Textbook of Lifestyle Medicine - Labros S. Sidossis

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replaces them in the diet.

      In populations following Western dietary habits, it has been shown that when 5% of the energy derived from SFAs is replaced by PUFAs, LDL cholesterol concentrations decrease. In turn, this change can generate a decrease in CHD occurrence and deaths. Males from the Health Professionals Follow‐up Study and females from the Nurses' Health Study (NHS) were followed prospectively for 24–30 years; people with the highest consumption of PUFAs had 20% lower CHD risk compared to those who consumed a diet low in PUFAs. Notably, for every 5% decrease of energy coming from SFAs, the CHD risk decreased by 25% when an equal amount of energy was replaced by PUFAs. Similarly, combined scientific data from randomized controlled trials (RCTs) have demonstrated that individuals with increased PUFA intake, instead of SFAs, were 20% less likely to develop CHD, compared with those following a higher SFA diet. The protective effect against CHD incidence was 10% for every 5% of energy replacement by PUFAs, and the magnitude of this beneficial effect was contingent on the duration of the intervention.

      Mixed results have been reported when total carbohydrates replace SFA, showing either no overall benefit, reduction, or even increased CVD risk. However, when separating whole grains from refined carbohydrates, isocaloric substitution of whole grains for SFA is associated with a decreased risk of CHD; CHD risk does not change in the case of isocaloric substitution of refined starches/added sugars for SFA.

      Current guidelines recommend decreasing saturated fat intake to improve blood lipids and reduce cardiovascular risk. Dairy products have been thought to increase the risk of CVD, due to their high SFA, cholesterol, and calorie content. Indeed, most of the existing dietary guidelines for the prevention and management of cardiometabolic risk recommend low‐fat or nonfat dairy consumption. However, robust evidence from prospective studies shows no increase or even a small benefit in CVD risk from high dairy consumption (e.g., yogurt and cheese). The potential mechanisms of the attenuating effects of dairy foods remain to be fully elaborated but seem to involve food matrix effects on fat bioavailability, changes in the gut microbiome, and glucose, insulin, and other hormonal responses.

       Key Point

      Robust evidence from prospective studies shows no increase or even a small benefit in CVD risk from high dairy consumption.

      TFAs are present in foods such as meat and dairy products from ruminant animals (i.e., cattle, sheep, goats, and camels). However, more TFAs are generated during the manufacturing process of partially hydrogenated vegetable and marine oils, such as margarines, confectionary fats, and fat spreads. Foods that commonly contain margarine (such as deep‐fried foods, baked goods, and snacks) are therefore high in TFAs. Compared to animal fats, hydrogenated vegetable oils are more stable and less likely to become rancid during repeated deep‐frying processes and have greater stability at room temperature. Thus, they are widely used for commercial purposes.

      However, TFA intake has been positively and robustly associated with increased risk of CHD and related mortality. The Zutphen Elderly Study showed a positive correlation between intake of TFAs and 10‐year risk for CHD. It was shown that for every 2% increase in TFA‐derived energy at baseline, there was 28% greater risk to develop CHD within the next decade. In the NHS, the 20‐year CHD risk for the women with high trans‐fat intake was associated with 1.3‐fold, i.e. 130% greater risk, compared to their counterparts with the lowest TFA intake, particularly the younger women.

      The underlying mechanism by which TFAs increase CVD risk is probably related to changes in lipoprotein profile. Even moderate levels of TFA intake may lead to increased LDL concentrations, while high‐density lipoprotein (HDL) concentrations usually decrease. A meta‐analysis of RCTs exploring the impact of either naturally occurring or industrially produced TFAs on plasma LDL to HDL ratio revealed that, independently of their source, all TFAs can lead to an increase in the LDL to HDL ratio. However, others have challenged these findings; they suggested that the high variability in types of oils and interventions used in the various studies precludes drawing safe conclusions on the effect of specific types of TFAs on lipoproteins levels and CHD risk (i.e., naturally occurring or industrially produced TFAs). Indeed, a systematic review and meta‐analysis of prospective studies found that industrially produced but not naturally occurring TFAs are associated with increased risk of CHD.

       Key Point

      Industrially produced but not naturally occurring TFAs are associated with increased risk of CHD.

      Another mechanism through which high TFA consumption can add to the CVD risk is by increasing inflammation and endothelial dysfunction. Data from the Nurses' Health Study I (NHS‐I) have shown that women who were free of CVD, cancer, and diabetes at baseline and who consumed a diet high in TFAs were more likely to have increased levels of inflammation and endothelial dysfunction. The positive relationship between TFA intake and systemic inflammation was also evident in an NHS‐II cohort; a modest mitigation of this association after controlling for serum lipid levels led to the hypothesis that TFAs impact on serum lipids may act as mediator of this positive association. In 2018, the WHO published an action package to reduce TFA use in the global food supply called the “REPLACE action package.” Based on a six‐step strategy, each country should implement actions to eliminate the industrially produced TFAs.

       Key Point

      Each country should implement actions to eliminate the industrially produced TFAs.

      The evidence linking simple carbohydrate‐rich foods with CHD is quite strong. High intake of refined carbohydrates, especially sugar‐sweetened beverages, has been consistently associated with increased risk of CHD. However, the characterization of carbohydrates according to their glycemic load (GL) may be a better way to categorize carbohydrates for predicting CHD risk, compared to the more simplistic categorization into “simple” and “complex” carbohydrates. Consumption of high GL meals has been associated with increased CHD incidence in female subjects followed prospectively for 10 years. Interestingly, those consuming a high GL diet had twice the likelihood to develop CHD, compared with those refraining from a high GL diet. In the NHS (76,000 female subjects), refined carbohydrates were associated with increased coronary heart disease, presumably due to increased dietary GL.

       Key Point

      Consumption of high GL meals has been associated with CHD incidence in female subjects followed prospectively for 10 years.

      Dietary fiber intake seems to be beneficial for human health. A meta‐analysis of 185 prospective studies yielded a 15–30% reduction in all‐cause and cardiovascular mortality, T2DM, and colorectal cancer in individuals with the highest dietary fiber intake, compared with those in the lowest consumption category. In the same meta‐analysis, 58 clinical trials were separately analyzed, showing significantly lower body weight, systolic blood pressure, and total cholesterol in people in the high dietary fiber category compared to the lower fiber category. The best outcomes were observed when daily intake of dietary fiber was 25–29 g. In another meta‐analysis of 17 prospective studies from 1997 to 2014, it was found that for every 10 g/day increase in fiber intake, there is a 10% decrease

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