Surplus body weight can lead to serious changes in plasma lipids and lipoproteins that raise the risk of atherosclerotic cardiovascular disease (CVD), which means that there are increases in triacylglycerols and small, dense LDL particles, with changeable increases in total LDL cholesterol, and reductions in high density lipoprotein (HDL) cholesterol. Atherogenic dyslipidemia associated with surplus adiposity is highly connected with decreased insulin sensitivity and is a crucial feature of the metabolic syndrome. Dietary carbohydrates, particularly simple sugars, are also able to promote atherogenic dyslipidemia, in huge part due to effects on the metabolism of plasma triacylglycerol-rich lipoproteins. HC, low-fat diets have been proven to encourage increased concentrations of small, dense LDL and expression of the small, dense LDL particle phenotype (LDL subclass pattern B) in a high proportion of healthy men.
Lately, attention has concentrated on the use of very-low-carbohydrate diets in order to attain weight loss. The reduction of the consumption of dietary carbohydrate in such diets is attained both by decreasing total calorie consumption and by substitution of protein, fat, or both. Metabolic changes resulting from this include: reductions in plasma triacylglycerol and decrease or a lack of increase in LDL cholesterol, in spite of pretty high dietary contents of saturated fat and cholesterol. The major objective of the current research was to examine the effects of moderate declines in carbohydrate consumption followed and not followed by weight loss on atherogenic dyslipidemia in overweight and slightly obese men. Additionally, the scientists examined the extent to which modifications in lipoprotein with declines in carbohydrate consumption are affected by variations in saturated fat content.
All participants were asked to consume the basal diet (54 per cent of energy as carbohydrate) for one week, and after that they were assigned randomly to the basal diet or 1 of the 3 LC diets. After three weeks (first stable-weight period), weight loss was encouraged by a decrease of approximately 1000 kcal per day in each diet for five weeks, after which energy intake was tailored to stabilize weight for four weeks (last stable-weight period). The subjects were free-living and were recommended not to change their physical activity in the course of the research. Frozen, prepared entrees fortified with vitamins and minerals to meet the suggested dietary allowances were offered both for lunch and dinner. The subjects had to prepare their own breakfasts and snacks in accordance with menus, and they were weighed each week by the staff, who tailored energy intakes if necessary. Obedience and loyalty were enhanced through frequent telephone contacts and weekly meetings with the dietitians. Compliance was evaluated through analysis of a every-day checklist of foods consumed. None of the participants were eliminated for noncompliance (that is defined as daily diet deviations averaging >5 per cent of total energy).
The 26%-carbohydrate, low-saturated-fat diet decreased the level of such substances as triacylglycerol, apolipoprotein B, small LDL mass, and total:HDL cholesterol and raised LDL peak diameter. These alterations were considerably different from those with the 54%-carbohydrate diet. After consequent weight loss, the alterations in all these variables were considerably bigger and the reduction in LDL cholesterol was considerably higher with the 54%-carbohydrate diet than with the 26%-carbohydrate diet. With the 26%-carbohydrate diet, lipoprotein alterations with the higher saturated fat intakes were not considerably diverse from those with the lower saturated fat intakes, with the exception of LDL cholesterol, which declined less with the higher saturated fat intake due to an increase in mass of large LDL.
In the current research, the scientists examined separately the effects of moderate declines in carbohydrate consumption and body weight on the components of atherogenic dyslipidemia in mildly overweight and moderately obese but generally healthy men in middle age. Like it has been demonstrated for diets with more extreme declines in carbohydrate, placing men on a diet with 26 per cent carbohydrate brought about reductions in plasma triacylglycerol concentrations, consistent with the well-known consequences of carbohydrate intake for the metabolism of triacylglycerol-rich lipoproteins. Lower carbohydrate consumption has also been demonstrated to be connected with decreased plasma apo B concentrations and a decreased ratio of total cholesterol to HDL. The decrease in these variables as a function of carbohydrate consumption was relevant only for the 26%-carbohydrate diet group. Whenb comparing the 54%- and 26%-carbohydrate, low-saturated-fat diets, there is no possibility to discriminate the consequences of the addition of protein and monounsaturated fat from those caused by the decrease in carbohydrate. Though, while the monounsaturated fat content of the 26%-carbohydrate, low-saturated fat diet was decreased from 27 per cent to 20 per cent, mainly by replacement with saturated fat, the alterations in triacylglycerol, apo B, and total:HDL cholesterol were not considerably diverse. This result indicates that these changes were not due primarily to the higher monounsaturated fat content of the diet.
There was a drop in LDL cholesterol with the 26%-carbohydrate, low-saturated-fat diet, even though the dissimilarities in comparison to the higher-carbohydrate diets were of borderline statistical importance. Analysis of alterations in LDL subfraction distribution, though, demonstrated that the low-carbohydrate diet led to drastically lower concentrations of small, dense LDL. Furthermore, the reductions were considerably connected with decreased plasma triacylglycerol concentrations, consistent with the pathways linking triacylglycerol-rich lipoproteins to the production of small, dense LDL. Therefore, the general effects of low-carbohydrate diets on the standard LDL-cholesterol measurement depend largely on the degree to which such diets differentially change the metabolism of larger in comparison to smaller LDL subclasses. The investigators also discovered that, along with weight loss, there were declines in the most important lipid and lipoprotein indicators of CVD risk (LDL cholesterol, triacylglycerol, apo B, total:HDL cholesterol, and small, dense LDL), and that these declines were much higher with the higher- than with the lower-carbohydrate diet.
Fears concerning carbohydrate limitation include the potential for insufficient consumption of certain advantageous dietary components, such as fiber and some vitamins, and the likelihood of reduced effectiveness over time. Though, with reasonable carbohydrate restriction, such as the 26%-carbohydrate, low-saturated-fat diet analysed in the current research, it is possible to meet the suggested dietary allowances for all necessary nutrients and to maintain sufficient fiber intake with proper supplementation. Remember that increased physical activity without dietary carbohydrate decline may also lead to improvements in the components of atherogenic dyslipidemia and can have the supplementary benefit of helping to preserve reductions in body weight.
