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View Full Version : Meta-analysis of prospective cohort studies evaluating the association of saturated f



MaxBrenner
19-10-2011, 04:11 PM
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 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824152/?tool=pubmed)

MaxBrenner
19-10-2011, 04:22 PM
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 (http://www.ajcn.org/content/92/2/458.long)

MaxBrenner
19-10-2011, 04:44 PM
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 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950931/?tool=pubmed)

MaxBrenner
19-10-2011, 05:04 PM
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? (http://www.ajcn.org/content/93/4/684.long)

TLS
19-10-2011, 05:08 PM
Hey Max. Have you thought about adding a Max's Conclusions section after the article?

MaxBrenner
19-10-2011, 05:11 PM
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 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974193/?tool=pubmed)

DKD
19-10-2011, 06:21 PM
You had me at 'meta-analysis'.

MaxBrenner
19-10-2011, 06:30 PM
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 :D

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.

MaxBrenner
19-10-2011, 06:48 PM
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? (http://jn.nutrition.org/content/134/1/187.full)


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.

MaxBrenner
19-10-2011, 06:49 PM
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 (http://www.ajcn.org/content/75/2/333.full)

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.

MaxBrenner
19-10-2011, 06:51 PM
Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet.
Mutungi G, Ratliff J, Puglisi M, Torres-Gonzalez M, Vaishnav U, Leite JO, Quann E, Volek JS, Fernandez ML.
Source
Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
Abstract
Carbohydrate-restricted diets (CRD) significantly decrease body weight and independently improve plasma triglycerides (TG) and HDL cholesterol (HDL-C). Increasing intake of dietary cholesterol from eggs in the context of a low-fat diet maintains the LDL cholesterol (LDL-C)/HDL-C for both hyper- and hypo-responders to dietary cholesterol. In this study, 28 overweight/obese male subjects (BMI = 25-37 kg/m2) aged 40-70 y were recruited to evaluate the contribution of dietary cholesterol from eggs in a CRD. Subjects were counseled to consume a CRD (10-15% energy from carbohydrate) and they were randomly allocated to the EGG group [intake of 3 eggs per day (640 mg/d additional dietary cholesterol)] or SUB group [equivalent amount of egg substitute (0 dietary cholesterol) per day]. Energy intake decreased in both groups from 10,243 +/- 4040 to 7968 +/- 2401 kJ (P < 0.05) compared with baseline. All subjects irrespective of their assigned group had reduced body weight and waist circumference (P < 0.0001). Similarly, the plasma TG concentration was reduced from 1.34 +/- 0.66 to 0.83 +/- 0.30 mmol/L after 12 wk (P < 0.001) in all subjects. The plasma LDL-C concentration, as well as the LDL-C:HDL-C ratio, did not change during the intervention. In contrast, plasma HDL-C concentration increased in the EGG group from 1.23 +/- 0.39 to 1.47 +/- 0.38 mmol/L (P < 0.01), whereas HDL-C did not change in the SUB group. Plasma glucose concentrations in fasting subjects did not change. Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS.

Full Text - Dietary Cholesterol from Eggs Increases Plasma HDL Cholesterol in Overweight Men Consuming a Carbohydrate-Restricted Diet (http://jn.nutrition.org/content/138/2/272.long)

Christian
05-11-2011, 10:00 PM
Dont listen to him saturated fat raises LDL and LDL is bad and kills you!

Yet from the same perspective why dont the dimwits say that sugar raises blood glucose and insulin and high blood glucose kills you... Seems to be just as retarded a way of thinking.

Thanks for this im not at home and on my phone and needed a reference to repy to this

"and i dont care what studies you show up, if thats wrong then our entire cardiac department needs to change all of their literature, which is based on solid references which i have personally reviewed (some of not all of them).
"

