How I Conquered High Cholesterol Through Diet and Exercise
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Dallas: American Heart Association. Specifically, egg consumption was limited to three whole eggs per week. This recommendation was based on several lines of available scientific evidence at that time. Early animal experiments conducted in rabbits fed with milk and egg yolks 44 or pure cholesterol showed a hypercholesterolemia and severe atherosclerosis. Subsequent nonhuman primate experiments noted that feeding egg yolks to rhesus monkeys elevated the plasma cholesterol level, which led to development of atherosclerotic lesions similar to that of human atherosclerotic plaque after months of feeding Reversibility of atherosclerosis was investigated in egg-yolk-induced hypercholesterolemic rhesus monkeys Feeding monkeys with cholesterol-free diets resulted in regression of atherosclerosis as demonstrated by significant reductions in occlusions of coronary arteries and in cholesterol content of atherosclerotic plaques.
Epidemiological observations have reported an association between dietary cholesterol intake and CHD risk and feeding with a high-cholesterol diet increased serum cholesterol concentrations Subsequent metabolic experiments in human subjects have documented an effect of dietary cholesterol on plasma TC and LDL-C levels Research over the last a few decades, however, has produced significant amount of data supporting a minimal or no effect of dietary cholesterol on blood cholesterol level or CHD risk.
The recent to edition of Dietary Guidelines for Americans contains no recommendation for dietary cholesterol intake In addition to an early study by Keys et al.
Analyses of epidemiological data have failed to find a significant impact on CHD risk by dietary cholesterol within populations As reviewed by Ravnskov 68 , in 11 reports from the prospective and retrospective epidemiological studies, dietary cholesterol was not different between cases and controls. Data also indicate that cholesterol feeding does not alter number of LDL particles — instead it increases cholesterol content of these particles leading to formation of large buoyant LDL Other nutritional components of a food, such as fats, can modulate the effects of dietary cholesterol on plasma levels.
Particularly, SFA is a major factor and acts synergistically with dietary cholesterol to induce hypercholesterolemia Addressing this topic, Keys et al. Similarly, significant associations between dietary cholesterol and CHD risk were abolished after covariates, including SFA, were taken into account 51 , A meta-analysis of prospective cohort studies found no evidence of an association between egg consumption and risk of CHD or stroke A similar meta-analysis of prospective cohort studies concluded that up to one egg daily may even contribute to a decreased risk of total stroke and that daily egg intake was not associated with CHD risk Thus, a considerable interindividual variation in response to a diet high in cholesterol has been observed.
As reviewed by McNamara et al. However, HDL-C appears to be less affected by this phenomenon An increase in non-HDL-C concentration was observed in lean and insulin sensitive individuals but not in lean and insulin resistant or obese and insulin resistant individuals after a 4-wk intervention with four eggs per day Overall, individual dietary recommendation with consideration of differences in response to dietary cholesterol intake as well as genetic variability influencing cholesterol metabolism is important to achieving prevention and treatment goals for hypercholesterolemia and to reducing CHD risk.
The strategy of reducing dietary saturated fat intake raises a critical question about what kinds of nutrients should be used to replace saturated fat, and several major macronutrients, such as carbohydrates and cis -unsaturated fatty acids, including PUFA and MUFA, have been tested in many investigations.
Meta-analyses of short-term controlled dietary trials have shown a favorable influence of PUFA on the ratio of atherogenic vs. Thus, TC, LDL-C and apoB levels were not different between women who consumed diets high and low in saturated fat, but with similar ratios of polyunsaturated to saturated fat In addition, in nonhuman primates, replacement of dietary saturated fat with PUFA 92 but not with MUFA 93 was shown to reduce coronary artery atherosclerosis. However, it could be postulated that the actual effects on overall CHD risk may be greater, considering that PUFA reduces inflammation and improves insulin resistance Furthermore, the amount of cholesterol consumed in the diet modulates the effects of saturated fat, as the increase in LDL-C at lower intakes of cholesterol was minimal compared to the substantial increase of LDL-C at higher intakes of cholesterol The average duration was 8 years, and the participants were men with a mean age of 65 years.
