The changing roles of dietary carbohydrates: from simple to complex

The dietary recommendations made for carbohydrate intake by many organizations/agencies have changed over time. Early recommendations were based on the need to ensure dietary sufficiency and focused on meeting micronutrient intake requirements. Because carbohydrate-containing foods are a rich source of micronutrients, starches, grains, fruits, and vegetables became the foundation of dietary guidance, including the base of the US Department of Agriculture's Food Guide Pyramid. Dietary sufficiency recommendations were followed by recommendations to reduce cholesterol levels and the risk for cardiovascular disease; reduction in total fat (and hence saturated fat) predominated. Beginning in the 1970s, carbohydrates were recommended as the preferred substitute for fat by the American Heart Association and others to achieve the recommended successive reductions in total fat and low-density lipoprotein cholesterol (LDL-C). Additional research on fats and fatty acids found that monounsaturated fatty acids could serve as an alternative substitution for saturated fats, providing equivalent lowering of LDL-C without concomitant reductions in high-density lipoprotein cholesterol and increases in triglycerides witnessed when carbohydrates replace saturated fat. This research led to a sharper focus in the guidelines in the 1990s toward restricting saturated fat and liberalizing a range of intake of total fat. Higher-fat diets, still low in saturated fatty acids, became alternative strategies to lower-fat diets. As the population has become increasingly overweight and obese, the emergence of the metabolic syndrome and its associated disruptions in glucose and lipid metabolism has led to reconsiderations of the role of carbohydrate-containing foods in the American diet. Consequently, a review of the evidence for and against high-carbohydrate diets is important to put this controversy into perspective. The current dietary recommendations for carbohydrate intake are supported by the evidence.     

Diet, lipids, and coronary heart disease

This review has highlighted some of the experimental studies in animals and humans that have shown an important link between dietary change and atherosclerosis. This relationship was further supported by population studies showing a key role for saturated fat intake in the determination of serum cholesterol level and the prediction of CHD. Recent data linking dietary cholesterol independent of serum cholesterol level to the prediction of CHD were discussed as well. Various components of the diet and their effects on lipid and lipoproteins were reviewed. The chief factors in the diet which raise cholesterol and low-density lipoprotein cholesterol (LDL-c) are dietary cholesterol, saturated fat, and excess calories leading to obesity. Dietary factors useful in lowering cholesterol and low-density lipoprotein cholesterol include monounsaturated fats, polyunsaturated fats, and dietary fiber, which can be substituted for saturated fats. The usefulness of a special class of polyunsaturated oil, the omega-3 fatty acids, in both lowering triglyceride levels and preventing thrombosis was also discussed. Although alcohol raises the HDL-c level, it is not clear that its use offers protection against CHD, and its risks clearly outweigh its advantages in this regard. Regular aerobic exercise is recommended as a healthier alternative to raising high-density lipoprotein cholesterol. Also discussed was postprandial lipemia, which may prove to be another indicator of risk of CHD. Finally, the recent NCEP dietary guidelines were discussed along with practical suggestions as to their implementation.     

Genetic factors associated with response of LDL subfractions to change in the nature of dietary fat

