemic load of a mixed meal and the calculated glycemic load based on the component parts is about .987, something like that, so it's very high, so you can predict with a good deal of accuracy what the glycemic load of a mixed meal is if you know what the components are, and it does change, absolutely.
DR. DWYER: Just one other -- we just put together an issue, a journal on this topic, and it's very popular in Australia, for example. Australia doesn't have food labels like we do so, you know, it's harder to find out these things. I just wonder if in the future if we're going to consider this it might be possible to get a representative of the Diabetes Association or some other group of endocrinologist who deal with this every day.
CHAIRMAN GARZA: I've got three people, Richard, Ellis and Rachel, so I want to assure everyone that I will get to the three of you in just a minute.
Richard.DR. DECKELBAUM: I think, you know, in our discussions also on the sugar working group this came up. And, you know, one of the questions we have to look at, we have to look at this also in terms of the whole guidelines because it's -- let's say it's 100 percent right. Let's say it's 100. It's still -- it's very controversial, and there are a lot of people out there who don't -- you know, who were not quite keen on glycemic index, so it may be a gradual process. And one thing I think we'd have to consider with the whole group is -- you know, if you get sort of a big noise about one aspect of the new guidelines, how would that affect the whole report, and so that's something we have to weigh.
And I think when we deliberate this afternoon, we'll be bringing this in to, you know, where it should be, if it should be, but where should it be and in what manner because I think we have to make sure that we look at the whole and not, you know, have some kind of topic that may bring up a major controversy which will affect the whole report.
We spent a lot of time on this, but I did bring up some other questions, so I'd prefer, if it's okay, not to discuss glycemic index anymore. We can bring it up again tomorrow when we report, but there were some other issues that we looked at as I reviewed, and that included nuts, and that included separation of grains from vegetable and fruits, and I'd like to get some comments from the committee before we break into our working groups this afternoon.DR. JOHNSON: I'll just follow up quickly as part of the sugar group. I did have conversations with Dr. Xavier Pesuniet, Dr. Gerald Reven and Dr. Denny Beer about the glycemic index, and I have all of my notes of those calls with me so I can share some of their opinions.
DR. LICHTENSTEIN: I was going to comment on the glycemic index, but what I'll do is first ask my question about nuts -- free speech. But just with nuts, are peanuts included with the nut group?
DR. STAMPFER: Yes.
DR. LICHTENSTEIN: Okay. Okay, peanuts are a legume and then nuts, most of the other nuts grow on trees.
(Laughter.)DR. LICHTENSTEIN: Okay. So is it -- I guess what I'm getting at, is it the nuts themselves or s it the fatty acid pattern that's common to those foods? And then if it's peanuts, is there anything unique that distinguishes peanuts from other legumes? So that are we really talking about nuts in this conglomerate of these two -- I don't know if they're called species or whatever, rely on the food scientists, or is it the fatty acid pattern or some other pattern, the protein pattern, amino acid pattern that's associated with those foods?
DR. STAMPFER: Well, if you look at the composition of peanuts, it looks a lot like nuts, and so the common parlance of nuts, peanuts being considered nuts actually makes more sense than the laneon classification of where they all came from. I don't think we should be hung up on the --
DR. JOHNSON: Which components of the nuts? I guess, what aspects of the nuts?
DR. STAMPFER: In terms of the protein and fatty acid composition of peanuts. They look like other nuts and peanuts, in our study we separated out peanuts from other nuts, and they are both have the similar effect. And you might say, well, what about peanut butter? And peanut butter, if it's just made from peanuts, presumably has the same effect. But a lot of peanut butter has trans added to it, trans fatty acids to keep the fats from separating, so that probably detracts from the benefits.
DR. JOHNSON: But I guess that's -- I'm getting at something a little bit different. Is it specifically that people should increase their nut consumption or should they increase their consumption of a diet that's consistent with the fatty acid profile of the nuts as far as advice?
DR. STAMPFER: Well, I think -- I don't know. I mean, these are the observations that people who eat nuts have a lower risk of coronary disease, and they also have a better lipid profile. You could get that lipid profile by feeding them oils instead of the nuts.
But I think the main message is a simple one, that we should remove the astigmia from nuts. Instead of considering them bad, because they are a high fat food, we should consider them according to what their health effects really are.CHAIRMAN GARZA: We have at this rate -- I'll just let the committee know -- we will be leaving tomorrow at about eight p.m.
(Simultaneous conversation.)CHAIRMAN GARZA: And so that I will caution you to pay attention to Dr. Deckelbaum's request as to what the group is going to need guidance from you. He mentioned two or three points, so make sure that your questions are targeted to that so that we can be of assistance to the working group.
DR. DECKELBAUM: Well, let me ask it in a different way. Is anyone against including nuts, you know, somewhere --
DR. DWYER: I have a question.
CHAIRMAN GARZA: Let's make sure that of the ones are targeted.
DR. DWYER: The question is, you know, I've heard about a lot of single groups, some of which apparently risks enormously in these analyses, some of which decrease risk by large amounts. Risk go down to .6, .4, whatever. How much of this is confounded?
DR. STAMPFER: Oh, these are -- these are adjustments for --
DR. DWYER: I know they are, but I'm still asking the question.
DR. STAMPFER: I think -- I mean, we measure diet, we try to assess diet, we assess coronary risk factor, we adjust as well -- you know, is there some residual confounded? Yeah, probably there is. Is it all correct? Well, it's a guess. These analysis I presented are after multiple adjustments. Obviously, you can't fully adjust --
CHAIRMAN GARZA: Meir, can you get closer to the microphone because people cannot --
DR. STAMPFER: The question is are these findings due to confounding, and obviously that's our bread and butter. We pay a lot of attention to confounding and try to avoid it as much as we can recognizing that there is residual confounding which could explain part of it. But it seems very unlikely that it can explain these effects to a very great extent, either the adverse or the beneficial ones.
CHAIRMAN GARZA: All right, we are going to do everything. Right now every single committee member has their hand up, so I'm just going to go around the table.
Scott?DR. GRUNDY: I want to address your question about the separation. I know that's on your list, and I think it's a very good idea to do that, and I think it's a very fundamental idea for this whole guidelines because in the past the linkage of those two together has been part of the whole idea of a high carbohydrate diet, and to separate those is -- is conceptually a very good idea, and it refocuses on the role of carbohydrate as a separate issue from fruits and vegetables, so I would strongly support it.
CHAIRMAN GARZA: Dr. Murphy.
DR. MURPHY: Since I'll only get one turn, probably I'm going to make a couple of comments.
First, on the nuts issue, I think certainly nuts are a nutritious food, and I have no problem encouraging consumers to eat more nuts. I'm not sure I think they're a fruit or a vegetable or a grain, and I would prefer, if we can, to see the nut issue addressed as a protein food, and in the context then of variety or maybe in our introduction that is now going to be as long as the original report, but I don't -- I don't think it's necessary that it be in with fruit, vegetable and grains.
A second comment I'd like to address, I think, is whether "whole" should be in the grain guideline, and whether it's separate or whether it's combined. I think we need to be careful about discouraging consumption of non-whole grain products for many of the reasons that Richard has already summarized. But I do think it would be good to focus more on variety. If we're going to take it out as a separate guide, it should be emphasized more in these guideline or guidelines. And certainly if we could just get consumers to do 50/50 whole grain/non-whole grain, we'd be many times better off than we are right now.
So my personal preference would be to see some focus, some additional focus on specificity, particularly with whole grains. Could we even say try to make half your grains whole grains? That would be my preference.
And I would also like to see potatoes on the fruits and vegetable because the pyramid is based on certain calculations that assume that all your vegetables are not potatoes, and we don't want people to eat all of any one fruit or any one vegetable. And so at least in the text we say things like eat dark green or colored vegetables frequently or more or whatever. Maybe we need to be more specific about that, at least once a day or whatever. So I would encourage the group to think about both variety and specificity within these guidelines.CHAIRMAN GARZA: Rachel?
DR. JOHNSON: No.
Roland?DR. WEINSIER: Just a quick comment. First of all, I agree with Alice. I think she has proposed a reasonable addition to the guidelines in terms of splitting fruits and vegetables from the grains. Conceptually, I think it's a good idea. In terms of adding the number of servings or whatever, I'm a little uncomfortable.
On the second issue very briefly, Meir suggests that perhaps potatoes, which seems to be the standout in terms of the vegetable group, be considered as part of the grain, perhaps the starch group, and one of the compelling reasons picks up on what Suzanne is saying, and that is that I think the figure yesterday was about 25 percent of the vegetable intake comes as potatoes, and I think the group should strongly consider putting it in the grain/starch group with consideration from people such as Suzanne, whether it in fact is more like a starch grain or is it more like a vegetable from a nutritional standpoint. So I'm just raising this for consideration. I think it's a good point to consider of people such as Suzanne, you know, think that it is more comparable to the grain group in terms of nutritional content than the vegetable group.CHAIRMAN GARZA: Shiriki?
DR. KUMANYIKA: I think separating the fruit and vegetable guideline is a good idea. I wanted to emphasize the need to encourage fruit consumption because the data suggests that that's much more of a problem, vegetable consumption, I think, even if you subtract the potatoes.
The other issue that comes up, I think, most because of these extreme guideline is the range of servings. I'm now convinced, based on totally anecdotal evidence, that most people don't understand the servings as they appear in the pyramid, and it's very easy to elicit a conversation with a consumer who thinks that they should try to get 11 servings of grains, even if they're appropriate at the 1600 calorie level.
And the way the information is put in the book aggravates it in the same way that you have to go hunting. You have to really hunt for the information that that range means different calorie levels because I went looking for it, and I almost thought it wasn't in here for a minute, and then I found it. But it's very submerged. So however we do the servings, I think we should pick up that issue of what this number means for people who are eating different -- one base range and then say something else later.
And I would go for moving the potatoes. I think we have a tendency to use the guidelines to reenforce traditional wisdom rather than really tell the public things that make sense based on the way we look at the data, and I think moving potatoes would be a good sign.CHAIRMAN GARZA: Richard?
DR. DECKELBAUM: Well, I think we would like some input from USDA. First of all, are we allowed to move potatoes?
I mean, I can just see -- I don't know --
(Simultaneous conversation.)DR. DECKELBAUM: No, seriously, but that's a -- I think some of these things -- some of these things are history.
CHAIRMAN GARZA: You may not like the answer.
DR. DECKELBAUM: The other point, I think the working group would like some input just to remind us on the history of why grains, vegetables and fruits are together. And I think, you know, this may have come up at previous meetings. And why was a decision made not to separate them. We need to know, we need to have that kind of information.
CHAIRMAN GARZA: Let me, before turning it over to USDA, let me try once again to remind the group the pyramid is not our responsibility. You can make recommendations certainly. I mean, you can move potatoes, add t-bone steak, but that's what it is; it's a recommendation.
DR. DECKELBAUM: Put steak with milk.
(Laughter.)CHAIRMAN GARZA: You can do anything you wish -- only if you're concerned about --
(Laughter.)CHAIRMAN GARZA: And I guess you'd move shell fish as a stand-alone group anyway.
(Laughter.)CHAIRMAN GARZA: Let me ask for the history and then we'll turn to Johanna on why grains, fruits and vegetables were put in the same -- that antedates my involvement so I don't know whether anyone whose memory goes --
DR. KENNEDY: Can I before I answer that question talk about -- I think there is a fairly straightforward reason why potatoes are where they are, and it's based on the -- I think, Richard, your question or comment -- the nutrient profile of potatoes fits more in the vegetable group than it does in the grain group.
Now, having said that, Shiriki's issue, and I think it's one that as we in both departments think about how we're actually going to promote the guidelines once the next edition is released, I think there are serious issues related to how consumers see the guidelines.
I mean, an example: We all know that botanically tomatoes are fruit, yet we put them in the vegetable group. And why do we do that? The overriding reason, I think, we do it is because that's the way most consumers see tomatoes. They see them as vegetables rather than fruits.
But from the point of view of Dr. Garza's comment, well taken, that the guidelines as they will emerge guide the one part of any revision on the food guide pyramid that would take place, but they are only one part of it. The other two parts I keep coming back to are what will emerge from the new DRI because that clearly is the second key building block of the pyramid, and the third part is American's latest consumption patterns, which will be based on the '94 - '96.
So get back to comments made yesterday, Alice's point about what do you do with calcium fortified orange juice. Well, to the extent, in proportion to how it's showing up in consumption patterns, it gets fed back in our algorithm into the composites that are used to look at here is where we are, here is where we need to be as far as having an adequate diet. So it is very complicated.
I would suggest maybe if this plays to some of the issues which are being discussed, that maybe at the next Dietary Guidelines Advisory Committee we set aside a period of time where someone goes through what actually has to be done to modify the food guide pyramid because it is a very tedious, sometimes frustrating, but an awful lot of what the staff say to me is grunt work going into the revisions that are necessary for the food guide pyramid is not, as people who were involved in the '95 guidelines, it's not two or three people sitting down one day and pulling something out the air. There is a lot more thought that went into it.CHAIRMAN GARZA: Johanna.
DR. DWYER: I wanted to support provisionally the notion of thinking about two guidelines for fruits and vegetables and for grains, and express my reservations as a person of Irish descent at a time -- the potato suggestion. I'm not sure it isn't beyond our scope, and I'd like to hear a lot -- a lot more about the food composition, the reasons why it was put there originally before precipitous action is taken.
CHAIRMAN GARZA: Well, remember --
DR. DWYER: I just don't have a --
CHAIRMAN GARZA: -- there is no precipitous action that will be taken at today's meeting. We are still in the information gathering stages, and all of these are just suggestions.
Linda and then Alice.MS. MEYERS: I'm responding to your, or trying to respond to your comment about historically what was the reason behind keeping them together, the fruits and vegetables and grains together, and I'll bring in the '80, '85, '90, the wording, so you can see that tomorrow, because I think that gives some idea of how it's changed.
I'm blanking on what the 1980 said, whether it was the avoid times, but clearly it wasn't an avoid starch, but it was a starch and fiber emphasis at that time and I recall, so that was -- it was in the context of this was the first time you were making -- the government was making recommendations related at all to chronic disease prevention, so there was clearly attention to fats and lowering fats and lowering sodium and someone, sugars, I guess, and keeping carbohydrates and starch up, so everything was just sort of lumped there. But I'd be happy to bring those in so you can see it, unless Katherine may have them here.DR. JOHNSON: Yeah, the 1980 and 1985 guidelines were "to eat foods with adequate starch and fiber," the focus was on that. The 1990 changed to "choose a diet with plenty of vegetables, fruits and grain products."
CHAIRMAN GARZA: Okay.
UNDER-SECRETARY WATKINS: I was not going to come to the table because I thought it was more fun sitting back listening to the comments, until you talked about separating potatoes out.
But I thought you better get to the table quick.
I think, Dr. Deckelbaum, you asked the question what kind of fire storm would this raise, and I think it would be a -- one that the Forest Service couldn't handle.
(Laughter.)DR. DECKELBAUM: Why?
UNDER-SECRETARY WATKINS: I think the people on the other side of the house in the producing community, just knowing as much as I know about what they would say, I think you'd have tremendous opposition to moving potatoes from a vegetable/fruit category and putting it into some other category. I think you'd have -- if you think about how you're going to move the dietary guidelines, if that question is raised, and if anybody gets any inkling that you're talking about moving it, I think you're going to have a lot of controversy about the dietary guidelines.
And whatever you do on that issue, you would certainly want to make certain, if you talk about moving it, that it truly is science-based and that you have some real rationale for moving it.
The other issue that I will mention very quickly is how you connect the dietary guidelines and the food guide pyramid, and there seems to have been a disconnect. People really don't know. If you ask the question, do you know what the dietary guides are, they really don't. Do you know what the food guide pyramid is, yes. We need to connect the two, and what we're hoping is that when the dietary guidelines are approved that the food guide pyramid's revision will be right on the heels of that. I really would like to see them come out almost simultaneously. Then people start to connect the two. Then we can do something about the changes in diet of people.
But when they are two separate entities, and people are not connecting them, I think we have a real problem in this country, and we need to address that. So we'd like to look at how can we move the two simultaneously, and I know the staff is just about dying when we talking about that, but I think that's kind of the way it needs to move.CHAIRMAN GARZA: Remember we're talking about three different steps. One is whether, to the degree that we want to emphasize whole grains in any guideline, to the degree that we want to separate the two, the issue of potatoes is an extraneous one because that can be embedded in the text as to how we convey either of those two guidelines, all right. But we don't have a separate potato guideline.
(Laughter.)DR. DECKELBAUM: Could we get --
UNDER-SECRETARY WATKINS: I'm going to pass.
DR. DECKELBAUM: In terms of separation of the guidelines, is that something that you would think would -- would be -- would there be -- do you envision opposition from certain groups there?
UNDER-SECRETARY WATKINS: I don't think so. I think anything you can do to make it easier for people to understand the dietary guidelines is going to be acceptable. I think anything that helps make it easier and helps us to get the message out, I think, is going to be critical.
CHAIRMAN GARZA: All right, on that positive note we have five minutes for our break.
(Whereupon, a recess was taken.)CHAIRMAN GARZA: We are now approximately an hour and a half late, which makes any excessive, compulsive individual very nervous, and I'm assuming we have at least eight or nine around the table that fit that category.
VOICE: You could say 100 percent safely.
CHAIRMAN GARZA: So we should have a lot of stressed individuals.
I'm going to challenge Dr. Johnson to get us through this one very, very efficiently.DR. JOHNSON: No problem.
CHAIRMAN GARZA: And the committee to be yet more insightful and inciseful in your comments.
CHAIRMAN GARZA: Concise.
(Laughter.)VOICE: And decisive perhaps.
DR. JOHNSON: Are we ready? Ready to roll? Okay, we're ready to roll with sugar.
First, I've chaired the subcommittee on the sugar guideline, and I'd like to thank Dr. Lichtenstein and Dr. Deckelbaum for their assistance and input, as well as the USDA staff, Dr. Garza and I'm very sorry that I left Shanthy Bowman off this slide because she was tremendously helpful in some work that we did that you'll see in a minute.
May I have the next slide, please?
The 1995 guideline said, "Choose a diet moderate in sugars," and the text elaborated by saying, "Sugar should be used in moderation by most healthy people and sparingly by people with low calorie needs."
Next slide, please.
the first thing the subcommittee did was grappled with the definition of what is a sugar, and according to the World Health Organization's 1995 report, or 1997, I'm sorry, report on carbohydrates in human nutrition, they say that "Sugars are conventionally described as the monoendysaccharides."
Next slide, please.
Unfortunately, this broad definition becomes problematic in the context of the dietary guidelines because it includes sugars like fructose, which are naturally present in high amounts in fruit, and lactose, which is present in dairy products. In fact, in the ILSI report done by Dr. Geiger, consumers reported being confused by what the guideline means by sugars, and they reported being uncomfortable with having one guideline that limits sugars and another in the same list of guidelines encouraging them to eat fruit which contain sugars.
Next slide, please.
Some of this dilemma, I think, led to the introduction of a number of terms which have been since developed to help further classify sugars. For example, in the U.K., the Department of Health uses the term "intrinsic" and "extrinsic" sugars to differentiate between those sugars which occur within the cell walls of plants and those which are added to foods.
Next slide, please.
The USDA has begun using the term "added sugars" when analyzing the nutrient intake of Americans, particularly with CSFII surveys. And added sugars have been defined by USDA as "all sugars used as ingredients in processed and prepared foods, such as breads, cakes, candies, soft drinks, jam and ice cream, as well as sugars eaten separately or added to foods at the table," and there is a list here specifically of which sugars are included in that definition of added sugars.
To me, the definition is quite clear cut and straightforward, and it has been well defined. It's important to note that added sugars do not include naturally occurring sugars, such as the lactose in milk or the fructose in fruit.
Next slide, please.
Next, I'd like to get into consumption or trying to answer the question exactly how much sugar is America eating. The Economic Research Service of USDA collects food supply data for caloric sweeteners which is comprised primarily of sucrose and corn sweeteners, including high fructose corn syrup, and total consumption has risen steadily since 1970, as you can see here. In 1997, Americans consumed on average 154 pounds of caloric sweeteners compared to the 122 pounds per person in 1970.
Using the USDA definition which I just gave you, added sugar intake varied with age and gender in the U.S. population. This chart shows the number of teaspoons of added sugar consumed by participants in the '94, '95, '96 CSFII surveys. Adolescent males had the highest intakes at 35 teaspoons of added sugar per day, and older females had the lowest intakes at 12 teaspoons per day.
Added sugar intakes ranged from 12 percent of total calories in females 51 and above, to 20 percent of total calories in adolescents, and this was true for both males and females between the ages of 12 and 18.
Now I wanted to move into looking at sources of added sugar. Clearly the most important source of added sugar in American's diets is regular calorie soft drinks, which accounts for one-third of all added sugar intake in the CSFII. Sugars and sweets were second in importance at 16 percent of added sugars and sweetened grains were third, contributing 13 percent of added sugars, regular calorie fruit aids and drinks were also important sources of added sugars, and together these four food categories were the source of three-fourths of all added sugar intake.
Okay, now, the next question is, okay, how does sugar intake relate to diet quality or the nutrient composition of the diet.
