Scientific Report of the 2015 Dietary Guidelines Advisory Committee

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Part D. Chapter 5: Food Sustainability and Safety - Continued

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Food Safety

The DGAC reviewed evidence of food safety topics was limited to usual coffee/caffeine consumption, high dose caffeine consumption, and aspartame. Coffee is one of the most widely consumed beverages in the U.S. and represents a major source of caffeine.63 The effects of coffee/caffeine consumption have not been evaluated by any prior DGAC. The Committee reviewed the evidence on normal and excessive coffee/caffeine intake and health outcomes. In addition, the DGAC reviewed evidence on health outcomes and aspartame; the most widely used nonnutritive sweetener.

Given the importance of food-borne illness prevention, the Committee reviewed the 2010 DGAC report content related to consumer behaviors and updated the key food safety behavior principles.

Question 5: What is the relationship between usual coffee/caffeine consumption and health?

Source of Evidence: Overview of systematic reviews and meta-analyses

Coffee/Caffeine and Chronic Disease


Strong and consistent evidence shows that consumption of coffee within the moderate range (3 to 5 cups/d or up to 400 mg/d caffeine) is not associated with increased risk of major chronic diseases, such as cardiovascular disease (CVD) and cancer and premature death in healthy adults. DGAC Grade: Strong

Consistent observational evidence indicates that moderate coffee consumption is associated with reduced risk of type 2 diabetes and cardiovascular disease in healthy adults. In addition, consistent observational evidence indicates that regular consumption of coffee is associated with reduced risk of cancer of the liver and endometrium, and slightly inverse or null associations are observed for other cancer sites. DGAC Grade: Moderate


Moderate coffee consumption can be incorporated into a healthy lifestyle, along with other behaviors, such as refraining from smoking, consuming a nutritionally balanced diet, maintaining a healthy body weight, and being physically active. However, it should be noted that coffee, as it is normally consumed, frequently contains added calories from cream, milk, and added sugars. Care should be taken to minimize these caloric additions. Furthermore, individuals who do not consume caffeinated coffee should not start to consume it for health benefits alone.

Review of the Evidence

Total Mortality

Evidence suggests a significant inverse relationship between coffee consumption of 1 to 4 cups/day with total mortality, especially CVD mortality. This evidence is based on three meta-analyses of more than 20 prospective cohort studies.64-66 In general, results were similar for men and women. The risk reduction associated with each cup of coffee per day was between 3 to 4 percent. In addition, Je and Giovannucci found a significant inverse association between coffee consumption and CVD mortality.65 This association was stronger in women (16 percent lower risk) than in men (8 percent lower risk). However, no association was found for cancer mortality. Crippa et al. found that the lowest risk was observed for 4 cups/day for all-cause mortality (16%, 95% CI: 13, 18) and 3 cups/day for CVD mortality (21%, 95% CI: 16, 26).64

Cardiovascular Disease

A large and current body of evidence directly addressed the relationship between normal coffee consumption and risk of CVD. The evidence included 12 systematic reviews with meta-analyses, all of which had high quality ratings (AMSTAR scores 8/11 – 11/11). CVD incidence and mortality, as well as CHD, stroke, heart failure, and hypertension were assessed by meta-analyses that consisted primarily of prospective cohort studies. Intermediate outcomes such as blood pressure, blood lipids, and blood glucose were assessed by meta-analyses of randomized controlled trials.

CVD risk was assessed by a current meta-analysis of 36 prospective cohort studies on long-term coffee consumption.67 This analysis showed a non-linear association, such that the lowest risk of CVD was seen with moderate coffee consumption (3 to 5 cups/day), but higher intakes (>5 cups/day) were neither protective nor harmful. Overall, moderate consumption of caffeinated, but not decaffeinated, coffee was associated with a 12 percent lower risk of CVD.

Results from the assessment of CHD risk in three meta-analyses were not entirely consistent.67-69 Ding et al. found 10 percent lower CHD risk with moderate coffee consumption (3 to 5 cups/day) in a meta-analysis of 30 prospective cohort studies, whereas Wu et al. and Sofi et al. in meta-analyses of 21 and 10 prospective cohort studies, respectively, found no association between coffee consumption and CHD risk. 67-69 However, in sub-group analysis, Wu et al. found that habitual moderate coffee consumption (1 to 4 cups/day) was associated with an 18 percent lower risk of CHD among women.69 Overall, the meta-analyses of Sofi et al. and Wu et al. were conducted with smaller bodies of evidence and Ding et al. assessed several more recent studies.67-69 Of note, coffee brewing methods have changed over time and the filter method has become more widely used, replacing unfiltered forms of coffee such as boiled coffee that were more widely reported by participants in earlier studies. Thus, the findings by Ding et al. are more up to date, reflecting health effects of coffee consumed in recent cohorts.

Risk of stroke was assessed in two systematic reviews with meta-analyses of prospective cohort studies with consistent findings.70, 71 Kim et al. found that coffee intake of 4 or more cups/day had a protective association on risk of stroke.70 Larsson et al. documented a non-linear association such that coffee consumption ranging from 1 to 6 cups/day was associated with an 8 percent to 13 percent lower risk of stroke, and higher intakes were not associated with decreased or increased risk.71 The inverse associations were limited to ischemic stroke and no association was seen with hemorrhagic stroke.

Regarding blood pressure, three meta-analyses evaluated the effect of coffee and caffeine on systolic and diastolic blood pressure using controlled trials.72-74 The most recent meta-analysis of 10 randomized controlled trials by Steffen et al. showed no effect of coffee on either systolic or diastolic blood pressure. Similarly, in another meta-analysis of 11 coffee trials and 5 caffeine trials, caffeine doses of <410 mg/day had no effect on systolic and diastolic blood pressure, while doses of 410 or more mg/day resulted in a net increase.73 A third meta-analysis showed that among individuals with hypertension, 200 to 300 mg of caffeine (equivalent to ~2 to 3 cups filtered coffee) resulted in an acute increase of systolic and diastolic blood pressure.72 Additionally, two meta-analyses quantified the effect of coffee on incidence of hypertension74, 75 and found no association between habitual coffee consumption and risk of hypertension. However, Zhang et al. documented a slightly elevated risk for light to moderate consumption (1 to 3 cups/day) of coffee compared to less than 1 cup/day.75

Regarding blood lipids, meta-analyses of short-term randomized controlled trials revealed that coffee consumption contributed significantly to an increase in total cholesterol and LDL-cholesterol, but cholesterol-raising effects were primarily limited to unfiltered coffee and filtered coffee appeared to have minimal effects on serum cholesterol levels.76, 77

In a meta-analysis of observational study data, including prospective, retrospective, and case-control studies, higher amounts of coffee or caffeine had no association with risk of atrial fibrillation, but low doses of caffeine (<350 mg/day) appeared to have a protective association.78 In addition, coffee consumption of 1 to 5 cups/day was found to be inversely associated with risk of heart failure in a meta-analysis of five prospective studies.79 A non-linear association was documented and the lowest risk was observed for 4 cups/day.79