A preponderance of dense low density lipoprotein (LDL) particles is associated with an increased risk of coronary heart disease. It has been shown that dense LDL levels can be modified by diet. We investigated the contribution of polymorphisms in the genes for apolipoprotein (apo) B, apo AIV, lipoprotein lipase (LPL) and cholesterol ester transfer protein (CETP) to variation in the changes in plasma concentrations of dense LDL between a high saturated and a high polyunsaturated fatty acid diet. A total of 46 freeliving individuals (19 men and 27 women) completed a crossover trial with two dietary interventions of 4 weeks each, a high saturated fat diet (providing 21% energy from saturated fat and 3% energy from polyunsaturated fat) and a high polyunsaturated fat diet (providing 11% energy as saturated fat and 10% energy as polyunsaturated fat). Overall, the change in dense LDL between the saturated and polyunsaturated fat period was 0.17+/-0.33 mmol/L and this change was similar in men and women. Of the polymorphisms studied only variation in the apo AIV gene causing the substitution of histidine for glutamine at position 360 (Q360H) was associated with significant differences in the change in dense LDL concentration. Apo AIV Q/H individuals (n=6) showed a three-fold greater change in dense LDL cholesterol unadjusted for Lp(a) levels than Q/Q individuals (0.46+/-0.27 versus 0.12+/-0.31 mmol/L, p=0.02). The greater decrease in dense LDL cholesterol with an increase in polyunsaturated fat seen in those with the apo AIV H360 variant, who represent roughly 10% of the general population, suggests that they may benefit most from a PUFA rich lipid lowering diet.     

Effects of a low-fat diet on plasma lipoprotein levels

Lowering the intake of fat to decrease serum cholesterol levels has unknown effects on the proportion of cholesterol in low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Twenty normolipidemic nonvegetarians were given dietary instruction and supervision in a low-fat, semivegetarian diet for three months. Mean consumption of total fat, saturated fat, and cholesterol decreased, whereas intake of carbohydrate increased significantly on a low-fat diet. Plasma LDL levels decreased by 18% and HDL levels by 7% from prestudy baseline levels. The LDL/HDL ratio declined by 11%. Plasma triglyceride levels and body weight were unchanged. In individual subjects, the decrements in consumption of saturated fat and the increments in ingestion of polyunsaturated fat were each significantly correlated with decreases in LDL. One year after the subjects had returned to a self-selected diet, levels of dietary saturated fat and cholesterol and the plasma LDL/HDL ratio remained significantly below prestudy levels. This study and others suggest that a low-fat, high-carbohydrate diet favorably affects the plasma LDL/HDL proportion by decreasing LDL on a percentage basis 2 1/2 to three times more than it decreases HDL.     

Ern?hrung bei diabetischer Dyslipid?mie

Dyslipidemia in diabetes is characterized by low high-density lipoprotein (HDL) cholesterol, high triglyceride levels and higher concentrations of atherogenic lipoprotein molecules. Various interventions are of importance in the nutritional therapy of dyslipidemia. An increased intake of unsaturated fatty acids from vegetable oils at the expense of saturated fatty acids lowers low-density lipoprotein (LDL) cholesterol. Trans-fatty acids (food sources: fat spreads and foods with partially hydrogenated fat, fried foods, fat-rich baked goods and sweets) cause an even more detrimental lipoprotein profile compared to saturated fatty acids and their intake should be limited. Significant reductions of LDL cholesterol are also achievable by fiber-rich foods and foods enriched with plant sterols and stanols. A reduction of body weight, an increase in physical activity and a limitation of alcohol consumption to moderate amounts are effective interventions to control triglyceride and HDL cholesterol levels. Triglycerides can also be reduced by supplementation with long-chain ??3 fatty acids (fish oil). Higher proportions of dietary carbohydrates cause higher triglyceride levels, therefore, moderation of carbohydrates in favor of unsaturated fatty acids can be an effective dietary strategy and the major focus is to limit the consumption of foods and beverages with added saccharose or fructose.     

Evidence-based guideline of the German Nutrition Society: carbohydrate intake and prevention of nutrition-related diseases