There were a couple of earlier studies which I show here that examine total sugar intake and nutrient adequacy, and the conclusion from these studies in both children and adults were that high amounts of total sugar do not necessarily lead to a poorer quality diet in comparison with consumers with low sugar intakes. It's important to realize that these studies included natural occurring sugar, such as fructose and lactose which are present in foods with generally high nutrient densities.
For example, in one study dairy foods contributed 31 percent of the total sugar intake in children, and fruits contributed 17 percent of the total sugar intake for all ages.
With the new CSFII database, there is now public access to data on the added sugar content of foods, and this allows for investigations into the impact of added sugar intake on nutrient quality. And with Dr. Bowman's assistance, we conducted analyses for the association of added sugar intake and diet quality in the '94, '95, '96 CSFII surveys. We statistically adjusted for age, sex and total energy intake to look at the association between added sugar intake and the total unsaturated fat, protein fiber, the essential vitamins and minerals, and we also looked at food groups.
And as you can see on this slide, after statistically controlling for age, sex and total caloric intake, added sugar intake was negatively associated with intakes of total unsaturated fat, protein fiber, the vitamins listed there, A, E, C, riboflavin, niacin, B 6 volute, B 13 and the minerals, calcium, phosphorus, irons, zinc and magnesium. It was also negatively associated with the number of servings of grains, fruits, vegetables, meats and dairy products.
And Meir and I were talking just before this, clearly what this shows is that when you add added sugar to the diet, which is not accompanied by any nutrients, any other nutrient will be negatively associated because you're simply adding empty calories, and so the impact will be negative on really any other nutrient, which is different than the analyses that you get when you look at total sugar intake, which is included -- which accompanies food that have some nutrient density.
Okay, I did want to point out one last thing about that slide, which was -- sorry -- that note the total unsaturated fat intakes are inversely related to sugar intake, and this is true both with total and added sugar intake. This has been referred to as the fat sugar see-saw such that as sugar goes up, fat goes down. But it's also important to notice that high consumers of added sugars were also more likely to have low intakes of shortfall or problem nutrients such as fiber, Vitamins A, C, folate, calcium, iron and zinc. So we have that interesting disparity there.
Okay, next slide, please.
I wanted to move into looking at beverage patterns among U.S. children because they've changed remarkably over the past decade, and I'm showing some data here from a paper by Morton and Guthrie that in the Family Economics and Nutrition Review just late in '98.
I know you can't see this well but it's just important to see the different bar graphs, and this shows what's happening in terms of dairy product intake; that basically low fat milk is remaining stable, whole milk consumption is going down, skim milk and other dairy product intake is going up slightly.
But it's important to note that overall milk consumption did decline in the period between '89 and '91, from 422 grams per day down to 396 grams a day in the '94, '95 surveys, so milk consumption is going down, and there has been some change in the type of milk that is consumed as well.
At the same time that milk consumption was declining major changes occurred in other beverage patterns. The largest increase occurred in the soft drink category, which increased from 198 grams per day up to 279 grams per day in the '94, '95 surveys. Male adolescents increased their consumption of soft drinks from a mean intake of 352 grams in '89 - '91, to 580 grams, which is almost 20 ounces a day of soda in '94-95, and this just shows the change and this is tea and breakfast drinks; soft drinks, you can see the big jump. This is fruit, aids and non --VOICE: It looks like "other."
DR. JOHNSON: Thank you, Joanne. Other drinks. The author is over here so I knew she would know.
And on that note, I wanted to share with you an article which Dr. Lichtenstein very kindly brought to me. This is from the Boston Globe, March 1. it says, "Here is the so-called problem, the kids in the Colorado Spring schools just aren't drinking enough Coke, or so says John Bushy, an area superintendent, for 13 schools who signs his correspondence `The Coke Dude.' The Colorado District was hard up for money for extras like band competitions and debates, so in 1997, they signed a 10-year contract in which it would get eight to 11 million dollars from Coca-Cola in return for giving the soft drink giant exclusive rights to sell Coke and other beverages in school vending machines. Sales of Coke products have been so sluggish that Bushy wrote to school officials in September, and I quote `We need to all work together to get next year's volume up to 70,000 cases,'" and the articles goes on. But this is the situation that's occurred in some school districts in our country with regards to soda and access by your young people.
Next slide, please.
Why are we concerned about this change in beverage patterns in U.S. Children? Calcium is concerned a problem nutrient among most age and sex groups in the U.S. Particularly problematic are adolescent and adult women, the majority of whom do not meet current calcium recommendations.
There has been research, some research by Gunthur, who was with USDA, established that carbonated beverages tend to displace milk in the diets of teenagers with negative implications for diet quality. This displacement effect has also been shown in adults. Joanne Guthrie found adult women whose diets failed to meet calcium recommendations, drank significantly more regular calorie sodas than those with diets meeting recommendations.
And as we've discussed yesterday, the DRIs did recently increase calcium recommendations over and above the 1980 RDA. So in my view or in the subcommittee's view, this ongoing trend for calcium-rich beverages to be displaced by beverages high in added sugars is a concern.
There is little evidence suggesting diets high in total sugar promote weight gain when consumed in amounts that do not exceed energy requirements. There is some evidence, however, that soda consumption is a major factor in the increased energy intakes of children and adults between the '89, '94 and '94-95 USDA surveys. And, in addition, a meta-analysis by Dr. Rick Matters at Purdue suggested that beverages high in carbohydrates have a low society effect, leading to a poor regulation of energy intake and subsequent weight gain.
In terms of sugar and diabetes, we looked at the Nurses' Health Study report which has already been talked about today, so I won't elaborate on that. Basically, at this time the sugar subcommittee felt that there was a paucity of evidence making it difficult to determine diets high in sugar ar linked with the etiology or causality of non-insulin dependent diabetes. There are many papers on the use of glycemic index for the treatment of diabetes but a real scarcity of papers on the actual etiology.
I did want to point out there is a paper in this month's issue of Pediatrics, which I will get and circulate to the committee. It was done in Susan Roberts lab in Tufts, and she demonstrated that when teenage boys consumed a lunch with a high glycemic index, they consumed nearly twice as much food afterwards in comparison with a low glycemic index lunch. And they suggested that meals with a high glycemic index set off a chain of actions that caused overeating and potentially could lead to subsequent obesity, so that's a new paper that I think we'll want to consider in our deliberations.
Again, I won't spend a lot of time on this. Dr. Byers mentioned this earlier, and I mentioned it in my comments that the World Cancer Research Fund is recommending limited consumption of refined sugars for cancer prevention.
Very quickly, because I mentioned this in September when we got together, there has been a meta- analysis of 23 studies over a 12-year period, leading to the conclusion that there is little evidence that sugar has any significant influence on either behavior or cognitive performance in children. So this idea of sugar and hyperactivity in children has pretty much been put to rest, at least scientifically, with these data.
Next slide, please.
Clearly, there is a role for dietary sugars in the development of dental carries and between milk consumption of sugar remains a risk factor for occurrence of dental carriers, and the recommendation now is that we focus on fluoridation, adequate oral hygiene and not just on sucrose intake alone.
Wanted to show you some data on low calorie sweeteners. The USDA Economic Research Service collected food supply data on low calorie sweeteners from 1970 to 1992. There are no data available after '92, primarily because low calorie sweeteners are used as constituents in other products like soft drinks and food manufacturers consider this proprietary information and it's difficult to get. But between 1970 and '92, consumption increased from an average of five pounds per person to 24 pounds per person per year, so there has been a dramatic jump in the use of sugar substitutes.
When we did a literature study for sugar substitutes, we find this one study in George Blackburn's study done in George Blackburn's lab that showed some evidence that multidisciplinary weight controlled programs that included Asparte, a sugar substitute, enhanced or facilitated long-term weight maintenance, but we could only find that one study so the evidence, again, is fairly sparse.
So, in review, I'd just to review these key points that I've raised. There is consumer confusion about what we mean when we say to eat diet moderate in sugar, and it particularly seems to be problematic as it relates to the fruit group. Since '975, USDA has defined, created a definition of "added sugar" which now allows us to do analyses of food consumption data of the USDA database which look at added sugar and its impact on diet quality. Sugar intake is clearly increasing. A third of all added sugars now comes from soft drinks. I showed you some new data that we had on sugar and diet quality, the sugar/fat see-saw which I talked about, and the fact that added sugar intake was negatively associated with a number of those problem or scarcity nutrients in the food supply.
And I also reviewed the evidence that we've looked at with sugar and weight, diabetes, cancer, behavior, dental carries and sugar substitutes. So thanks very much.
I think in terms of the committee and what it would be nice to have some comments about are what we're really grappling with is this question of added sugars and whether or not the guideline needs to reflect the nature of some of the data that I've showed.
Thanks.CHAIRMAN GARZA: Alice?
DR. LICHTENSTEIN: I think you did a nice job of summarizing the group's work.
I think that -- I agree, I think that there needs to be a mechanism for distinguishing sugar that comes from fruit and milk from other kinds of sugar, and added sugar really sounded like a way of doing that.
However, what I think we really need to know is what the public's perception is of the word "added sugar," if it's just sort of sprinkling it on some breakfast cereal, and it seems like the major contributor in soft drinks, and I wonder how that's actually perceived terminology was because that may not be perceived as added sugar, and whether there are any suggestions on alternate terminology that would really capture that issue.DR. JOHNSON: Right.
CHAIRMAN GARZA: You want to respond now?
DR. JOHNSON: Well, I think that's a good point, and I don't have the answer. I know in the focus group study they said they're confused how the general public would perceive the term "added sugar."
DR. LICHTENSTEIN: I just think we need to get the information.
DR. JOHNSON: I think that's a good question, yeah.
DR. LICHTENSTEIN: Yeah.
DR. JOHNSON: I think I'll sit down if that's all right.
CHAIRMAN GARZA: Meir.
DR. STAMPFER: I think it's clear that the added sugar is having a big impact on diet even though we can't pin much in the way of specific diseases to this, but its adverse effect in -- main adverse effect is that it's displacing foods that do provide nutrients. So I think this might make a good model case to consider as one of the sort of second tier guidelines, if we got to that proposal that several people had made of distinguishing sort of top tier and second tier guidelines, that this, I think, should remain as a guideline, and perhaps the text could be shrunk a little bit, and it could go into the second tier where maybe some other guidelines might go.
CHAIRMAN GARZA: Any other? Johanna?
DR. DWYER: Just a -- thank you for an interesting presentation.
One thing it seems we need a little more work on is cariogenecity, and it seemed to me in a brief review of the literature a couple of months ago that it might be helpful to think of all of these variables, these various diseases as which ones seem to be most associated with whatever this thing is, extrinsic or whatever you want to call it, and what isn't.
Certainly with cariogenecity there are two issues. One is something to do with the composition of food with respect to sugars. Another is the carbohydrate, the cooking of the carbohydrate so that the starch is also associated with cariogenecity. And then there are all of these other things about when you eat it, what you do afterward and so forth. Do you have a toothbrush afterward?CHAIRMAN GARZA: Johanna, can you speak closer to the mike?
DR. DWYER: It would seem to me it would be helpful if we could just array them as we ponder this issue.
The other thing, Rachel, was I wasn't sure what you were -- the group was suggesting. Is it change the existing guidelines to choose a diet moderate in added sugars?DR. JOHNSON: That's one option that we've considered.
DR. DWYER: And what are the others?
DR. JOHNSON: We're looking for help. That was our primary option that we considered, was whether or not we wanted to use that term "added sugar" in the guideline itself.
I mean, I suppose another option is do we need a sugar guideline.CHAIRMAN GARZA: Dr. Kumanyika?
DR. KUMANYIKA: I think that the presentation is very convincing that a guideline is needed on something like food and beverages with added sugars, which is different from what it says now, which is "moderate in sugar." So you get into the "avoid" issues. And if you said then you're back to the limit, foods and beverage with added sugar, but something in that spirit is much clearer this round than I've remembered in the past because it's very clear that it's a displacement issue and it's not that you're trying to link sugar in the diet itself to the health problems, but it's part of the pattern, that it's not -- that it's replacing things that are needed, so maybe that word could give someone an inspiration for how to --
DR. JOHNSON: Say that again, Shiriki? Food is?
DR. KUMANYIKA: Foods and beverages with added sugars, because then it doesn't matter who adds them. People know it's been added.
CHAIRMAN GARZA: Any other comments or suggestions?
Dr. Dwyer?DR. DWYER: Yeah, I still have concerns about the "added" business, and I guess the first thing is something that Dr. Lichtenstein brought up, which is what does that mean. Does that mean to most people sugar from the sugar bowl or does it mean corn syrup? It strikes me that maybe there is more focus group information we haven't seen, but I'd really like to see that.
And the second things is I'm having trouble remembering all the things you said and which ones are related to "total." For instance, cariogenecity, I know from our own work that vegetarian children who eat a lot of raisins get just as high carries as kids who were non-vegetarians who ate a lot of added sugar. So that it would help me to array those things and think of them before I made a decision.CHAIRMAN GARZA: Dr. Deckelbaum and then Dr. Kumanyika.
DR. DECKELBAUM: I guess added sugars was a major part of our discussions and how to define it. And I guess in the simplest way, because it's added sugars by food producers or its added sugars in the home. But I think that it's where you add simple sugars, as a first step add simple sugars to food, to sort of natural food either in home or industrially. So I guess if you were a soft drink manufacturer and you put it in the mix, that would be an added sugar. Similarly at home by adding it to tea or coffee or whatever would be an added sugar.
We didn't really discuss too much about corn syrup and corn syrup solids, but, again, those added sugars, and we had some discussion on that yesterday, are in large part small glucose polymers. Corn syrup, I think the mean sort of size of a glucose polymer is about 15 glucose molecules together and they're not very sweet, so they're not added -- they're not added --DR. DWYER: I take issue --
DR. DECKELBAUM: They're not added for sweetness.
DR. DWYER: Okay. I take issue with the importance, I take issue with that statement, but I also take issue with the question that they are not important. I think they are very important and we need to see some breakout data because it strikes me that a lot of --
DR. DECKELBAUM: It's not important.
DR. DWYER: A lot of the corn syrup solids, sweeteners, I think a lot of what's added to the soft drinks that Dr. Rachel mentioned are corn syrup, it's not -- isn't it?
DR. JOHNSON: Well, remember that soda is the number one source.
DR. DWYER: So they're not added to the make up --
(Laughter.)CHAIRMAN GARZA: Dr. Kumanyika, on that.
DR. KUMANYIKA: I just wanted to pose the question of if the goal of this guideline would shift to being foods and beverages with added sugar or sweeteners or whatever, then it might not be the place to address some of the issues of total sugar or total carbohydrates. It's just -- I mean, we think about some carbohydrate issues as part of another guideline. If this one could be clearer, focusing on this added sugar displacement problem.
CHAIRMAN GARZA: Carole, is there either plans within the department to do some focus groups --
MS. DAVIS: Yes.
CHAIRMAN GARZA: -- before, that one could explore at least the meaning to consumers of added sweeteners, added sugars, a variety of various messages such as the one that Shiriki suggested?
MS. DAVIS: Yes, we have plans -- I don't know if this is on or not. We have plans to do that. it's going to be very limited, and we're using this to get other things that you want to -- to have us study, and we just hope the timing will be right. We're in the process now of going through all of our clearances that we have to do.
CHAIRMAN GARZA: Because what the group might want to do is to focus its attention on the rationale for modifying the current guideline either as a first or second tier, and then coming to some judgment later on, based on that evidence and the added input of the focus group, as to what would be the best wording, and then making a final recommendation based on the basis of both types of evidence. Is that --
DR. LICHTENSTEIN: I think that's a very good idea. I think when the subcommittee was deliberating, you know, we came up with the word "added," and we all -- we're just abnormal, but it all seemed real clear to us what we were, you know, talking about, and it wasn't until I actually heard the presentation and then relooked at the contribution of sugar that I realized that it probably wouldn't be perceived as added sugar, and I also think we need to find out more about corn syrup because if you taste corn syrup it's sweet. If the mean polymer size is 15, one wouldn't predict it to be --
CHAIRMAN GARZA: That's a smaller size though. It's not --
DR. LICHTENSTEIN: Right. One wouldn't predict thought that it would be sweet because even the monosaccharides would be glucose, which have less sweetening, relative sweetening that fructose. I just think we need to find out, but that's something that's sort of a factual thing. But it seems in a lot of the food labels that you look at, a lot of it is corn syrup and not sucrose.
CHAIRMAN GARZA: Okay. Can we move on to the next one?
DR. DWYER: It seems to me it depends on what the meaning of "is" is.
(Laughter.)CHAIRMAN GARZA: That was Dr. Dwyer. Can you tell me why?
(Laughter.)CHAIRMAN GARZA: It's gotten to be an internal joke among the committee.
All right, let's move on then.
Kathryn?MS. MCCURRY: i'm sorry. I just wanted to remind the committee that if you're taking about distinctions between added versus intrinsic sugars, and thinking about guidance to the consumers, virtually every processed food label is "added" in terms of total grams of sugars per serving, and that would account for all forms of sugar that are added, although I believe there are distinctions in terms of -- I think it monoendysaccharides that are labeled, although there is some --
CHAIRMAN GARZA: You're saying that the term "added sugar" is on the food label?
MS. MCMURRY: No. Total sugars.
CHAIRMAN GARZA: Total sugars.
MS. MCMURRY: Total sugars is what's on the label, although there is --
CHAIRMAN GARZA: We'll get somebody to clarify.
All right then let's move on then to another noncontroversial guideline. Dr. Kumanyika is going to provide us with untold wisdom in about 30 minutes. In 30 minutes we will have this guideline resolved.DR. KUMANYIKA: I actually think this is going to be short. What time is lunch? You think you can get two more in before lunch to catch up?
CHAIRMAN GARZA: At the present time there is no lunch.
DR. KUMANYIKA: Okay.
CHAIRMAN GARZA: But we'll see what we can do.
DR. KUMANYIKA: All right. Okay.
DR. DECKELBAUM: It's the hour and a half that we went over.
DR. KUMANYIKA: The sodium subcommittee consists of myself and Drs. Dwyer and Stampfer, and Joan Lyon, who is giving us staff support and very helpful in keeping us on track.
What I'm going to do is just highlight what we've been doing and some of the issues that we think are important for sodium this time. If we leave that one for awhile, the key issues in sodium are whether to keep the guideline at all, and then if we decide to keep it, what should it say. And the reason I say whether to it at all is because it has been suggested, for example, yesterday that we drop the guideline, so I think the committee needs to consider that since the challenge is put before us of whether this guideline should continue.
What we did after the last meeting was to go through and identify all of the issues that had anything to do with either the validity of the guideline or the reasons for supporting the guideline, the evidence. And we had the sort of unusual situation of having the National Hot Line of Blood Institute convene a conference on this topic between the two meetings. So rather than -- and I certainly am not going to try to summarize the proceedings of the conference, because I think we needed to have a two-day conference where, fortunately, our entire subcommittee was present for the whole time, so we've heard a review of the evidence on the topic. I'm going to go through what was covered at the conference first. Then as Drs. Dwyer and Stampfer to give their impressions of whether -- the question I posed to them is whether anything that they heard in the presentations at the conference alters their understanding of the supporting evidence.
Before I do that, I want to read off a list of questions that I raised about this guideline because there is a sense that this case may not be strong or may not be existent. So one of the questions is if the cases for sodium reduction as a guideline is not strong, why is it not strong? And here is the list. I don't have this on the side.
One is, is it not strong compared to that for other guidelines, which would mean it's a second tier type of guideline or something? Is it not strong compared to the case for other dietary factors that might influence blood pressure, which is a different issue? And some of the arguments that are made are that it's not strong because by itself it won't do as much as other factors and therefore we don't need it.
Thirdly, is it not strong simply because the methodology to address the issue is limited, which means that people think it's there but because urinary sodium, 24-hour urinary sodium is hard to collect and dietary doesn't get sodium? It just not strong because the type of evidence we have is by its very nature inconclusive. Another reason it might not be strong is because the studies that would tell you if the case is good haven't been done yet, and I'm going to mention a little bit later one of the studies that's currently in the field. Or is it not strong because the evidence is actually equivocal and, you know, the case isn't there?
And, finally, is it not a strong case because there's a lot of noise in the system, which I take to mean to mean that it is actually a strong case, but there are -- people put noise in the system by trying to cite odd and invalid evidence to confuse whether there is a strong case or not.
So why don't we put up the next overhead.
I think this actually summarizes the sense that we had at one of our conference calls, but this is still open to discussion; that the guidelines says there is a role for sodium reduction in the general population, and that there is a defensible case for that based on the evidence.
At the NHLB conference, which was chaired by Drs. Martha Hill and Aram Chobanian, we had an overview of the relationship between sodium and blood pressure by Dr. Paul Whelton; differences in the blood pressure responsiveness to sodium intake, which was the salt-sensitivity issue, by Dr. Myron Weinberger, and that was discussed -- there were discussants: Drs. Margo Denke, John Flack and Steven Hunt; and Dr. Frank Sacks talked about the interactions between sodium, potassium, magnesium and calcium, and gave a little DASH advocacy at the end of his presentation. He's one of the main players in the DASH study and we had that discussed by Drs. Ted Kotchen, David McCaron and Laura Svetkey.