Type 2 Diabetes

Coffee consumption has consistently been associated with a reduced risk of type 2 diabetes. In four meta-analyses of prospective cohort studies80-83 and cross-sectional studies,83 coffee consumption was inversely associated with risk of type 2 diabetes in a dose-response manner. Compared to non-drinkers, risk for type 2 diabetes was 33 percent lower for those consuming 6 cups/day in the analysis by Ding et al. while the risk was 37 percent lower for those consuming 10 cups/day in the analysis by Jiang et al.67, 82 Using a sub-set of the prospective cohorts in the Ding et al. and Jiang et al. meta-analyses, Huxley et al. documented that each cup of coffee was associated with a 7 percent lower risk of type 2 diabetes.81 Similarly, van Dam and Hu noted that consumption of ≥6 or ≥7 cups/day was associated with a 35 percent lower risk of type 2 diabetes.83 Three meta-analyses80-82 also found protective associations for decaffeinated coffee. Moderate decaffeinated coffee consumption (3 to 4 cups/day) was associated with a 36 percent lower risk of type 2 diabetes.81 Each cup of decaffeinated coffee was associated with a 6 percent lower risk80 while every 2 cups were associated with a 11 percent lower risk.82 Both reports also documented a dose-response association between caffeine and type 2 diabetes risk such that every 140 mg/day was associated with an 8 percent lower risk in the Ding et al. meta-analysis, while every 200 mg/day was associated with a 14 percent lower risk in the analysis by Jiang et al.80, 82 However, it remains unclear if this inverse association is independent of coffee consumption, as Ding et al. indicated that none of the studies included in the caffeine dose-response analysis adjusted for total coffee.

Only one systematic review of nine randomized controlled trials examined the effects of caffeine on blood glucose and insulin concentrations among those with type 2 diabetes.84 Ingestion of 200 to 500 mg of caffeine acutely increased blood glucose concentrations by 16 to 28 percent of the area under the curve and insulin secretions by 19 to 48 percent of the area under the curve when taken before a glucose load. At the same time, these trials also noted a decrease in insulin sensitivity by 14 to 37 percent. Although no study has examined whether the effects of caffeine on blood glucose and insulin persist in the long term, evidence from prospective cohorts indicates that the acute effects of caffeine do not translate into long-term risk of type 2 diabetes. Furthermore, the inverse association between decaffeinated coffee and diabetes risk suggests that the observed benefit is likely to be due to other constituents in coffee rather than caffeine.


Several systematic reviews and meta-analyses examined the association between coffee consumption and risk of cancer. Types of cancer examined by the DGAC included total cancer, cancers of the lung, liver, breast, prostate, ovaries, endometrium, bladder, pancreas, upper digestive and respiratory tract, esophagus, stomach, colon, and rectum.

In a quantitative summary of 40 prospective cohort studies with an average follow-up of 14.3 years, Yu et al. found a 13 percent lower risk of total cancer among coffee drinkers compared to non-drinkers or those with lowest intakes.85 Risk estimates were similar for men and women. In sub-group analyses, the authors noted that coffee drinking was associated with a reduced risk of bladder, breast, buccal and pharyngeal, colorectal, endometrial, esophageal, hepatocellular, leukemic, pancreatic, and prostate cancers.

Tang et al. evaluated five prospective cohorts and eight case-control studies and found that, overall, those with the highest levels of coffee consumption had a 27 percent higher risk for lung cancer compared to never drinkers or those with least consumption.86 An increase in coffee consumption of 2 cups/day was associated with a 14 percent higher risk of developing lung cancer. However, because smoking is an important confounder, when analyses were stratified by smoking status, coffee consumption was marginally protective in non-smokers and was not associated with lung cancer among smokers. When estimates from two studies that examined decaffeinated coffee were summarized, a protective association with lung cancer was seen. No association was seen with lung cancer when only case-control studies were considered.

Results from two meta-analyses indicate that coffee consumption is associated with a 40 to 50 percent lower risk of liver cancer,87, 88 when considering both cohort and case-control studies. In one meta-analysis, the associations were significant in men but not in women.87

Three meta-analyses of observational studies found no association between coffee consumption,89-91 caffeine consumption, or decaffeinated coffee consumption and risk of breast cancer. In all three reports, each 2 cup/day of coffee was marginally associated with a 2 percent lower risk of breast cancer. However, in sub-group analyses, coffee consumption was protective against breast cancer risk in postmenopausal women,89 BRCA1 mutation carriers,89 and women with estrogen receptor negative breast tumors .90

The association between coffee consumption and risk of prostate cancer was mixed. Cao et al. and Zhong et al. found that regular or high coffee consumption, compared to non- or lowest levels of consumption, was associated with a 12 percent to 17 percent lower risk of prostate cancer in prospective cohort studies.92, 93 Further, each 2 cups of coffee per day was associated with a 7 percent lower risk of prostate cancer. However, no associations were seen with case-control data alone or when these studies were examined together with prospective cohort studies. Using a combination of both prospective cohort and case-control data, Discacciati et al. found that each 3 cups/day of coffee was associated with a 3 percent lower risk of localized prostate cancer and an 11 percent lower risk of mortality from prostate cancer.94 On the other hand, after summarizing data from 12 prospective cohort and case-control studies, Park et al. found a 16 percent higher risk of prostate cancer.95 However, in sub-group analyses by study design, the higher risk was observed in case-control but not in cohort studies.

Consumption of coffee was not associated with risk of ovarian cancer in a meta-analysis of seven prospective cohort studies with more than 640,000 participants.96 Two meta-analyses confirmed an inverse association between coffee consumption and risk of endometrial cancer.97, 98 In the most recent and updated meta-analysis of prospective cohort and case-control studies, compared to those in the lowest category of coffee consumption, those with the highest intakes of coffee had a 29 percent lower risk of endometrial cancer.98 Each cup of coffee per day was associated with an 8 percent lower risk of endometrial cancer. Similar results were found in the meta-analysis by Bravi et al. that included a sub-set of the studies in Je et al. and documented a 20 percent lower risk of endometrial cancer overall, and a 7 percent decrease for each cup of coffee per day.97, 98 However, the association was significant only in case-control studies but not in cohort studies, most likely due to lower statistical power.

A recent meta-analysis of 23 case-control studies by Zhou et al. found coffee was a risk factor for bladder cancer. There was a smoking-adjusted increased risk of bladder cancer for those in the highest (45 percent), second highest, (21 percent), and third highest (8 percent) groups of coffee consumption, compared to those in the lowest intake group.99 No association was, however, seen in cohort studies.

Two meta-analyses of coffee consumption and pancreatic cancer risk provided mixed results.85, 100 Using both prospective cohort and case-control studies, Turati et al. found that coffee consumption was not associated with risk of pancreatic cancer.100 However, an increased risk was seen in case-control studies that did not adjust for smoking. Using a sub-set of prospective cohorts included in the Turati et al. meta-analysis, Dong et al. found that coffee drinking was inversely associated with pancreatic cancer risk but did not separate studies based on their adjustment for smoking status.101 Sub-group analyses revealed a protective association in men, but not in women.