Retardos

MaxBrenner
05-11-2011, 11:12 PM
Do we really need to minimize saturated fat?
By Alan Aragon __________________________________________________
Intro & background
If you conduct a simple word association game with just about anyone, “saturated fat” would immediately be linked to “bad” or “heart attack.” Any way you slice it, saturated fat (SFA) has earned an automatic partnership with the risk for cardiovascular disease (CVD). This conditioned response isn’t surprising, considering that SFA has been heavily touted as a CVD risk factor for roughly the last 40 years. To the present day, major public health organizations concur that SFA should be proactively minimized. The latest USDA Dietary Guidelines for Americans limits SFA intake to less than 10% of total calories.1 The same recommendation is shared by the joint committee of the FAO/WHO.2 The American Heart Association (AHA) is even more prohibitive, limiting SFA to less than 7% of total caloric intake.3
With all the big guys claiming that SFA intake is a significant risk factor for CVD, it’s easy to assume the current body of research evidence supports their recommendations. But does it? This question is the crux of the controversy surrounding SFA. In this article, I’ll attempt to provide answers, as well as reasons why the answers are far from simple. Before we dive in, let me clarify that coronary heart disease (CHD), characterized by atherosclerosis, angina, and heart attack, is the most common type of CVD. According to the AHA, CHD is currently the leading cause of death in the US.4
Observational research origins
Beginning in the late 1950’s, the Seven Countries Study, led by Ancel Keys, aimed to investigate the relationship between diet and CVD.5 Keys showed a positive correlation between elevated serum cholesterol and CVD. By proxy, dietary intake of saturated fat and cholesterol were also indicted via their association with increased serum cholesterol levels.6 This so- called “lipid hypothesis” has perhaps been the most influential factor in shaping the current paradigm of dietary recommendations.
But alas, science never sleeps. The fact remains that the Seven Countries data was observational, as opposed to being derived from randomized controlled trials (RCTs), thus unable to establish causal relationships – only associations. These correlations are wide-open to questioning because they’re subject to a multitude of confounding variables.
Challenging age-old assumptions
In recent years, researchers have re-examined the relationship of saturated fat & CVD, casting considerable doubt upon its clinical significance. A poignant example is a review by Volk, examining the methodology of the studies implicating saturated fat in the development of heart disease.7 He concluded that CHD does not appear to be due to an increased intake of saturated fat
and cholesterol, which have been major components of the human diet for thousands of years. Volk leans more toward blaming on the agricultural boom and its associated processing of foods that conflict with our hunter-gatherer genome. This, along with a widespread sedentary lifestyle shift, combine to exacerbate the prevalence of heart disease – not an increase in saturated fat per se. Volt eloquently concludes the following regarding the early research basis for the lipid hypothesis:
“The many problems associated with research into fats and CHD make it logical to conclude that the lipid hypothesis of atherosclerosis is based on several false premises, including linear causation, fallacious national mortality statistics, biased age and subject selection, and methodological inaccuracies.”
Battle of the recent meta-analyses & systematic reviews
A large enough body of evidence has accumulated over the past few decades to allow investigators to make quantitative attempts at summing up the situation. It would be nice and simple if there were no disagreements, but that’s not the case. Siri-Tarino et al conducted a meta-analysis of prospective epidemiologic studies, and found no significant association between SFA and increased risk of CHD or CVD.8 However, Scarborough et al criticize this study for adjusting for serum cholesterol, which is associated with CHD and CVD.9 In their view, serum cholesterol is an integral part of the causal link between SFA intake and heart disease, therefore, adjusting for this variable erroneously altered the outcomes. To quote them,
“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.”
Adding food for thought to the findings of Siri-Tarino et al, a meta-analysis by Mozaffarian et al determined that replacing the consumption of SFA with polyunsaturated fatty acid (PUFA) would significantly reduce rates of CHD.10 Specifically, each 5% increase in the proportion of energy from PUFA reduced the risk of CHD events by 10%. Importantly, only RCTs were included in the analysis, whereas Siri-Tarino et al looked at observational studies. But keep in mind that Mozaffarian et al admit that the trials in their study have several limitations, including a lack of double-blinding, questionable compliance, variable methods of estimating/reporting intake, and open enrollment where participants were allowed to drop in & drop out during the trial. Nevertheless, when examining nutrients in isolation, PUFA (from non-hydrogenated vegetable sources) appears to have the strongest evidence basis as a replacement for SFA.
Variable consequences of SFA intake replacement
During the past few decades, the persistent public health recommendation to lower total fat intake has led to a decrease in SFA consumption, which as been replaced by an increase in carbohydrate more so than PUFA or MUFA.11 In a recent review on this particular topic, Siri-Tarino et al warn that the primary emphasis on SFA reduction needs to be reevaluated, since it neglects to provide any specific recommendation of what to consume in its place.12 The replacement of SFA with carbohydrate generally appears to have no benefit. The authors
Alan Aragon’s Research Review – April 2011
[Back to Contents] Page 2assert that certain subsets of the population (i.e., those with diabetes and/or insulin resistance) might not benefit, and actually incur harm by replacing SFA intake with carbohydrate – particularly refined carbohydrate, which can contribute to atherogenic dyslipidemia.
Replacing SFA with MUFA has yielded inconsistent results. This is likely due to differences in the constituents of MUFA- containing foods. Vegetable-derived MUFA is often accompanied by phytochemicals & phenolic compounds that provide health benefits independently of the fatty acids within the MUFA-containing plant foods.13 Further direct investigation in this area is required to clear up the inconsistencies. One of the alternatives with clearly adverse cardiovascular health consequences is replacing SFA with an excess of partially hydrogenated vegetable oils, which have a high concentration of trans fatty acids (TFA).14,15