As you might know if you know this literature from some of the names, we had almost all of the antagonists and protagonists there except that, as Dr. Lenfant mentioned in his opening remarks, Dr. Mickey Alderman chose to be out of the country during the days that we had the conference. That's the way that Dr. Lenfant put it. And so he was not there. Someone else presented some of his data that he's published.
We went to sodium and blood pressure in the young. Dr. Ron Prineas talked about the effects of neonatal sodium intake. Dr. Bonita Falkner, Sodium and blood pressure in children, which was discussed by Dr. Gerry Berenson, Clarence Grim and Julie Ingelfinger.
We looked at the clinical trials and studies. Dr. Graudal presented his meta-analysis of trials of sodium reduction. Richard Grimm talked about subpopulations by age, race and gender. Janice Douglas, prevalence of sodium sensitivity in postmenopausal women, and I talked about sodium reduction and quality of life issues, and we had discussants including Larry Appel, David Freedman, Diana Petitti, James Robins and Michael Stoto. And by this time it was really a very lively meeting with, I think, people who hadn't all been in the same room together to discuss these issues actually having a chance to hear each other's arguments and agree with them or rebut them at that time.
Paul Elliott presented by INTERSALT data, and then Dr. Chris Sempos talked about the cohort studies that have some long-term data and mortality data, so he presented Alderman's Work Site Cohort Study and the NHANES I analysis that Dr. Alderman has published, and the Scottish Heart Health Study data, so those were the three -- three of the studies that have relationship, some relationship between sodium and mortality.
And then Dr. Jerome Cohen presented the mortality data from the MRFIT-Follow-up. So that's a fourth source of mortality data; and we had Dr. Nancy Cook, Kesteloot, Graham MacGregor and Louis Tobian to discuss that.
The role of sodium in non-cardiovascular conditions was a topic on the second day. Dr. Dan Jones addressed that. We talked about sodium in left ventricular mass, Richard Devereaux, and Jay Cohen, Ed Fruhlich and Lew Kuller discussed that.
Dr. Suzanne Oparil was at the -- gave a presentation on the renin-angiotensin system. The sympathetic nervous system was discussed by Allyn Mark, and then Plasma insulin, cholesterol and coagulation factors. So this was really an exhaustive discussion not designed for the Dietary Guidelines Committee, but certainly more than we ever wanted to know about the details of the topic.
The basic research in the area was discussed and the future studies, clinic and epidemiological research and the question was posed as a discussion topic of whether there should be a randomized clinical trial on sodium reduction and blood pressure with morbidity or mortality as an outcome.
At the end we had a presentation by Dr. Michael McGinnis on dietary guidance public policy, and Drs. Dwyer Stampfer both were discussants, Dr. Bill Harlan and Marion Nestle all talked about some of the policy considerations.
In the hallways, some of the people who were present actually revealed that they thought it was a consensus conference, and they thought we were going to take a vote at the end of the conference, and some of the NHLBI people, and Dr. Hill, certainly made it clear that the purpose of this meeting was not to have a consensus, but it was just to really describe the evidence and have people have a chance to hear the arguments and hear the arguments about the arguments so that we could make up our minds.
So I think I'll stop there and just ask for whatever comments that the other two subcommittee members from the DJAC want to make, and then I'll go into the talk about what we would have in the guideline if there will still be a guideline.
Do you want to come up here or use your mike there? As long as people can hear you.DR. DWYER: I thought you gave a good summary there. Just a couple of observations.
The first was the level of heat was considerable, the level of vipe was also considerable in this conference, but I thought that the data were very well reviewed. Some impressions I had was that one of the problems is the data aren't as strong as some of the other things we've been talking about, like saturated fat. Nevertheless, I think what your side says, Dr. Kumanyika, is correct; there is a role. The problem is not exaggerating on either end of the debate.
That slide from DASH is interesting, and certainly it will be of great interest to follow the community-based intervention, but a feeding study with the facts is not the same as what we're after, which is more what happens if you give dietary advice or recommendations to federal officials or other officials. Nevertheless, it does seem to be safe. Any concerns I had on that were dispelled by what I heard.
The question is how effective it is and how big an effect, what people can do, can make.DR. KUMANYIKA: Thank you.
Meir?DR. STAMPFER: Those pretty much were my sentiments after going to the meeting. I think first on the safety issue, we can basically completely dismiss any important concerns on all of safety of low salt diet. That turned out not to be a credible issue.
I think the evidence is actually pretty good for modest effect, and I think the evidence for big effect is weak. So my take on it is that I agree there is a role for sodium reduction in the general population, and where to rank it in the hierarchy of advice is open to question, you know. If we want to tell Americans some number of things that they can do in their diet to improve their health, I think sodium fits in there, but it's not in the top tier of recommendations.
So my bottom line take would be to keep the guideline, perhaps shrink the text, and like with sugar, to put it in the second tier. But I wouldn't weaken it in the sense of relaxing the recommendation at all. I think the evidence is good for a modest but important effect on a population level.DR. KUMANYIKA: Okay, thank you.
So if there will be a sense that there is no scientific evidence that's been put forth since 1995 that warrants dropping this guideline, then the question is what should we say in the supporting evidence, and is there something we can put in the text that would make it clearer to people.
Put up the next.
So we went through the points that are made in the current guideline, and have just summarized the things that the committee has discussed and will be working on according to those points.
These three bullets, "Sodium and salt are found mainly in processed food, processed and prepared foods" is currently one of the lead-off points in the bulletin, and will probably remain in the bulletin, and one question will be would we suggest that it be in that section? Is that really the main point? And this is, again, this is foods with added salt. It's less likely to add salt to beverages although there are some liquid foods that have salt added. So this would be one to retain and maybe elaborate.
The next is "How much sodium or salt should the average adult consume?" This is one where the 1995 committee has been criticized for being vague. What 's there now is a statement, "Most Americans consume more salt than needed," and then in the advice for today, it says that the food label says 2400 as a daily value.
So one question for you is should we then have this section on how much sold, or sodium or salt should the average adult consume, and then address head on things like where we get -- where the recommendation would come from, like what requirements are; point out that the average adult includes a lot of people who, like the hypertension, more than 50 percent of adults who are trying to reduce their sodium intake have been so advised; comment on children, lower limits.
The other thing that we've wondered is whether we should come and explicitly on the type of people who would be accepted from any recommendation we would make about the amount of sodium. Do we mention conditions, salt-losing conditions or something where people would know that they're not in the general healthy population, because some of the criticism that's come about adverse effects really talks about populations that are not healthy, that have some condition where you would not restrict their salt, where you might even want to give them salt, and that's mixed in in a way that I think frightens a lot of people, or certainly confuses them. So we could help consumers perhaps by saying there are certain people from whom sodium reduction is not recommended and say who they are.
In terms of how much sodium Americans eat, I was -- on our table this morning is a report from the USDA, "Away From Home Foods." Some of you have it. The committee has it. And there are three tables on sodium that I thought were interesting, so this is too small for you to see the details. I'll tell you what the bylines are for these graphs.
I thought this was interesting. I hadn't seen data put together this way before, and I would like ultimately to know from someone who's been involved in the analysis how this information was derived.
The first one is that American sodium intake remains high above the recommended level, and it shows that the -- over time that sodium intake is -- this is in milligrams per 1,000 calories, that it's been remaining high. It hasn't gone down. The food away from the home actually has a little blip there. I just had looked at this this morning during the meeting so I'm not that familiar with it. And if the author is here, you will be free to comment if the Chair would permit it. So that's all food and food at home.
And then this benchmark on sodium density is showing that it's going down because calorie intake in these data sets has gone up, and so the sodium intake being relatively flat by this estimation is from less per 1,000 calories. That's a little bit confusing, I mean, because sodium intake sometimes tracks very well, correlated about .6 with calories, so I'm not sure where that comes from.
But this Figure 10, Restaurant of foods contain much more sodium than other away from home foods," this is interesting, certainly something that consumers are not able to figure out themselves how much sodium is in restaurant foods. And this graph suggests that it's going down since about 1991, but it's still higher than foods from other sources. This is new information that might give us a handle on how to advise consumers.
And the third is showing the percent of people meeting recommendation. I'm assuming this is data that includes discretionary salt, but if not, then it would be probably an over-estimation of the people meeting the recommendation. So it gives the average intake over time and shows that -- and it's gone from 41 percent meeting new recommendation down to 34.
And I've seen NHANES data put forth differently that implied that sodium intake is going up, and I haven't been sure whether that's because of a better probe being in the more recent dietary assessments, or if we actually feel confident that sodium intake is going up and the fewer people are meeting the recommendations.
That would certainly address one of the issues related to whether we need a guideline, because in the absence of a guideline, or if the guideline is downplayed, you may not stay level; you may actually have sodium intake increase and what is the health effect of that.
Okay, I also had just -- some of our discussion, we talked about behaviors and sodium-related behaviors. We have this "Advice for Today" section, and you could replace that or add a section of new habits that can reduce sodium intake in the interest of how and maybe positive behaviors that have the effect of reducing sodium intake instead of the avoid.
I also wondered when I looked at this and listened to the discussion yesterday if anyone has ever tried to standardize the rest of the bulletin, because the "Advice for Today" seems to be the only section that appears in all of the guidelines at the end. But when somebody was talking about the alcohol and they said, well, you made the statement about historical use in alcohol but you didn't make it for anything else, and so I just wondered if anybody had ever thought about having the same categories as you go through the guidelines, and one would be what behaviors will get you there and another might be what's the history behind this or whatever.
But we could focus on habits because there are types of habits that people in some of the clinical trials have adopted to help them reduce their sodium intake, and that could be made more prominent so it's more of a "how-to" guideline as to necessarily a blood pressure guideline, which is the way it reads to some people.
Let's put the next one up.
The next key point in this guideline has it appears now is that sodium is associated with high blood pressure, and some of the criticism that have come up relate to the fact that it is not the only factor related to blood pressure and maybe is not the main factor related to high blood pressure in the population. So one possible way of addressing that would be to talk about the two things that are shown here: to mention that it's an important factor associated with high blood pressure, but not imply that it's the only factor; and then describe where sodium intake fits in to the overall eating pattern, which would be a place where you could mention something like a DASH diet and cross-reference to other fruits and vegetables.
Text like that appears there now, but it's framed as other factors also affect blood pressure, and one way to think about it is, you know, where does sodium fit in with other dietary factors, which is not quite the same thing, but it would allow you to put the same information there.
I wanted to comment on the DASH II study because I think that the ultimate question about the short-term effect of the DASH eating pattern on blood pressure and its relationship to sodium reduction will be answered in this study and we might even in the supporting evidence describe the study even though the results will not be available. So I'm just going to review the design of that which Joan got from the worldwide web and it's available there for those of you who don't have a copy.
That study is contrasting the DASH dietary pattern, high fruit and vegetable, dairy dietary pattern with the control pattern, and then people will be crossed over on three levels of sodium intake so DASH 50, 100 and 150 per day.
So as I understand the design, there will be four centers and each one will have 100 -- there has, there has. I think the actually finished data collection in November, and will be able to look at 50, 100 and 150 without the DASH diet and also be able to look at the effects of 50, 100 or 150 with the DASH diet using people as they are on controls, and the cross-over design with like a two-week washout in between.
They began that in August 1997. Recruitment, began the experimental diets in January of 1998, and eventually, perhaps for the 2005 dietary guidelines committee, would be able to address the issue of dietary pattern of sodium in blood pressure in a more coherent fashion.
I probably mentioned that to say that until that's type of study is done there won't be any way to tell much about additive benefits of DASH and sodium intake because the DASH held sodium intake constant at a moderate level of three grams per day.
There is also a study that is planning -- planning stages now which is called "Permier." It's an investigator-initiated study, it will test the DASH diet with weight reduction and sodium reduction in a free living population, and that might answer the test of what you could expect if you put everything actually in the dietary guidelines together, except with the DASH pattern being a little bit more aggressive on fruits and vegetables than the traditional pattern, so some of this is just to say that we don't know much more about the role of sodium and its ultimate benefits than we did in 1995, but we can describe it a little bit differently, and we may know down the line.
May I have the last slide? It's about consistency with other recommendations.
Reduction of sodium or salt is recommended in the Surgeon General's report on nutrition and health, the National Research Council, the Report on Diet and Health, and that is like six grams of salt per day. The Surgeon General's report doesn't have a numeric goal or didn't have a numeric goal. Then the daily value is 2400 both for the 2000 and 2500 kilo-calorie intakes. The level of sodium reduction hasn't been -- maximum sodium intake hasn't been changed by calorie level.
The requirement is listed as 500 milligrams of sodium per day in the 10th Edition of the RDA as a safe minimum intake. As some of you will remember, the 9th Edition had a range for adults of 1100 to 3300 milligrams per day of sodium but that was not repeated in the 10th Edition of the RDA.
The healthy people 2010 objectives are moving towards a total sodium objective, but I don't know what it is yet. It may not have been formulated. The 2000 objectives, some of the text that the committee has says that the objectives were met, which is an error, but the 2000 objectives were behavioral objectives that had to do with the addition of salt, preparing foods without adding salt, buying low salt foods and avoiding adding salt at the table.
There is, I think, no data on the food preparation goal. The goal was 65 percent of people preparing foods without added salt. But the use of salt at the table, the goal is 80 percent rarely or never using, and the 1996 data shows 62 percent rarely or never using salt at the table, which also emphasizes that it's going to be food sodium. And then adults who regularly purchased foods with reduced salt, the goal was 40 percent, and the 1995 data say 19 percent.
But I think that there is a move to change because those behaviors by themselves may not add up to a low sodium intake because they only deal with discretionary additions or buying certain products, so if there is a new healthy people 2010 guideline that's quantitative, we might want to see when that's going to be available, and if we can align ourselves with that.
That's all I wanted to say about this -- well, one more thing. We've looked at adverse affects and other issues and have reviewed this iodine issue. Dr. Dwyer had some comments about that in one of our conference calls and mentioned that the HLBI conference, and since then we've obtained a report from a CDC conference on the iodine issue. And right now I think that it means we might want to make sure we describe the role of iodized salt and current levels and the fact that they're going to be monitored in the population more clearly in the supporting evidence and in advice to consumers, and I don't know if you want to say anymore about what you think we should say because, I mean, the concern is that if iodized salt is an important source of iodine, we need to take that into account when we are recommending limited use of discretionary salt.DR. DWYER: I think on that iodine issue, that there are two issues. One is that it appears from the work of Powell, I think it is, et al., and we can show you the slide tomorrow if you wish, that there is a sizeable proportion of people who don't seem to be getting enough in terms of their urinary iodide, and maybe some of that has to do with the characteristics of these particular people and their use of various foods and salting and so forth.
Then there is another group of people who probably get more than they need or too much, and so it's like the three bears: too much, not enough, just right. And what we'd want to do is as we ponder these issues is to think more about how we can help on that.
The other issue is the second issue that is a hangover from the '95 guideline discussions, and I don't think we have really discussed this in depth yet, Shiriki, but the question of quantifying sodium or salt guidelines means that we think the evidence is very great that there is reasons to quantify, doesn't it?
And the only recommendations, I think, in '95 that are quantified now are saturated fat and total fat.DR. KUMANYIKA: I don't know. I think we need to hear comments on that. The best reason for quantifying, at least with the range or some limit, to me s that consumers won't be able to use the guideline without that. But whether or not that makes it easy to quantify it and be correct about it is a different story.
DR. DWYER: But how can consumers use it even if we quantify it?
DR. KUMANYIKA: Well, I mean, I'm thinking about like the old cholesterol guideline that was 300 because it was half of what people were consuming. Do you know what I'm saying?
If people -- if we decided that people should eat less than their -- without saying that this is their physical threshold that will have an effect on your blood pressure, but just that there is a greater relationship.CHAIRMAN GARZA: Shiriki, was there anything that any of you might have learned that would bring greater specificity to the recommendation in terms of who might benefit? Or at the NHLBI conference are there characteristics of the population that would help us provide guidance beyond saying, well, if you're human, you know, and regardless of whether you're 90 years old or five years old?
As we look at other guidelines, we're trying to make them wherever we can as specific as possible. Any new data that we should be paying attention to along those lines?DR. KUMANYIKA: I think if my hearing of the conference was that the only basis for doing that would be a lifestyle basis in terms of how has lifestyles or eating patterns that are most likely to put them at risk of eating a lot of sodium to people who have -- I mean, family history type issues. But the salt sensitivity discussion -- well, some of the discussions were very disappointing because they really didn't tell you anything more than you knew before, even though we had hoped to come to a new level of discussion. I didn't hear anything new about salt sensitivity. Many people think it is not a dichotomy and that it's confusing to make it sound like a dichotomy.
But we have a list of specific issues that we've done a literature review on but we haven't, you know, read through everything and discussed it. I don't know if we're going to get anything new or not of that, but that's one of the issues that we have and we've posed some questions in our outline that we might be able to turn into special analyses of data or modeling of how many people -- you know, how far would people have to reduce their sodium to move the blood pressure distribution into a better range? How many people in certain studies have actually lowered their blood pressure if they reduce their sodium intake? Just different ways of looking at data that haven't been exactly done in published reports that we might be able to get a better handle on the likelihood of the average person responding.
But at the conference, I think it was a population argument, so it's not really responder/non-responder type of argument, and Johanna may want to comment.DR. STAMPFER: I agree.
DR. DWYER: The question I've got though is I don't think -- I think the RDAs for sodium, for all those electrolytes, are they coming up soon? Are they going to be reviewed soon?
CHAIRMAN GARZA: They are going to be reviewed. I don't anticipate reviewing -- is Alice, is Alice on the floor here?
The last is that there is at least a year and a half, two years away. I don't see them coming up before then.DR. DWYER: From starting.
CHAIRMAN GARZA: From starting, that's right, unless the federal group can bring us more current information.
MS. SUTOR: Part of that -- part of that depends though, doesn't it, on whether the DRI committee sees that it would be more important or more useful to do the electrolytes as their next group rather than the macro nutrients.
CHAIRMAN GARZA: And there is so much pressure now to do macro nutrients that I doubt if that's going to be reordered.
Rachel, and then Scott.DR. JOHNSON: I just wanted to comment on the quantification of the sodium guideline. It seems that there is this driving need for people to have a number. And if I can remember correctly, there really never was a number, and then diet and health came out, what, in the mid eighties or late eighties, and they said six grams of salt, which we all immediately translated to 2400 milligrams of sodium and that sort of became the magic number and then it was on the food labels, and everyone uses that as the cutoff in diet quality research to say what percent of the population meets t.
So I think, you know, that seems to be the number that's sort of out there. So whether or not we concur with that or not, I think in the absence of the dietary guidelines giving a number, there will be a number that's used as a cutoff for the population.CHAIRMAN GARZA: Scott.
DR. GRUNDY: The current terminology is moderate, and I think -- I think that might have a moderating effect on the population. And, you know, one of the questions is going from moderate to low, which seems like it has a questionable effect, but it's -- you know, it's also a little unrealistic.
What about if you totally eliminated any comment about sodium and let's say the levels doubled in the population because for whatever reason people no longer paid any attention to it, and you were taking in 12 grams a day or 13 or 14 grams like some populations? Is there any evidence that that would be harmful?DR. KUMANYIKA: I think there is -- I mean, we would have to follow the population, but the presumption is, from the evidence associating from salt data and those kind of comparisons, and from the ability to reduce the incidence of hypertension and lowering sodium in people with high normal blood pressure, the assumption is that more people would be at a high sodium intake and then more of those who are predisposed would convert over into hypertension at an earlier age and so forth.
So the assumption is that it goes both ways, that you could say in the similar way that the weight of the population increased. One of the problems in the blood pressure literature is that blood pressure in pharmacologically controlled in the churn data, and that we did a paper trying to model the impact to see if the incidence of high blood pressure is actually going up, and that we just suppressing it with medication, and the only way we could do that was to impute the people who were on meds, to put them in the high part of the distribution and then look at it churn over time.
But that's one of the problems, people -- because the treatment -- well, see, and for blood pressure about 25 percent of people who know they have blood pressure and taking medications have blood pressure in the desirable range, so that's another like 50 to 70 percent of the adult middle age population who might have a harder time controlling their blood pressure if they were to be consuming more sodium.
This is such a passive issue from the point of view of consumers because you saw the discretionary data. It's not that convincing. Now, this is something consumers are doing, but this guideline is always a little bit circuitous because the message is really to the say catering industry or some of the people who feel that consumers want this amount of sodium and therefore put it in their food, not because consumers what it, and I don't know what you do with that, but at least this is a platform for working with industry on how to keep it at a moderate level.CHAIRMAN GARZA: Alice?
DR. LICHTENSTEIN: I have two comments about the guideline itself.
First, right now it says "Choose a diet maturate in salt and sodium." And I'm wondering, I didn't look at the consumer focus group data on that, but what is the perception, you can't do one without the other as far as salt and sodium, and, you know, historically were they always both -- those both terms included and then is that confusing or is that actually helpful?DR. KUMANYIKA: My impression is that historically, when it was sodium, that nobody had any idea what that meant. So you have to say "salt" because people don't --
DR. LICHTENSTEIN: Right, but then is it necessary to say "sodium" or is it confusing just as far as the message goes?