Turati et al. quantified the association between coffee consumption and various upper digestive and respiratory tract cancers using data from observational studies.102 Coffee consumption was associated with a 36 percent lower risk of oral and pharyngeal cancer but not with risk of laryngeal cancer, esophageal squamous cell carcinoma, or esophageal adenocarcinoma. In a meta-analysis of prospective cohort and case-control studies, Zheng et al. noted that coffee was inversely, but non-significantly, associated with risk of esophageal cancer.103 Regarding gastric cancer, no association between coffee consumption and risk was seen in a meta-analysis of observational studies by Botelho et al.104

Three meta-analyses on the association between coffee consumption and colorectal cancer risk have yielded mixed findings.105-107 Results from case-control studies suggested coffee consumption was associated with lower risk of colorectal (15 percent lower) and colon cancer (21 percent lower), especially in women. However, this inverse association was non-significant for cohort studies. Using all but one of the case-control studies, Galeone et al. arrived at similar conclusions as a Li et al. analysis, although associations were in general stronger.105, 107 Galeone et al. also provided suggestive evidence for a dose-response relationship between coffee and colorectal cancer such that each cup of coffee was associated with a 6 percent lower risk of colorectal cancer, 5 percent lower risk of colon cancer, and 3 percent lower risk of rectal cancer.105 Using several prospective cohort studies, as in the Li et al. meta-analysis, Je et al. found no significant association of coffee consumption with risk of colorectal cancer.106, 107 Interestingly, no differences were seen by sex but the suggestive inverse associations were slightly stronger in studies that adjusted for smoking and alcohol.

For additional details on this body of evidence, visit: Appendix E-2.39a Evidence Portfolio, Appendix E-2.39b Systematic Review/Meta-Analysis Data Table [Excel - 56KB], and References 64-107

Caffeine and Neurodegenerative Disease


Consistent evidence indicates an inverse association between caffeine intake and risk of Parkinson’s disease. DGAC Grade: Moderate

Limited evidence indicates that caffeine consumption is associated with a modestly lower risk of cognitive decline or impairment and lower risk of Alzheimer’s disease. DGAC Grade: Limited


Moderate coffee consumption can be incorporated into a healthy lifestyle, along with other behaviors, such as refraining from smoking, consuming a nutritionally balanced diet, maintaining a healthy body weight, and being physically active. However, it should be noted that coffee as it is normally consumed can contain added calories from cream, milk, and added sugars. Care should be taken to minimize these caloric additions. Furthermore, individuals who do not consume caffeinated coffee should not start to consume it for health benefits alone.

Review of the Evidence

Parkinson’s Disease

Evidence from two systematic reviews108, 109 and one quantitative meta-analysis110 confirmed an inverse association between coffee, caffeine, and risk of Parkinson’s disease. Qi et al. evaluated six case-control studies and seven prospective articles and documented a non-linear relationship between coffee and risk of Parkinson’s disease, overall.110 The lowest risk was observed at about 3 cups/day (smoking-adjusted risk reduction was 28 percent). For caffeine, a linear dose-response was found and every 200 mg/day increment in caffeine intake was associated with a 17 percent lower risk of Parkinson’s disease. Using a combination of cohort, case-control, and cross-sectional data, Costa et al. summarized that the risk of Parkinson’s disease was 25 percent lower among those consuming the highest versus lowest amounts of caffeine.108 Like Qi et al., Costa et al. documented a linear dose-response with caffeine intake such that every 300 mg/day was associated with a 24 percent lower risk of Parkinson’s disease. In both reports, associations were weaker among women than in men.


Two systematic reviews111, 112 and one meta-analysis112 examined the effects of caffeine from various sources, including coffee, tea, and chocolate, on cognitive outcomes. Arab et al. systematically reviewed six longitudinal cohort studies evaluating the effect of caffeine or caffeine-rich beverages on cognitive decline.111 Most studies in this review used the Mini Mental State Examination Score as a global measure of cognitive decline. The review concluded that estimates of cognitive decline were lower among caffeine consumers, although there was no clear dose-response relationship. Studies also showed stronger associations among women than men. In a meta-analysis of nine cohort and two case-control studies, caffeine intake from various sources was associated with a 16 percent lower risk of various measures of cognitive impairment/decline. Specifically, data from four studies indicate that caffeine is associated with a 38 percent lower risk of Alzheimer’s disease.

For additional details on this body of evidence, visit: Appendix E-2.39a Evidence Portfolio, Appendix E-2.39b Systematic Review/Meta-Analysis Data Table [Excel - 56KB], and References 108-112

Caffeine and Pregnancy Outcomes


Consistent evidence from observational studies indicates that moderate caffeine intake in pregnant women is not associated with risk of preterm delivery. DGAC Grade: Moderate

Higher caffeine intake is associated with a small increased risk of miscarriage, stillbirth, low birth weight, and small for gestational age (SGA) births. However, these data should be interpreted cautiously due to potential recall bias in the case-control studies and confounding by smoking and pregnancy signal symptoms. The DGAC recognizes that there is limited data to identify a level of caffeine intake beyond which risk increases. Based on the existing data, the risk of miscarriage, stillbirth, low birth weight, and SGA births is minimal given the average caffeine intake of pregnant women in the United States. DGAC Grade: Limited


Overall, the evidence supports current recommendations to limit caffeine intake during pregnancy as a precaution. Based on existing evidence, women who are pregnant or planning to become pregnant should be cautious and adhere to current recommendations of the American Congress of Obstetricians and Gynecologists regarding caffeine consumption, and not consume more than 200 mg caffeine per day (approximately two cups of coffee per day).

Review of the Evidence

Two SRs/MA assessed observational studies on the association of caffeine intake with adverse pregnancy outcomes.113, 114 The pregnancy outcomes included miscarriage, pre-term birth, stillbirth, SGA, and low birth weight. The most recent SR/MA by Greenwood et al. quantified the association between caffeine intake and adverse pregnancy outcomes from 60 publications from 53 separate cohort (26) and case-control (27) studies.113 The evidence covered a variety of countries with caffeine intake categories that ranged from non-consumers to those consuming more than 1,000 mg/day. They found that an increment of 100 mg caffeine was associated with a 14 percent increased risk of miscarriage, 19 percent increased risk of stillbirth, 10 percent increased risk of SGA, and 7 percent increased risk of low birth weight. The risk of pre-term delivery was not increased significantly. The magnitude of these associations was relatively small within the range of caffeine intakes of the majority women in the study populations, and the associations became more pronounced at higher range (300 mg/day). The authors also note the substantial heterogeneity observed in the meta-analyses shows that interpretation of the results should be cautious. In addition, the results from prospective cohort studies and case-control studies were mixed together. Because coffee consumption is positively correlated with smoking, residual confounding by smoking may have biased the results toward a positive direction.