Although these effects may be of a lesser magnitude than those associated with PUFA, they were of a similar magnitude to those associated with carbohydrates 84 , , Triglycerides were significantly elevated with the carbohydrate diet, but tended to be lower with the MUFA diet.
In addition, plasma lipoprotein a , Lp a , concentrations were elevated with both diets, with a slightly larger increase observed for the carbohydrate diet Overall, these findings suggest that replacement of saturated fat with MUFA is a preferable regimen when compared to strategies using carbohydrate or protein as a replacement.
In line with these findings, a meta-analysis reported a modest but consistent lower TG level on the diets high in PUFA vs. It was noted that any dietary recommendations for the use of PUFA or MUFA in preference to the other should be based on outcomes other than cholesterol concentrations. The findings related to replacement of energy from saturated fat with carbohydrates have been much more complex.
Carbohydrate foods differ substantially in their quantitative and qualitative features with regard to micronutrients, phytochemicals, fibers, and other bioactive substances, which could in turn have differential effects on plasma lipids and CHD risk. SFA intake was lower in the intervention group vs. Among healthy subjects, replacement of saturated fat with carbohydrates resulted in reductions of TC and LDL-C across sex and ethnicity Triglyceride concentrations tended to be lower with the MUFA diet, but were significantly higher with the high carbohydrate diet.
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Of note, the dietary lipid responses varied on the basis of baseline lipid profiles, but they did not differ by metabolic syndrome or insulin resistance status Mixed results have been reported in diabetic patients with respect to the effects of dietary carbohydrates on plasma lipids A recent systematic analysis of 17 clinical trials among obese subjects reported that low-carbohydrate diets were associated with significant decreases in TG and increases in HDL-C, without impacting LDL-C Studies replacing saturated fat with carbohydrates have investigated the impact of carbohydrate intake on LDL particle size, which has been associated with CVD endpoints Individuals with pattern B have a higher proportion of small dense LDL particles, and thus more likely to have atherogenic dyslipidemia.
The amount of dietary carbohydrates was associated with a decrease in LDL particle size and an increase in LDL density, contributing to the atherogenic dyslipidemia Of note, proportions of saturated vs. One third of these individuals converted to pattern B on this diet. Thus, it was suggested that reduced fat consumption replaced with an increased intake of carbohydrates modifies lipid and lipoprotein profiles towards atherogenic dyslipidemia.
On the other hand, reductions in dietary carbohydrate, even in the context of a diet high in saturated fat, have been associated with increases in large and medium LDL particles, and decreases in small, dense LDL particles These observations indicate that dietary carbohydrates may be a driving force for atherogenic dyslipidemia. Another study in overweight men provided a more detailed view with respect to the effects of varying carbohydrates and saturated fat, as well as weight loss, on lipid profiles In this study, comparing low-carbohydrate diets with a high vs.
A 9-month intervention study in overweight and obese adults reported significantly increased LDL particle size after a low-carbohydrate diet, whereas there was no difference after a low-fat diet Of note the change in body weight was similar between these two groups. A Mediterranean-style diet with reduced energy intake from carbohydrate and fat but with increases in MUFA intake and increased energy intake from protein has been shown to reduce small LDL Overall, these findings suggest that dietary fat content may not have a major impact on atherogenic dyslipidemia, that carbohydrate metabolism impacts LDL particle quality rather than its quantity and that diets low in carbohydrate may help to improve LDL quality.
However, lower-fat and higher-carbohydrate diets, compared to higher-fat and lower-carbohydrate diets, may induce greater reductions in LDL-C concentrations particularly in individuals starting with pattern B.