I mean, people don't eat sodium. They do eat salt, and salt is listed on the ingredient label, not sodium. So I think that's something that should be considered.DR. KUMANYIKA: Sodium. On the ingredient list?
DR. LICHTENSTEIN: Yes. But on the nutrient label, I guess, it's different.
DR. KUMANYIKA: Unless it's another sodium compound.
DR. LICHTENSTEIN: Right, yeah.
The other point is right now the way the guide --the commentary to the guideline is written it says, "Consuming more fruits land vegetables also increase potassium intakes which may he help to reduce blood pressure." That sort of comes out of the blue, and then there is a box that talks about some good sources of potassium.
You didn't mention potassium, but I'm wondering, given that we have a limited amount of space in the booklet, is that particularly useful to the consumer with respect to the guideline?CHAIRMAN GARZA: Is that a rhetorical question or is that what you wish us to say?
DR. LICHTENSTEIN: I guess I'm really interested because, you know, being either a normal or abnormal consumer, I'm a little confused.
DR. JOHNSON: Maybe when we promote fruits and vegetables, and as the effect of the DASH diet, you know, you could say something about blood pressure in the fruit and vegetable part. That's where your potassium --
DR. LICHTENSTEIN: But we need information. I mean, I didn't hear anything about potassium. Do you think that potassium should be here and then the box should be devoted to potassium-rich foods as it's written?
DR. KUMANYIKA: Yeah, I can, and maybe we didn't have anybody we thought would be the best to invite this time to talk about some of these issues, but from this discussion maybe we will come up with the right person for next time.
The blood pressure literature makes it hard to distinguish between whether it's sodium itself or the sodium potassium ratio, but potassium doesn't come out as standing on its own as a risk factor, and potassium supplementation seems to -- they do more in certain populations if potassium intake is low; like African-Americans have low potassium intake, and there have been couple studies showing that supplementation will help, also the same with calcium.
So this has been the holding place, just like calcium is mentioned here and there and other reasons, this has been a place for mentioning factors that don't stand alone, and that's why I was thinking that maybe we would change some wording about sodium in the diet, and the committee hasn't had a chance to discuss this, but there may be a better way to do it because it does sound silly if you don't know why it's there, and you don't know the sodium/potassium ratio literature, it looks like --DR. LICHTENSTEIN: No, no, no. I know some of the literature and I know there have been reports that there is a relationship. I'm trying to put myself in the shoes of just a regular old consumer, and it's sort of buried in a sentence. I'm looking at a guideline that's referring to salt and sodium, and what I see as a visual in a box which I might just focus on is potassium, and I'm just wondering how much of an impact that actually has because it's not part of the guideline, which was maybe to, you know, read it, so that's why. There may be a good reason for it but I think it's a good question.
CHAIRMAN GARZA: Richard and then Roland.
DR. DECKELBAUM: Actually, just to -- the potassium box is the first box you see in the guideline.
DR. LICHTENSTEIN: Yes.
DR. DECKELBAUM: I wasn't going to bring that. I was going to suggest that quantifying, I guess that would be a number.
(Laughter.)CHAIRMAN GARZA: I hope that's not a reflection of our glycemic index now.
(Laughter.)DR. DECKELBAUM: But from what I understand, and correct me, that the dietary guidelines have been food-based and not number-based, and use numbers when other may other organizations provided them, much like it's used in the current guideline. I think quantifying, just, you know, putting it in as a number is just going to give a lot of area for controversy because you're going to have to spend a lot of time finding that exact number and, you know, maybe the -- so I would let the DRI committee or other committees worry about it, but we don't -- I don't think we have to worry about a number in our verdicts.
CHAIRMAN GARZA: Okay, Roland.
DR. WEINSIER: As it comes across now, it seems that sodium is punitive primarily for risk of hypertension, and I wonder if your committee has or would want to consider including here the relationship of sodium intake to calcium loss and bone health.
I think that there is as accumulating body of literature -- did I miss it?DR. KUMANYIKA: It's in the guideline, yeah, in a sort of catch-all category.
CHAIRMAN GARZA: Okay, I'm going to take one or two questions. Let me tell you what the plan is before everyone decides what they need to say needs to be said now. We're going to take the next guideline before we break for lunch, and we're going to be back by 1:15.
Otherwise, we're not going to get through what we need to do this afternoon, to make sure that the groups meet in the afternoon and start wrestling with these issues, because we have to come back tomorrow and deal with outlines and begin to make your work more concrete.
So as long as everybody is aware of what you will be doing to your lunch break, then we can proceed.VOICE: Can we get sandwiches or something brought in?
CHAIRMAN GARZA: And work through lunch?
CHAIRMAN GARZA: Yes, that would be a great -- because when we can just break for 10 minutes or five minutes and have lunch brought in.
Is everyone agreeable to do that?
(Chorus of ayes.)VOICE: We heard you, we heard you.
CHAIRMAN GARZA: All right, good. Let's just plan to do that.
VOICE: And it's still snowing out.
(Simultaneous conversation.)CHAIRMAN GARZA: All right, let me ask Shanthy or someone in the staff if they can bring in a menu or something, then we'll just pass the menu around.
VOICE: Give us two choices, give a variety.
DR. LICHTENSTEIN: I would just say one thing about if the subcommittee is considering a number, just remember that the guidelines are for individuals two and above, so with the fat it's 20 percent of calories, but little people may -- it may be more appropriate for them to have higher or lower total amounts of sodium than big people.
CHAIRMAN GARZA: Any other comments?
Linda?MS. MEYERS: The salt and sodium, you're quite correct that the -- when salt was added, it was because nobody understood sodium. Sodium wasn't deleted only because it was on the food label, and I think probably it had an hour's discussion, so it wasn't based on a lot of analysis about what people would understand.
DR. LICHTENSTEIN: But do we have -- did any of the focus groups deal with that?
MS. MEYERS: I can find out. I don't know the answer to that.
CHAIRMAN GARZA: Carole?
DR. LICHTENSTEIN: Connie is nodding yes.
CHAIRMAN GARZA: Connie, can you comment a bit more than just yes?
VOICE: The majority of the consumers do not know the difference between sodium and sodium chloride. They don't understand why they are put there. Some, very sadly, consumers --
CHAIRMAN GARZA: Okay.
DR. LICHTENSTEIN: I would like to ask Constance about added sugar as long as we have her up.
Do you know if there is consumer data on their perception of added versus the term "sugar".VOICE: We did not in our, our study ask that.
CHAIRMAN GARZA: Okay. There are a number of others that have questions and I may have stifled them. All right, caloric restriction may be a very adequate strategy for the next guideline and we're -- so Dr. Weinsier here, would you like to go on then and over on to the next one?
DR. WEINSIER: Since the attention span is --
CHAIRMAN GARZA: You need to either -- there should be either a --
DR. WEINSIER: Is that on now? Yeah.
Okay, I think I can shorten this considerably. Some of the issues that were raised, before I get into this category, and I say "raised" by some people that spoke yesterday, letters that we've gotten, comments made within and outside of our committee, basically focusing on four areas of concern or suggestion. One was the title; second was the etiology of obesity, and should we address this in this guideline; third, the methods, methods for assessment of body fat and methods for assessment of body composition or body fat distribution; and, fourth, emphasis on physical activity.
Basically, the working group consist of Rachel Johnson, Shiriki, Joan, Kathryn, myself. The general considerations in our working model was to look at new evidence 1995, focus on general concepts to be emphasized, recommendations should be appropriate for the population at large rather than too prescriptive, and this is a though one for us, and then information should obviously be practical for dealing with the public at large.
In terms of the first issue and concerns that were expressed, the title has raised a number of questions. this is one possibility, but others have been suggested. The previous title was "Balance the food you eat with physical activity, maintain or improve your weight." Apparently the word "improve" in focus groups has given people pause and concern because apparently the definition of "improve" is not clear. Does that mean gain weight? Or other issues have been raised, but it was not clear.
A second issue that's come up, and I'm not sure it's addressed in this proposed title, is the word "Balance the food you eat with physical activity." The implication for some has been, well, I'm heavy, but I'm balancing the food I eat with my activity, so I'm doing what I should do when it should be "imbalanced" at that point. So I'm not sure that this deals with it, but we're open to suggestions.
One that has been proposed is more focused, simply "Achieve a healthy body weight." The word "healthy," our committee seem to fee fairly comfortable as a word we might want to have repeatedly within the guideline.
In terms of areas of new evidence, actually I was going to go into some detail on this, but I'm going to skip probably a fairly large number of overheads and discussion and simply come back and give you a feeling here of one way we might want to deal with this.
But the other things we need to look on, I think there are new data that we need to consider in terms of methodologies for measuring percent body fat or body fat, as well as distribution. We need to look at the relationship of fatness; the fat pattern medical risk, we have new information here; the guidelines, as before, who should lose weight probably should be retained. In terms of weight loss goal, we may want to rethink this a little bit in terms of weight loss approach, eating pattern and physical activity may just need some tweaking and not major changes.
With regard to the first, that is, the etiology, just allow me to skip way ahead, and if you really feel strongly, I'll come back and discuss these. I think it's a very important area, but it may not be necessary for our discussing right now.
The reason they came up, at least as I understand that it came up is that there is concern that the public has a feeling that with so much emphasis on the genetics of obesity certainly in recent years, since '95 when the OB gene was discovered, that there is a perception that it is now really out of our control for many of us. It's in our genes or it's not in our genes. If it is, then it's not a modifiable factor. This was raised -- this concern was raised to me by Dr. Goldman, the editor of the Annals of Internal Medicine, just several weeks ago when he expressed concern that of his 100,000 readership, he feels strongly that a vast majority of them -- these are medical folks -- fee that obesity is determined by genes and therefore it's not modifiable.
So jumping past all the data on one side and the other, one thing we might consider on the basis of my understanding of the literature is that there are non-modifiable genetic influences. I mean, this is absolutely a given. I think the data is absolutely solid that there are genetic influences and there are certainly variations of energy requirements, which you can say are inherent, perhaps genetically determined, plus we have the changing environment and these pose challenges for weight control.
But it still appears that for the general population weight changes are determined, underline the word "determined," not by our genes or environment, but the causative or cause/effect relationship is based upon the behaviors. And so I think we have thee flexibility and should try to encourage the readership of the guidelines that it may be difficult, but we still have modifiable behaviors that are still under our control, so you may want to come back and discuss that, make suggestions to our committee, but that's the approach that we're currently taking.
Methods to assess body fatness, we do have some new guidelines. The BMI seems to be useful for categorizing degrees of obesity and the association of health risk. Proposed recommendations based upon the WHO and the NIH reports, the NHLBR report suggest these guidelines for normal. They used the term "normal." We suggest the possibility of substituting "healthy weight" as the BMI, these numbers proposed overweight, the number here proposed, and obesity greater than 30 kilograms squared.
It's also been suggested the NHLBR guidelines, that the same BMI cutoff for obesity is justified for all gender and race groups.
So our suggestive revision is, without showing you a picture of it, but the last, the '95 guidelines based on weight for height, it was like several graded areas that you could trace your weight for your height. One consideration is to perhaps use the BMI, the Body Mass Index, rather than weight for height based upon the newer reports.
With regard to health risk and the other parameter, assessment of body fat pattern, the BMI appears to be associative of increasing health risk in a graded fashion, so we have to be careful that when we talk about BMIs and cutoffs that the interpretation is not that if my BMI is 24.9, I am perfectly healthy. If mine is 25.1, I've got real problems; that it is a graded association.
Waist circumference appears to be an independent risk factor, at least up to actually a BMI of 35, for various disease, including cardiovascular disease, diabetes, hypertension. So there is good reason to consider in the guidelines giving the public information about how to assess waist circumference as well as BMI.
Since body fat pattern is determined in part by modifiable risk factors, such as exercise reported in this study in '95, waist circumference is to some extent modifiable, so this has to be taken into account. If it's not modifiable, maybe we shouldn't push this on the public. But on the basis that it may well be modifiable, then we should consider focusing on waist circumference as another measure.
In contrast to BMI, waist circumference cutoffs differ between genders, so this does have to be taken into account. So in our revision we may want to consider using the waist circumference -- previously it was the weight to height ratio -- excuse me, waist to hip ratio -- consider using waist circumference as a reference replacing the WHR.
And we might want to consider a table such as this or a box such as this. It's based upon the NHLBI clinical guidelines report. We might want to substitute the word "healthy" for "normal" BMI. We may want to consider rounding off a number here to make it consistent, but these are things that need to be discussed. But basically the point is that to figure out -- to estimate your weight status and risk of disease, to give some guidance in terms of what your BMI is, how to measure it, and where the waist circumference fits in to figuring out your relative risk of disease.
And in terms of controlling weight, who should lose weight, it's important that, as in the previous guideline, that we emphasize that not everyone, you know, has to lose weight. And the BMI is greater than or equal to 25, that in itself may not be an indication that medically the person needs to lose weight. However, if the BMI is greater than 25, the data do suggest that we consider looking for a BC-related considerations. As well, if the waist circumference is greater than 88 in women or greater than 102 in men, we look for obesity-related conditions.
Our suggested revision maybe include a reference table about who should lose weight and try to emphasize the distinctions of who should and who should not lose weight, and I won't read all of this now, but this is an example of what a box might look like in terms of who should lose weight. The main point, regardless of the wording, is that you may not need to lose weight even if you are in the overweight category, i.e., a BMI greater than 25, or between 25 and 29.9, or even if your waist circumference has increased, i.e., greater than 35 for women or 40 inches for men, however, risk factors should be assessed and then perhaps have some guidelines for who should consider losing weight based upon BMI, waist circumference, number of risk factors.
Now, in terms of how to go about it, i.e., what are some reasonable guidelines for the weight control or achieving a healthy weight, the previous guidelines emphasized the five to 10 percent weight loss. By weight loss of five to 10 percent can reduce but may not eliminate co-morbid conditions.
One thing to consider and this is, in part, based upon the NHLBI report, but also more recent, the CLEM report, looking at the registry of individuals who have lost significant amounts of weight and kept it off for an average of five years, is that medical risk is assumed to be maximally improved by achieving a normal body weight. So if we're talking about maximal improvement, then the guideline should be achieve a normal body weight. Thus, the ultimate goal might be to achieve what we're calling a healthy or normal body weight rather than leaving the impression that five to 10 percent takes care of it. It's a good initial goal, but we need to think about the wording and consider whether we want to emphasize normal weight because it's a goal that most people will probably not achieve.
Does that mean it should be taken out of the guidelines or do we want to leave it in? Weight reduction can improve health, the ability to function and quality of life for overweight or obese individuals at any age, so age is a consideration to think about in this guideline, certainly for the elderly population or the older adult population.
The suggested revision, five to 10 percent, is an appropriate initial goal, ultimate goal, a healthy body weight is something we may want to consider.
In terms of dietary pattern for weight control, there are some data that have been published since 1995 that we probably want to consider. They come out -- they come from the same group. Bell and Barbara Rolls are both at Penn State. But these studies are meticulously conducted, at least in my view, and are compelling in terms of short-term control of energy intake. Anyway, the data suggests that energy intake is determined more by the volume and the weight of the food consumed rather than the fat content. these studies, as I say, were very carefully conducted. Lower energy intake occurs spontaneously with use of the lower energy dense food. Reducing dietary fat alone without reducing calories is not sufficient for weight loss.
So just taking account of some of this data, most of it new, some of it not so new, we may want to consider the possibility of giving guidelines that relate to the foods at the base of the pyramid; that is, the whole grain foods, the plant foods, vegetables and fruits, which are going to be relatively low in energy density, and at least in the short term, seem to be a primary determinant of energy intake.
Above findings are consistent with emphasis on intake of foods at the bottom of the pyramid, as I say, which are low in energy density and fat content.
Suggested revisions: The 1995 guidelines are primarily focused, at least in my view, on negative advice. There were six of seven on one box given, six of seven at the advice statements were negative in the sense that they're saying "eat less....", "eat smaller...", "eat without...", it's all things that we should not be doing, and I'd like to think through, if it's okay with the subcommittee and the entire committee, on ways to emphasize positive statements, perhaps by putting the emphasis on the majority of intake being derived from minimally processed whole grains and cereals, vegetables and fruits at the base of the pyramid, enabling advice for weight control which is positive as well as appropriate for overall health. So it's a consideration I'd like for us to remember.
And, finally, with regard to physical activity, physical activity benefits only modestly the weight loss. So in terms of inducing weight loss, I think it's pretty well documented it's not going to contribute a great deal. It does, however, improve cardiovascular fitness and it certainly appears to improve weight loss maintenance, may have a specific effect on decreasing abdominal and inter-abdominal fat.
Individual's success with long-term weight control, according to the Weight Loss Registry, have physical activity levels that are about three times that of the American College of Sports Medicine Recommendation. So those individuals who seem to be successful in achieving a large amount of weight loss and maintaining it for a long period of time seem to be more active than would be recommended by the American College of Sports Medicine.
In older adults, preserving strength is particularly important to reduce risk of falls and fractures.
So the bottom line, in terms of suggestive revisions we might want to consider, physical activity is an important part of a weight control program, being highly, and I highlighted the word "highly," highly active favors long-term success in overall health. We need to be thinking about where and how to emphasize "highly," not to mislead people that just becoming a little more active may healthier, may be more helpful, but, again it's like achieving a healthy weight versus a five to 10 percent intake. We try to set a goal a little bit higher which may not be realistic for most.
So that's basically the comments that I have based on the input from the committee. But, Shiriki, Rachel, please jump in.DR. JOHNSON: I just wanted to add that we did talk about children as well, and I think it's something we definitely need to include with obesity increasing at the rate that it is among American's children. And I know we talked about some behavioral things, primarily based on Leanne Burges' work on what happens when you coerce or force children to eat, and the negative impact that can have over the long term. So I'm hoping that we're going to be able to put some behavior tips for parents and caregivers related to children and really emphasize physical activity in regard to the pediatric population.
CHAIRMAN GARZA: Other comments or questions?
Meir?DR. STAMPFER: Yeah, I thought that was a really thoughtful and measured set of recommendations. I just had a few comments.
One was, in terms of the diet composition that promotes or doesn't promote weight loss, those studies, I agree, they're careful, but they are very short term. They are really based mostly on meals in terms of the energy density, and I think you can gain weight on just about anything that has calories, as long as you don't balance them, and I don't think the evidence for energy-dense foods as especially promoting weight gain or being against weight loss is very compelling.
My second point I think may be more important, the notion about should you try to lose weight when you're over a BMI of 25. I think our emphasis should be on prevention of these conditions, like blood pressure, adverse lipids and diabetes, and so I don't think we should tell people to wait until they have an adverse condition and then try to lose weight. It's much harder to lose weight than it is to maintain weight. So I think we should stress prevention, not waiting until these things.
I think just about anybody over 25, unless they are in a very unusual body builder type with a big muscle mass, is probably going to need to lose weight, and I think we should stress that there are exceptions, but most of those people by far should be losing weight, and they'll improve their lipids and their glucose tolerance and their blood pressure even before they reach a critical level where they need treatment.
Likewise, even people who are within, sort of at 24.8, some of those people ought to be losing weight too, depending on their lean body mass and so on, and I think there should be more emphasis on weight gain during -- trying to avoid weight gain during adult life. if you've gained weight from say age 20, on the average you're overweight, and the -- for most people the weight that you've gained is adipose.
So those are my two main comments.CHAIRMAN GARZA: Alice?
DR. LICHTENSTEIN: I have a comment on the wording of the guideline. It seems like the important point is to maintain or improve your weight. I'm wondering, there is a lot in that guideline, and, again, going back to the focus groups and what we know about perception, balance of food you eat with physical activity, as pointed out in the beginning, is a -- I mean, it can be interpreted a lot of different ways. I'm wondering if we consider just the -- you know, consider the wording, and that perhaps if the basic, the most important message is to maintain or improve your weight, that's what the guideline should say, and then the text should be more explicit regarding how to do it.
CHAIRMAN GARZA: Johanna?
DR. DWYER: Just two, two points.
The first is it would be helpful, I think, to include instead, if we're worried about space, a little formula to calculate BMI from inches and pounds, because it's clear that we're not going that track. It's also clear that most people do not know how to calculate this, and so it becomes a magic, yet another magic medicalized thing that we tell people.
The second thing is is the issue of the BMI drift, and the problem, certainly the same BMI for all gender and age groups may be appropriate for adults, but it's certainly, I don't think you would want to be including children in that BMI, would you?
Perhaps you would, but I don't think so from what I know serum cholesterol values at the 85th and 95th percentile are different and the believe the VMIs are too. So I think you need to reconsider that for kids over the age of two but under the age of 19.
I also would like to endorse Meir's suggestions with respect to the prevention. In terms of the treatment, we really do have to realize that where we are with this after 50 years is still with cure rates that are about the same as cancer of the stomach, right? Ten percent cure rates at five years. So we need to be, I think, modest in our promises to people about what we can do.CHAIRMAN GARZA: Richard?
DR. DECKELBAUM: Just one point, I think, that will help in terms of the genetic contribution of the argument. I don't think the gene pool in the United States has changed that much between NHANES I and NHANES III. Obesity is doubling and tripling in some populations and that's certainly a major argument, that there has been some other change besides genes.