MaxBrenner
05-11-2011, 11:12 PM
Results from a recent symposium
On May 28-29, 2010, an invitation-only scientific consensus meeting was held at the Department of Nutrition at the University of Copenhagen. To the benefit of the uninvited, the results of the symposium were published in the American Journal of Clinical Nutrition.16 Conclusions from this momentous symposium, which focused on the relationship between SFA & CHD, are as follows:
␣ In the Seven Countries Study, the higher risk of CHD mortality associated with intake of SFA may be biased because of many potential confounding factors. Thus, it can only be viewed at best as hypothesis-generating.
␣Most randomized controlled trials (RCTs) have been statistically underpowered and poorly designed, but some have supported the benefits of substituting PUFA for SFA.
␣ The weight of the evidence indicates that substituting PUFA for SFA is beneficial for improving blood lipids and CHD prevention, but there is no evidence to support the benefit of substituting refined carbohydrates for SFAs. Furthermore, the quality of carbohydrate source in relation to replacing SFA has not been adequately investigated.
␣Replacing SFA with low-GI (or less-refined) carbohydrate foods may lower the risk of CHD. Carbohydrates are likely to have fewer adverse effects on blood lipids and CHD risk in healthy and physically active individuals than in overweight/sedentary folks with insulin resistance.
␣ There’s insufficient evidence the replacement of SFA with MUFA on CHD risk mainly because the research on MUFA are confounded by the food sources of MUFAs (e.g., dairy and meats) in Western dietary patterns.
␣Industrially derived trans fatty acids (TFAs) are strongly associated with a higher risk of CHD than SFAs, but interestingly (and unfortunately for Paleo fans), the lowest
risk was found for diets high in n−6 PUFA and low in TFA.
␣ Although LDL cholesterol is the most widely accepted lipid biomarker for CHD risk, evidence from the Prospective Studies Collaboration meta-analysis supports that the ratio of total cholesterol to HDL cholesterol is a more powerful predictor than LDL alone.
␣Apolipoprotein B and non-HDL cholesterol are also important biomarkers of clinical risk assessment, particularly in individuals with the metabolic syndrome. Specific LDL subparticles can contribute to CHD risk, but their levels tend to be correlated with other lipid measures.
␣The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. A comprehensive assessment of multiple biomarkers of CHD risk, including total and HDL cholesterol, blood pressure, body fatness, glucose tolerance, and inflammatory markers, can substantiate the effects of diet on CHD risk.
␣Food-based recommendations are more practical for the general public than nutrient-based dietary advice. The total matrix of a food is more important than just its fatty acid content when predicting the effect of a food on CHD risk. For example, the effect of SFA from cheese on blood lipids and CHD may be counterbalanced by the content of protein, calcium, or other components in cheese known to provide multiple health benefits.
␣ Specific types of SFA may actually impart health benefits; therefore blanket indictments of SFA are unwarranted. For example, rumenic acid, trans vaccenic acid, and short-chain fatty acids may modify the effect on CHD risk. Another example is stearic acid, which reduces risk factors of CVD.
␣ Most epidemiologic studies and several intervention studies support the benefits of Mediterranean dietary pattern (which is low in SFA and high in MUFA) on CVD risk factors and concrete outcomes.
␣ The data indicating the cardiovascular risk-lowering benefits of other dietary patterns, such as traditional Asian diets which are very low in SFA, are mainly derived from observational studies, not RCTs. However, evidence from both epidemiologic studies and RCTs indicate that long- chain omega-3 fatty acids prevent CHD.
␣To effectively communicate current findings, the dietary pattern that decreases CVD risk should be delivered in practical terms. A healthy dietary pattern is primarily plant- based and low in SFA, but can include lean meats and low- fat dairy products in small-to-modest amounts.
␣Because CVD is the leading cause of death in most countries, the relation of diet to CVD should be a prominent aspect of dietary recommendations. However, other crucially important health issues (obesity, cancer, and osteoporosis) should also be considered; currently there is no clear relation of SFA intake to these outcomes.*
*I bolded the above for emphasis.
Research gaps in the symposium & beyond
As acknowledged by the authors of the symposium’s conclusions, research on the effect of SFA replacement with specific food types & sources is lacking. Genomics, although currently in its infancy, may be important in explaining variable responses to diet. Unaddressed in the symposium summary was the potential impact of exercise & athletic goals on the relationship between SFA & CVD. In addition, questions still
[Back to Contents] Page 3
Alan Aragon’s Research Review – April 2011
remain about the effect of energy balance – specifically, chronic hypocaloric versus hypercaloric states common to the sports & fitness-oriented populations.
Further gaps in the current literature involve the impact of the optimization of macronutrient amounts, with specific emphasis on protein. However, toward answering these questions, Clifton et al recently pooled together the results of three 12-week RCTs comparing the effect of a high-protein diet (110g; 27% of total kcals) with a standard-protein diet (60g; 16% of total kcals) in obese men & women with elevated triacylglycerols (TAG).17 Total weight and fat loss on the whole were not significantly different, but the high-protein treatments caused greater TAG reduction. In subjects whose TAG was above the median, greater reductions in TAG, bodyweight, abdominal fat, and total cholesterol occurred in the high-protein treatments.
Notably, none of the three studies in Clifton et al’s pooled analysis exceeded 10% of total kcals from SFA. In contrast, Wycherley et al compared the long-term (12-month) effects of a high-SFA/low-carb diet with a low-SFA/high-carbohydrate diet in overweight and obese subjects.18 The high-SFA/low-carb diet caused a greater reduction in triacylglycerol (TAG), and increases in HDL-C & total cholesterol.