The relative contribution of nutrition-related chronic diseases to the total disease burden of the society and the health care costs has risen continuously over the last decades. Thus, there is an urgent necessity to better exploit the potential of dietary prevention of diseases. Carbohydrates play a major role in human nutrition - next to fat, carbohydrates are the second biggest group of energy-yielding nutrients. Obesity, type 2 diabetes mellitus, dyslipoproteinaemia, hypertension, metabolic syndrome, coronary heart disease and cancer are wide-spread diseases, in which carbohydrates could have a pathophysiologic relevance. Correspondingly, modification of carbohydrate intake could have a preventive potential. In the present evidence-based guideline of the German Nutrition Society, the potential role of carbohydrates in the primary prevention of the named diseases was judged systematically. The major findings were: a high carbohydrate intake at the expense of total fat and saturated fatty acids reduces the concentrations of total, LDL and HDL cholesterol. A high carbohydrate consumption at the expense of polyunsaturated fatty acids increases total and LDL cholesterol, but reduces HDL cholesterol. Regardless of the type of fat being replaced, a high carbohydrate intake promotes an increase in the triglyceride concentration. Furthermore, a high consumption of sugar-sweetened beverages increases the risk of obesity and type 2 diabetes mellitus, whereas a high dietary fibre intake, mainly from whole-grain products, reduces the risk of obesity, type 2 diabetes mellitus, dyslipoproteinaemia, cardiovascular disease and colorectal cancer at varying evidence levels. The practical consequences for current dietary recommendations are presented.     

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.     

Effects of dietary fats versus carbohydrates on coronary heart disease: A review of the evidence

Recommendations arising from the traditional diet-coronary heart disease (CHD) paradigm, which focuses on effects of total and saturated fat on serum total and low-density lipoprotein cholesterol, may have failed to reduce CHD risk and inadvertently exacerbated dyslipidemia, insulin resistance, and weight gain, particularly among individuals who are older, female, sedentary, or obese. A suitable dietary paradigm must consider types and qualities of fats and carbohydrates consumed, their effects on a range of intermediary risk factors, and characteristics that may modify individual susceptibility. Based on current evidence, replacement of total, unsaturated, and even possibly saturated fats with refined, high-glycemic index carbohydrates is unlikely to reduce CHD risk and may increase risk in persons predisposed to insulin resistance. In contrast, a diet that is 1) rich in whole grains and other minimally processed carbohydrates; 2) includes moderate amounts of fats (approximately 30%–40% of total energy), particularly unsaturated fats and omega-3 polyunsaturated fats from seafood and plant sources; 3) is lower in refined grains and carbohydrates; and 4) eliminates packaged foods, baked goods, and fast foods containing trans fatty acids, will likely reduce the risk of CHD.     

Effects of exercise, dietary cholesterol, and dietary fat on blood lipids

Exercise, a low fat diet, or a diet low in saturated fat content can each lower plasma total cholesterol and low-density lipoprotein (LDL) cholesterol. We investigated whether these factors together could prevent the lipid-raising effects of dietary cholesterol. Ten healthy, athletic, normolipidemic male volunteers were studied. Two diets of 4 weeks duration each were compared in a randomized, blind crossover design. Diets were identical except for cholesterol content: one contained 600 mg/d; the other 200 mg/d. Both diets contained 15% of calories as protein, 55% as carbohydrate, 30% as fat, and the polyunsaturated fat to saturated fat ratio was 1.5. Exercise level and body weight were kept constant in each subject. As compared with plasma values obtained following the 200-mg/d cholesterol diet, mean values following the 600-mg/d cholesterol diet significantly increased for LDL cholesterol and apolipoprotein B by 10% and 13%, respectively. Mean plasma triglycerides, high-density lipoprotein 2 and 3, and apolipoprotein A-1 levels did not change significantly. Individual responses, however, were highly variable. Three subjects increased LDL cholesterol by more than 25%; 2 subjects increased LDL cholesterol by 10% to 25%; and 5 subjects had 5% or less change in LDL cholesterol. A dietary cholesterol increase can significantly elevate plasma LDL cholesterol and apolipoprotein B in certain normolipidemic, healthy men even when they are exercising regularly and consuming a moderately fat restricted, low saturated fat diet. Dietary cholesterol restriction may therefore be justifiable even when other life-style and dietary measures to minimize blood cholesterol are undertaken.     