I think if we look where we're going with the different risk factors and chronic diseases, this is the one where we have the greatest failure. I think I'm right, Paul, in that statement. And therefore, with the knowledge of coma morbidities and even obesity as an independent factor, it's the one that I really think as a group we must focus on in a very integrated fashion throughout the guidelines because it represents the greatest failure of, you know, risk factor control that's actually happening now in the United States.
And in doing so we have to have, I think, very careful integration throughout the related guidelines, and somewhere, either in the introduction or a variety or wherever it's going to be, in terms of, you know, pulling all the data together that we're hearing, we're hearing some of it. You know, if the science base is out there that kids who have a lot of sugar at lunch are going to eat more later on in the afternoon with their snacks and during the day, we really must gather that kind of evidence wherever we can, and we -- even -- we've really got to, I think, take this factor in terms of appetite control, because this is what we're really talking about, it's appetite control, and one of the factors that contribute to appetite control, and we've had very little of that at this meeting, but I think it's something I think we should be considering in our deliberations, and perhaps we can get someone to help us on that because we really -- there are people who know a lot about appetite control, but we have, except for very little, we've had very little discussion on it, but that's a major factor in the number of calories is how do you control your appetite.CHAIRMAN GARZA: Do you know of any data that relates -- measures appetite control to clinical outcomes?
I know the theory, but is it -- getting back to Meir's question, I mean, do we have any data that would give us any sense that this is related?DR. DECKELBAUM: I don't know. Again, this isn't my major field. There may be some things out there, but if you can just take -- take the big increase in soft drink consumption, which does have sort of simple sugars in it, and if there is some data on simple sugar consumption and appetite later during the day, it's something we should be considering even if -- even if the direct link isn't -- hasn't been made yet. Certainly if you look at cholesterol and heart -- cholesterol levels and heart disease, the initial links were made before the data was in, showing that lowering cholesterol, in fact, lower risk of heart disease.
CHAIRMAN GARZA: But the point I thought Meir was making is that the data are in there, at least people have looked in terms of looking for diet composition. I mean, they've looked for fat, they've looked for carbohydrates and not been able to link it because, in fact the idea is that you somehow compensate the following day. Is that --
DR. STAMPFER: My read of the long-term data is that diet composition isn't a terribly important predictor of weight gain or weight loss. But there are data on satiety and how you feel after a meal.
Now, linking that to obesity is logical, but I'm not aware of the data that's done that.CHAIRMAN GARZA: is it because of a lack of
then -- do you compensate the following day, and that's the dynamic that we don't have a good handle on.DR. GRUNDY: I wanted to say something about this eating out of the base of the pyramid. Let's say the pyramid, you know, if all of our food came in the form of little pyramids like Hershey's Kisses, and that's the way you said it, we'd just take a bite out of the bottom of those and throw away the top. And I think what I think we ought to do is to eat the whole thing, eat the whole pyramids, but just eat less of them. It wouldn't be eating the total diet, so I have a problem with that concept.
DR. WEINSIER: I may have misstated. I did not intend to say that the foods selected should be limited to the base of the pyramid. I didn't intend to say that. I was trying to imply --
DR. GRUNDY: I mean, the pyramid should be structured so that you eat the whole pyramid, right? That's what I'm saying?
DR. WEINSIER: Well, I look at it as a guideline to food selection. So if an individual is going through a smorgasbord line and they have to make choices, that in the back of their mind they've got this image of a pyramid where, I guess, most of the food on my plate should come from the grains, the fruits and vegetables, and then I have the option to choose some additional foods from the protein group, from the dairy group. So you've got some reference point at what to put on your plate as you're going through the cafeteria line.
Does that make sense?DR. GRUNDY: I have a feeling that in your case you'd never get to the top of the pyramid when you went through that line the way you describe it. I'm not saying that's bad, but I think our pyramid ought to be constructed in a way that most people eat the whole pyramid.
DR. WEINSIER: Well, that's what I said, I didn't mean to intend --
DR. GRUNDY: Yeah.
DR. WEINSIER: -- to exclude any food because I don't practice that when I treat patient.
CHAIRMAN GARZA: Before we continue with a discussion, let me tell you what's being passed around. You have the menu. Please put your initials by whatever you want. Then I want to reassure the transcriber that we are going to take a 20-minute break at the end of this discussion and that will give everybody a chance, give them a chance to rest up a bit and you a chance to stand up and stretch. But I want these filled out, otherwise, you may not get your food in a timely manner. So do that as we speak, okay?
Johanna, then Suzanne.DR. DWYER: Richard, just back to your intriguing remarks. I was trying to remember, and perhaps someone in the audience or at the table knows of the study. This was a study that we done at your institution in the early 1970s by a wonderful investigator who died prematurely by the name of Kathy Porocoust, and she did this study with Tadbee in Italy, and it was one of the few, as I remember, long-term studies of regulation of food intake over months rather than weeks.
Barbara Roll's study, as Dr. Stampfer has pointed out, are acute studies. They are not as long as that.
And as I remember, the results were not very compelling. The results were compelling but the effects were very small. But I may be wrong and it's in your library some place.CHAIRMAN GARZA: There are the Labinsky studies as well for three months, and there are some longer term studies.
DR. JOHNSON: I just had a couple of points. I wanted to follow up on Johanna and Meir's plea for an emphasis on prevention. I agree with that, and I think what I would like to see us really emphasize is physical activity and some behavioral tips that are commonly used in behavioral weight control programs, and with some particular emphasis on portion sizes.
I think we also need to be careful about the definition of "healthy," because if you recall when the NIH guidelines came out they were broadly misinterpreted in the media to say that anyone with a BMI over 25 needed to lose weight, and that's not what they say. They say a BMI between 25 and 29, with two additional risk factors. There is going to be a lot of debate about what is healthy if we come out and define that.
I mean, if we're going to define over 25 as not healthy, we need to be on very firm footing, I think.
Shiriki, you were on that NIH panel, weren't
you --DR. KUMANYIKA: Um-hmm.
DR. JOHNSON: -- for the weight guidelines, so maybe you could help us out there.
CHAIRMAN GARZA: Hold on, let me ask -- let me ask Suzanne because she's been trying to get in a comment.
DR. MURPHY: If it's directly related to what Rachel just said, go ahead.
I too want to chime in about physical activity. I think that is the biggest purpose of this guideline, and all the weight discussion in the world should take second place to focusing on physical activity.
I also wanted to ask maybe somebody who knows more about the chart than I do that's in Figure 3, I had always thought that was calculated based on a BMI of 25, 30, et cetera. Is that true?
And in that case, isn't that much easier for consumers than giving them a formula? Why wouldn't you just keep Figure 3 the way it is?MS. MEYERS: It was actually calculated with a simple Excel spreadsheet.
CHAIRMAN GARZA: If you track back, it comes out to the same BMIs, is that what you're saying, Linda?
DR. KUMANYIKA: What did you think it was based on? I notice when you were saying, I had the feeling that you thought this was based on something?
DR. MURPHY: He said height for weight.
DR. WEINSIER: Yeah, weight for height, but not weight of height squared.
DR. MURPHY: Okay.
DR. LICHTENSTEIN: That last two guidelines have basically taken BMI cutoffs and converted them to weight for eight squared for the table.
DR. MURPHY: I think anything we can do to simplify these things for the readers is great. And along that line, there is also a statement about if their waist is bigger than your hip, you need to worry. I like that sort of easily implemented approach. It may not be theoretically quite a correct as giving them the centimeters, but it sure is a lot easier for people to understand.
DR. STAMPFER: I just wanted to respond to Rachel. I think, you know, for a cutoff of 25, I think that's basically what the current WHO cutoff is as defining a desirable weight. And I think there is just plenty of data to support that. I don't think we're on thin ice at all to use a 25 cutoff. There is just lots of data out there for diabetes and blood pressure and other risk factors, mortality. I think we're quite comfortable on that.
DR. KUMANYIKA: I didn't hear all of your comment. You asked me -- what were you suggesting instead?
DR. JOHNSON: Well, when the NIH guidelines came out, my understanding of the interpretation is they don't say everyone with a BMI over 25 needs to lose weight; that between 25 and 29, they say with two additional risk factors.
Am I not interpreting that correctly?DR. KUMANYIKA: NO, it -- but it says that they are overweight, and it says that that's a window of concern and that that's a -- should be trying not to gain anymore weight. Those are clinical guidelines meant for people to really talk to individuals, and what's factored in there is that the person may not want to lose weight. And so I think that I agree basically with the 25 mention there because it is first level of concern about weight. It's just that what a clinician does with that person may vary depending on their --
DR. JOHNSON: See, you're comfortable with saying that everything over 25 is not a healthy weight. If you say anything under 25 is healthy, the implication is that anything over 25 is not healthy.
DR. KUMANYIKA: Well one of the DJAC report from 1995 also had a list of BMI range, which was based on BMI 25, and all that made it into the final booklet was the chart, but this chart is based on a BMI of 25, which was somewhat controversial at the time for people who had noticed it, and then it showed the gradation, and probably not on -- I'm not sure now, Linda probably knows where the shading changes, if it changes at 32 or 30.
But I think the point was that, yeah, once you're over 25, you should pay more attention to your weight than below, than below 25, so I would change it from 25, but also change the 1995 dietary guidelines.CHAIRMAN GARZA: Johanna.
DR. DWYER: Just two things.
One is i didn't hear anything with aging, so it's going to be flat for aging.
And secondly, I don't think we -- something needs to be said about the appetite suppressing drugs. One is on the market, one was withdrawn from the market, and a third is hoping again to go on the market. It seems to me to simply ignore it, you can't.CHAIRMAN GARZA: All right. On that rather controversial note.
DR. LICHTENSTEIN: Well, I would point out those are prescription drugs.
DR. DWYER: Right.
DR. LICHTENSTEIN: So it's not that it -- so there are other issues.
Just on the comment that Rachel made. Desirable, healthy, what's the word? Because if it's a desirable weight, then it doesn't sound so bad if you're above or below 25.DR. JOHNSON: Well, I just know we will get arguments. I mean, if you want controversy, we'll get arguments from people who say that if your blood pressure is normal and you don't have diabetes, then all these other things, and your BMI is 27, are you unhealthy.
CHAIRMAN GARZA: Scott.
DR. GRUNDY: I think we have to be quite careful about that BMI of 25. You know, when that NHLBI guideline came out, we got a tremendous amount of flack about that from people who were saying that a lot of healthy, young men have BMIs above 25 and they're not overweight and are not obese, and that is very true.
And my argument in defense of that was that was like you said, Shiriki, a clinical guideline, and it's one in which physicians can look at the patient and say something about it.
Now, it's true that probably 90 percent of people whose BMI is over 25 are overweight, but there has to be some caveat in there that there will be some people who are not over -- are not obese or have too much total body fat at a BMI of 25.CHAIRMAN GARZA: Shiriki?
DR. KUMANYIKA: I'm going to try to look at the aging literature again and see if we know how the wording should be for older people. It's not -- it's not easy to figure out what wording there is. We weren't thinking about changing the guidelines, but we want to have language there.
I think, even though I've been participating in getting things to this point, I still have a feeling that this guideline is missing something that consumers need, so I just wanted to say that. I had actually mentioned to Roland before he presented that we might be so bold as to consider a separate guideline for physical activity and allow this one to be more of a "how do you eat to manage your weight," because as I look through what we have in the old version, and probably the new one, it's just like even the box that you wanted to fix about what you could eat, if you look at Box 6, it really doesn't say you have to eat less food except in the most subtle -- I mean, it just doesn't say that. And I think that this issue of portion sizes that someone mentioned, to become much more specific in terms of the fact that the size of a container is not the size of a portion. It would really help consumers understand where all the extra food is coming from, and to mention that weight has gone up in the population, and try to get that prevention message a little stronger.
And this one, we've talked about this, it still feels more clinical than it could be for the purpose of a dietary guidelines, and the question is what should be added. And I think, Mary, your comment about making the prevention message stronger would be a place to start, and I think also talking more about what to eat, how to eat as opposed to only the losing weight, which is a weight control guideline, but it minimizes -- it minimizes food.CHAIRMAN GARZA: The only other issue that I have not heard anyone raise, and probably would want to include in the secretary's report, is if there is any new data on the consequences of losing and gaining weight, because that was one of the -- I think if I think back on the two, two principal drivers that ended up with the wording that in fact many have criticized as being awkward was the point that Johanna raised that in fact the success rate of losing weight and keeping it off looks so low that if we focused on achieving a healthy weight, that we were going to be asking half of the population, given the percent that's overweight, to constantly be losing and gaining and losing and gaining because we know that so few gain -- or rather, lose and keep it off.
So we probably would have to update that database to say has yo-yo dieting --DR. WEINSIER: But this was addressed fairly recently. Van, what was the date of or NIDDK report on weight cycling? But it was within the last two years that there's basically a data --
CHAIRMAN GARZA: No, I was saying included in
our -- I'm not saying it hasn't been reviewed.VOICE: There is no other -- there is no newer data out.
CHAIRMAN GARZA: Right, it's since '95.
DR. WEINSIER: Yeah.
CHAIRMAN GARZA: What we need to do is include that consensus document or the evidence that led to that. That's the one piece that I saw was missing. There might be others.
DR. LICHTENSTEIN: How does that compare, losing/gaining, losing/gaining, how does that compare to gaining/gaining/gaining? Is there any evidence -- no, with all seriousness, is there any --
DR. WEINSIER: No, that's never an option. It is either maintained -- that was how the issue of maintaining your weight got there.
DR. LICHTENSTEIN: Oh, I understand that, but I guess what I'm concerned about is that in taking the people that gain/lose, gain/lose, what would happen if they were advised not to do that?
CHAIRMAN GARZA: The guideline was crafted in a way that would say, look, you have to focus peoples' attention, focus their attention on at least maintaining their weight and not gaining any more weight rather than focusing their attention on losing weight -- this is a bad pun because we know that's a losing proposition.
DR. GRUNDY: I would like to raise a point that Shiriki brought up and expand on it, and ask whether it's possible to associate physical activity here in these guidelines from body weight?
There are so many other advantages of physical activity that go beyond body weight, and, in fact, you know, you can eat in a minute what you can run off in three hours. So, you know, there has -- it's not the solution to the obesity problem, but it is a solution to a lot of other problems that we have. I mean, I don't know whether this is out of our purview or not to get into putting that in as a separate thing, but to highlight it as a separate valuable thing for health, you know, I think you could make a strong argument for that.
Is that going to be something we could do?CHAIRMAN GARZA: Well, we could consider it.
DR. GRUNDY: Yeah.
CHAIRMAN GARZA: I mean, the issue of whether or not divorcing it from the diet fall under purview is something that we need to think about carefully.
DR. GRUNDY: It would be divorced from the diet entirely if you made it a separate item, but that it would have benefit on a lot of other risk factors that relate to diet beyond body weight, that's what I'm saying.
CHAIRMAN GARZA: I have to agree with -- I mean, I think this is -- physical activity is a major issue that we can't afford to overlook, and how we deal with it, either with a separate guideline or strengthening the present guideline, I mean, is something the group can certainly come back. Either choice is available to us.
DR. JOHNSON: I had a discussion with Allison Yates about the macro nutrients in the DRIs which I thought was very interesting that may shed some light on this, and she was saying that when you look at the DRI for energy, we know from doubly labeled water energy expenditure data that expenditures are lower than current recommendations.
The problem is if you get the recommendations down to low, you can't easily meet micro nutrient needs, so there may be sort of a paradigm shift where we need to look at what do we need to get our activity levels up to in order to be physically active enough that we can balance that with an energy intake that we can reasonably meet our nutrient needs at, so I think that just adds strength to the argument to really emphasize activity.CHAIRMAN GARZA: Alice and then Meir.
DR. LICHTENSTEIN: Just to get back to the point about emphasis on maintaining, I think it should also be on prevention in children; that there may be even a separate section on that because that seems to be where some of the problem is starting.
CHAIRMAN GARZA: We will give you the last word and then we'll break. I'm sure the transcribers will be very grateful for that.
DR. STAMPFER: Just to second the thoughts on the physical activity. Scott and I were talking in the hall and he was pointing out that caloric intake in China is substantially higher than it is here even though their typical BMIs are 20 or 21 due to physical activity.
And I think I agree with you, Scott, that it's not the solution to losing weight, but I think it is either the solution or it's necessary but not sufficient for maintaining weight loss, and those few 10 percent that do succeed several studies have shown that it's with physical activity.
So I think it's pretty intrinsically bound in --DR. GRUNDY: I'm not denigrating it's role in that regard, but I think it has so many other damages beyond weight control that it might deserve a separate identity.
DR. STAMPFER: Thereby linking it solely on weight control.
CHAIRMAN GARZA: All right, well, then, let's try to convene at 1:20. And if your sandwich has arrived, you can start eating it before then. But if not, we will eat after we convene.
(Whereupon, at 12:55 p.m., the meeting was recessed, to reconvene at 1:20 p.m., this same day, Tuesday, March 9, 1999.)
A F T E R N O O N S E S S I O N
(1:35 p.m.)DR. GRUNDY: Okay, what I would like to do while you're eating your low fat meal is to just say a few words briefly about the summary of our recommendations, and then we can open this up for discussion. I would also like to thank Kathryn McMurray, who helped so much and helped putting this together. And after I make a few comments, then Alice and Richard will also say something, and Meir also wanted to comment on trans fatty acids.
If you look in quantitative terms, look at the numbers, I don't think the recommendations that we come up with are going to be a lot different than they were before, but there clearly is going to be some difference in emphasis if we follow the recommendations that we've outlined here, and that's what I would like to go through with you briefly.
And if you have that before you what our summary is, you can see that the priority of the recommendations are saturated fat and dietary cholesterol and trans fat, and then percent of energy from fat.
In the previous guidelines, it started out to chose a diet low in fat, then saturated fat and cholesterol, but we feel that if you take a look at the scientific evidence, we are stronger on saturated fat than percent of energy from fat or a diet low in fat, if that implies a low percentage of fat.
So we think the guidelines should emphasize saturated fat for chronic disease, coronary heart disease and stroke, and this link is primarily through the effect of saturated fats to raise cholesterol levels and promote arteriosclerosis, and there is a broad base of evidence to support that recommendation, which I think most of you are familiar with. And we felt that dietary quantities of saturated fat should be less than 10 percent of calories.
Now, dietary cholesterol intakes, currently the recommendations have been on the books for a long time for most groups in this country have been for dietary cholesterol intakes of less than 300 milligrams per day. As we read the data in this area, we think that still is a reasonable recommendation.
We heard yesterday some evidence that dietary cholesterol may have less effect than we may have thought in the past, and I think it is quite clear that the effects of dietary cholesterol in humans is not as great as it is in animals on raising the plasma cholesterol level. But, in our view, to some extent the quantitative effect depends on the way you analyze the data, and which studies that you take for analysis.
There have been a large number of studies in this field that are not terribly well controlled, and then are some tightly controlled metabolic studies. And if you rely more on the carefully done metabolic studies, you will see a somewhat greater increment in cholesterol levels in plasma than what Don McNamara showed yesterday, but clearly the effect is not great. But if you add it all up, say going between 300 and 500 milligrams of cholesterol like it used to be, in our view that would raise cholesterol levels by about six to eight milligram per DL, which, I think, is not trivial.
It also might be noted that we had a decline in cholesterol levels in the population in the past 20 years or so, and that has paralleled a reduction in dietary cholesterol intake. In fact, the decrease in dietary cholesterol may be the major factor, not the only factor, but perhaps the major factor contributing to the decline in cholesterol levels in the population. We can't be sure of that but the data are consistent with the metabolic studies.
Now, we also recommended that trans fats should be mentioned in the text under the saturated fats section. Now, there might be one view, and maybe Meir would espouse that view that trans fats should be listed as a separate category separate from saturated fat. You know, that's somewhat controversial and can be discussed. I think it was the view of our group that the trans fat probably has about the same effect as saturated fat, but the total intake is quite a bit less, and therefore it might be contained under the recommendation for saturated fat and sort of lumped together as saturated fat and trans fat in some way which we'll have to discuss. This is not to minimize the importance of trans fat because it clearly raises cholesterol levels in the same way as saturated fat.
Now, we thought that total energy intake should be discussed in terms of the -- total fat intake in terms of total energy intake, including carbohydrates. Now, this is, in our view, would be a major shift, a paradigm shift for the guidelines. But it seemed to us from reviewing the literature that a case cannot be made for a very low fat diet or a low fat diet being a major factor responsible for obesity or for control of obesity in the population, and it may be a more balanced recommendation to include those together and to emphasize for the public the need to curtail intake of total calories, whatever their source, both to prevent the development of obesity and to reduce excess body weight, and I'm sure that will be an interesting point for discussion.
For unsaturated fatty acids, we really didn't differentiate between the monounsaturated and the polices. The more recent data may give a new lease on life to polies, although probably in practical terms polyunsaturates may be pretty much at the maximum intake available -- that is possible now. But in any case, we put those together for simplicity and called the unsaturated fatty acids, and we recognize that they don't lower serum cholesterol levels and they should be limited to maintain appropriate energy levels. But I think at the same time they do represent an important source of calories and one that should not necessarily be targeted for reduction preferentially.
Among the omega 3 fatty acids are complicated and we didn't get into those too much, and maybe it's not necessary in these guidelines to emphasize those particularly. Their intakes currently are low and the appropriate intake is not clear.