MaxBrenner
05-11-2011, 11:13 PM
The low-carb group had a non-significantly greater weight loss. Unfortunately, body composition was not assessed. A potentially important finding was that although both diets caused improvement in pulse wave velocity (PVW – an indirect measure of aortic stiffness), a 2% reduction in flow-mediated dilation (FMD) occurred in the low- carb group by the end of the trial. Since FMD is an index of endothelial function, this raised concerns about an increased risk of adverse cardiovascular events in the low-carb group.
In contrast to the above findings by Clifton et al, a previous 12- month study by Keogh et al found that FMD was not affected by either a high- or low-carb diet.19 However, both diets were low in SFA (7% in the low-carb, 4% in the high-carb diet). Another difference was that the low-carb group in Clifton et al’s study consumed 20-40g carbs per day, while Keogh et al’s low-carb subjects consumed substantially more carbohydrate (appx 140g vs. 20-40g/day). This presumably allowed more room for the consumption of cardioprotective, yet carb-dominant foods (i.e., fruits & vegetables).
After their 12-month study comparing low-SFA diets, Keogh et al compared a high-SFA/low-carb diet with a low-SFA/high- carbohydrate diet in overweight and obese subjects.20 The high- SFA/low-carb diet caused a greater reduction in bodyweight and abdominal fat, but importantly, this diet did not impair flow- mediated dilation (FMD). The latter outcome is in direct conflict with those of Wycherley et al.18 Nevertheless, what the design lacks in trial length (2 months vs. 12 months), it compensates for in its assessment of regional changes in body fat. The greater reduction in abdominal fat in the high-SFA/low-carb group is an outcome whose implications are arguably at least equally important as a reduction in FMD.21
A systematic review that warrants special attention
Hession et al did a systematic review of RCTs comparing the effects of low-carb vs. Low-fat/low-calorie diets on obesity and CVD risk.23 Their findings were rather eye-opening. Unlike
meta-analyses that have limited their investigation to the associations between SFA and biomarkers of CVD, this one cut straight to the chase by also comparing the macro-effects and subjects’ ability to adhere to the diets. The outcomes are summarized as follows:
␣ Low-carb/high-protein (LC/HP) diets are more effective at 6 months and are as effective, if not more, as LF diets in reducing weight and CVD risk up to 1 year.
␣LC/HP diets are generally more effective at increasing HDL-C, and decreasing triacylglycerol levels & systolic blood pressure.
␣ A higher attrition (drop-out) rate in the low-fat compared with the LC/HP groups suggests a patient preference for the latter approach instead of the public health recommendation of a low-fat/high-carb diet.
␣ Overall, the systematic review concludes that LC/HP diets are more effective at 6 months and are as effective, if not more, than low-fat diets for lowering bodyweight and cardiovascular disease risk in trials lasting up to 1 year.
It’s important to note that the diets in this review varied in terms of both macronutrition and food choices. The authors themselves acknowledge that there’s currently a lack of consistent and robust study designs, and thus there’s no cohesive definition of a LC/HP diet. Another limitation is the use of obese, sedentary subjects minus a structured training protocol. Trained subjects involved in regular or progressive exercise would almost certainly alter the outcomes, and this remains to be investigated. Unfortunately, as much as it’s relevant to our interests, there’s no pressing clinical need to study these effects in the healthy/athletic population.
Conclusions & applications
Going back to the original question, does the current body of research evidence support the authoritative public health recommendations to minimize saturated fat intake? There isn’t a definitive yes or no answer for this. After examining the full range of evidence, the best answer (aside from the old standby of “it depends”) is not really. To begin with, at approximately 12% of total calories, the general population is not consuming prodigious amounts of SFA beyond what’s recommended.22 This alone challenges the urgency of the ‘official’ public health guidelines to force SFA intake further down.
According to the latest stats from the USDA,1 the primary dietary sources of SFA in the American diet are full fat cheese (9% of total SFA intake), pizza (6%), grain-based desserts (6%), chicken and chicken-mixed dishes (6%), and sausage, franks, bacon, & ribs (5%). The full breakdown is at the bottom of page 26 of the latest USDA-DGA. While it’s possible that a diet predominated with these foods could cause health problems, it’s doubtful that SFA per se would be the main culprit. To reiterate, the problem would more likely be the lack of whole foods causing a disproportionately high calorie density, and corresponding lack of essential nutrition. I’m referring to both macro- and micronutrition, as well as beneficial phytonutrients & zoonutrients present in whole & minimally processed foods.
Alan Aragon’s Research Review – April 2011
[Back to Contents] Page 4
A recent review by Micha and Mozaffarian suggests that placing the focus on reducing SFA intake is not likely to produce the intended benefits.13 They make the important point that even the evidence-based tactic of replacing SFA with PUFA pales in importance compared to other dietary CVD threats such as insufficient intake of omega-3 fatty acids, low intake of fruits & vegetables, and a high intake of trans fats & salt. The concluding statement of their paper is worth quoting since it captures the importance of seeing the big picture & not fixating on isolated details:
“Finally, although investigation of individual nutrients provides important information on potential underlying mechanisms of health effects, people make decisions about eating whole foods that contain multiple macro- and micronutrients in various amounts. Thus, food-based scientific research and policy recommendations may be most relevant in the modern era to understand and reduce the pandemics of chronic disease occurring in nearly all nations.”
A simple solution is to stay physically active and hit your macronutrient targets over a reasonable variety of mostly whole and minimally processed plant & animal foods. Neurotically checking every food label for SFA and basing food choices on its absence or minimization would be missing the forest for the trees. A parallel example of this erroneous move would be avoiding fruit due to its fructose content, or avoiding nuts due to their high proportion of fat. Because of the neglect of context, neither of these tactics is inherently preventive of CVD. The same applies to focusing on SFA while blurring out the surrounding factors.