Carbohydrate restriction and cardiovascular risk

Originally developed as a strategy for weight loss, diets based on restriction of carbohydrates were traditionally of concern because of the assumed increased cardiovascular risk if the carbohydrates were replaced with fat. It now appears that such diets are associated with an improvement in markers of cardiovascular risk, even with higher saturated fat intake and even in the absence of weight loss. Various evidence supports this paradigm shift: 1) carbohydrate restriction improves markers of atherogenic dyslipidemia (triglycerides, high-density lipoprotein cholesterol, apolipoprotein B-apolipoprotein A-1 ratio) and reduces the more atherogenic small, dense low-density lipoprotein cholesterol; 2) high amounts of dietary carbohydrates increase de novo fatty acid synthesis and plasma triglycerides; and 3) large, long-term studies of traditional dietary fat reduction continue to fail to demonstrate the predicted improvement in cardiovascular disease risk. Cardiovascular disease is the leading cause of morbidity and mortality in the Western world. It seems appropriate to consider carbohydrate reduction as a useful, if not the preferred, alternative to low-fat diets, which have met with limited success.     

Dietary fats, fatty acids, and their effects on lipoproteins

All saturated fatty acids, with the notable exception of stearic acid (C18:0), raise low-density lipoprotein (LDL) cholesterol levels. A few less ubiquitous fatty acids also have LDL cholesterol effects. Trans-monounsaturated fatty acids, at equivalent doses of saturated fatty acids, raise LDL cholesterol. Polyunsaturated fatty acids, at three times the dose of saturated fatty acids, lower LDL cholesterol. Higher intakes of most fatty acids raise high-density lipoprotein (HDL) cholesterol, with the notable exception of trans-monounsaturated fatty acids, which lower HDL cholesterol to the same extent as carbohydrate when either is substituted for other dietary fatty acids. Conjugated linoleic acids containing both cis and trans bonds and cis-monounsaturated fatty acids neither raise nor lower cholesterol concentrations of lipoproteins. The omega-3 fatty acids from fish lower triglyceride levels. Although dietary composition remains an important, modifiable predictor of dyslipidemia, overconsumption of any form of dietary energy may replace overconsumption of saturated fat as the primary factor that increases lipid and lipoprotein levels.     

A moderate-fat diet for combined hyperlipidemia and metabolic syndrome

A low-fat diet is recommended for hyperlipidemia. However, low-density lipoprotein (LDL) responses depend on the type of hyperlipidemia (ie, simple hypercholesterolemia or combined hyperlipidemia). In combined hyperlipidemia, which is typical of patients with metabolic syndrome, LDL levels are only one third as responsive to fat and cholesterol as simple hypercholesterolemia. The diminished dietary sensitivity of combined hyperlipidemia is explained by diminished intestinal absorption of cholesterol, a feature of metabolic syndrome. In turn, combined hyperlipidemia is caused by heightened lipid secretion by the liver. A moderate-fat, moderate-carbohydrate diet employing allowable fats has the promise of reducing endogenous lipoprotein production in combined hyperlipidemia. Triglyceride, LDL, and small-dense LDL should be lower, and high-density lipoprotein, apoprotein A-I, and buoyant LDL should be higher. A test of this dietary strategy on lipoproteins and downstream benefits on inflammatory mediators, oxidative stress, and vascular reactivity is now underway.     

Apolipoprotein E polymorphisms, dietary fat and fibre, and serum lipids: the EPIC Norfolk study.