We also thought it was important to emphasize foods rather than fat per se as sources of particular fatty acids. The discussion of nuts this morning was a good example of that. These are rich in unsaturated fatty acids, and it was pointed out how they may be a useful component of the diet, and that's one way that we might emphasize foods rather than particular fatty acids.
I think those -- well, perhaps one other recommendation. We thought they should focus on individuals and not populations, and that's the aim of the guidelines is for individuals, and that's been a subject of some confusion in the past.
There also needs to be some consideration for children. There was emphasis given in the previous guideline, I believe, for children under age two with regard to dietary fat, but I believe Richard wants to make a case for perhaps cutting that out of this particular guidelines and making a more general statement for children.
Now, perhaps Alice might want to say something and then Richard, and then we could open, and Meir, and then have a discussion.DR. LICHTENSTEIN: My comments actually are going to be limited to omega 3 fatty acids and fish that I think there may be some reason to include a recommendation that fish be consumed, even on a weekly basis, something like that, because I think there is epidemiological evidence to support a relationship between decreased incidence of cardiovascular disease and fish consumption.
I think there is some clinical data to support it, that levels of omega 3 fatty acids in red blood cells correlate inversely with risk of sudden death after a heart attack, and that there is some work on a more basic level suggesting there omega 3 fatty acids may be involved with arrhythmias, heart arrhythmias.
I also think a recommendation like that is not particularly radical and also would be consistent with some of the other recommendations because recommending something like fish would most likely displace other types of foods that will be high in saturated fats. So do something for consideration. I think that the amount of evidence has increased between 1995 and now with regard to that point.
Otherwise, I totally concur.DR. GRUNDY: Richard.
DR. DECKELBAUM: Just a short comment on children. I think in the previous guidelines it was written that children between the ages of two and five should gradually adopt a diet to what would meet 30 percent whole fat and 10 percent saturated fat.
I think that, you know, in terms of implementation, we're spending a lot of time on implementation, it's hard to give guidelines for gradual implementation, and I think the good news is that there is certainly new data since the previous guidelines have been published showing the safety of diets that are moderate in fat, 30 percent or even lower, and there is the DISK studies, a number of papers which are in older children, but something that's ongoing right now is the -- which is outside of the United States, but it's quite an exciting study. It's the STRIP study, and I can't remember exactly what it stands for. Meir, do you want to -- but in this study, this is children in Finland, a relatively large cohort. I think about 2,000 who were randomized after leaning to a low fat diet, which is about 28 - 29 percent, about 28 percent total fat, and low in saturated fat as well by nutritional guidance compared to the normal control, some other kind of guidance.
And now the initial STRIP cohorts are about five and six years old, and they've done a lot of work on not only lipid levels with the experimental group with the low fat group, but quite important data has been accumulated to show that there is absolutely no adverse effects on cognitive or other development signs, so that these are kids who were getting 27 to 29 percent fat beginning at the age of, depending on when weaning is, four to seven months, and there is no adverse effects and outcome.
And I know that they have some unpublished data which is actually quite exciting with regards to how the prevalence of obesity in five - six year olds, depending on what group they were in. I don't have the data, but you can guess.
So I would just encourage that you pretty much go with the concept that children over the age of two can pretty much follow the rest of the guideline for fat, and I don't think there needs to be any qualifiers for children over the age of two.
Under the age of two, I'm not sure that's within the charge of the USDA, so that I think we would just stay away from it and not include it as part of our mission.DR. GRUNDY: Okay, Meir.
DR. STAMPFER: It's part of the USDA but it's not part of this committee.
CHAIRMAN GARZA: While Meir is going to get up to the table, I can brief you on at least the way that language that Richard was referring to came into the guideline was the sense that it was not safe, and there were some of us on the committee that argued that, in fact, couldn't understand the lack of safety given the normal weaning pattern. So the data are not very surprising, but it was in the end a compromise among those on the committee who felt that extending those fat guidelines to the age of two was not a problem, and those who felt very strongly than, in fact, that might have been -- I think they were concerned we would be stumping children and also causing cognitive problems.
DR. DECKELBAUM: I just want to add one thing and this comes up repeatedly in terms of kids and children over the age of two. I don't think there is anyone who promotes these moderate fat intakes who says to achieve this that dairy products should be excluded, so that these guidelines do not mean decrease in the intake of dairy products in children. What they do mean though is encouragement of low fat dairy products.
DR. LICHTENSTEIN: Can I talk about children just --
CHAIRMAN GARZA: Well, go ahead and then we will go to Meir.
DR. LICHTENSTEIN: Okay. That I think also that Richard's proposal is very reasonable because now that the school lunch program, so that when the kids hit school at age five, they're adhering to the recommendations of less than 30 percent, less than 10 percent saturated fats. So there is no phase-in at that point.
DR. STAMPFER: Yes, I just wanted to say a couple of words about trans. Trans is unique because not only does it raise LDL but it lowers HDL, and we haven't talked much about HDL, and I guess there is some degree of controversy over how much causality to attribute to HDL, but it's certainly a very strong predictor. The higher HDL is associated with lower risk of heart disease. So something in the diet that does both bad things, raising LDL and lowering HDL, we have to be very cautious.
This is a summary by Alberto Escharia, and it's a figure from a paper that's under review that I will distribute to the people around the table and ask that you don't pass it around because it's not published. But this summarizes all the studies that have compared saturated fat with trans on the impact on the LDL to HDL ratio, and what one finds is that trans is about twice as bad as saturated fat is in terms of this ratio. Both saturated and trans raise LDL, but because trans also lowers HDL, it has a much worse impact.
Now, the second point is that the increase in risk associated with trans is actually higher than what you would predict just based on the lipid changes in the epidemiologic studies. For example, this is from the nurses, and admittedly this is just one study, but the bottom bar here projects what the change in risk would be if the two percent of energy from trans were replaced with two percent of energy from unsaturated fat, and it basically cuts the risk approximately in half, which is far more than you would predict based on the lipid levels. And this makes sense biologically because trans can interfere with the metabolism of essential fatty acids.
Two final points: One is that the natural replacement of trans is polyunsaturated fats, which are beneficial, and the clinical trials that have shown a benefit of lowering saturated fat by replacing with polies have shown benefit in contrast to the clinical trials that just reduce fat.
And the final point is that this easy to do because a lot of the trans that we get comes from manufactured product, baked goods, and fast food, fried food, and there are replacements that are available at higher cost but not astronomically higher cost. Trans is basically pretty much being phased out in Europe. We can do it here in the U.S., so that consumers can reap a dietary benefit with very little effort on their part.
And also just to make a second to what Alice was saying about the omega 3's. I think that's another point that we should consider, whether the data is strong enough to emphasize. I think that they are strong enough to mention.DR. GRUNDY: What kind of a recommendation would you make for omega 3, that they are strong enough? I didn't quite understand what you were saying there.
DR. STAMPFER: Whether we should distinguish that from just unsaturated fats is all.
DR. GRUNDY: You think we should?
DR. STAMPFER: I think we should talk about it.
DR. GRUNDY: Okay. Are you going to lead the -- yes.
DR. LICHTENSTEIN: I would like to say something about the trans fatty acid issue.
I don't agree that we should put a lot of emphasis on trans fatty acids for a couple of reasons. Although the epidemiological data does so, an association with a greater risk with trans fatty acids as opposed to saturated fatty acids, the clinical data doesn't necessarily support that because there have been two very extensive studies on trans fatty acids and blood clotting, and they both turned out to be negative. There have been two studies published on trans fatty acids and acceptability of LDL toxidation. However, we feel that should be taken into consideration and those are negative.
So although there is some -- or no effect. And although there is some basic work suggesting an effect of trans fatty acids on essential fatty acid metabolism, there has been no biochemical abnormality or change to date that's actually been associated with it, but I guess my concern is that right now it's been estimated that the trans fatty acid intake in the U.S. is about 2.2 percent energy intake whereas the saturates is about 12 to 14, but we're not near where the goal of 10 percent was set years ago.
And I think that there is not too much room for play as far as discretion goes in trans fatty acid intake of individuals. I think the food supply is going more towards lower in trans fatty acids, and I certainly agree that the impact of trans fatty acids on LDL cholesterol is similar to saturated fatty acids, whereas saturated fatty acids do raise HDL. I think trans may not quite lower them but have no effect so that the ratio is a little bit worse, but I think when you look at the relative portion of intake in the U.S. diet and what the impact of the message has, I would hate to see a lot of focus on trans and lose the focus on sats. whereas I think we can make the most or the biggest impact if we could get saturated fat intake lowered, the biggest impact on risk for cardiovascular disease.CHAIRMAN GARZA: Any other questions or comments from the group?
Go ahead.DR. DWYER: I thank Scott for his presentation. i share, with less knowledge from direct experimental work, Alice's concerns about trans, over-emphasizing it and not just sort of lumping it under saturated.
What I wasn't clear about, however, Scott, and I wanted a little more from the committee is it seems awfully heavily weighted to cardiovascular coronary heart disease end points. And on the total issue, it would seem to me there might be reason to focus on other issues as well as those.
So I find the second page of the possible way to go a little coy. If there is a way to -- one of the biggest randomized trials in the world is now being carried out with American postmenopausal women on dietary fat, total fat. It might be worth us at least reviewing the reasons for putting that particular intervention into the -- into the study, the Women's Health Initiative. I realize that we heard one presentation this morning that suggested, well, maybe 10 years later they wouldn't have done it or he wouldn't have done it. But these recommendations are extant both from the National Academy of Sciences for low fat and also they are now in play in a very large clinical trial, and wondered if perhaps those concerns might be better reflected by a little broader approach.DR. GRUNDY: I think we're certainly aware of the issue, and, you know, maybe we didn't highlight it adequately for the whole, total fat discussion. I think that the evidence that was presented today was pretty much the way our committee read the evidence; that certainly when we're talking about 30 percent fat in the diet, that is a moderate to relatively low fat intake, and in a way it was where we put the emphasis.
One of our concerns, I guess, had to do more with the obesity issue than it did with the cancer issue, which, you know, I think is a little problematic. But the obesity area, it seems like that maybe our emphasis on low percentage of at may have backfired on us, and that perhaps we would be wiser to go forth with a message that was across the board calories rather than just emphasizing fat. if we stick with the 30 percent fat recommendation, that ought to be adequate to lead to a good body weight if people would pay attention to their diet and control all the components in the diet. So I guess that we thought the obesity thing was perhaps a little more in the fore in this regard than the cancer issue.
Now, also, from what we have heard and seen from the literature about the cancer issue is that saturate fat seemed to rise to the top among the different components of the fat story that led to the cancer. So there again by reducing saturated fat the evidence seemed to point more towards saturated fat than it did total fat, so that was another reason, I guess, but maybe we didn't articulate that adequately. Maybe you don't even disagree with that conclusion either but --DR. DWYER: No, I don't disagree with putting saturated first. I think that's good. What I do disagree with a lot is mentioning trans fat five times and mentioning total fat once.
DR. GRUNDY: Uh-huh.
DR. DWYER: And only in the context of coronary heart disease.
DR. GRUNDY: Okay. Well, I think that's a valid point, that we have to make an appropriate argument for our position considering all the different factors.
Now, you still may not agree with the conclusion even if we -- even if we did it in a logical fashion like you outline. I mean, I guess -- I'm sure that's going to be a point of discussion, and I expect that, and I think we should discuss that.
Go ahead, yeah.DR. STAMPFER: Maybe Johanna -- maybe you could elaborate a little. What adverse health effect is reliably attributed to higher total fat that's not specifically related to animal fat or saturated fat?
What adverse outcome is there for say more mono or poly where there is credible data?DR. DWYER: Well, I guess what I'd suggest is that I'm concerned a little about your -- and perhaps you have data that you could show us that would alleviate those concerns.
DR. STAMPFER: You mean --
DR. DWYER: Yes. I'm not sure it's a subtle issue. You know, I think that it's a legitimate debate about whether it's fine to go to 35 or 40. You know, we're really right back where we were in 1971 and '2, when they were formulating the Mr. Fipp study when the decision was made to go with a higher fat level instead of going down.
DR. GRUNDY: Well, I don't think we're going to 35 or 40. I mean, I think we have to --
DR. DWYER: Well, you give one mention of 30.
DR. GRUNDY: Yeah, I think we have to make that clear that 30 is -- I mean, we're not changing -- that's why I said at the very beginning -- we're not changing the numbers; we're just changing the emphasis more to -- and hope by changing the emphasis as the message gets out there, that the final result will be a more balanced result.
CHAIRMAN GARZA: Alice, did you want to say something?
DR. LICHTENSTEIN: No, I was going to --
CHAIRMAN GARZA: Rachel.
DR. JOHNSON: There is some data in children, referring to what Johanna said, in a paper by Manose that's in Pediatrics that analyzed USDA's survey data when the children reached a high fat level, 35 - 40 percent, it does affect adequacy. Only in the context of the U.S. diet when you see somebody with 35 - 40 percent diet, it's not from olive oil generally in the U.S. diet. So I think in the context of as the guidelines fit into our culture there could be adequacy problems at fat intake levels, getting upwards of 35 and 40.
CHAIRMAN GARZA: Meir.
DR. STAMPFER: One other quick question. There seems to be a contradiction in the text where for unsaturated fat you say "must be limited only to maintain appropriate levels of total energy intake."
How do you reconcile that with the -- do you intend to maintain a 30 percent from calories limit for fat, and if so, one of those two statements don't go together?DR. GRUNDY: Okay. You know, I guess the answer to that -- I think that's a good question, and if I understand it correctly, let me try to answer it.
If you reduce saturated fat, that carries with it a reduction of certain categories of fat, and that also reduces some unsaturated fat that's carried along with that. So that opens the door for a lot of replacement with vegetable oils. So probably you're not going to -- if you get the saturated fat down to the level we want, you're not going to get too much above 30 percent unless, you know, you turn into, you know, somebody from Crete or some place like that. But most of the time the Mediterranean area where that kind of diet is followed, I think it's around 30 to 35 percent; isn't that correct?CHAIRMAN GARZA: What about the arguments that are made by some of the individuals in the cancer field, for example, in the American Cancer Institute report that suggested, in fact, 30 percent is too high; that we ought to be aiming at lower fat levels if we really are going to deal with some of the cancer nutrient links? Do you feel that date is just not sufficient to make public policy, that it's wrong? Because that's the only other issue that I can imagine we will be faced with is, well, why are we maintaining 30. I mean, has the database not changed since 1995?
DR. GRUNDY: Okay, we had a good review of that today, I thought, and, you know, personally I thought that was an adequate review of the diet/cancer fat/cancer link. I agree, as I tried to question the speaker, that, you know, what is -- what are the data that supports these earlier claims and earlier positions, and he wasn't able to articulate those very well, and I think we're still waiting to hear those put forward in a clear-cut manner. I think they basically related to cross-cultural studies in certain populations that have very low fat intake there is a relatively low cancer incidence. But, you know, there are some animal studies that support that too, but I think like you say, we may not be on firm enough ground there to make public health recommendations.
Maybe after the women's health trial is over, if it turns out we're soundingly positive, you know, we might have to reconsider that issue.CHAIRMAN GARZA: There was one trial at NCI that was attempting to use low fat on the polyp prevential trial. That's been completed, but I don't know if that's been published.
DR. DWYER: It will be published by June, won't it?
CHAIRMAN GARZA: Yes. Perhaps we could have them come then at our next meeting if it hasn't been published and review that data. That's the only trial that I'm aware of that was aiming at possibly lower levels of fat.
Either anyone on the committee or in the audience who have any other trials that have been completed in the last five years?DR. DWYER: There are two that are in progress. One is the Women's Health Initiative.
CHAIRMAN GARZA: Yes, but that's not going to be finished by --
DR. DWYER: No, it won't be finished, and there won't be interim results on it.
I think Ross Preniss has written a paper that outlines the rationale for that. I know certainly members of the committee disagree with what he said, but basically it's written there.
The other trial that's a secondary prevention is that WINN's -- what is it called -- WINN's? That's a cancer adjuvant therapy trial in women who have breast -- postmenopausal women who've had breast cancer, so it's a little different than primary prevention.CHAIRMAN GARZA: Yes. This one was also a polyps a secondary prevention of polyps.
DR. GRUNDY: I want to make one other comment about that, is I think we have to be careful not to let disease-specific, diseases that are relatively rare in terms of the total population drive a total dietary guideline. I mean, even if a lower fat reduced colon polyps, that wouldn't necessarily mean that we would change our guideline, but it could be noted. I mean, every little possible health problem, even though it's important to the person that got it, might not be enough to justify driving the whole guideline.
CHAIRMAN GARZA: Rachel.
DR. JOHNSON: I just would like you to address, it can be briefly, but the work, you know, by Dean Ornish that says that seven to 10 percent fat diet actually leads to regression of atherosclerosis and I think he had some more end plinths in terms of MIs and just address that. Certainly that's a very, very low fat diet.
DR. GRUNDY: That's a very low saturated fat diet. If you just -- you know, we used to give people in metabolic studies diets that were very high, 40 percent corn oil diets, and their cholesterols fell just as much as what he would obtain from those very low. It's the saturated fat is what would raise the cholesterol unless you believe that there is something magic about just low fat in terms of etherial genesis, which some people have claimed, you know, that's certainly something that's never been proven. So I think it's that they lower cholesterol levels quite effectively.
They can get -- they also in those metabolic settings they have patients lose weight in addition to that, and they get levels of LDL deduction similar to what's obtained in clinical trials with drugs. And when you get kind of reductions and you can induce some regression of lesions, there is no doubt about that.
But, you know, whether those kind of diets justify making a recommendation that we all eat five percent fat, you know, that's a totally different issue, I think.CHAIRMAN GARZA: Shiriki?
DR. KUMANYIKA: I wanted to comment on the fish issue just so it doesn't get lost.
For say low income populations, urban areas, that's going to mean a fish sandwich, a fried fish sandwich at a -- well, when we make the recommendation, we have to make clear what kind of fish we're talking about because for a lot of people, that's menu choice that would -- they would interpret as something to increase, and so it's not quite a simple as eat more fish. It will be, you know, eat certain types of fish or whatever we would want to say.
But I know in scoring diets in studies with African-Americans we have to change the way we score the fats instrument because if people increase their fish consumption, they're supposed to get a better score. But it's always fried.CHAIRMAN GARZA: That's a good point.
DR. LICHTENSTEIN: I'd like to say something about the Owen studies, or study with about 35 people in it and no control group, adequately matched control group; that there were really three components to that. One was an extremely low fat diet, and as Scott pointed out, drastically low in saturated fat. There is also an exercise component that was supervised, and there was a stress reduction component of it where they met with a psychologist multiple times per week.
What's also interesting with that is they lost about 22 pounds during the first year, which also helped with the dramatic reduction in plasma lipid levels which I'm sure accounted for a lot of the regression in addition to the decrease in saturated fat and cholesterol intake.
But interestingly, if you look at the follow-up data over the next five years, they claim good adherence to the diet and weight was flat because I know issues have come up with body weight and total fat intake.
So that's the data. It's one single study and a small group of individuals.CHAIRMAN GARZA: I would ask Suzanne for the last comments so we can move on to the alcohol guideline. Then I'm going to be leaving at 2:30 on the Dietary Guideline Advisory Meeting and Suzanne will chair, and we'll work -- we'll be in working group sessions after the food safety.
so Suzanne.DR. MURPHY: Just a quick question that we probably don't want to take a lot of time to discuss right now, but am I understanding that your group is proposing taking total fat out of the guideline wording?
DR. GRUNDY: There is two ways to look at fat. One is percentage of fat and one is absolute amount. And we wanted to change the emphasis of total fat to the absolute amount and combine that with an emphasis on the absolute amount of carbohydrate, and put that as the emphasis for people to pay attention to rather than trying to figure out what percentage of fat is in the diet, because if you're eating a low percentage, you're eating a high carbohydrate diet. So if you eat a low fat diet the way it's written now, you'd have to say "eat a low fat, high carbohydrate diet," and that's what we don't what.
DR. MURPHY: But the wording in our notebook
does -- all the options say nothing about total fat in the guideline itself; is that correct? Alice is nodding.DR. GRUNDY: Well, not --
DR. LICHTENSTEIN: According to the way it's written.
DR. GRUNDY: It says total, "total fat intake should be discussed in terms of total energy intake, including carbohydrate."
DR. MURPHY: But not in the wording of the guideline at all. I think that's something we need to --
DR. GRUNDY: Well, let's see here.
DR. MURPHY: -- revisit.
DR. GRUNDY: What page?
DR. MURPHY: It's under "Detailed Outline," the page that has -- and you have A through F?
DR. GRUNDY: Um-hmm.
DR. MURPHY: And one of the options, it says "Total fat."
DR. GRUNDY: Okay, I'm looking here.
No, jump over there to the -- on the next page it says, "Choose a diet low enough in fat and carbohydrate calories to achieve appropriate body weight."DR. MURPHY: So that's a new guideline? I just don't -- I'm confused about what's in the guideline and what's in the text.
DR. GRUNDY: What's in our -- what we're proposing to be in the new guideline?
DR. LICHTENSTEIN: Yeah, the new guideline; not in the guideline, but the absolute guideline itself.
DR. STAMPFER: The picky statement that we are going to be making.