MaxBrenner
05-11-2011, 11:14 PM
References
1. UDSA Center for Nutrition Policy and Promotion. Dietary guidelines for Americans. Jan 2011. [USDA-CNPP]
2. Holt R. The Food and Agriculture Organization/World Health Organization expert report on diet, nutrition and prevention of chronic diseases. Diabetes Obes Metab. 2003 Sep;5(5):354. [Medline]
3. Lichtenstein AH, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006 Jul 4;114(1):82-96. [Medline]
4. American Heart Association. Cardiovascular disease statistics. [AHA]
5. Kromhout D, et al. Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May;49(5):889- 94. [Medline]
6. Mancini M, Stamler J. Diet for preventing cardiovascular diseases: light from Ancel Keys, distinguished centenarian scientist. Nutr Metab Cardiovasc Dis. 2004 Feb;14(1):52-7. [Medline]
7. Volk MG, et al. An examination of the evidence supporting the association of dietary cholesterol and saturated fats with serum cholesterol and development of coronary heart disease. Altern Med Rev. 2007 Sep;12(3):228-45. [Medline]
8. Siri-Tarino PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46. [Medline]
9. Scarborough P, et al. Meta-analysis of effect of saturated fat intake on cardiovascular disease: overadjustment obscures true associations. Am J Clin Nutr. 2010 Aug;92(2):458-9; author reply 459. [Medline]
10. Mozaffarian D. et al. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252. [Medline]
11. Centers for disease Control & Prevention. Trends in intake of energy and macronutrients: United States, 1971–2000. Morb Mortal Wkly Rep 53(04):80-2 [CDC]
12. Siri-Tarino PW, et al. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):502-9. [Medline]
13. Micha R, Mozaffarian D. Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids. 2010 Oct;45(10):893- 905. [Medline]
14. Mozaffarian D, et al. Health effects of trans-fatty acids: experimental and observational evidence. Eur J Clin Nutr. 2009 May;63 Suppl 2:S5-21. [Medline]
15. Mozaffarian D, Clarke R. Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils. Eur J Clin Nutr. 2009 May;63 Suppl 2:S22- 33. [Medline]
16. Astrup A, et al. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr. 2011 Apr;93(4):684-8. [Medline]
17. Clifton PM. et al. High protein diets decrease total and abdominal fat and improve CVD risk profile in overweight and obese men and women with elevated triacylglycerol. Nutr Metab Cardiovasc Dis. 2009 Oct;19(8):548-54. [Medline]
18. Wycherley TP, et al. Long-term effects of weight loss with a very low carbohydrate and low fat diet on vascular function in overweight and obese patients. J Intern Med. 2010 May;267(5):452-61. [Medline]
19. Keogh JB, et al. Effects of weight loss on a low- carbohydrate diet on flow-mediated dilatation, adhesion molecules and adiponectin. Br J Nutr. 2007 Oct;98(4):852- 9. [Medline]
20. Keogh JB, et al. Effects of weight loss from a very-low- carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. Am J Clin Nutr. 2008 Mar;87(3):567-76. [Medline]
21. Seifalian AM, et al. Obesity and arterial compliance alterations. Curr Vasc Pharmacol. 2010 Mar;8(2):155-68. [Medline]
22. German JB, Dillard CJ. Saturated fats: what dietary intake? Am J Clin Nutr. 2004 Sep;80(3):550-9. [Medline]
23. Hession M, et al. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev. 2009 Jan;10(1):36-50. [Medline]
Alan Aragon’s Research Review – April 2011
[Back to Contents]
Page 5