The other SR/MA assessed pre-term birth and the results were in agreement with Greenwood et al.113 Maslova et al. reviewed 22 studies (15 cohort and 7 case-control studies) and found no significant association between caffeine intake and risk of pre-term birth in either case-control or cohort studies.114 For all of the observational studies assessed across the SRs/MA, most studies did not adequately adjust for the pregnancy signal phenomenon, i.e. that nausea, vomiting, and other adverse symptoms are associated with a healthy pregnancy that results in a live birth, whereas pregnancy signal symptoms occur less frequently when the result is miscarriage. Coffee consumption decreases with increasing pregnancy signal symptoms, typically during the early weeks of pregnancy, and this severely confounds the association.115 Greenwood et al. state that this potential bias is the most prominent argument against a causal role for caffeine in adverse pregnancy outcomes.113 Only one randomized controlled trial of caffeine/coffee reduction during pregnancy has been conducted to date.116 The study found that in pregnant women who consumed at least three cups of coffee a day and were less than 20 weeks pregnant, a reduction of 200 mg of caffeine intake (~ 2 cups) per day did not significantly influence birth weight or length of gestation, compared to those with no decrease in caffeine consumption. The trial did not examine other outcomes.

For additional details on this body of evidence, visit: Appendix E-2.39a Evidence Portfolio, Appendix E-2.39b Systematic Review/Meta-Analysis Data Table [Excel - 56KB], and References 113, 114

Question 6: What is the relationship between high-dose coffee/caffeine consumption and health?

Source of Evidence: Systematic reviews117, 118


Evidence on the effects of excessive caffeine intake on the health of adults or children (>400 mg/day for adults; undetermined for children and adolescents) is limited. Some evidence links high caffeine intake in the form of energy drinks to certain adverse outcomes, such as caffeine toxicity and cardiovascular events. Randomized controlled trials (RCTs) on the relationship between high-caffeine energy drinks and cardiovascular risk factors and other health outcomes report mixed results. Evidence also is limited on the health effects of mixing alcohol with energy drinks, but some evidence suggests that energy drinks may mask the effects of alcohol intoxication, so an individual may drink more and increase their risk of alcohol-related adverse events. DGAC Grade: Limited


Early safety signals consisting of case reports of adverse events associated with high-caffeine drink consumption, including increased emergency room visits, indicate a potential public health problem. The DGAC agrees with the American Academy of Pediatrics and the American Medical Association that until safety has been demonstrated, limited or no consumption of high-caffeine drinks, or other products with high amounts of caffeine, is advised for vulnerable populations, including children and adolescents. High-caffeine energy drinks and alcoholic beverages should not be consumed together, either mixed together or consumed at the same sitting. This is especially true for children and adolescents.


According to the FDA, the upper limit of moderate caffeine intake in healthy adult populations (barring pregnant women) is 400 mg/day, with intakes higher than this being considered excessive caffeine consumption. The FDA has not defined moderate and excessive intake levels for children and adolescents. However, according to Health Canada, children should not consume more than 2.5 mg of caffeine per kg bodyweight per day.119 Although this guideline pertains only to children up to the age of 12 years, in the literature it is usually applied to children and adolescents of all ages. A caffeine threshold of 2.5 mg/kg/day would translate into around 37.5 mg/day for children ages 2 to 5 years with an average weight of 15 kg, 75 mg/day for youth ages 6 to 12 years with an average weight of 30 kg, and 137.5 mg/day for youth ages 13 to 17 years with an average weight of 55 kg.

The main sources of caffeine among both adults and children are coffee, tea, and carbonated soft drinks. Another product, which has received a lot of attention recently as a potential source of excessive caffeine intake, especially among younger populations, is energy drinks.120 An energy drink is a beverage that contains caffeine as its active ingredient, along with other ingredients such as taurine, herbal supplements, vitamins, and sugar. It is usually marketed as a product that can improve energy, stamina, athletic performance, or concentration.121 Energy drinks are relatively new to the market and have evaded oversight and regulation by the FDA due to their classification as dietary supplements, or because their components are generally recognized as safe.121 Overall, these drinks are highly variable in caffeine content and some products have excessively high caffeine content (from 50 to 505 mg per can/bottle, with caffeine concentrations anywhere between 2.5 to 171 mg per fluid ounce).122

Health organizations including the American Academy of Pediatrics, the International Society of Sports Nutrition, and the American Medical Association have issued position statements on energy drinks, advising limited or no consumption among children and adolescents. Given the increasing evidence pointing toward harmful effects of excessive caffeine consumption,105-107 the FDA requested the IOM to convene a workshop examining the science behind safe levels of caffeine intake. A report summarizing this workshop was recently published.123 Its main conclusions were: 1) Children and adolescents are a potential vulnerable group, in whom caffeine intake could have detrimental health consequences. This is particularly important given insufficient data on caffeine consumption in this demographic, which is increasingly getting exposed to new modes of caffeine intake such as energy drinks, 2) not enough is understood about potential interactions between caffeine and other ingredients commonly found in caffeine-containing foods and beverages, and 3) more research is needed to identify individual differences in reactions to caffeine, especially in vulnerable populations, including children with underlying heart conditions and individuals with genetic predispositions to heart conditions.

The Center for Disease Control (CDC) recently reported on trends in caffeine intake over the past decade (1999-2010) among U.S. children, adolescents, and young adults.124 The CDC found that although energy drinks were not widely available before 1999, energy drinks made up nearly 6 percent of caffeine intake in 2009-2010, indicating fast growth in U.S. consumption over a short period of time. When energy drink consumption was assessed in a nationally representative sample of U.S. secondary school students,125 35 percent of 8th graders, 30 percent of 10th graders, and 31 percent of 12th graders consumed energy drinks or shots, and consumption was higher for adolescent boys than girls. Furthermore, energy drink use was associated with higher prevalence of substance use, as assessed for all grades of U.S. secondary students.

Furthermore, a serious issue of public health concern has been the popular trend of combining energy drinks with alcoholic beverages. In 2010, the FDA determined that caffeine added to alcoholic beverages was not generally recognized as safe (GRAS), leading to withdrawal of premixed, caffeinated alcoholic beverages from the market.126 Currently, Health Canada caps caffeine levels for energy drinks at 100 mg/250 ml (~1 cup) and has determined that an energy drink container that cannot be resealed be treated as a single-serving container, because the total volume is usually consumed. They also have mandated that manufacturers add a warning to labels that energy drinks should not be combined with alcohol. Recently, the CDC has made public statements on the dangers of mixing alcohol and energy drinks. They indicate that high amounts of caffeine in energy drinks can mask the intoxicating effects of alcohol, while at the same time having no effect on the metabolism of alcohol by the liver. Therefore, high amounts of caffeine in energy drinks may result in an “awake” state of intoxication, thus increasing the risk of alcohol-related harm and injury (, March 2014).127

Review of the Evidence

Several case reports of adverse events related to energy drink use have been published. A recent systematic review of case reports of adverse cardiovascular events related to consumption of energy drinks documented 17 such published case reports.118 The cardiovascular events documented included atrial fibrillation, ventricular fibrillation, supraventricular tachycardia, prolonged QT, and ST elevation. In 41 percent of the cases, the person had consumed large amounts of energy drinks, and 29 percent of the cases were associated with consumption of energy drinks together with alcohol or other drugs. In 88 percent of the cases, no underlying cardiac condition was found that could potentially explain the cardiovascular event, although other cardiovascular risk factors co-occurred with energy drink consumption before the onset of the event in most cases. Of the cases that presented with serious adverse events, including cardiac arrest, the majority occurred with either acute heavy consumption of energy drinks or consumption in combination with alcohol or other drugs. Overall, the authors concluded that causality cannot be inferred from this case series, but physicians should routinely inquire about energy drink consumption in relevant cases and vulnerable consumers should be cautioned against heavy consumption of energy drinks or concomitant alcohol (or drug) ingestion. This systematic review is consistent with a recent report from the Drug Abuse Warning Network (DAWN) on energy drink-related emergency room visits that showed U.S. emergency room visits temporally related to energy drink consumption doubled between 2007 and 2011.128 These visits were attributed mainly to adverse reactions to energy drinks, but also to combinations with alcohol or drugs. It is generally agreed that adverse events associated with energy drink consumption are underreported.

