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Thread: Meta-analysis of prospective cohort studies evaluating the association of saturated f

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    Default Meta-analysis of prospective cohort studies evaluating the association of saturated f

    Background: A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.
    Objective: The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.
    Design: Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.

    Results: During 5–23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.

    Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

    Full Text - Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease





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    Meta-analysis of effect of saturated fat intake on cardiovascular disease: overadjustment obscures true associations.

    The recent article by Siri-Tarino et al (1), which reported on a meta-analysis of prospective cohort studies evaluating the association of saturated fat with coronary heart disease (CHD), stroke, and cardiovascular disease (CVD) observed that “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” This finding has generated some interest in the media (2, 3). However, we believe that the interpretations of the results presented in this article are overstated and could be a result of flaws in the methodologic design of the study.

    The meta-analysis involves data from 16 studies that evaluate the effect of saturated fat intake on CHD incidence or mortality and from 8 studies that evaluate the effect of saturated fat intake on stroke incidence or mortality. The results for CVD include any events for either CHD or stroke.

    The authors state that “wherever possible, risk estimates from the most fully adjusted models were used in the estimation of the pooled [relative risks].” It is well established that saturated fat intake is associated with increased concentration of serum cholesterol (4), and that serum cholesterol concentrations are associated with CHD and CVD (5).

    Therefore, serum cholesterol concentrations lie on the causal chain between saturated fat intake and CHD and CVD and to adjust for serum cholesterol concentrations in a meta-analysis will obscure the effect of saturated fat intake on these health outcomes.

    Yet 7 of the 16 studies included in the meta-analysis of CHD events, and 4 of the 8 studies included in the meta-analysis of stroke events, were adjusted for serum cholesterol concentrations. These studies accounted for nearly half of all CHD and CVD events included in the meta-analyses (see Table 1). Adjustment for serum cholesterol concentrations will inevitably bias the estimates of effect of saturated fat intake toward the null hypothesis. A meta-analysis of nonadjusted data would have produced different (and more informative) results.

    Siri-Tarino et al (1) do not mention this as a potential limitation of their study, nor do they calculate estimates of the effect of saturated fat intake on CHD and CVD using unadjusted data from the identified cohort studies. Without this further analysis, the conclusion that, “our meta-analysis showed that there is insufficient evidence from prospective epidemiologic studies to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD” is unsupported.

    Full Text - Meta-analysis of effect of saturated fat intake on cardiovascular disease: overadjustment obscures true associations


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    Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence.

    Abstract
    Dietary and policy recommendations frequently focus on reducing saturated fatty acid consumption for improving cardiometabolic health, based largely on ecologic and animal studies. Recent advances in nutritional science now allow assessment of critical questions about health effects of saturated fatty acids (SFA). We reviewed the evidence from randomized controlled trials (RCTs) of lipid and non-lipid risk factors, prospective cohort studies of disease endpoints, and RCTs of disease endpoints for cardiometabolic effects of SFA consumption in humans, including whether effects vary depending on specific SFA chain-length; on the replacement nutrient; or on disease outcomes evaluated. Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid. However, insufficient evidence exists for different chain-length-specific effects on other risk pathways or, more importantly, disease endpoints. Based on consistent evidence from human studies, replacing SFA with polyunsaturated fat modestly lowers coronary heart disease risk, with ~10% risk reduction for a 5% energy substitution; whereas replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.

    Full Text - Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence


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    The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?

    Abstract
    Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.

    Full Text - The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?


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    Hey Max. Have you thought about adding a Max's Conclusions section after the article?
    Curb weight: 78 kg
    DL 84 x 8; SQ 67 x 10 49 x 20; BR 67 x 8; PC 45 x 10; MP 39 x 7; BP 57 x 10
    1RM. DL - 139 PC-FS - 67 BP - 57 (not tested)


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    Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet.