AIMS: To investigate whether blood lipid response to dietary fat and fibre vary according to the apolipoprotein E (APOE) gene locus. METHODS AND RESULTS: Regression analysis of intake of dietary fat and lipid fractions according to APOE gene loci was assessed by Pyrosequencing and validated with restriction fragment length polymorphism in 22 915 participants of the Norfolk arm of the European Prospective Investigation of Cancer. There were significant (P < 0.001) differences in serum lipids according to genotype, highest total and low-density lipoprotein (LDL) cholesterol, and lowest high-density lipoprotein and triglycerides in epsilon4/epsilon4 individuals. There were positive associations between total and saturated fat and serum total and LDL cholesterol, and significant inverse associations (P < 0.001) between polyunsaturated fat and dietary fibre and lipid fractions overall. Associations were in the same direction for epsilon2, epsilon3, and epsilon4 expressing individuals with no significant interactions between diet and genotype group on blood lipids, except in the 3% individuals expressing epsilon2/epsilon4 (P < 0.05) in whom the associations were doubled. CONCLUSION: In this largest study to date, ApoE gene loci status does not confer exemption from population targets to reduce dietary saturated fat and increase dietary fibre in order to reduce blood lipids and risk of coronary heart disease.     

Dietary factors and Alcoholic Cirrhosis

Mortality from cirrhosis in many countries deviates markedly from that expected for a given per capita alcohol intake. We investigated the possibility that dietary factors might explain the deviation expected and actual mortality rates in different countries. Deviations from expected cirrhosis mortality was calculated as a percentage for 17 different countries, all of whom had carrier rates for hepatitis B virus of less than 2%. The percentage of deviation was correlated with dietary intake of saturated fat, polyunsaturated fat, cholesterol, and also with mortality from ischemic heart disease. The percentage of deviation correlated inversely with dietary cholesterol (r = -0.86, p 0.001) and saturated fat (r = -0.80, p 0.001) and positively with polyunsaturated fats (r = -0.55 p 0.05). This suggests that both saturated fat and cholesterol protect against alcoholic cirrhosis while polyunsaturated fats promote cirrhosis. The correlation between percentage of deviation and ischemic heart disease (r = -0.78, p 0.002) suggests that those factors that promote ischemic heart disease protect against alcoholic cirrhosis.     

Improvement of the omega 3 index of healthy subjects does not alter the effects of dietary saturated fats or n-6PUFA on LDL profiles

Background and AimsDietary fat composition is known to modulate circulating lipid and lipoprotein levels. Although supplementation with long chain omega-3 polyunsaturated fatty acids (LCn-3PUFA) has been shown to reduce plasma triglyceride levels, the effect of the interactions between LCn-3PUFA and the major dietary fats consumed has not been previously investigated.MethodsIn a randomized controlled parallel design clinical intervention, we examined the effect of diets rich in either saturated fatty acids (SFA) or omega-6 polyunsaturated fatty acids (n-6PUFA) on plasma lipid levels and lipoprotein profiles (lipoprotein size, concentration and distribution in subclasses) in subjects with an adequate omega 3 index. Twenty six healthy subjects went through a four-week pre-supplementation period with LCn-3PUFA and were then randomized to diets rich in either n-6PUFA or SFA both supplemented with LCn-3PUFA.ResultsThe diet rich in n-6PUFA decreased low density lipoprotein (LDL) particle concentration (− 8%, p = 0.013) and LDL cholesterol (LDL-C) level (− 8%, p = 0.021), while the saturated fat rich diet did not affect LDL particle concentration or LDL-C levels significantly. Nevertheless, dietary saturated fatty acids increased LCn-3PUFA in plasma and tissue lipids compared with n-6PUFA, potentially reducing other cardiovascular risk factors such as inflammation and clotting tendency.ConclusionImprovement on the omega 3 index of healthy subjects did not alter the known effects of dietary saturated fats and n-6PUFA on LDL profiles.     

Progressing Insights into the Role of Dietary Fats in the Prevention of Cardiovascular Disease

Dietary fats have important effects on the risk of cardiovascular disease (CVD). Abundant evidence shows that partial replacement of saturated fatty acids (SAFA) with unsaturated fatty acids improves the blood lipid and lipoprotein profile and reduces the risk of coronary heart disease (CHD). Low-fat diets high in refined carbohydrates and sugar are not effective. Very long-chain polyunsaturated n-3 or omega-3 fatty acids (n-3 VLCPUFA) present in fish have multiple beneficial metabolic effects, and regular intake of fatty fish is associated with lower risks of fatal CHD and stroke. Food-based guidelines on dietary fats recommend limiting the consumption of animal fats high in SAFA, using vegetable oils high in monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA), and eating fatty fish. These recommendations are part of a healthy eating pattern that also includes ample intake of plant-based foods rich in fiber and limited sugar and salt.     