dave
05-11-2011, 11:30 PM
They make the important point that even the evidence-based tactic of replacing SFA with PUFA pales in importance compared to other dietary CVD threats such as insufficient intake of omega-3 fatty acids, low intake of fruits & vegetables, and a high intake of trans fats & salt.

Well I'm screwed.

MaxBrenner
05-11-2011, 11:34 PM
Dave you are screwed far beyond those realms :D

dave
05-11-2011, 11:39 PM
If we go into any more details you may have to put a NSFW disclaimer in the thread title.

Got any studies in your collection on fibre, fruit/veg intake etc on ldl/hdl level with no change in SFA intake?

Too lazy to search myself.

MaxBrenner
05-11-2011, 11:49 PM
Too lazy to search myself.Got some but, This :D

Its way past my bed time to be doing this shit :D

MaxBrenner
05-11-2011, 11:52 PM
Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Saturated fat and cardiometabolic risk factors, coron... [Lipids. 2010] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/20354806)


Micha R (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Micha%20R%22%5BAuthor%5D), Mozaffarian D (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mozaffarian%20D%22%5BAuthor%5D).
Source

Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

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.

MaxBrenner
05-11-2011, 11:54 PM
Saturated fat, carbohydrate, and cardiovascular disease. Saturated fat, carbohydrate, and cardiovascul... [Am J Clin Nutr. 2010] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/20089734)


Siri-Tarino PW (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22%5BAuthor%5D), Sun Q (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22%5BAuthor%5D), Hu FB (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22%5BAuthor%5D), Krauss RM (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22%5BAuthor%5D).
Source

Department of Atherosclerosis Research Children's Hospital Oakland Research Institute Oakland, CA, USA.