    Abstract
    We recently showed that a hypocaloric carbohydrate restricted diet (CRD) had two striking effects: (1) a reduction in plasma saturated fatty acids (SFA) despite higher intake than a low fat diet, and (2) a decrease in inflammation despite a significant increase in arachidonic acid (ARA). Here we extend these findings in 8 weight stable men who were fed two 6-week CRD (12%en carbohydrate) varying in quality of fat. One CRD emphasized SFA (CRD-SFA, 86 g/d SFA) and the other, unsaturated fat (CRD-UFA, 47 g SFA/d). All foods were provided to subjects. Both CRD decreased serum triacylglycerol (TAG) and insulin, and increased LDL-C particle size. The CRD-UFA significantly decreased plasma TAG SFA (27.48 ± 2.89 mol%) compared to baseline (31.06 ± 4.26 mol%). Plasma TAG SFA, however, remained unchanged in the CRD-SFA (33.14 ± 3.49 mol%) despite a doubling in SFA intake. Both CRD significantly reduced plasma palmitoleic acid (16:1n-7) indicating decreased de novo lipogenesis. CRD-SFA significantly increased plasma phospholipid ARA content, while CRD-UFA significantly increased EPA and DHA. Urine 8-iso PGF(2α), a free radical-catalyzed product of ARA, was significantly lower than baseline following CRD-UFA (-32%). There was a significant inverse correlation between changes in urine 8-iso PGF(2α) and PL ARA on both CRD (r = -0.82 CRD-SFA; r = -0.62 CRD-UFA). These findings are consistent with the concept that dietary saturated fat is efficiently metabolized in the presence of low carbohydrate, and that a CRD results in better preservation of plasma ARA.

    Full Text - Limited Effect of Dietary Saturated Fat on Plasma Saturated Fat in the Context of a Low Carbohydrate Diet


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    You had me at 'meta-analysis'.


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    Quote Originally Posted by TLS View Post
    Hey Max. Have you thought about adding a Max's Conclusions section after the article?
    My conclusion won't be as interesting the article's conclusion

    This is just a little bit of reading material showing a few different sides to the whole saturated fat debate.

    Quite simply my basic view is -

    Saturated fat is not the devil.

    It has many uses within the human body and is required for optimum function on all levels.

    A correlation between a high saturated fat intake and cardiovascular diseases have been found but there are also numerous other factors that play apart in that.

    As with most diseases or epidemics, the finger is pointed to ONE factor and the all of a sudden it is seen as being the cause and or bad.


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    Are the Current Dietary Guidelines Regarding Egg Consumption Appropriate?
    Kristin L. Herron1 and Maria Luz Fernandez2
    Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269

    Full Text - Are the Current Dietary Guidelines Regarding Egg Consumption Appropriate?


    Despite being considered a good or excellent source of 11 nutrients (1), egg intake accounted for only 1.3% of the total energy consumed by the average American in 2000 (2). The perception of cholesterol-rich eggs as a "forbidden food" developed in response to the highly publicized 1970s recommendation by the American Heart Association (AHA) to restrict egg consumption and limit dietary cholesterol intake to ≤300 mg/d. The dietary cholesterol guidelines are similar in the most recent AHA report; however, their position regarding egg intake has become more specific (3). This new report states that the intake of one yolk a day would be acceptable, if other cholesterol contributing foods were limited in the diet (3). Although this recommendation may be useful for certain individuals with a history of elevated plasma cholesterol or established coronary heart disease (CHD),2 it is unwarranted for the vast majority of the population and may actually have negative nutritional implications. This commentary evaluates the controversy and consequences of the dietary recommendations regarding eggs. The elderly high-risk demographic is utilized to illustrate the health benefits of consumption and the functionality of individual egg nutrients.

    As a whole food, eggs are an inexpensive and low calorie source of nutrients such as folate, riboflavin, selenium, choline and vitamins B-12 and A. Eggs are also one of the few exogenous sources of vitamins K and D. Furthermore, eggs are a source of high quality protein, and the lipid matrix of the yolk serves to enhance the bioavailability of nutrients such as lutein and zeaxanthin. However, despite these benefits, to gain popular acceptance the controversy surrounding the dietary cholesterol content of eggs must be revisited and revised.