Ad libitum intake of low-fat diets rich in either starchy foods or sucrose: effects on blood lipids, factor VII coagulant activity, and fibrinogen

People are advised to reduce their intake of saturated fat and replace it by carbohydrate to avoid coronary heart disease. It is unknown whether sucrose and starchy foods, two major sources of carbohydrates, have similar effects on cardiovascular risk markers if incorporated as a replacement for saturated fat into diets eaten ad libitum. We served 20 healthy, normal-weight women aged 21 to 52 years three strictly controlled diets ad libitum: FAT, high in total fat (46% of total energy [E%]) and saturated fat (21 E%); STARCH, high in total carbohydrates (59 E%) and low in sucrose (2.5 E%); and SUCROSE, high in total carbohydrates (59 E%) and sucrose (23.2 E%). The diets were eaten in randomized order for a period of 2 weeks. Blood lipids, factor VII coagulant activity (FVIIc), and fibrinogen concentrations were measured with subjects in the fasted state (9:45 AM) and the postabsorptive state (6:00 PM). STARCH was associated with lower total cholesterol (mean difference, 0.34 mmol/L; 95% confidence interval [CI], 0.18 to 0.50), low-density lipoprotein (LDL) cholesterol (0.25 mmol/L; 95% CI, 0.13 to 0.37), fasting triglycerides (0.15 mmol/L; 95% CI, 0.07 to 0.23), nonfasting triglycerides (0.44 mmol/L; 95% CI, 0.30 to 0.58), and nonfasting FVIIc (9.8%; 95% CI, 3.8 to 15.8) than SUCROSE. Compared with FAT, STARCH resulted in a desirable decrease of LDL cholesterol and nonfasting FVIIc. STARCH was also associated with a minor weight loss (0.7 kg) that was not found on the other 2 diets. We conclude that starchy foods with a natural content of dietary fiber can be recommended as substitutes for saturated fat in the dietary prevention of coronary heart disease. According to the present short-term findings in healthy females, substitution with sucrose is not advisable.     

Effects of dietary polyunsaturated and saturated fats on lipoproteins in the baboon

The effects of 2 different dietary fats (40% of calories from corn oil or coconut oil), in the presence of high-dietary cholesterol (1.7 mg/kcal), on the lipoprotein profiles of baboons (Papio cynocephalus sp) were studied by analytic ultracentrifugation, gradient gel electrophoresis (GGE), and heparin-manganese chloride precipitation. Relative to the corn oil (polyunsaturated fat) diet, the coconut oil (saturated fat) diet significantly increased total serum cholesterol by 43% (P less than 0.001) by increasing non-precipitable cholesterol (HDL-C) 58% (P less than 0.001) and precipitable cholesterol (VLDL + LDL-C) 35% (P less than 0.001). Analytic ultracentrifugal observations indicated that the increase in HDL-C was due to considerable increases in both HDL-I (baboon HDL of size 100-125 A and hydrated density 1.063-1.120 g/ml) and F1.20 degrees 9-28 lipoproteins (material of size 125-220 A and hydrated density 1.03-1.08 g/ml, and containing HDL apolipoproteins and apo E). Concentrations of other HDL subpopulations were unaffected by the dietary saturated rat. The increase in VLDL + LDL-C was due to increased LDL (S degree F 5-12 lipoproteins) and, to some extent, F1.20 degrees 9-28 lipoproteins because the larger, faster floating subspecies of the F1.20 degrees 9-28 lipoproteins were precipitable by heparin-manganese. In contrast, saturated fat (relative to polyunsaturated fat) induced lower concentrations of IDL (SF degree 12-20) and VLDL (SF degree 20-100). Lipoprotein size distributions by GGE indicated 5 HDL subpopulations and 2 or more LDL subpopulations in the sera of most baboons. The type of dietary fat did not affect the particle size range of each of the the HDL or LDL subpopulations. The results indicate that dietary fat markedly modulates the distribution of cholesterol between apo A-I-containing (HDL and F1.20 degrees 9-28) and apo B-containing (IDL and VLDL) lipoproteins without altering the presence of subpopulations based on particle size.     