Several short-term RCTs have examined the health effects of energy drink consumption. All of these have been carried out in adult populations, probably due to ethical constraints in providing energy drinks to children. Burrows et al. recently published a systematic review of RCTs examining this question.117 They found 15 such RCTS, examining the effect of variable doses of energy drinks (mean dose: one and a half 250 ml cans per study session) with differing ingredient combinations and concentrations on a number of different health outcomes. The high variability in exposure and outcome definitions made a meta-analysis infeasible. Overall, they found no consistent effects of energy drinks on cardiorespiratory outcomes (heart rate, arrhythmias, blood pressure), pathological outcomes (blood glucose, blood lactate, free fatty acids, clinical safety markers), and body composition, with some studies showing positive, some inverse, and some no associations. For many of these outcomes, consistent results could not be stated due to only one study reporting on them. There was a slight indication of a potential positive effect of energy drinks on physiological outcomes (run time to exhaustion, peak oxygen uptake, resting energy expenditure). However, the authors concluded that more studies were needed before arriving at a definitive conclusion. Two of the studies assessed the simultaneous ingestion of alcohol and energy drinks.129, 130 One found that when compared with the ingestion of alcohol alone, the addition of an energy drink reduced individuals’ perception of impairment from alcohol, while at the same time, objective measures indicated ongoing deficits in motor coordination and visual acuity.129 Nor did energy drinks reduce breath alcohol concentration, indicating no change or increase in alcohol metabolism by the liver. Another study on energy drinks in combination with alcohol and exercise showed that during post-exercise recovery there was no effect on arrhythmias within 6 hours of energy drink ingestion in healthy young adults.130

Many of the these studies have methodological limitations, such as lack of a true control group (water or no drink), a very short follow-up duration of only a few hours, and small sample sizes, which could explain the inconsistent findings. In addition, many of these studies did not report whether they were commercially funded. Several of those that did report funding sources had financial conflicts of interest. Lastly, the doses of energy drinks used in these studies were not too high, resulting in caffeine intake levels that fell within the normal range. It is possible that excessive caffeine intake due to heavy energy drink consumption adversely affects several health outcomes, but this hypothesis was not clearly addressed by these studies. Hence it is difficult to ascertain the impact of excessive caffeine intake on health outcomes on the basis of these RCTs. In addition, very little data are available on the health effects of excessive caffeine consumption in pediatric populations.

For additional details on this body of evidence, visit: Appendix E-2.40 Evidence Portfolio and References 117, 118

Question 7: What is the relationship between consumption of aspartame and health?

Source of Evidence: Scientific Opinion on the re-evaluation of aspartame (E 951) as a food additive (2013), European Food Safety Authority (EFSA) Panel on Food Additives and Nutrient Sources added to Food 29


The DGAC generally concurs with the European Food Safety Authority (EFSA) Panel on Food Additives that aspartame in amounts commonly consumed is safe and poses minimal health risk for healthy individuals without phenylketonuria (PKU). DGAC Grade: Moderate

Limited and inconsistent evidence suggests a possible association between aspartame and risk of some hematopoietic cancers (non-Hodgkin lymphoma and multiple myeloma) in men, indicating the need for more long-term human studies. In addition, limited and inconsistent evidence indicates a potential for risk of preterm delivery. Due to very limited evidence it is not possible to draw any conclusions on the relationship between aspartame consumption and headaches. DGAC Grade: Limited


If individuals choose to drink beverages that are sweetened with aspartame, they should stay below the aspartame Acceptable Daily Intake (ADI) of no more than 50mg/kg/day (a 12-ounce diet beverage contains approximately 180 mg of aspartame).131 To be cautious, adults and children should be aware of the amount of aspartame they are consuming, given the need for more long-term human studies. Currently, most Americans are well below the ADI.132


Aspartame is the most common low-calorie sweetener used in the United States. It is found in numerous dietary sources. Although most commonly associated with low-calorie/low-sugar versions of carbonated and non-carbonated beverages, it also is found in low-calorie/low-sugar versions of canned fruits and juices; instant cereals; baked goods; ice cream and frozen ices; candy and chocolate products; jams, jellies, syrups, and condiments; yogurt; and beer. Non-nutritive sweeteners are regulated by the FDA. The FDA has concluded that aspartame is safe as a general purpose sweetener in food.133 Given the high interest of the public in the safety of aspartame, the DGAC reviewed the EFSA report on the sweetener and health outcomes.

Review of the Evidence

The most recent European Food Safety Authority report on the re-evaluation of aspartame as a food additive was used to address this question.29 The EFSA report based its evaluation on original study reports and information submitted following public calls for data, previous evaluations, and additional literature that became available up until the end of public consultation on November 15, 2013. The DGAC focused on results from human studies, not animal studies or studies conducted in vitro. The Mode of Action (MoA) analysis on reproductive and developmental toxicity of aspartame also was included. Although the EFSA report considered both published and unpublished studies, the DGAC considered only published studies.


A relatively limited body of evidence on human studies has directly addressed the relationship between aspartame consumption and cancer risk. The most consistent finding in six U.S. and European case-control studies134-139 was the absence of an adverse relationship between consumption of low-calorie sweeteners, including aspartame, and risk of some cancers. An exception was one study in Argentina that found a positive association between long-term use (≥10 y) of artificial sweeteners and risk of urinary tract tumors (UTT), compared to non-users; although for short-term users, no association was observed.134

The findings of two prospective cohort studies140, 141 were not consistent. Lim et al. examined a large cohort of men and women from the NIH-AARP Diet and Health study and found no association between consumption of aspartame-containing beverages and risk of overall hematopoietic cancers, brain cancers, or their subtypes.140 A second large prospective cohort study by Shernhammer et al. involved the Nurses’ Health Study (NHS) and Health Professionals Follow-up Study (HPFS) cohorts followed over 22 years with dietary intake measured every 4 years.141 In this study, the highest category of aspartame intake (≥143 mg/day from diet soda and aspartame packets) was associated with significantly elevated risk of non-Hodgkin lymphoma (NHL) and of multiple myeloma in men, but not in women. Both of the prospective cohort studies that addressed cancer risk had limitations regarding generalizability. The NIH-AARP cohort had an age range of 50 to 71 years and was, therefore, not generalizable to the overall adult population. Additionally, the Panel considered the positive findings in Shernhammer et al. to be preliminary and require replication in other populations because the positive association between aspartame consumption and NHL was limited to men and lacked a clear dose-response relationship.29

Further investigation should be considered to ensure that no association exists between aspartame consumption and specific cancer risk.