    Eggs and cholesterol

    Cholesterol is a dietary component that has elicited much public and scientific interest in conjunction with CHD. Extensive research has failed to establish a definite link between dietary cholesterol intake and disease progression (4). Numerous population studies have clearly demonstrated the lack of a relationship between egg intake and CHD (5). A recent study, which examined the intake of 117,000 nurses and health professionals over a 14-y period, found no difference in the relative risk for CHD between those who consumed less than one egg a week and those who ate more than one egg a day (6). Furthermore, clinical studies have clearly shown that plasma compartment changes resulting from dietary cholesterol consumption are regulated by a vast number of genes, which allow for extensive individual variation in response. The classification of individual genetic differences may allow for the future identification of those who would respond favorably to dietary cholesterol restriction and those who are hyporesponsive to intake. It has been suggested that ∼70% of humans are hyporesponsive to excess dietary cholesterol consumption (4). In addition, those individuals who hyperrespond generally experience elevations in both LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) (7) allowing for the maintenance of the LDL-C/HDL-C ratio, an important marker for CHD risk (8,9). This evidence suggests that for healthy individuals, the nutritional benefits clearly outweigh the concern surrounding the 213 mg of dietary cholesterol provided by one large egg.

    Current recommendations do not benefit the elderly population

    By the year 2020, the number of people worldwide over the age of 60 y is expected to reach one billion. This generation, born between 1946 and 1964, will also represent ∼25% of the U.S. population. Therefore, the incidence of age-related disease will continue to increase, further burdening the already strained U.S. health care system. It has been estimated that each year the treatment of chronic disease accounts for 75% of all health care costs in the U.S. Furthermore, of the total money spent each year to treat conditions such as CHD, cancer, stroke and diabetes, approximately $33 billion of the medical and $9 billion of the lost productivity costs can be attributed to poor nutrition (10).

    Widely accepted risk factors that have been identified for CHD may not be applicable to elderly populations. Although elevated total cholesterol values have been shown to predict CHD risk in middle-aged individuals, this parameter does not seem to be relevant for the elderly demographic (11). The difficulty that surrounds this finding is that the low fat diet is commonly prescribed to many elderly individuals in an attempt to lower elevated total cholesterol concentrations. Unfortunately, restriction of fat and cholesterol from the diet often results in the inclusion of foods high in simple sugars. This change in diet composition can be detrimental, causing increases in triglycerides (TG), which are generally accompanied by low HDL-C levels. Low HDL-C has been identified as the best lipoprotein indicator of CHD risk in elderly individuals (12). Furthermore, the consumption of a diet high in simple sugars can cause changes in lipoprotein metabolism that result in the production of smaller more dense LDL particles (13). These LDL particles, identified as the pattern B subclass, are considered to be more atherogenic than the larger cholesteryl ester-enriched fraction (14). A predominance of LDL particles in this pattern B subclass has been shown to be associated with a threefold increase in CHD risk (14,15), which may be due to the easy entry of the particle into the arterial wall and its high susceptibility to oxidation (14). Oxidized LDL possess increased atherogenicity due to unregulated uptake by macrophages and their role in foam cell production. Furthermore, it has been suggested that the consumption of a low fat diet by elderly individuals may promote insulin resistance. Insulin resistance and obesity are conditions that are accompanied by increased LDL-C and TG, and decreased HDL-C. Studies have shown that these dyslipidemias are inherent to insulin resistance and not attributable to diet because there appears to be a diminished response in these individuals to dietary saturated fat and cholesterol (7). Therefore, because insulin resistance is considered an independent risk factor for CHD (16), energy restriction as opposed to fat and cholesterol limitations appears to be a better treatment option for this population. Contrary to the current recommendations, these findings suggest that low energy (17.5 kJ/large egg) eggs could be included in a heart healthy diet for this population.