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Therefore, beneficial effects of a high or a low carbohydrate diet on cardiovascular health remain to be clarified. Dietary sugar is a major source of carbohydrates, and research focused on sugar consumption has provided much evidence supporting a role of sugar in the development of cardiometabolic disease. Different kinds of sugar impact differentially on the lipid profile and its contribution to atherogenic dyslipidemia. Fructose is known to increase TG levels and impair insulin sensitivity, and has been shown, in several recent studies, to more adversely impact LDL particle subclass profile than glucose.
In a wk study among overweight and obese individuals, indices of postprandial TG h area under the curve, TG exposure and postprandial peak, but not fasting TG increased after fructose, but not after glucose intake Of note, fructose also increased small dense LDL particles.
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High fructose corn syrup HFCS has become a major source of fructose intake, and a recent study investigated whether there are differences in the lipid profile after consumptions of HFCS, glucose, or fructose alone These changes were comparable to the ones seen with fructose, but were greater than those seen with glucose In addition, among overweight schoolchildren, fructose intake predicted LDL particle size Consumption of carbohydrates with a higher GI was associated with an increased plasma TG concentration in a large observational study, and this observation was independent of age, BMI, exercise, and the intake of other macronutrients A meta-analysis of observational studies reported an association between the consumption of lower GI foods and lower TG and higher HDL-C concentrations A high GI was associated with an unfavorable lipoprotein subclass profile as determined by a nuclear magnetic resonance spectroscopy A Cochrane meta-analysis of 21 RCTs among subjects with at least one major CVD risk factor or a CHD diagnosis, where subjects were provided either dietary instruction or food for a minimum of four weeks, concluded that there is no significant effect of the GI value of the diet on fasting glucose, insulin, HbA1c, HDL-C, and TG concentrations In contrast, a meta-analysis of RCTs comparing studies that supplied at least one meal per day with a high or low GI value found significant reductions in TC [ It is important to distinguish between RCTs where participants were provided only dietary instructions to modify their dietary GI values, and those where some or all foods i.
To address these issues, Kristo et al. Two cross-over studies designed to maintain weight reported contradictory results , Studies by Stanhope et al. The GI of fructose is 23 compared with for glucose. In their studies, the calculated relative GI of the baseline complex-carbohydrate diet, the high-glucose intervention diet, and the high-fructose intervention diet, consumed during the 24 h blood collections, was 64, 83, and 38, respectively , , As expected, glucose and insulin excursions of the diets paralleled the GI, with exposure being highest on the glucose diet, intermediate on the complex-carbohydrate baseline diet, and lowest on the fructose diet.
However, individuals consuming the high-fructose diets with the lowest GI index and glycemic exposure exhibited increased visceral abdominal adipose tissue and decreased insulin sensitivity , and increases of LDL, apoB, and postprandial TG , In contrast, when individuals consumed high-glucose diets, postprandial plasma glucose and insulin excursions increased substantially , , however, insulin sensitivity and postprandial TG exposure, LDL, and apoB remained unchanged , , These findings underscore the importance of accurately assessing glucose and fructose content in study diets.
The authors noted that dietary fructose may be an important contributor to the inconsistent reported effects of dietary GI on metabolic risk factors, and that this together with other differences e.
It is likely that the fructose, and not the glucose, component of sucrose and HFCS is primarily responsible for their adverse metabolic effects There was a modest but direct association of coronary events with replacement of the same amount of energy with carbohydrates and no association of MUFA with coronary risk. Mozaffarian et al. Study duration was an independent predictor of risk reduction, with studies of longer duration showing greater benefits.
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A meta-analysis of 21 prospective cohort studies using a random-effects model, which allows heterogeneity of variance between studies, reported no significant association of saturated fat intake with CHD, stroke, or CVD Evaluation of the subset studies that adjusted for total energy, which has been shown to be relevant in evaluating nutrient-disease relations , yielded similar results.