Preterm Delivery

Two European cohort studies were used in this evaluation. A large prospective cohort study by Halldorsson et al.142 from the Danish National Birth Cohort investigated associations between consumption of artificially sweetened and sugar-sweetened soft drinks during pregnancy and subsequent pre-term delivery. Also, a large prospective cohort study of Norwegian women by Englund-Ögge et al.143 investigated the relationship between consumption of artificially sweetened and sugar-sweetened soft drinks during the first 4 to 5 months of pregnancy and subsequent pre-term delivery. In addition, La Vecchia combined these two studies in a meta-analysis that the Panel considered.144

Regarding the Halldorsson study, significant trends in risk of pre-term delivery with increasing consumption of artificially sweetened drinks (carbonated and non-carbonated) were found, but not for sugar-sweetened drinks.142 In the highest exposure groups (≥ 4 servings/d) the odds ratios relative to non-consumption were 1.78 (95% CI: 1.19-2.66) and 1.29 (95% CI: 1.05-1.59), respectively, for carbonated and non-carbonated artificially sweetened drinks. Associations with consumption of artificially sweetened carbonated drinks did not differ according to whether delivery was very early (less than 32 weeks) or only moderately or late pre-term.142 The EFSA Panel noted that the prospective design and large size of the study sample were major strengths, and that the methods used had no important flaws.29 The Panel agreed with the authors who concluded that replication of their findings in another setting was warranted.

Regarding the Englund-Ögge study, no significant trends were found in risk of pre-term delivery with increasing consumption of artificially sweetened drinks or sugar-sweetened drinks.143 Small elevations of risk were observed with higher consumption of artificially sweetened soft drinks, but after adjustment for covariates, these reached significance only when categories of consumption were aggregated to four levels, and then the odds ratio for the highest category (≥ 1 serving/day) was 1.11 (95% CI: 1.00-1.24) compared with non-consumption. This was driven by an increase in spontaneous but not medically induced pre-term delivery. Associations with sugar-sweetened soft drinks tended to be stronger, with an adjusted odds ratio of 1.25 (95% CI: 1.08-1.45) for consumption of at least 1 serving per day. The Panel noted that effects may have been underestimated because of inaccuracies in the assessment of dietary exposures, but the method was similar to that used by Halldorsson et al., and the same for sugar-sweetened as for artificially sweetened soft drinks.29

Behavior and Cognition


Two RCTs146, 146 and two non-randomized controlled trials147, 148 conducted in the United States were included in the evidence on effects of aspartame on behavior and cognition in children. Wolraich et al. compared diets high in sucrose to diets high in aspartame in 25 preschool and 23 primary school-age children and found that even when intake exceeded typical dietary levels, neither dietary sucrose nor aspartame affected children’s behavior or cognitive function.146 Shaywitz et al. examined the effect of large doses of aspartame (10 times usual consumption) on behavioral/cognitive function in children with attention deficit disorder (ages 5 to 13 years) and found no effect of aspartame on cognitive, attentive, or behavioral testing.146 Roshon and Hagan examined 12 preschool children on alternate experimental days with a challenge of sucrose- or aspartame-containing drinks and found no significant differences in locomotion, task orientation, or learning.148 Lastly, Kruesi et al. investigated the effect of sugar, aspartame, saccharin, and glucose on disruptive behavior in 30 preschool boys on four separate experimental days.147 There was no significant difference in scores of aggression or observer’s ratings of behavior in response to any of the treatments. The limitations of this evidence were that all of the trials were approximately 20 to 30 years old, all had small sample sizes, and all were conducted over the short-term (1 day to 3 weeks). Overall, the Panel noted that no effects of aspartame on behavior and cognition were observed in children in these studies.29


Seven studies on the effect of aspartame on adult behavior and cognition were included in this body of evidence. Five RCTs, one non-randomized controlled trial, and one case-control study were conducted in the United States. Two of these trials examined a single experimental dose of aspartame on one day.149, 150 Lapierre et al. examined 15 mg aspartame/kg body weight in 10 healthy adults and found no significant differences between aspartame and placebo in cognition or memory during the study.149 Ryan-Harshman et al. tested 13 healthy adult men and found no change in any behavioral effects measured.150 A third randomized crossover trial examined 48 adults over 20 days; half of the participants were given high dose aspartame (45 mg/kg/d) and half were given low dose aspartame (15 mg/kg/d).151 This study found no neuropsychologic, neurophysiologic, or behavioral effects linked to aspartame consumption. Two trials were conducted with pilots or college students to test cognitive abilities related to aviation tasks.152, 153 In the first study, 12 pilots were given aspartame (50 mg/kg) or placebo and tested for aviation-related information processing after a single treatment on one day. The authors detected no performance decrements associated with exposure to aspartame. In the follow-up study, college students were given repeated dosing of aspartame (50 mg/kg for 9 days) and tested for aviation-related cognitive tasks. No impaired performance was observed. One non-randomized crossover trial examined the effects of aspartame on mood and well-being in 120 young college women and found no difference in changes in mood after consuming a 12-ounce water or aspartame-sweetened beverage on a single day.154 Lastly, a case-control study was conducted with 40 adults with unipolar depression and a similar number of subjects without a psychiatric history.155 Participants were given aspartame (30 mg/kg) or placebo for 7 days and individuals with depression reported an increase in severity of self-scored symptoms between aspartame and placebo; whereas the non-depressed matched subjects reported no difference. This suggested that individuals with mood disorders may be sensitive to aspartame. Overall, the Panel noted the limited number of participants, the short duration of the studies, and the inconsistency of the reporting of the results in all adult studies. However, despite these limitations, the Panel concluded that there was no evidence that aspartame affects behavior or cognitive function in adults.29

Other (Headaches, Seizures)

Several studies examined headaches and seizures. A number of RCTs were conducted to assess the incidence of headache after consumption of aspartame. One RCT tested the effects of aspartame within 24 hours of consumption (30 mg/kg) on 40 subjects with a history of headache and found no difference in the incidence rate of headaches.156 Another RCT looked at the effect of aspartame on frequency and intensity of migraine headaches in 10 subjects with medical diagnosis of migraine headaches over 4 weeks.157 The authors found an increase in the frequency of migraine headaches with the aspartame treatment. In an RCT of 18 subjects with self-described sensitivity to aspartame, the participants reported headaches on 33 percent of the days, compared with 24 percent with placebo.158 The authors concluded that a subset of the population may be susceptible to headaches induced by aspartame. Lastly, in a survey study of 171 patients at a headache unit, 8 percent reported that aspartame was a trigger of headaches compared to 2.3 percent for carbohydrates and 50 percent for alcohol.159 Overall, the Panel concluded the possible effect of aspartame on headaches had been investigated in various studies which reported conflicting results, ranging from no effect to the suggestion that a small subset of the population may be susceptible to aspartame-induced headaches.29 The number of existing studies was small and not recent and several studies had high dropout rates. The Panel noted that because of the limitations of the studies, it was not possible to draw a conclusion on the relationship between aspartame consumption and headaches.