DR. GRUNDY: Well, I think it would be "Choose a diet low enough in fat..." Isn't that what we want to propose?
DR. MURPHY: Well, the proposals right now are "Choose a diet low in saturated fat and carbohydrate. Choose a diet low in saturated fat, or choose a diet low in saturated fat, trans and cholesterol."
DR. GRUNDY: No, that's just the option for the saturated fat and cholesterol component of that. That's not for the whole -- that's not for the total thing. That's just for that component.
VOICE: Well, what do you propose it to cover?
DR. GRUNDY: Well, I don't know. I didn't know we were supposed to propose a cover.
DR. MURPHY: No, I'm not implying --
DR. GRUNDY: No.
DR. MURPHY: I thought you had proposed --
DR. GRUNDY: No, we have not.
DR. MURPHY: -- it in these A through F.
DR. GRUNDY: No, that's not the total. Yeah, I think we're just trying to give some options there for the saturated fat and cholesterol component --
CHAIRMAN GARZA: For one of the headings.
DR. GRUNDY: Yeah, that component.
DR. MURPHY: All right.
CHAIRMAN GARZA: Thank you very much --
DR. GRUNDY: Sure.
CHAIRMAN GARZA: -- Scott, and to the other members of the group. That was very helpful.
All right, we'll move on then to the alcohol guideline, Dr. Stampfer.DR. STAMPFER: I would like to start with just a little bit of data, commenting on some of the issues raised by Dr. Gordis and then I'll talk about some of the issues that -- I'm going to use this in a minute.
But just, first of all, to comment on a couple of his points. These are data from the Health Professional Follow-up Study.DR. MURPHY: Meir, I can't hear you. I don't know if you're mike is not on or if there is too much distraction.
DR. STAMPFER: It's on, isn't it?
DR. MURPHY: Thank you.
DR. STAMPFER: I'm showing these data to stress two points. First, to underscore that this idea of the sick quitter as an explanation for the lower risk of coronary disease can be pretty much dismissed because you can see those two lines. One is the total cohort, one is with men who have no preexisting important health conditions and they are super-imposable.
And the second point I want to raise with this slide is to show the magnitude of the reduction, and it's in the neighborhood of 35 to 40 percent for coronary heart disease, so this does fit in quite nicely with the data that we were presented yesterday regarding the 22 percent reduction in total mortality. It does hang together.
His second point was that, well, maybe wine drinkers eat tofu and have a healthy lifestyle and that could be the explanation. This slide shows the characteristics of people in this study, the men, and this is true in women too according to their average alcohol intake, and you can take a look that, for example, if you look across the BMI column, they are all -- mean BMIs are all around 25. They're not especially lean, the drinkers. if you look at smoking, it's well know that people who drink more tend to smoke more. So it's not the case that moderate alcohol consumption is a marker for a healthy lifestyle in this and many, many data sets.
In fact, when you adjust for the other risk factors, the protection gets even stronger. And actually, in the -- now, for total mortality, these are date from the Nurses' Study. You can see that CHD mortality is reduced by 40 percent among the most moderate drinkers. Total mortality is reduced by about 30 or so percent.
But if you -- if you look at women who don't have coronary risk factors, and this is actually a minority of women because risk factors are so prevalent, you don't see much in the way of a reduction in total mortality. So this really supports the biology that it's due -- that the benefit, what there is of it, is due to reduction in coronary disease. And then at the higher levels of drinking, you see an increase in risk as you've explained.DR. DWYER: Meir, is that absolutely alcohol?
DR. STAMPFER: This is grams per day of alcohol, right.
DR. DWYER: Absolute?
DR. STAMPFER: Right.
DR. DWYER: So it's one to four grams of absolutely alcohol?
DR. STAMPFER: right, so that's about -- so the first category would be up to about half a drink per day. The next category is about a drink per day or a little bit less. Right, this is alcohol, not averaged over the different sources of beverage.
Now, this is -- here is another -- this is data from a beer drinking population. Again, you see all cause mortality or CHD mortality. You see that U-shaped curve. it's not just the tofu eating, wine drinkers. This is from Germany. And, again, you see with high levels of consumption, much higher than what we are -- what we have in our guidelines as a limit, there is an increase, but you see a very substantial reduction compared to the non-drinkers either for total or for CHD, either CHD incidence or all-caused mortality. It's big, it's a big effect.
This is incidence rate. The vertical access is incidence either of all-caused mortality or CHD incidence, and comparing no alcohol intake to different, different amounts of alcohol. That's from Germany.
And this is just to emphasize -- these are the -- this is an old slide, but this is the only limited prospective studies of alcohol and coronary disease, 34, and there are actually probably another six or seven since then, and almost all show this, this is remarkably consistent, and with huge body of data. This is looking at SACCO that was mentioned earlier, the moderate alcohol and ischemic stroke, you see the same kind of J-shaped curve with the lowest levels, the lowest incidence at moderage levels of consumption. Then it actually exceeds the level of never drinkers.
But pay attention to the axes too. It's a big reduction in the odds ratios going down to say a 40 - 45 percent reduction in risk. These are not small.
This is the AC study, an earlier version of the one presented earlier. I'm going to skip through this in the interest of time. There are too many slides here.
This is one of many, many experiments showing the effect of alcohol on HDL, percent increase. You can see big, big league increases in HDL. These are not subtle, and HDL, this is one of many, many studies. This is from Framingham looking at the relation between HDL and cardiovascular risk compared to average risk. You can see changes in HDL or differences in the level of HDL are associated with very marked differences in risk. So it's clearly a very important marker. Whether it's causal is controversial. I believe that it is causal.
And in terms of mechanism, about 60 percent of the apparent reduction can be explained through changes in HDL and Apo-A1. Insulin sensitive is reduced and hemostasis. I think that's -- oh, just the last slide to again get back to this healthy wine drinker concept. Basically all the studies that looked at moderate consumption, whatever the beverage of moderation is, that's the one that is associated with the most reduction in risk. In fact, in the Health Professional Follow-Up Study, spirits was the best predictor, even better than wine.
And this slide just depicts studies that have looked at beer, wine and liquor. it's the number of studies that show this reduction in risk, and basically the studies that looked at different beverages simultaneously pretty much find that alcohol per se is the one that's associated with lower risk.
Okay, now, let me turn to the issues that have been raised that we can talk about, and I'll try to be brief on this.
So these are some of the issues that have been raised in terms of how we might modify the guidelines if we want to modify them. Perhaps -- and I'll go through each of these, to say a couple of words about each of those topics.
The first adverse effect, "Should more stress be placed," and these are all phrased in the form of questions, not recommendations. "Should more stress be placed on the adverse effects of excess intake?" This is something we should consider.
And one point that was raised a couple of times is this sentence, which is now the third sentence of the current guidelines, "Alcoholic beverages have been used to enhance enjoyment of meals by many societies throughout human history. Should this be altered?"
I think some people have said, well, you can say the same about sugar. You can say the same about salt, and so this should be taken out. The reason that this was put in, I went back to look at the guidelines' report, the reason that this was in originally was to emphasize alcohol as a food in these dietary guidelines rather than as a drug, and I think that was the rationale for it, and we could talk about whether we think that's a reasonable rationale or not. It's certainly not factually incorrect. Nobody could argue that this is false. But whether this has a place in the guidelines, we could discuss.
The second point, pregnancy, "Should it be more broadly targeted to women who may become pregnant rather than just pregnant? Should we tighten the language?"
Right now it says "Fetal alcohol syndrome has attributed to heavy drinking. Should we consider tightening that to perhaps saying `causes.'"
Here is another statement that the question had been raised whether this should remain in the guidelines. "Lack of conclusive evidence that an occasional drink is harmful to the fetus." Dr. Gordis pointed out that accumulating evidence suggests that perhaps a lower and lower threshold is -- would be in order so that perhaps this ignorance is no longer present.
Another point that several have raised, individuals, using medications. Right now we say, the guidelines state that if you're using medications, you shouldn't drink. Most older people are using medications of some sort, and is it appropriate that we just on a blanket basis exclude them from any alcohol? I think that's an overstatement and we should consider how to amend that because that's clearly not scientifically defensible.
Several people have raised the issue of age targeting for this guideline, and the question is, "Should we emphasize the risk of abuse and lack of benefit for young people?" There is now really good data, I think, showing that the earlier people start drinking regularly, the greater their risk of alcohol abuse later in life. And since the benefit appears to be pretty much for cardiovascular disease, it's not a -- it's a situation where the young really don't benefit and only have a potential for harm in terms of their health risk.
Breast cancer, this has been raised a few times. i was actually surprised that Dr. Gordis characterized this as a non-event. I think Tim thought this was a good basis for providing specific guidance to the population, and I think that's something we should talk about.
On the benefit side for cardiovascular disease, several people have commented on the phrase "in some individuals." The current guidelines say that "Moderate alcohol consumption is suggested to reduce risk of coronary disease in some individuals," and whether we should define this a little more explicitly because it's kind of left hanging. Again, should we specify that the older individuals more likely to benefit from reduction of CHD, and we could talk about the specifics of the wording.
Finally, there are other health benefits of moderate alcohol consumption that we haven't really talked about. Some studies find decreased osteoporosis. This is not completely consistent data. For non-insulin dependent diabetes, actually this is quite a consistent finding, although there are not that many studies, but the ones that have looked do find reduction in non-insulin dependent diabetes, and in short term studies find a better -- better insulin sensitivity with moderate alcohol consumption, and there is a reduction in gallstones with moderate drinking.
So I guess the question is should any of those be mentioned or not.
Definition of "moderation," some people have claimed that this is hard to understand and should we alter this somehow and I guess we could think about what sorts of recommendations we might make with that.
And should we change the summary guideline statement? Actually, there hasn't been much, either from the alcohol -- I wouldn't want to characterize anyone as an alcohol advocate, but for the people who favor the benefits of moderate consumption or the people who worry a lot about the adverse effects, there hasn't -- doesn't seem to be a strong sentiment for changing the actual slogan of the guideline, and we could talk about it, but my sense would be to leave well enough alone.
These are some issues that Dr. Sutter raised. How can we estimate the effects of alcohol on motor function? In particular, will moderate alcohol consumption promote the possibility for old people to fall and break their hips and that sort of thing?
Actually, I don't know of any data supporting an association of moderate alcohol consumption with fractures in the elderly.
Are there effects of alcohol related to the duration of the dietary patterns that include alcohol? And this question also raises the question that had come up earlier about how long do you need to be drinking for a benefit to accrue, and are there any specific potential for abuse among individuals who initiate consumption after the age of 40? And I think it's a very good question, and I don't think there is any data to answer that in any particular group of individuals.
So that concludes what I thought seem to be some of the issues that had been raised, but I'm sure there are other. We can talk about it for awhile.DR. MURPHY: Thank you. Questions?
Dr. Weinsier.DR. WEINSIER: If I don't drink, but I want to reduce my risk of having a myocardial infarction and death from cardiovascular disease with moderate, reasonable intake, how much time would it take me to recognize that benefit?
DR. STAMPFER: It's unknown. There does seem to be a short-term benefit, and several studies have looked at this and found that the alcohol that you did or didn't drink last night may be related to your risk of coronary disease today based on platlett function and thrombolytic function. And epidemiologic studies support that an acute -- an acute beneficial effect, so part of the effect would kick in the next day.
But in terms of the HDL, if that's truly causal, then my guess is that it would take a couple of years to kick in.
I think -- pardon? Oh, you'd see the HDL rise in a few weeks, but the benefit of an elevated HDL on clinical outcomes probably would take, I'm guessing now, a couple years, but I don't think it would take decades. I think even though arteriolosclerosis is a long-term process we know that if you lower cholesterol through drugs, two years after that you start to see clinical benefit. So I think we don't need to start when we're young and build up.DR. WEINSIER: I'm just trying to put it in the context of, you know, the recent data suggesting that, and actually older data suggesting that arteriolosclerosis starting at a very early age, and we're now looking at the beset way to reduce that risk. Do we want to start at younger ages rather than later ages when we're in advanced stages of atherosclerosis. So I'm trying to put it in the context of your suggestion, if I interpreted it correctly, or your questions, whether this should be recommended for the older population rather than the younger population? Are we really at the wrong end of the spectrum, and if so, can you justify it in the younger from the other health standpoint, accident, risk, et cetera, that Dr. Gordis has raised?
DR. MURPHY: Dr. Deckelbaum.
DR. DECKELBAUM: Just in terms of arteriolosclerosis, you know, beginning at a young age, but there is a number of factors that play into the development of arterioscleroses, you know, through the decades. And then for the final event, we heard some evidence yesterday that they may be, you know, related to the -- the acute event may be related to coagulation factors or sort of ruptured plaques and that kind of thing, so that I think in terms of young people we know that for young people that alcohol intake is a major risk, and I don't think we want to balance, you know, the other approaches that we can have to reduce arteriosclerosis with adding another way just which would affect ADL in this young age group because for that young age group it's a major cause of morbidity and mortality because of accidents and other causes of deaths, so I don't think we really have to concern ourselves that much in the young age group with alcohol intake, except to say that it should be avoided.
DR. MURPHY: Dr. Dwyer.
DR. DWYER: I want to thank you for a nice presentation, Meir.
I didn't hear -- I heard him say "in the evidence," but I didn't hear what the evidence was for Dr. Gordis's statement that an occasional drink causes harm to the fetus. I heard a lot about -- but I didn't hear anything about that, and I think before we take on the one shot a day during pregnancy, we've got to be very sure that the data are there.
The second thing is on breast cancer risk I'm still not clear about that from the presentations, and I think we need a little more clarification perhaps on that.
And the final thing is I would have -- that we somehow come out very strongly and say that the definition of "moderation" for those who have problems with drinking is zero. You can't sort of fool around with it. You just cannot drink.DR. STAMPFER: Let me just briefly respond to those three.
I think for the first one, in terms of the pregnancy, I don't think that there is data for the occasional drink, and I don't think that's what Dr. Gordis was intending, but there are two points of accumulating data.
One is that in terms of the threshold for regular consumption there is, I think, more data now -- I can't cite it to you right now, but I can get it to you -- that even low levels of regular consumption are harmful, but we don't have data for, you know, the occasional glass of wine.
But the other point of data is an interesting survey that -- in the pack of material that was sent to me where it was a survey of pregnant women asking them about what their understanding was of alcohol during pregnancy, and basically they -- their take on this was that it was actually okay to drink levels. When alcohol was supposed to be limited during pregnancy, the interpretation was limited to, you know, two or three drinks and day and basically not to get drunk very often when you're pregnant. So there is a widespread --DR. DWYER: I need to see that data because I don't remember reading anything at all like that.
DR. STAMPFER: Yeah. Well, I'll send you the paper.
Basically, there was a striking, striking to me, striking lack of appreciation of the importance of limiting alcohol during pregnancy, and I think if we had a statement that was interpreted as permissive, this could be taken out of context. So that was the -- but I agree with you, I don't know of any data for harm of an occasional glass of Chardoney or even Zinfendel.
Let's see, the second was the breast cancer, and I think there is controversy here. My read of the data is basically the same as what Tim presented, which is a real increase in risk of about 10 percent or so with the one drink a day level, and to me, a 10 percent increase in risk of breast cancer is not a non-event; that that's an event. We don't know how to -- we don't know of very many ways to lower breast cancer risk.
I think we should consider putting something in the guidelines to inform women, or we should at least discuss it anyway.
And the third point about problem drinking, I agree with you entirely. They should be in a category of don't drink at all.DR. MURPHY: Dr. Lichtenstein.
DR. LICHTENSTEIN: I would just say as women in child-bearing age it's probably reasonable to err on the side of caution because they tend to have low HDL, or excuse me, low LDL and high HDL levels, so there is probably not much progression of disease in that specific age group.
I guess I would take some, or question the assumption that alcohol intake via HDL could have an impact on disease risk in short, relatively short period of time because I don't think it's particular comparable to the data on drug intervention and disease risk where you may see an effect in two years because the effect with drugs are so much more dramatic on LDL than one would expect to see with alcohol in HDL.
And lastly, I'm just wondering, is there -- not all HDLs are the same, HDL particles. And I'm just wondering, is there any HDL data, I mean, there is a classification on the basis of density, HDL-2 and 3 and we know that there are differences with respect to reverse cholesterol transport, and then there is another classification depending on whether there is A2 on the particle versus just A1 only on the particle, again, differences with respect to HDL function? Is there anything known about that? Would that at all be helpful with respect to this issue?DR. STAMPFER: Yeah, alcohol raises HDL-2 and HDL-3. It raises HDL-3 proportionately more. The relevance for risk of heart disease is not -- it's controversial. Some studies, including mine, find reduction for both HDL-2 and HDL-3 in relation to risk of heart diseases. But, yeah, both types.
In terms of the APOS, I have to go back and check.DR. MURPHY: Dr. Grundy?
DR. GRUNDY: I wanted to make a general comment. First, outside the evidence, I think, and the literature suggest that alcohol raises CETP, which is not supposed to be such a protective event, but anyway that's kind of an aside.
You know, when Dr. Gordis was here I asked him the question of what the recommendation ought to be, and he said we ought to leave it what it is. Now, I don't know how you feel about that. I'd like to ask you that, whether that's an adequate recommendation that we have now. But in thinking about this and let me just propose this and see if you agree with me or not. It almost seems like we have kind of maxed out in this country on the benefit that can be derived from alcohol, if there is a benefit. About two-thirds of the people drink, what we heard, and maybe one-third don't, and the two-thirds that do, they will have gotten the benefit that there is to get. The one-third that don't at least, you know, a portion of those, that probably half of that, maybe a sixth of people are not going to drink no matter what. They have strong beliefs that they shouldn't and maybe there are alcohol problems in their family, so they're not going to.
So you're left -- if you're going to be positive about it, a very small portion of the population would derive some benefit from a positive statement. But this moderation statement almost seems like it covers both sides adequately. I just wanted to throw that out and see if you agree with that as a general comment.DR. STAMPFER: Yes, I do. I think there are -- I would not propose to change this slogan of the guideline, but I think there are a few places, just minor tinkering where we could just clarify the issues a bit. But since you asked my opinion about it, I think it's pretty close to where I'd like to see it.
DR. MURPHY: Okay, Dr. Deckelbaum.
DR. DECKELBAUM: Just two points relating to women actually. You brought up an interesting point and I don't know if there is any data on it, is that, you know, benefits of folic acid and other micro nutrients probably come before conception. And you brought up the point whether alcohol risk. Is there any data about alcohol, you know, prior to conception or post-conception in terms of the risk?
And the other factor related to women, I think you may have addressed it in the September meeting, but I don't really, is it's a very striking cutoff between men and women in terms of one drink versus two, two drinks is moderate for men and one for women. So do body fat and weight differences account for women being discriminated against here with one versus two?DR. GRUNDY: I'm afraid we're --
DR. DECKELBAUM: You can see which side I'm on.
DR. KUMANYIKA: I'm under the impression that both the dilution's base and the first pass metabolism are working against women there, so there may be enough factors for that to be a real, a real difference by gender.
But I had another comment unless somebody else wants to contribute to the one versus two.DR. MURPHY: Go ahead.
DR. DECKELBAUM: Is there a science base for that?
DR. STAMPFER: No, it's --
DR. DECKELBAUM: It's 100 percent --
DR. STAMPFER: Yes, it's -- it's both body size. cholesterols Shiriki was saying, there is evidence for that. It's not just pulled out of thin air.
DR. DECKELBAUM: I know, but when you look at
your --DR. STAMPFER: And in fact, when we look at our data on the protective side, you also see difference in that the reduction of risk of coronary disease, as Johanna was pointing out on that side, you could see the one to five grams a day. That's half a drink per day, you've already saw pretty substantial reduction of risk of coronary disease in women. But in men, it's shifted over. So for both benefit and risk, inebriation and so on, women are more sensitive.
DR. LICHTENSTEIN: Can I comment on that specific one?
DR. MURPHY: Sure.
DR. LICHTENSTEIN: Aren't also the enzymes that are on metabolized alcohol, they are inducible, so there are a lot of other factors besides just first pass and just body water space, because if you're a habitual drinker, you're going to end up clearing it a lot faster than if you're a binge drinker.
DR. DECKELBAUM: But the other point in terms of conception and alcohol.
DR. STAMPFER: Well, with folate, it's a time
of -- specific time that the fetus is developing at the very, very early stage. I don't know of any data. Does anybody know of data that's sort of specific for the very early --DR. LICHTENSTEIN: Yes, Richard, the 1990 committee set the two and one for the first time, and they based it on -- I don't remember whose work it was, but it was reported in The Diet and Health Study, but I believe it was only one study at that time, and it was confirmed during their deliberations by some work by Charles Lieber, and we could get you that paper. There may have been work since then, but that was the basis on which they did the initial two and one, I believe.
DR. MURPHY: Okay, Dr. Kumanyika.
DR. KUMANYIKA: The other point that I had has to do with the way this guideline is framed, not the statement but the text. It discusses alcohol consumption as if the main reason for deciding whether to drink or how much has to do with the fact that it's a food or a beverage. And the other information about whether one would decide to drink or not is a -- you know, after you've thought about all the health benefits or risk, then there area certain people who shouldn't partake of this because of, you know, children, adolescents and so forth. And it seemed to me after listening to Dr. Gordis that it would be okay to talk about alcohol consumption as a more general factor, and then say that for those who consume alcohol, there may be these health issues, because right now it just seems -- it seems backwards in terms of the social consequences of alcohol consumption, the discussion is basically dietary, even though it's a dietary guideline, but there could still be an opening paragraph or something to talk about the decision to consume alcohol and what that might do to you, and then talk about specific health issues.