As the authors noted, due to insufficient information in the component studies with respect to dietary carbohydrates or PUFA, the meta-analysis did not asses the effects on CVD risk of replacing specific amount of saturated fat with either carbohydrate or PUFA. The meta-analysis stated that there is insufficient evidence from prospective epidemiological studies to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD.
In these studies, however, PUFA was supplied as safflower oil margarine to substitute for animal fats, which may contain trans fatty acids. Trans fatty acids significantly increase CHD risk, and were not evaluated in these studies.
CHOLESTEROL DOES NOT CAUSE HEART DISEASE
Trans fatty acids originate from two independent dietary sources: industrially produced and naturally occurring i. In , a systematic review and meta-analysis of 13 RCTs assessed the impact of ruminant trans fatty acids intake on changes in cardiovascular risk factors No relationship was seen between intake of ruminant trans fatty acids up to 4.
It was concluded that trans fatty acids from natural sources, up to 4. In , a systematic review and meta-analysis of data from long-term prospective observational studies of a broad range of both dietary and biomarker fatty acid FA measures in coronary disease was published The meta-analysis then concluded that current evidence does not clearly support cardiovascular guidelines that encourage high consumption of PUFA and low consumption of total SFA. Another recent observational finding by Virtanen et al. Numerous meta-analysis and comprehensive reviews have evaluated the effects of marine —derived n-3 PUFA EPA and DHA on primary and secondary prevention of CVD and all-cause mortality, with many reporting beneficial effects for the former but not for the latter.
Another meta-analysis of RCTs in patients with a history of CVD did not find sufficient evidence of a secondary preventive effect of n-3 PUFA supplementation against cardiovascular events A subgroup analyses indicated significant associations between higher intakes of olive oil and reduced risk of all-cause mortality, cardiovascular events, and stroke, whereas the MUFA subgroup analyses did not reveal any significant risk reduction Taken together, these findings underscore the complexity of assessing the effects of dietary interventions on cardiovascular risk and that there are likely many factors contributing to the variability in observations.
These factors may include the presence of substantial heterogeneity in study settings and designs, publication biases, issues related with self-reported measures of dietary intakes as well as adherence measurements to study diet, a limited number of studies focused on certain types of diet or dietary composition, the approaches used to dissect the effects based on studies where substantially different approaches have been used, and many more. Lifestyle changes recommended for those with high cholesterol levels include smoking cessation, limiting alcohol consumption, following a low saturated fat diet, avoiding trans -fat, increasing physical activity, and maintaining a healthy weight Dietary advice given by health professionals in practice can provide only a modest decrease in cholesterol levels, and may be sufficient in the treatment of mildly elevated cholesterol In a systematic review of 19 RCTs, the efficacy of individualized dietary advice to modify fat intake to lower TC levels in free-living subjects and the efficacy of different dietary recommendations were evaluated The percentage reduction in TC attributable to dietary advice after at least six months of intervention was 5.
Including both short- and long-term studies, the effect was 8. The latter diet was of similar efficacy to diets that aimed to lower total fat intake or to raise the polyunsaturated to saturated fatty acid ratio. It was concluded that individualized dietary advice for reducing cholesterol concentration is modestly effective in free-living subjects, and more intensive diets achieve a greater reduction in serum cholesterol concentration Failure to comply fully with dietary recommendations is the likely explanation for this limited efficacy. An updated Cochrane database systematic review analysis of 44 randomized studies with at least three months duration, excluding trials to reduce weight or those involving dietary supplementations assessed the effects of providing dietary advice to achieve sustained dietary changes or improved cardiovascular risk profile among healthy adults Compared to no advice, dietary advice reduced TC by 0.
In addition, dietary advice increased fruit and vegetable intake by 1. It was concluded that dietary advice appears to be effective in bringing about modest beneficial changes in diet and cardiovascular risk factors over approximately 12 months, but longer-term effects are not known. A systematic review and meta-analysis of five RCTs in diabetic individuals compared individualized nutrition therapy with dietary advice At short term 6 or 12 months , nutrition therapy compared with dietary advice was associated with a 0.