Several small studies assessed seizures. One RCT in children investigated whether aspartame would induce the occurrence of petit mal seizures.160 Ten children were given one treatment of aspartame at the ADI of 40 mg/kg and that treatment exacerbated the number of electroencephalogram spike waves per hour for these children without a history of seizures. In a second RCT, aspartame (34 mg/kg) was administered to 10 epileptic children over 2 weeks to examine the induction of seizures.145 No difference was found in the occurrence of seizures between aspartame and placebo exposure. Another RCT studied 18 subjects who claimed to have experienced epileptic seizures due to aspartame.161 One treatment (50 mg/kg) was administered on a single day and the authors reported no seizures or other adverse effect from aspartame treatment in this group. Overall, the Panel concluded that the available data do not provide evidence for a relationship between aspartame consumption and seizures.29

Pregnancy Outcomes: Mode of Action (MoA) analysis

The EFSA Panel considered that adverse effects on reproduction and development reported for aspartame in animal studies could be attributed to the metabolite phenylalanine.29 They undertook a formal Mode of Action (MoA) analysis of the putative role of phenylalanine in developmental toxicity (as seen in animal studies).

Risk characterization was based on comparison of plasma phenylalanine levels following aspartame administration with plasma phenylalanine levels associated with developmental effects in children born from mothers with PKU. Current clinical practice guidelines recommend PKU patients restrict dietary intake of phenylalanine to keep plasma levels below 360μM. The EFSA Panel noted that intakes of aspartame as a food additive could occur at the same time as other dietary phenylalanine sources. Therefore, they considered the threshold used for comparisons should be lowered to allow for simultaneous intake of aspartame with meals. So plasma phenylalanine from the diet (120μM) was subtracted from 360μM to determine the maximum safe plasma concentration of phenylalanine that can be derived from aspartame (240μM).

The Panel considered that given these conservative assumptions, realistic dietary intake of aspartame and the confidence intervals provided by the modeling, the peak plasma phenylalanine levels would not exceed the clinical target threshold of 240μM when a normal individual consumed aspartame at or below the current ADI of 40 mg/kg body weight/day. Therefore, the Panel concluded there would not be a risk of adverse effects on pregnancy in the general population at the current ADI.29

For additional details on this body of evidence, visit: Appendix E-2.41 Evidence Portfolio and Scientific Opinion on the re-evaluation of aspartame (E 951) as a food additive (2013), European Food Safety Authority (EFSA) Panel on Food Additives and Nutrient Sources added to Food. Available at

Question 8: What Consumer Behaviors Prevent Food Safety Problems? (Topic update from 2010)

Introduction and Methods

Food safety continues to be an issue of public health importance. Foodborne illness is a preventable, yet common issue affecting the U.S. population. Each year, approximately 1 in 6 people in the U.S. population become ill, 128,000 are hospitalized, and 3,000 die of foodborne illness.162 It is critical to educate consumers and food producers on good techniques and behaviors for preventing food borne illness.

The 2010 DGAC conducted NEL systematic reviews for the Food Safety and Technology chapter and provided in-depth guidance on foodborne illness prevention. The 2015 DGAC reviewed the content related to consumer behavior and the prevention of food safety problems. The Committee determined that the majority of the 2010 food safety guidance was current and that only minor updates were necessary. For more information on the evidence review on food safety, refer to the DGAC 2010 report, Food Safety and Technology Section: ( [PDF - 670 KB]).

The four food safety principles—Clean, Separate, Cook, and Chill are the foundation of the Fight BAC!® campaign ( and are reemphasized in this report. Data from the Centers for Disease Control and Prevention,30 Food and Drug Administration,31 and the Food Safety and Inspection Service32 were used to update the 2010 DGAC tables on the following topics related to consumer behavior and food safety:

CLEAN and SEPARATE (Tables D5.1, D5.2, D5.3)

  • Techniques for hand sanitation, washing fresh produce, and preventing cross-contamination.

COOK and CHILL (Table D5.4)

  • Temperature control during food preparation and storage.

Table D5.3 includes updated guidance on preventing cross-contamination from shopping to serving foods. Table D5.4 lists recommended internal temperatures for meat, seafood, eggs, and leftovers. Additionally, Tables D5.5 and D5.6 provide recommended techniques for using food and refrigerator/freezer thermometers. Specific changes made to the 2010 tables are detailed in the footnotes of the tables.

Food Safety—Tables

Table D5.1. Recommended procedures for hand sanitation

When washing hands with soap and water:

  • Wet your hands with clean, running water (warm or cold), turn off the tap, and apply soap.1
  • Lather your hands by rubbing them together with the soap. Be sure to lather the backs of your hands, between your fingers, and under your nails.2
  • Scrub your hands for at least 20 seconds. Need a timer? Hum the “Happy Birthday” song from beginning to end twice.3
  • Rinse your hands well under clean, running water.
  • Dry your hands using a clean towel or air dry them.4

If soap and clean, running water are not available, use an alcohol-based hand sanitizer that contains at least 60% alcohol5. Hand sanitizers are not as effective when hands are visibly dirty or greasy.6 How do you use hand sanitizer:7

  • Apply the product to the palm of one hand (read the label to learn the correct amount).
  • Rub your hands together.
  • Rub the product over all surfaces of your hands and fingers until your hands are dry.

Updates to the 2010 DGAC table

1 Water temperature “warm or cold” and a conservation recommendation of ‘turn off the tap’ were added.

2 The soap is to be help while lathering one’s hands, then rub all together. “Scrub all surfaces” was clarified to “the backs of hands, between fingers, and under nails.”

3 “At least” was added to the 20 seconds time frame. To give a time reference, the suggestion to” hum the Happy Birthday song…” was added.

4 The word ‘paper’ was removed as a modifier for towel, and instead it was specified to be a ‘clean’ towel. The option to ‘air dry them’ was added and the option of using an air dryer was removed from the phrase. Also removed was the direction to use your paper towel to turn off the faucet.

5 The words ‘clean’ and ‘running’ were inserted in the directions for when water is not available. ‘Hand sanitizer that contains at least 60% alcohol’ replaces ‘gel’.

6 This guidance was added.

7 The following step was added, “Read the label to learn the correct amount.”

Source: Adapted from Accessed June 2, 2014.30

Table D5.2. Recommended techniques for washing produce

When preparing any fresh produce, begin with clean hands. Wash your hands for at least 20 seconds with soap and warm water before and after preparation.

Cut away any damaged or bruised areas on fresh fruits and vegetables before preparing and/or eating. Produce that looks rotten should be discarded.

Wash all produce thoroughly under running water before eating, cutting or cooking. This includes produce grown conventionally or organically at home, or purchased from a grocery store or farmer's market. Washing fruits and vegetables with soap or detergent or using commercial produce washes is not recommended.

Even if you plan to peel the produce before eating, it is still important to wash it first so dirt and bacteria are not transferred from the peel via the knife to the fruit or vegetable1

Scrub firm produce, such as melons and cucumbers, with a clean produce brush.

Dry produce with a clean cloth towel or paper towel to further reduce bacteria that may be present.