    Egg protein and resistance training

    As people age they may experience the loss of skeletal muscle mass, a condition termed sarcopenia (17). Furthermore, it has been well documented that on average adults generally experience a 1.8–2 lb (0.82–0.91 kg) weight gain each year (18). Decreased fat-free mass and elevated fat mass are associated with lower total energy expenditure, lower resting metabolic rate and altered protein metabolism (19), which further increases the risk for the development of chronic diseases such as type II diabetes, osteoporosis and CHD. However, the adoption of resistance training programs for older adults has proven to be effective in increasing skeletal muscle mass (20). In addition, dietary protein may have a profound effect on the results of training. Acute increases in protein intake can effectively reduce the rate of protein breakdown, whereas long-term (1–2 wk) elevations in intake result in an increase in whole-body protein turnover (21). Consumption of a 133-kJ supplement drink, which contained 17 g/100 g protein, by healthy men between the ages of 61–72 who were engaged in a 12-wk resistance-training program, significantly (P < 0.01) increased muscle hypertrophy (22). This finding can be further explained by a study that found increased protein intake by aging individuals has an effect on the uptake and utilization of nitrogen during resistance training (23). These results led to the speculation that it may be possible to enhance the skeletal muscle synthesis that is seen with resistance training by modifying the quality of dietary protein consumed. The source of protein in the diet may also have an effect on protein metabolism in older adults. A study by Campbell et al. (24) reported that consumption of an omnivorous diet results in greater increases in fat-free mass after 12 wk of resistance training compared with those increases achieved with a lactoovovegetarian diet. This finding was further explored by Pannemans et al. (25) who determined that values for protein flux, protein oxidation and protein synthesis are not different between elderly women who consume either a high animal or high vegetable protein diet for a period of 2 wk. However, they did find that protein breakdown decreases (although not significantly; P < 0.08) during the high animal protein diet period. The data from these studies suggest that vegetable protein may not efficiently suppress protein breakdown.

    The intake of a high protein meal provides a large number of amino acids to the labile protein pool. However, homeostasis of this pool is maintained within narrow limits by increasing protein synthesis, decreasing protein breakdown or elevating the rate of protein oxidation. The productivity of this postabsorptive phase can be enhanced by increasing the concentration of essential amino acids in the pool and this can be achieved by changing the source of dietary protein. Diets high in vegetable protein contribute less essential amino acids to the labile pool; therefore, they are less capable of inhibiting breakdown and initiating synthesis. An analysis of the amino acid composition of both eggs and soy milk resulted in the determination that eggs provide a greater amount of both the essential and branched chain amino acids (Table 1). Although, eggs were found to have lower amino acid content compared with beef, the biological value of egg protein is greater.


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    TABLE 1Nutrient composition of whole eggs, soy milk and ground beef1, 2
    Egg carotenoids and age related macular degeneration (AMD)

    The leading cause of irreversible blindness in the U.S. is AMD (26). This condition develops from long-term oxidative damage caused by the exposure of the eye to intense light. Furthermore, the retina itself has been shown to have a high rate of oxidative metabolism. Lutein and zeaxanthin accumulate in the macular region of the retina (27); therefore, because of their chemical properties, these two carotenoids may function to reduce the risk for development of AMD. As antioxidants, lutein and zeaxanthin may reduce the degree of oxidation or minimize the resulting damage by decreasing the permeability of the membrane to oxygen (28). Epidemiological data support this protective role suggested for lutein and zeaxanthin. Those individuals who consumed a greater number of foods rich in lutein and zeaxanthin had a lower risk for AMD (29), as were those who had the highest level of intake (30), or had increased concentrations of the two carotenoids in plasma (31) or in the retina (32). The lipid matrix of the egg yolk has been shown to enhance the bioavailability of lutein and zeaxanthin. One yolk has been found to provide between 200 and 300 µg of these carotenoids (31). In a study that measured the total carotenoid content of several foods, lutein represented 15–47 mol/100 mol of the total found in various dark green leafy vegetables, whereas eggs were found to contain 54 mol/100 mol (33). Furthermore, increased consumption of foods rich in these carotenoids has been directly associated with elevated serum concentrations of lutein and zeaxanthin and increased macular pigment density (34).

    Lutein and zeaxanthin intake also may be associated with a decrease in the risk for CHD by reducing arterial plaque formation. The expression of adhesion molecules, which are needed for monocyte association with the artery, may be inhibited by carotenoid consumption (35). In addition, lutein has demonstrated antioxidant function in vivo as a scavenger of peroxynitrite, the reaction product of nitirc oxide and superoxide (36). Peroxynitrite, in the presence of LDL, can destroy lipid-protein complexes creating a particle that is more susceptible to uptake by the macrophage scavenger receptor. Studies have shown that the consumption of foods high in lutein can increase the concentration of this carotenoid in the plasma and the LDL particle (37). Furthermore, two epidemiological studies, which examined carotid intima thickness as a measure of CHD, showed that high levels of plasma lutein produce a significant reduction in disease risk (38,39).