Abstract

A focus of dietary recommendations for cardiovascular disease (CVD) prevention and treatment has been a reduction in saturated fat intake, primarily as a means of lowering LDL-cholesterol concentrations. However, the evidence that supports a reduction in saturated fat intake must be evaluated in the context of replacement by other macronutrients. Clinical trials that replaced saturated fat with polyunsaturated fat have generally shown a reduction in CVD events, although several studies showed no effects. An independent association of saturated fat intake with CVD risk has not been consistently shown in prospective epidemiologic studies, although some have provided evidence of an increased risk in young individuals and in women. Replacement of saturated fat by polyunsaturated or monounsaturated fat lowers both LDL and HDL cholesterol. However, replacement with a higher carbohydrate intake, particularly refined carbohydrate, can exacerbate the atherogenic dyslipidemia associated with insulin resistance and obesity that includes increased triglycerides, small LDL particles, and reduced HDL cholesterol. In summary, although substitution of dietary polyunsaturated fat for saturated fat has been shown to lower CVD risk, there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate. Furthermore, particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.

MaxBrenner
05-11-2011, 11:56 PM
Dietary Carbohydrate Modifies the Inverse Association Between Saturated Fat Intake and Cholesterol on Very Low-Density Lipoproteins. Dietary Carbohydrate Modifies the Inverse Ass... [Lipid Insights. 2011] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/21912485)


Wood AC (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Wood%20AC%22%5BAuthor%5D), Kabagambe EK (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kabagambe%20EK%22%5BAuthor%5D), Borecki IB (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Borecki%20IB%22%5BAuthor%5D), Tiwari HK (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Tiwari%20HK%22%5BAuthor%5D), Ordovas JM (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Ordovas%20JM%22%5BAuthor%5D), Arnett DK (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Arnett%20DK%22%5BAuthor%5D).
Source

Department of Epidemiology, University of Alabama at Birmingham, School of Public Health, Birmingham, AL 35294, USA.

Abstract

We aimed to investigate the relationship between dietary saturated fat on fasting triglyceride (TG) and cholesterol levels, and any mediation of this relationship by dietary carbohydrate intake. Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n = 1036, mean age ± SD = 49 ± 16 y) were included. Mixed linear models were run with saturated fat as a predictor variable and fasting TG, very low density lipoprotein cholesterol (VLDL-C), low density cholesterol (LDL-C) and high density cholesterol (HDL-C) as separate outcome variables. Subsequent models were run which included dietary carbohydrate as a predictor variable, and an interaction term between saturated fat and carbohydrate. All models controlled for age, sex, BMI, blood pressure and dietary covariates. In models that included only saturated fat as a predictor, saturated fat did not show significant associations with fasting lipids. When carbohydrate intake and an interaction term between carbohydrates and saturated fat intake was included, carbohydrate intake did not associate with lipids, but there was an inverse relationship between saturated fat intake and VLDL-C (P = 0.01) with a significant interaction (P = 0.01) between saturated fat and carbohydrate with regard to fasting VLDL-C concentrations. Similar results were observed for fasting TG levels. We conclude that, when controlling for carbohydrate intake, higher saturated fat was associated with lower VLDL-C and TGs. This was not the case at higher intakes of carbohydrate. This has important implications for dietary advice aimed at reducing TG and VLDL-C levels.

dave
05-11-2011, 11:58 PM
Obviously not that tired. Nice work.

MaxBrenner
05-11-2011, 11:58 PM
One-year effects of increasingly fat-restricted, carbohydrate-enriched diets on lipoprotein levels in free-living subjects. One-year effects of increasingly fat-r... [Proc Soc Exp Biol Med. 2000] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/11082213)


Knopp RH (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Knopp%20RH%22%5BAuthor%5D), Retzlaff B (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Retzlaff%20B%22%5BAuthor%5D), Walden C (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Walden%20C%22%5BAuthor%5D), Fish B (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Fish%20B%22%5BAuthor%5D), Buck B (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Buck%20B%22%5BAuthor%5D), McCann B (http://www.ncbi.nlm.nih.gov/pubmed?term=%22McCann%20B%22%5BAuthor%5D).
Source

Northwest Lipid Research Clinic and the Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington 98104, USA. rhknopp@u.washington.edu