Many pre-cut, bagged, or packaged produce items like lettuce are pre-washed and ready-to-eat. If so, it will be stated on the package and you can use the product without further washing.

If you do choose to wash a product marked “pre-washed” and “ready-to-eat,” be sure to use safe handling practices to avoid any cross-contamination (see Table D5.3).

Updates to the 2010 DGAC table

1 The following explanation was provided: “. . . so dirt and bacteria aren’t transferred from the knife onto fruit or vegetable.”

Source: Adapted from [PDF - 1.5 MB]. Accessed June 2, 201431

Table D5.3. Recommended techniques for preventing cross-contamination

When Shopping:

Separate raw meat, poultry, and seafood from other foods in your grocery-shopping cart. Place these foods in plastic bags to prevent their juices from dripping onto other foods. It is also best to separate these foods from other foods at check out and in your grocery bags.

When Refrigerating Food1:

Place raw meat, poultry, and seafood in containers or sealed plastic bags to prevent their juices from dripping

onto other foods. Raw juices often contain harmful bacteria.

Store eggs in their original carton and refrigerate as soon as possible.

When Preparing Food:

Washing raw poultry, beef, pork, lamb, or veal before cooking it is not recommended. Bacteria in raw meat and

poultry juices can be spread to other foods, utensils, and surfaces.

Wash hands and surfaces often. Harmful bacteria can spread throughout the kitchen and get onto cutting boards,

utensils, and countertops. To prevent this:

  • Wash hands with soap and warm water for 20 seconds before and after handling food, and after using the bathroom, changing diapers; or handling pets.
  • Use hot, soapy water and paper towels or clean cloths to wipe up kitchen surfaces or spills. Wash cloths often in the hot cycle of your washing machine.
  • Wash cutting boards, dishes, and counter tops with hot, soapy water after preparing each food item and before you go on to the next item.
  • A solution of 1 tablespoon of unscented, liquid chlorine bleach per gallon of water may be used to sanitize surfaces and utensils.

Cutting Boards:

Always use a clean cutting board.

If possible, use one cutting board for fresh produce and a separate one for raw meat, poultry, and seafood.

Once cutting boards become excessively worn or develop hard-to-clean grooves, they should be replaced.

Marinating Food:

Always marinate food in the refrigerator, not on the counter.

Sauce that is used to marinate raw meat, poultry, or seafood should not be used on cooked foods, unless it is

boiled just before using.

When Serving Food:

Always use a clean plate.

Never place cooked food back on the same plate or cutting board that previously held raw food.

Updates to the 2010 DGAC table

1This sentence was deleted, ““When not possible, store raw animal foods below ready-to-eat foods and separate different types of raw animal foods, such as meat, poultry, and seafood from each other so that they do not cross-contaminate each other.”

Source: Adapted from and Accessed June 3, 2014.32

Table D5.4. Recommended safe minimum internal temperatures

Cook to the minimum internal temperatures below, as measured with a clean food thermometer before removing meat from the heat source. For safety and quality, allow meat to rest for at least three minutes before carving or consuming. For reasons of personal preference, consumers may choose to cook meat to higher temperatures.1 c


Degrees Fahrenheit

Ground Meat and Meat Mixturesa

Beef, Pork, Veal, Lamb


Turkey, Chicken


Fresh Beef, Pork, Veal, Lamb a , 2

Steaks, roasts, chopsa



Chicken and Turkey, whole


Poultry breasts, roasts


Poultry thighs, wings


Duck and Goose


Stuffing (cooked alone or in bird)


Fresh Porka



Fresh (raw)3


Pre-cooked (to reheat)


Eggs and Egg Dishesa


Cook until yolk and white are firm.

Egg dishes


Fresh Seafood b



Cook fish until it is opaque (milky white) and flakes with a fork.


Cook shrimp, lobster, and scallops until they reach their appropriate color. The flesh of shrimp and lobster should be an opaque (milky white) color. Scallops should be opaque (milky white) and firm.

Cook clams, mussels, and oysters until their shells open. This means that they are done. Throw away the ones that didn't open.

Shucked clams and shucked oysters are fully cooked when they are opaque (milky white) and firm4.

Leftovers and Casserolesa


Updates to the 2010 DGAC table

1 An introductory paragraph was added on the topic of allowing for a three-minute rest period after cooking meat.

2 Pork was added to the list of fresh meats.

3Fresh (raw) ham was added to the table.

4Information on cooking status of shucked clams and oysters was added.


a handbook/ct_index. Accessed June 3, 2014.32

b Accessed June 3, 2014.31

c [PDF - 627 KB]. Accessed June 3, 2014.32

Table D5.5. Recommended techniques for food thermometers

To be safe, meat, poultry, and egga and seafoodb products must be cooked to a safe minimum internal temperature to destroy any harmful microorganisms that may be in the food.

A food thermometer should also be used to ensure that cooked food is held at safe temperatures until served. Cold foods should be held at 40°F or below. Hot foods should be kept hot at 140°F or above.a

Most available food thermometers will give an accurate reading within 2 to 4°F. The reading will only be correct, however, if the thermometer is placed in the proper location in the food. a

In general, the food thermometer should be placed in the thickest part of the food, away from bone, fat, or gristle.a

When the food being cooked is irregularly shaped, such as with a beef roast, check the temperature in several places. Egg dishes and dishes containing ground meat and poultry should be checked in several places.a

When measuring the temperature of a thin food, such as a hamburger patty, pork chop, or chicken breast, a thermistor or thermocouple food thermometer should be used, if possible. a

However, if using an "instant-read" dial bimetallic-coil food thermometer, the probe must be inserted in the side of the food so the entire sensing area (usually 2 to 3 inches) is positioned through the center of the food.a

To avoid burning fingers, it may be helpful to remove the food from the heat source (if cooking on a grill or in a frying pan) and insert the food thermometer sideways after placing the item on a clean spatula or plate.a

Food thermometers should be washed with hot soapy water. Most thermometers should not be immersed in water.a


a, Accessed June 3, 2014.32

b , Accessed June 3, 2014.31

Table D5.6. Recommended techniques for using refrigerator/freezer thermometers

For safety, it is important to verify the temperature of refrigerators and freezers.

Refrigerators should maintain a temperature no higher than 40°F.

Frozen food will hold its top quality for the longest possible time when the freezer maintains 0°F or below.

To measure the temperature in the refrigerator:

Put the thermometer in a glass of water and place in the middle of the refrigerator. Wait 5 to 8 hours. If the temperature is not 38 to 40°F, adjust the refrigerator temperature control. Check again after 5 to 8 hours.

To measure the temperature in the freezer:

Place the thermometer between frozen food packages. Wait 5 to 8 hours. If the temperature is not 0 to 2°F, adjust the freezer temperature control. Check again after 5 to 8 hours. An appliance thermometer can be kept in the refrigerator and freezer to monitor the temperature at all times. This can be critical in the event of a power outage. When the power goes back on, if the refrigerator is still 40°F and the freezer is 0°F or below, the food is safe1.

Updates to the 2010 DGAC table

1When referring to the correct freezer temperature, ‘or below’ was added after ‘zero degrees Fahrenheit.’

Source: , Accessed June 3, 2014.32

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