Thursday, 22 December 2011

40 Things You Should Know – The Science (part 9)

Point 44

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


 A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.


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.


 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.


 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.


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.

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


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.

Revisiting dietary cholesterol recommendations: does the evidence support a limit of 300 mg/d?


The perceived association between dietary cholesterol (DC) and risk for coronary heart disease (CHD) has resulted in recommendations of no more than 300 mg/d for healthy persons in the United States. These dietary recommendations proposed in the 1960s had little scientific evidence other than the known association between saturated fat and cholesterol and animal studies where cholesterol was fed in amounts far exceeding normal intakes. In contrast, European countries, Asian countries, and Canada do not have an upper limit for DC. Further, current epidemiologic data have clearly demonstrated that increasing concentrations of DC are not correlated with increased risk for CHD. Clinical studies have shown that even if DC may increase plasma low-density lipoprotein (LDL) cholesterol in certain individuals (hyper-responders), this is always accompanied by increases in high-density lipoprotein (HDL) cholesterol, so the LDL/HDL cholesterol ratio is maintained. More importantly, DC reduces circulating levels of small, dense LDL particles, a well-defined risk factor for CHD. This article presents recent evidence from human studies documenting the lack of effect of DC on CHD risk, suggesting that guidelines for DC should be revisited.

Rethinking dietary cholesterol.



The perceived notion that dietary cholesterol is associated with increased risk for coronary heart disease (CHD) has led to dietary recommendations of no more than 300 mg/day for healthy populations in the USA. This study will review the recent evidence that challenges the current dietary restrictions regarding cholesterol while it presents some beneficial effects of eggs (an icon for dietary cholesterol) in healthy individuals.


The European countries, Australia, Canada, New Zealand, Korea and India among others do not have an upper limit for cholesterol intake in their dietary guidelines. Further, existing epidemiological data have clearly demonstrated that dietary cholesterol is not correlated with increased risk for CHD. Although numerous clinical studies have shown that dietary cholesterol challenges may increase plasma LDL cholesterol in certain individuals, who are more sensitive to dietary cholesterol (about one-quarter of the population), HDL cholesterol also rises resulting in the maintenance of the LDL/HDL cholesterol ratio, a key marker of CHD risk.


The lines of evidence coming from current epidemiological studies and from clinical interventions utilizing different types of cholesterol challenges support the notion that the recommendations limiting dietary cholesterol should be reconsidered.

Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations.



Extensive research has not clearly established a link between egg consumption and risk for coronary heart disease. The effects of egg intake on plasma lipids and low-density lipoprotein (LDL) atherogenicity in healthy populations need to be addressed.


The lack of connection between heart disease and egg intake could partially be explained by the fact that dietary cholesterol increases the concentrations of both circulating LDL and high-density lipoprotein (HDL) cholesterol in those individuals who experience an increase in plasma cholesterol following egg consumption (hyperresponders). It is also important to note that 70% of the population experiences a mild increase or no alterations in plasma cholesterol concentrations when challenged with high amounts of dietary cholesterol (hyporesponders). Egg intake has been shown to promote the formation of large LDL, in addition to shifting individuals from the LDL pattern B to pattern A, which is less atherogenic. Eggs are also good sources of antioxidants known to protect the eye; therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts.


For these reasons, dietary recommendations aimed at restricting egg consumption should not be generalized to include all individuals. We need to acknowledge that diverse healthy populations experience no risk in developing coronary heart disease by increasing their intake of cholesterol but, in contrast, they may have multiple beneficial effects by the inclusion of eggs in their regular diet.

Point 33

Normal weight men and women overestimate exercise energy expenditure.



The limited potential of exercise to induce weight loss could be partly due to the overestimation of the energy cost of exercise. The objectives of this study were twofold: 1) to investigate whether men and women are able to accurately estimate exercise energy expenditure (EE); and 2) to determine whether they have the ability to accurately compensate for the EE of exercise during a buffet-type meal.


Sixteen (8 men, 8 women) moderately active (VO2 peak=45.4±7.7, normal weight (BMI=22.8±3.3 kg/m2) individuals, aged 20-35 years, were studied. They were blinded to two randomly assigned experimental conditions: a 200 and a 300 kcal (measured by indirect calorimetry) exercise sessions that were performed on a treadmill at the same intensity (50% of VO2 peak). At the end of each exercise session individuals were asked to estimate EE of the exercise sessions and to then eat the caloric equivalent of their estimated exercise EE from a buffet-type meal.


Estimated EE was higher than measured EE for both the 200 kcal (825.0±1061.8 vs. 200.1±0.7 kcal, P<0.05) and 300 kcal (896.9±952.4 vs. 300.2±0.7 kcal, P<0.05) sessions. Further, post-exercise energy intake was higher than measured EE for the 200 kcal (556.8±204.4 vs. 200.1±0.7 kcal, P<0.001) and the 300 kcal (607.2±166.5 vs. 300.2±0.7 kcal, P<0.001) sessions. Although post-exercise energy intake was lower than estimated EE, no significant differences were noted.


These results suggest that normal weight individuals overestimate EE during exercise by 3-4 folds. Further, when asked to precisely compensate for exercise EE with food intake, the resulting energy intake is still 2 to 3 folds greater than the measured EE of exercise.

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