Abstract

Restriction of all dietary fat is a popular strategy for restricting saturated fat intake to lower LDL cholesterol. Some authorities advise the restriction of fat intake to the extreme of less than 10% of daily energy on the assumption that more fat restriction is better. The two studies described herein address questions relating to whether increasing fat restriction produces proportionally increasing benefit on cardiovascular risk factors in hyperlipidemic subjects. The first study is the Dietary Alternatives Study (DAS). The DAS was conducted in 531 male Boeing employees over a 2-year period. Subjects were defined as hypercholesterolemic (HC) or combined hyperlipidemic (CHL) based on age-specific 75th percentiles for plasma LDL-C and triglyceride levels. Hypothesis test analyses were performed at 1 year. HC subjects were randomized to diets taught to attain fat intakes of 30, 26, 22, and 18% (Diets levels 1-4, respectively). CHL subjects (slightly fewer in number) were randomized to Diets 1-3. After 1 year, subjects' total fat intakes were 27, 26, 25, and 22% of energy (en%), resulting in saturated fat intakes of 8, 7, 7, and 6%, respectively. In HC subjects the greatest LDL-C decrease was with Diet 2 (mean of 13.4%) and in CHL subjects with Diet 1 (7.0%). Surprisingly, plasma triglyceride concentrations rose in HC subjects 20% and 40% above baseline on Diets 3 and 4, respectively, with reciprocal reductions in HDL cholesterol of 2.5% and 3%, respectively. Furthermore, apo B reductions were attenuated below Diet 2 in HC subjects and Diet 1 in CHL subjects, and no further reductions were seen in plasma glucose and insulin concentrations, blood pressure, or body weight. Measurements of plasma total fatty acid composition showed a slight increase in plasma palmitate, whereas stearate decreased slightly, supporting the idea that de novo synthesis of palmitic acid was increased in the chronic high-carbohydrate feeding condition. The second study asked if the most effective diet in HC subjects, Diet 2, has an equivalent effect in women and men. To answer this question, men and women Boeing employees were taught the closely similar National Cholesterol Education Program (NCEP) Step II diet. After 6 and 12 months, equivalent reductions in LDL cholesterol were observed in women compared with men. HDL cholesterol levels in men were unchanged from baseline at 6 and 12 months, but were reduced 8% in HC women, with accompanying decreases of 18% in HDL2-cholesterol and 5% in apoprotein A-I (all P < 0.01). These data indicate that intakes of fat below about 25 en% and carbohydrate intake above approximately 60 en% yield no further LDL-C lowering in HC and CHL male subjects and can be counterproductive to triglyceride, HDL-C, and apo B levels. This lack of benefit appears to be explained by an enhanced endogenous synthesis of palmitic acid, which negates the benefit of further saturated fat restriction. The HDL-C decrease in HC women may have a similar cause and points to an underlying male-female difference. Alternative dietary approaches to limit saturated fat intake deserve intensive study.

MaxBrenner
05-11-2011, 11:59 PM
Obviously not that tired. Nice work.
Got a second wind :D

dave
06-11-2011, 12:00 AM
Got a second wind :D

Too many mars bars as a late night snack.

MaxBrenner
06-11-2011, 12:02 AM
10 squares of cadbury choc!

MaxBrenner
06-11-2011, 12:31 AM
The complex and important cellular and metabolic functions of saturated fatty acids. The Complex and Important Cellular and Metabolic Functions of Saturated Fatty Acids (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974191/)


Legrand P (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Legrand%20P%22%5BAuthor%5D), Rioux V (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rioux%20V%22%5BAuthor%5D).
Source

Laboratoire de Biochimie-Nutrition Humaine, Agrocampus Rennes, INRA USC 2012, 65 rue de Saint-Brieuc, CS 84215, Rennes Cedex, France. philippe.legrand@agrocampus-ouest.fr

Abstract

This review summarizes recent findings on the metabolism and biological functions of saturated fatty acids (SFA). Some of these findings show that SFA may have important and specific roles in the cells. Elucidated biochemical mechanisms like protein acylation (N-myristoylation, S-palmitoylation) and regulation of gene transcription are presented. In terms of physiology, SFA are involved for instance in lipogenesis, fat deposition, polyunsaturated fatty acids bioavailability and apoptosis. The variety of their functions demonstrates that SFA should no longer be considered as a single group.