    Egg lecithin and choline

    As a polyunsaturated phosphatidylcholine (PPC), lecithin is a functional and structural component of all biological membranes. PPC function as the rate-limiting step in the activation of membrane enzymes such as superoxide dismutase. It has been suggested that ineffective activation of these antioxidant enzymes would lead to increased damage of membranes by reactive oxygen species, which could eventually lead to hearing loss if mitochondrial DNA were affected. A recent study (40) reported that lecithin supplementation for 6 mo safeguards cochlear mitochondrial function and prevents age-related hearing loss in rats.

    As a component of egg lecithin, choline is a required nutrient (41) that is essential for normal development of the brain (42). Choline has numerous important physiologic functions that include the synthesis of phospholipids, the metabolism of methyl and cholinergic neurotranmission. Eggs are one of the few food sources that contain high concentrations of choline (43). Studies in rats have demonstrated that supplementation of choline, during embryonic development or immediately following birth, can result in improved memory performance, which is maintained as the animal ages (44). Additional studies in humans are needed to verify these findings and to further determine the importance of dietary choline at differing life stages including pregnancy, infancy and old age.


    CONCLUSION
    If judged as a whole food, and not simply as a source of dietary cholesterol, the positive contribution of eggs to a healthy diet becomes apparent. Because eggs are a conventional food containing nutrients that play fundamental roles beyond basic nutrition, their promotion as a functional food should be considered. This discussion has examined the possible role of egg nutrients in the prevention and treatment of specific symptoms associated with chronic age-related diseases. Furthermore, evidence has been presented showing that the current blanket recommendations regarding dietary cholesterol and egg intake are unwarranted for the majority of people and are not supported by scientific data. The assumptions made by these recommendations are that dietary cholesterol consumption >300 mg/d translates directly into elevated plasma cholesterol levels and the development of CHD in all individuals. These assumptions are clearly flawed. First, a conservative estimate suggests that only 30% of the population would respond to dietary cholesterol. It has been determined that a reduction in dietary cholesterol of 100 mg/d would only slightly decrease plasma total cholesterol levels of those who are responsive. For example, if a responsive individual chose to eat two eggs in one day they would exceed the AHA recommended upper limit for cholesterol intake by 126 mg, which would suggest that they may experience a 0.05–0.07 mmol/L increase in plasma total cholesterol levels. However, as previously mentioned, persons who consume more than one egg a day do not have a greater relative risk for CHD than those who eat only one egg a week. There are populations that may benefit from decreasing dietary cholesterol intake such as those with diabetes who may possess an abnormality in the mechanism by which they transport cholesterol. However, the current recommendation is applied to the general population without taking individual differences into account. Furthermore, the revised guidelines only allow for eggs to be incorporated into a healthy diet if no other animal products are consumed. Because this guideline is unrealistic, it further promotes the public message that eggs should be avoided. The reality of the situation is that although egg intake has steadily declined since the original recommendations in the 1970s, CHD is still the leading cause of death in the U.S. today. Clearly, the current guidelines are not benefiting the public as a whole and may actually have negative nutritional implications.


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    Eggs and heart disease risk: perpetuating the misperception
    Donald J McNamara
    Egg Nutrition Center 1050 17th Street, NW Suite 560 Washington, DC 20036 E-mail: enc@enc-online.org
    Eggs and heart disease risk: perpetuating the misperception

    Although the report by Weggemans et al (1) confirms the findings from many recent reported analyses that dietary cholesterol has a small effect not only on plasma total and LDL cholesterol but also on plasma HDL cholesterol (2–4), their interpretation of the findings contradicts more than a decade of epidemiologic studies showing that dietary cholesterol is not a contributor to heart disease risk. The reviews by Howell et al (2), Clarke et al (3), McNamara (4), and Weggemans et al indicate that a 100-mg/d change in dietary cholesterol increases plasma total cholesterol concentrations by 0.06 mmol/L (2.3 mg/dL), LDL cholesterol by 0.05 mmol/L (1.9 mg/dL), and HDL cholesterol by 0.01 mmol/L (0.4 mg/dL). However, Weggemans et al conclude from their analysis that dietary cholesterol increases the ratio of total to HDL cholesterol and that adding an egg a day to the diet increases heart disease risk by 2%. This conclusion is difficult to accept given that a decade of epidemiologic studies indicates that eggs and dietary cholesterol are not significant factors in heart disease risk (5, 6).