Importance of diet in the treatment of familial hypercholesterolemia

The principal goal of dietary treatment of heterozygous familial hypercholesterolemia (hFH) is the reduction of the plasma low density lipoprotein (LDL) cholesterol. This is best accomplished by enhancing the activity of LDL receptors and, at the same time, depressing liver synthesis of cholesterol. Both cholesterol and saturated fat down-regulate the LDL receptor and inhibit the removal of LDL from the plasma by the liver. Saturated fat down-regulates the LDL receptor, especially when cholesterol is concurrently present in the diet. The total amount of dietary fat is also important. The greater the flux of chylomicron remnants into the liver, the greater is the influx of cholesterol ester. In addition, factors that affect LDL synthesis could be important. These include excessive calories (obesity) that enhance very low density lipoprotein (VLDL) and, hence, LDL synthesis, and weight loss and ω-3 fatty acids, which depress synthesis of VLDL and LDL The optimal diet for treatment of children and adults has the following characteristics: cholesterol (100 mg/day), total fat (20% of kcal, 6% saturated with the balance from ω-3 and ω-6 polyunsaturated and monounsaturated fat), carbohydrate (65% kcal, 67% from starch), and protein (15% kcal). This low-fat, high-carbohydrate diet can lower the plasma cholesterol 18–21%. A new concept, the Cholesterol-Saturated Fat Index, allows people to evaluate any foodstuff for its potential to elevate the plasma LDL cholesterol level. It is an antithrombotic diet, thrombosis being another major consideration in preventing coronary heart disease. Also, it contains significant amounts of antioxidants and fiber. Dietary therapy is the mainstay of treatment of hFH to which various drug therapies can be added.     

Influence of 4 weeks' intervention by exercise and diet on low-density lipoprotein subfractions in obese men with type 2 diabetes.

Insulin resistance is associated with dyslipoproteinemia characterized by increased serum triglycerides, reduced high-density lipoprotein 2 (HDL2) cholesterol, and increased small, dense low-density lipoprotein (LDL) subfraction particles. Physical activity and weight reduction are known to improve insulin resistance and dyslipoproteinemia, but their influence on LDL subfractions in diabetic patients is unknown. Therefore, we investigated the effect of a 4-week intervention program of exercise (2,200 kcal/wk) and diet (1,000 kcal/d: 50% carbohydrate, 25% protein, and 25% fat; polyunsaturated/saturated fat ratio, 1.0) on glycemic control and HDL and LDL subfractions in 34 obese patients with non-insulin-dependent diabetes (age, 49 +/- 9 years; body mass index [BMI], 33.1 +/- 5.1 kg/m2). Reductions in body weight (P < .001) and improvements in fasting blood glucose, insulin, fructosamine (P < .001), and free fatty acids (P < .01) by intervention were associated with reductions in serum cholesterol and apolipoprotein B (apo B) concentrations in very-low-density lipoprotein (VLDL) (P < .01), intermediate-density lipoprotein (IDL), and small, dense (>1.040 g/mL) LDL particles (P < .001). These data underlie the positive influence of weight reduction induced by exercise and diet on insulin resistance and lipoprotein metabolism in obese diabetic patients, particularly showing improvements of the LDL subfraction profile with a decrease of small, dense LDL particles. This is of particular importance, as these particles have been shown to be associated with coronary artery disease.