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Modification of plasma lipid profile by low-fat dietary interventions was dependent on menopausal status of women. In contrast, in a strict environment, such as metabolic ward studies dietary changes can induce a greater reduction in cholesterol concentrations. Denke et al. Similar efficacy was observed in six of the seven trials of diet for secondary prevention. The effectiveness of dietary therapy was enhanced when individualized counseling was used, follow-up was maintained, and weight reduction was achieved.
Responses of blood lipids and lipoproteins to individual SFA intake are heterogeneous. Cholesterol-raising effects of SFA depend on chain-length as these effects decrease as chain lengths increase. Overall effects of dietary cholesterol on blood cholesterol level are limited and modulated by other nutritional components. Founded on early observations on the relationship between occupational physical activity PA and chronic disease risk e. They found that the sedentary bus drivers had higher rates of CVD mortality than their active counterparts, the conductors, and postulated that physically active work had a cardioprotective effect.
This work was extended to postmen and postal clerks, where postmen who walked or cycled while delivering mail had much lower rates of heart disease than the postal clerks who had sedentary jobs Further, Morris et al. Around the same time, in , Ralph Paffenbarger et al. They found that the CVD death rate was significantly lower in the most active compared with sedentary workers. In , Paffenbarger et al.
Numerous other studies have documented an inverse association between occupational PA and CVD risk In , to test the hypothesis that PA outside the occupational domain would provide cardioprotective benefits, Morris et al. Another study of Morris et al. A low PA when combined with another risk factor i. Over the past few decades, there has been a substantial accrual of epidemiological evidence on the inverse relationship between leisure time PA and CVD. A recent meta-analysis of 26 prospective cohort studies , individuals and 20, CHD events with follow-ups of 4 to 25 years reported significant reductions in CVD mortality in both high and moderate levels of self-reported leisure time PA Although being used in the literature interchangeably, PA and exercise denote different concepts.
Physical Activity PA appears to impact CVD risk through beneficial effects on several factors, including adiposity, insulin sensitivity, glycemic control, type 2 diabetes incidence, blood pressure, blood lipids, endothelial function, hemostasis, and inflammatory defense systems After multivariate adjustments i.
Aadahl et al. PA intervention was based on lifestyle consultations and subjects on lipid-lowering medications were excluded from analysis. A 5-year follow up study by the same investigators demonstrated significant improvements in TC, LDL-C, and TG among 4, participants aged 30—60 years, with an additional significant improvement in HDL-C seen only in men In contrast, compared with the ref group, all-cause mortality risk was elevated in those who did not meet PA guidelines and whose HDL-C was either normal or low.
CVD mortality hazard ratios were similar, although confidence intervals were wider. At the end of the study, TC Compared to usual care, lifestyle interventions achieved significant improvements in TC Combined strategies had greater and significant effects on blood lipid profile than PA alone strategy. The authors noted that this finding may be related to methodological shortcomings in exercise-only interventions such as low adherence, insufficient exercise volume or length of intervention In addition, evidence suggests that it may take up to two years for a previously sedentary obese individual to attain enough volume of exercise to modify risk factors.
In addition, waist circumference and BMI were decreased. A recent small study among inactive older women with hypertriglyceridemia compared the effects of different patterns of walking on PP TG levels Aerobic exercise training AET includes cardiorespiratory endurance exercises such as jogging, running, and cycling In a wk shorter duration study of young women, LeMura et al. A review article examined the effects of AET on blood lipids in exercise training intervention trials of more than 12 wks The increase in HDL-C with AET was inversely associated with its baseline level, but there were no significant associations with age, sex, weekly volume of exercise, or with exercise-induced changes in body weight or peak oxygen effect VO 2max.