    The problem is that although dietary cholesterol–mediated changes in total, LDL-, and HDL-cholesterol concentrations are constant relative to the dose, changes in the ratio of LDL to HDL cholesterol are a function of the actual value of each variable. For example, patient X with LDL and HDL concentrations of 3.1 mmol/L (120 mg/dL) and 1.0 mmol/L (40 mg/dL), respectively, has an LDL-HDL ratio of 3.00. Theoretically, adding an egg a day to this patient's diet would increase LDL and HDL concentrations to 3.2 mmol/L (123.8 mg/dL) and 1.1 mmol/L (40.8 mg/dL), respectively, resulting in a ratio of total to HDL cholesterol of 3.03, similar to the ratio of 0.04 predicted by Weggemans et al. In contrast, patient Y with LDL and HDL concentrations of 4.1 mmol/L (160 mg/dL) and 1.0 mmol/L (40 mg/dL), respectively, has a ratio of 4.00. Adding an egg a day to this patient's diet would increase the LDL concentration to 4.2 mmol/L (163.8 mg/dL), the HDL concentration to 1.1 mmol/L (40.8 mg/dL), and the ratio of LDL to HDL cholesterol by 0.01–4.01, not the predicted change of 0.04. Thus, an individual with a very low risk of myocardial infarction could, theoretically, increase their risk by 1.5%, whereas an individual with a high risk could increase their risk by 0.5%. These values represent maximal estimates because, as shown by Weggemans et al, the response of plasma LDL cholesterol to dietary cholesterol was attenuated when the ratio of polyunsaturated to saturated fatty acids (P:S) in the background diet was >0.7 [an increase of 0.04 mmol/L (1.4 mg/dL) with a diet low in saturated fat compared with an increase of 0.06 mmol/L (2.2 mg/dL) with a diet high in saturated fat with each additional increase of 100 mg cholesterol/d], whereas the response of plasma HDL cholesterol is unchanged. Under these conditions there would be no measurable change in the ratio of LDL to HDL cholesterol in our 2 hypothetical patients after adding one egg a day to their diets (ratio: 3.00–3.01 in patient X and 3.99–4.00 in patient Y).

    More importantly, I am surprised at the unfortunate interpretation of Weggeman et al's finding that egg restriction can reduce the risk of heart disease. Statistical significance and biological importance must be viewed as distinct concepts. The assertion that eating an egg a day increases the risk of heart disease by 2% (but only in those with low ratios of LDL to HDL cholesterol and a low dietary P:S) needs to be put in perspective relative to other risk factors: 1) the 72% increase in risk associated with a body mass index (in kg/m2) of 25–28.9 relative to a body mass index < 23 (7), 2) the 42% decrease in risk associated with the replacement of 5% of energy from saturated fat with 5% from unsaturated fat (8), and 3) the 51% decrease in risk associated with 1.5 h of vigorous walking 1 d/wk (9).

    The fact that no studies in the past decade have reported a significant relation between either egg consumption or dietary cholesterol intakes and heart disease risk (5) is consistent with the view that the hypothesis that dietary cholesterol is a risk factor for heart disease should be dismissed. A small, statistically significant increase in the ratio of total to HDL cholesterol has little biological importance concerning heart disease risk when considered relative to those dietary and lifestyle factors that do in fact contribute to heart disease risk. Concerning the suggestion by Weggeman et al that eggs make no important contributions to the diet, I refer them to a recent supplement of the Journal of the American College of Nutrition (10) in which the merits of egg consumption are documented. In an evaluation of the relation between dietary cholesterol and the risk of heart disease, it is crucial to not only have accurate estimates of risk but also a practical perspective of what a risk estimate represents.


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