Do you -- you don't know what I mean?DR. STAMPFER: I'm not sure what you're suggesting.
DR. KUMANYIKA: Well, who should not drink, people who plan to drive and so forth? The emphasis seems wrong --
DR. JOHNSON: I get it.
DR. KUMANYIKA: Do you know what I mean?
DR. MURPHY: I think what she is saying that you should make the decision first if you're going to drink or not drink. And if you choose to drink, there are these added health benefits, but don't choose to drink for the health benefits if there is other issues like you're pregnant or you're planning to have a child or you have alcoholism in your family, I mean that should come first.
DR. STAMPFER: So you think who should not drink should come first; is that what you're saying?
DR. JOHNSON: Yeah.
DR. STAMPFER: Okay.
DR. KUMANYIKA: Or the decision to drink or something about what we know about drinking, and that's exactly what I meant; not to decide on the basis of your heart disease risk.
DR. GRUNDY: What you just said worries me; that if there should be any implication here that you should drink for health reasons, that bothers me. If you do drink, you know, maybe you get some benefit probably, but not to make a chose. I think Roland brought that up too. Anything in here that would encourage people to drink for health reasons bothers me. And I think it like Dr. Gordis. I don't know how you feel about that, but to start drinking for that purpose.
DR. STAMPFER: Well, I think it's too big of a risk. I think the science alone -- if I could be sure if I recommended a 60-year-old who didn't drink or a nation of people that old, if I could be completely sure that they would adhere to the guidelines and drink moderately, then I'd say the science support it. But we know that that's not true and we can't make up these guidelines in isolation from the real world, and therefore I agree with you. I don't think we should say in the slogan or the text to recommend drinking. I agree with you even though I think scientifically it could be justified.
DR. MURPHY: Okay. Who was first? Dr. Johnson. I don't know.
DR. JOHNSON: I just wondered if it makes sense in terms of the alcohol and breast cancer thing to somehow suggest that women need to assess their risk fort he different diseases. I mean, that's a lot to get into but there are certain known risk for breast cancer, there is known risk for heart disease. And as a woman, I suppose you have to balance those in making your decision.
Does that make sense?DR. STAMPFER: Yeah, it makes sense. I don't know how to put it in the text, but I welcome your suggestion.
DR. MURPHY: Dr. Weinsier.
DR. WEINSIER: Yes, real quick. Rachel keeps reminding us, and I think it's important, that with the limited calorie intake for the average U.S. population every choice has an impact and probably a critical impact. We're talking about here for women, maybe a five percent; you know, swing for men, maybe, you know, five, six or seven percent swing in calorie intake if you choose to drink moderately versus if not.
And I'm trying to think through what I would have to give up for the sake of taking this additional alcohol. In the studies that show a benefit -- in the studies, Meir, that show the benefit of short-term intake, what calories were substituted? How was the HDL increase demonstrated? WaS this addition over and above the basic diet and you're adding more calories?DR. STAMPFER: You mean in the controlled studies?
DR. WEINSIER: Yeah.
DR. STAMPFER: I don't recall. I think it was -- in the control studies, I'm not sure. I think it was carbohydrate. But in terms of what happens in populations there are data to -- there are data available. Basically, it's interesting. In women it's pretty much substituted for sugar, calorie for calorie on the average.
DR. WEINSIER: So when women choose to drink alcohol they are usually substituted for --
DR. STAMPFER: Their sugar goes --
DR. WEINSIER: Oh, for sugar?
DR. STAMPFER: Their sugar goes down. Sugar specifically, yeah. But for men, there is no specific change in the diet composition that goes along with drinking, so it seems to just substitute for just lower calories across the board.
DR. MURPHY: Okay, Dr. Grundy and then Dr. Dwyer.
DR. GRUNDY: You didn't know that alcohol doesn't, you don't have to substitute for either one. It doesn't add to weight gain. It's burned up independently of caloric intake.
DR. WEINSIER: If I recall those date, we've seen both sides. Doesn't it depend on the level intake? It's a Luzin study. That was eight years ago, give or take about a year. I thought that it did substitute it. The levels they were using which I think were in the --
DR. GRUNDY: Could substitute but, you know, we've done metabolic studies where we substitute 20 percent of calories and it has absolutely no effect on weight. It's burned up independently of the other calories. I mean, we probably don't need to get into that.
DR. STAMPFER: Yes, it's probably a separate issue. I was thinking about the nutrient content of the other foods, not so much the calories, but that's an important point too.
DR. MURPHY: Dr. Dwyer.
DR. DWYER: Just the same point, and maybe we could address it later, but it's the whole issue of appetite hunger and what these alcohol calories do. I believe it's Dr. Hall said it at Davis who suggested that there is a bypassing of satiety mechanisms, and so the question you asked about the substitution, maybe you've answered it metabolically, Scott, but it struck me that there is a literature on that; that it bypasses. So it sort of doesn't get counted by the mechanisms regulating food intake. And if that is in fact true, then there might be some problems in terms of weight.
DR. MURPHY: All right. We need to move on. Are there any final comments on the alcohol discussion?
Yes, Dr. Lichenstein.DR. LICHTENSTEIN: I think perhaps maybe there should be some advice also for individuals if they are uncertain to consult with their physician, because I'm thinking of individuals that are hypertensive. There is a relationship between alcohol consumption, blood pressure and individual that are hyperglycemic, that alcohol can exacerbate that situation. So perhaps just some cautionary note to consult the physician.
DR. MURPHY: That makes sense to me.
Okay, very good. Let's move on then, and is Dr. Dwyer ready to talk about food safety perhaps?DR. DWYER: I would like to thank Etta Saltos who up until today has been collecting references, and I believe she is going to pass out three that are somewhat relevant to some of the custodians that came up yesterday about the amount of -- the amount of foodborne disease, bacterial disease that you could contribute -- attribute to home-prepared, things going on in the home vis-a-vis the food system.
I'd also like to thank Joan Lyon and Shanthy, Dr. Johnson, whose gone through many drafts with me, Dr. Tinker who is in communicado, but I'm sure has been reading all of these drafts, and Dr. McMurry for collecting many things. In addition to that, someone who is not here right now, but who's been very helpful, has been -- has been the people in various other parts of USDA who deal with this on an everyday basis, such as Sandy Fansinoli, and the people at the National Agricultural Library.
The task force report is in your booklet here, and what I'd like to do is to go through very quickly the possible guideline or slogan, "Handle food safety from market to table." The list of the consultants is given in your books and it's about 20 people because this isn't something that's certainly my area.
Is there a clicker up here or do I click? That's fine. Thank you.
So I'll try to not duplicate what Dr. Woteki said yesterday -- thank you very much -- and just go quickly through this because I know you're all tired.
The first things that we thought needed to be considered in such a guideline should it be deemed appropriate would be to emphasize this whole notion of keeping food safe by handling them safely from market to table, and you'll notice that the various things that are suggested there -- clean, separate, cook, chill, follow the labels safely, and if you doubt, throw it out -- are pretty much in line with the Fight Back Campaign that Dr. Woteki talked about yesterday.
The second thing is to identify and define what foodborne illness is, and basically, as you know, there are many different kinds of foodborne illness, but this would focus primarily on bacterial, and I'll try to get around to why that would be in a few moments.
But basically, bacteria, bacterial foodborne disease is really the most common and it's probably the one, at least from existing data, not from maybe there is some data we haven't been able to find. It seems as though our experts felt that that was the easiest form of illness for consumers to do something about if you really believe this is something where consumers should have -- be able to do something rather than the various food safety branches of state, local and federal governments.
So that's basically it. The other kinds of things that would be covered in the page or two would be the rational -- the first essential for healthy eating be that food must be safe when they're produced but also they need to be handled after the time they are purchased, whether it's at a market or a store and eaten.
And, again, to emphasize continuity, it isn't that producers, distributors and preparers of food outside the home aren't important -- they are very important -- but consumers are a critical link in that chain as well.
The other thing is this enormous and probably growing recognition that foodborne illness is really quite a prevalent public health problem. The estimates are given in the text from the latest data we could find, and some more data is being passed out now.
The other thing we thought might be useful would be some kind of a little guide like this. It's in text in your books but here it is in graphics, just summarizing thoroughly cooking of foods.
People who need to be especially careful, certainly these groups -- pregnant women, very young children, older adults not only because of possible immunosuppression, but when you get above 85 where large numbers of people have problems with memory, if they are still living independently at home there are questions about how long things stay in the refrigerator, and then there is a large group of immunosuppressed people, both, I guess, the people who everyone thinks of right away is patients with HIV, but there are a large number of people in chemo therapy for various disorders, be it cerotic arthritis down to other things, organ transplants, renal disease, so forth, all sorts of weaken immune systems.
The section would conclude with a little bit about a few useful resources: web pages, local and state resources and the USDA hot line.
Now, that basically is -- that is pretty much what we've suggested. There are a couple of other -- in the course of interviewing about 100 people in all, a lot of people had different ideas about what a good slogan would be, and the slogan "Handle food safety from market to table" was one that I think that you and I felt probably was the best of all of them, but that doesn't mean that one of the others might not be more appropriate. Some of them are listed here. Some people thought "The fight back" was best, some "Eating a variety of foods," some -- this is the Supreme Court one that has everything in it. These are written by lawyers, these two. You can see that there is excess of verbiage. But they are all good. The question is whether they are actionable and whether they are memorable because they are so long.
So basically that's the kind of thing that we think might be useful in a separate guideline.
Now, what are some of the -- oh, I've got a few other suggestions. There are some others. They are all listed in your book with the name of the groups or group that recommended them.
Let me just spend five more minutes talking about a couple of issues that came up yesterday. The first is this issue about reporting, and in reading this literature it becomes apparent right away that reports of foodborne illness are really quite dramatically under-counted. And I think that this sort of bull's-eye diagram illustrates what we found.
There is a small group of cases, the center of the bull's eye, if you will, where the food, the agent and the causes are all known, and there are some cases where this all fits together.
There is a much larger group of cases where there are reports, but fecal samples haven't been taken, or there is no sample of the food available so you really can't tell what's going on. And then there is a very large group of cases where the level of suspicion is high but it's not clear.
Now, that center of the bull's eye includes a lot of cases in institutions, for example, in hospitals, getting to Dr. Grundy's very good question yesterday. How do you really know the percent of cases that are due to things people do after they buy the food or purchase the good in a store. You can answer that to some degree in a hospital or in another institution where the food is all produced andy you could take samples of the food and culture them theoretically, and then because the people are in an institution, if they get sick you can also easily get biological specimens and get some idea of what made them sick.
But aside from those sorts of situations it's very difficult for me to think of how to -- how to find out with a great deal of precision exactly how many cases of disease are caused by things where the food left the market pristine pure, and then it was contaminated later. So it's an issue with the techniques we've got right now that remains, I guess, with the Scottish verdict, unproven but highly suspicious.
The handouts that Dr. Saltos has been passing out, I guess, summarize the views of the IFTX expert panel of food safety and nutrition in 1995, and some other work by Allen Levy about what their view -- these people are experts and I certainly am not -- about this issue.
So we're pretty sure that foodborne illness, this bacterial foodborne illness particularly, is under-reported. We know that CDC investigations compared to estimates, such as the ones we heard yesterday, are quite dramatically different. Whether it's illness or death, this is illness, the CDC investigated over on the left estimates, the low estimate and then the high estimate, an enormous variability, but clear really very serious under-reporting
Public Citizen claimed in a recent manifesto that about one to five percent of foodborne illness was actually reported. That was their view.
Now, why is it that this under-reporting occurs? Some of the issues, I think, we've already talked about, but the CDC definition calls for a couple of cases of similar illness for ingestion of food. So if you're an old lady and you forgot that it's now March 8th or 9th and the turkey has been in the refrigerator since November 25th, believe me, I worked on a hot line in Massachusetts for about six years, and that is not a hypothetical question. We constantly got calls in March about what do you think about the Thanksgiving turkey, and that's what led to the "if in doubt, throw it out."
You have to have two or more cases for CDC to call that an event. The small outbreaks tend to be invisible. You tend to confuse them with the GI flu. We lack methods at present, and hopefully this won't be forever, to rapidly detect pathogens in food and in blood and in stools, so we don't have the easy techniques we do for some other things right now, and we have a voluntary reporting system where every state is not equally determined to find these problems. We have some states that are doing an admiral job, but it's a real problem.
The other problem is what happens as a result of this, how many of us are out of work because of events that take place. Again, our uncertainty because of the reasons I've already suggested is considerable, but the estimates are really quite dramatic in terms of lost productivity a year. This is about -- ranging from about 10 to 40 billion dollar a year, so we're not talking about small potatoes here -- wherever they go, whatever food group they go in.
The other thing, Richard Lavens at Harvard and others have talked about the constantly emerging, emerging changes in infectious disease, and one example perhaps of this is foodborne illness. The first reason, we know that foodborne illness is going to rise in the next 10 years, and I believe Dr. Woteki said this in her swearing in, is that we know that our statistics are getting better. So regardless of what -- even if we -- even if things are going along the same, as reporting gets better, the perception of foodborne illness rising will clearly be there.
The second reason why foodborne illness probably may be on an upswing is demographics. We have an aging population compared to 20 years ago, there are more people who are immunosuppressed today both because of HIV and transplants and chemo therapy than probably there ever were before.
And, finally, foodborne illness is small but I think preventable proportion, involves lack of consumer awareness and education.
There are other reasons too at different levels farther back in the food chain, but those three certainly may be important.
The other big reason why foodborne illness is probably on the increase is because of environmental exposures that are increased, and I've tried to outline them in the draft rationale we put together. Clearly, there are new strains of foodborne bacterial, and Cathy talked about some of them yesterday. We have sufe and other minimally processed foods in supermarkets. These are very high profit margin items, the suvid where you draw a vacuum and the food stays sanitary or safe for quite awhile. Then there are also things like partially cooked foods which are sold for take-out. All of those things increase environmental exposures. And then the issue of a global food economy, think Dr. Woteki talked about that. There isn't good evidence that foreign foods are less hygienic than ours, nevertheless it's a global economy now.
What's argued in the text is that interventions can prevent and lapses can cause foodborne illness, and these interventions include things that are under our own control as consumers, as well as things that must be controlled by our elected represented, and appointed representatives in government at other points in the food chain.
But there are four essentials that also can occur at one. One are bacterial cells as spores; second, the food vehicle; third, conditions allowing bacteria to survive and thrive; and, fourth, a vulnerable food consumer.
So basically, our lifestyles as well as our food-use patterns at home and in our daily lives can pose needless and preventable foodborne illness hazards, and it seems to me that we need to do something about it. We can avoid some of these problems with appropriate handling, both the food prepared outside the home and then food that's bought at the store where the handling depends on what we do to it.
So why bother to do all of this? First of all, it's an actionable measure that we can take to eat in a health way that really does make a difference in terms of morbidity as well as mortality. It's something where consumers are concerned, and where they are worried, and where they do need help. We need to bother about it because the dietary guidelines really weren't conceived at the very beginnings as solely for chronic degenerative disease. They are about health. They are not about a specific turf of the medical area.
And if we look at Healthy People 210, I think everybody got a copy of it, it's the great, big, fat, yellow book. If you look at Healthy People 210, it fits very well in with some of the things that experts in our various cabinet-level departments as well as thousands of experts in public health from all around the country are thinking of.
Now, another question that came up last time and that we've tried to answer in the 15 or so pages of text is what really works. Are there any examples of things that involve information to consumers that really work?
Well, the first thing that we talked about yesterday was the Fight Back Campaign, and that's only been up and running now for about a year, and so it's a little early to look at hard end points. They've got some interesting focus group data. They have some other data that's referenced in your text. But there is not too much yet on that campaign.
The other campaign that we saw fairly good data on, talking to Dr. Levy, I believe it was something out of the Department of Health and Human Services a fair number of years ago where there were demonstrable effects from a raw shell fish campaign, and those of you who are in FDA may be able to talk more about it, but it's basically the problem hepatitis associated with people eating raw shell fish. And if any of you come to Boston, you'll go to the Union Oyster House and see people eating raw shell fish there.
It turns out that people who do that on a chronic basis have very, very high risks of hepatitis, so the targeted group was those people, and they were able to show significant decreases in that particular behavior.
So does this kind of -- this kind of informational campaign work? I guess we'd have to say probably yes; more evidence probably is also going to be helpful.
In terms of some other questions that were asked by Dr. Sutor, some of those things were mistakes in the text and I think they are changed in the version of the text that you have. Thank you.DR. MURPHY: Thank you. Anybody have questions? Everybody is numb.
Dr. Stampfer.DR. STAMPFER: Johanna, this thing called Factoid Watch came around.
DR. DWYER: Yes, I'm sorry. I just got that too, Meir.
DR. STAMPFER: I'll be curious to get our reaction when you've had a chance to read it.
DR. SALTOS: We just got this from FSIS and they did give us some better references, journal articles that are more vigorous but we couldn't get copies for everybody, but we can get those.
DR. STAMPFER: It can wait until tomorrow then. You don't have to read it right now, Johanna.
DR. DWYER: Okay.
DR. MURPHY: All right, Dr. Grundy.
DR. DWYER: Very good. it says that food poisoning is a phony figure from the Columbia Journalism Review. Well, I don't know. We found all of the data we could, and I think that food poisoning is a real problem. I don't know what the exact numbers are, and I think, as I've indicated on the slides I showed you, that the confidence estimates are rather broad, but they are all far above levels of zero.
DR. GRUNDY: You know, I've noticed that most of the time when I get sick from eating food, it's from eating out and not from eating at home, and I know most of the emphasis here was on eating at home.
Is there any -- have you been thinking about having any comments about trying to avoid when you eat out?DR. DWYER: Well, Scott, the way we tried to go about it, and Dr. Johnson may want to comment too, was to pick the things where people really all agreed. It turns out, it's the same as heart disease. Until you get into it, you never realize how many arguments there are about it. And so to make a statement like "Don't be an idiot, don't eat sushi unless you know where its source is from," or "Don't eat shell fish unless you're sure" or something like that seemed to be less fraught with consensus, if you will, than what's in the draft that's presented there.
We tried to rely on our information experts from the CDC, the FDS, the FSIS, and universities around the country to try to get what it is that they all felt was the nub of agreement. There certainly are additional things, additional caveats that could be added, but I think what's here is sort of the kernel, if you will, of what everybody agrees on. They really -- there doesn't seem to be much dispute about that.
You will notice that I don't think we included any kinds of estimates of millions of people who were dying or dead as a result of this because, again, these are very difficult issues to resolve, so we stuck to what we know the best. That's the reason also for sticking with bacterial foodborne illness rather than including -- trying to get into things about pesticides and so forth. Again, it's just that the experts in this field, of which I am not one, seem to feel that those are the messages that are unlikely to be reversed in four or five years or 10 years.DR. JOHNSON: I just wanted to add that I think this is a case for us to really think about the broad policy implications of the dietary guidelines. In the conference calls that Johanna brought together, and she brought some really excellent people, and we kept hearing the message over and over again from people in local health departments who are clearly doing food safety programming, from people in the extension system that are doing food safety programming and the fact that they use the dietary guidelines as a teaching tool, that they felt that incorporating food safety in with the dietary guidelines really help, would help them in terms of strengthening some of their educational programs that they provide to the public.
And also thinking about the school nutrition programs as well, certainly food safety is an absolute critical component of any massive feeding program, of which nutrition is one, so I think they also felt that strengthening that aspect in the guidelines would help them in terms of overall policy.DR. DWYER: One final thing I didn't get a chance to do slides of because I didn't get it until yesterday, but you might enjoy a copy of it. Etta, I don't know if we can get copies --
DR. SALTOS: We can get copies.
DR. DWYER: Can we get copies?
What this does, it's called "The Food Safety Educator." It just came out, I guess. What it does is focuses on the interesting consumer research that's been done now on food safety education, and it goes into rather exhaustive detail about some of the questions that were also raised yesterday about the kind of food safety risks in homes, and it goes through a series of various consumer perceptions, and some of the things that people are not seemingly getting, if you will, with respect to this issue, people just don't seem to know, for example, that some people are at higher risk of foodborne illness than others. They don't seem to really understanding what to do about things like cross-contamination and so forth. So there is some pretty good consumer data now suggesting that this isn't just sort of nonsense.DR. MURPHY: Okay, any other comments?
All right, we're a tired group, I think. Nonetheless, we all have another large assignment. If you look at your agenda, we're next supposed to talk about a review of the third day of DGA. I think we recommend we skip that and we keep the third day just what it is, and
move on to the working groups that we're going to have, at least the members of the committee are going to have for the rest of the afternoon.
So, in effect, we are adjourning the public meeting for now but please, members, don't go away. We need to talk about the logistics as I look at Linda and hope that she has information on the logistics.
(Whereupon, at 3:28 p.m., the meeting was recessed, to resumed at 9:00 a.m., on Wednesday, March 10, 1999.)
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