Effects of dietary carbohydrate quality and quantity on the lipid triad of atherogenic dyslipidaemia in obese people – results from a randomized controlled trial (CARBFUNC)
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Introduction The link between obesity, especially abdominal or visceral adiposity, with dyslipidaemia and cardiometabolic diseases is well–established. The prevalence of overweight and obesity has increased dramatically worldwide during the last decades, and one of the earliest cardiometabolic risk factors that manifests with increasing body weight, is atherogenic dyslipidaemia. Atherogenic dyslipidaemia, which is one of the strongest cardiometabolic risk factors in obesity, is the combination of elevated triacylglycerol and small–, dense low–density lipoproteins, and low high–density lipoprotein cholesterol levels, and is characteristically seen in patients with obesity, metabolic syndrome, insulin resistance and type 2 diabetes. Several studies have reported that diets lower in carbohydrates and higher in fat were associated with favourable changes in the lipid triad of AD, while low–fat higher carbohydrate diets were associated with less favourable changes. However, there is still considerable uncertainty about how lipids and lipoprotein subclasses are affected by diets comparing differences in quality, and especially carbohydrate quality. It is also not known whether diet quality might reduce the effect of differences in macronutrient profile. Processed and especially ultra–processed foods versus whole foods is an area that still lacks research. In recent years, epidemiological studies have found possible support for an association between intake of ultra–processed foods and obesity, where refined foods that are carbohydrate–dense have been suggested to play a crucial role in the worldwide obesity epidemic. While carbohydrate quality has been assessed using low and high glycaemic index, results have been inconclusive, and it has been shown that e individuals can have large variances in glycaemic response. A hypothesis by Spreadbury (2012) implied that the degree of processing of a carbohydrate food could have health–related implications such as changes in the gut microbiota. By this, carbohydrates were classified where carbohydrate–dense foods that had been untouched of any processing and had all its cells intact, could be classified as a cellular carbohydrate source, and processed carbohydrates where cells are more or less disrupted as acellular carbohydrates. To our knowledge, no randomized controlled intervention trials have extensively tested this hypothesis on atherogenic dyslipidaemia and lipid–related metabolic risks, comparing cellular and acellular diets as well as compared to a low–carbohydrate high– fat diet. 8 Objective To examine the effects of three isocaloric, isoproteinic normo–caloric dietary patterns differing in carbohydrate quality and/or quantity, on changes from baseline to three–month follow–up in the lipid triad of atherogenic dyslipidaemia and lipid–and lipoprotein–related risk markers. Design and methods This thesis included data from baseline to three months follow–up for a subset of participants (block 2) in the randomized controlled trial CARBFUNC. 84 healthy obese (BMI>30kg/m2 ) men and women in block 2 were randomized to either a low–fat, high–carbohydrate acellular (LFHC–AC), low–fat, high–carbohydrate cellular (LFHC–C) or a low–carbohydrate, high–fat (LCHF) dietary pattern. The diets were designed to be similar in protein (17 E%) and with moderate energy content (women:8370kJ (2,000kcal), men:10 460kJ (2,500kcal)), but differed in carbohydrate quantity and/or quality. The carbohydrate and fat content were respectively, 46 E% and 37 E% for the LFHC diets and 8 E% and 75 E% for the LCHF diet. Body weight, height and waist circumference, fasting serum blood samples and self–reported compliance from questionnaire, among other measures were obtained at baseline and three months. Specific recipes for each diet group were made for all meals of the day, with calculated amounts of each ingredient, and adjusted to meet the planned macronutrient and energy intake. Results 51 participants in block 2 completed the three–months follow–up and had fasting serum samples and were included in this thesis (LFHC–AC n=14, LFHC–C n=18, LCHF n=19). For the AD triad, Triacylglycerols (TAG) and TAG to high–density lipoprotein–cholesterol (HDL– C) were significantly reduced in the LCHF group and HDL–C did not significantly change for any of the groups. There were no significant changes from baseline to three–months follow–up between the groups in any of these variables, although the average change in TAG/HDL–C was greater in the LCHF group as compared to the LFHC–C group (25% decrease vs 5% increase). There were no significant differences between any of the groups after three months in the absolute score change from baseline in total cholesterol (TC), low–density lipoprotein– cholesterol (LDL–C), nonHDL–C, TC/HDL–C ratio, nonHDL–C/HDL–C ratio and LDL– C/HDL–C ratio. Differential effects were observed between the groups for some lipoproteins. LFHC–C group significantly reduced TC, LDL–C and nonHDL–C (p<), while the LFHC–AC 9 group showed a trend of significant reduction in nonHDL–C, TC/HDL–C, nonHDL–C/HDL– C and LDL–C/HDL–C ratios. A subgroup of each diet group had available fasting serum apolipoproteins (LFHC–AC n=13, LFHC–C n=13, LCHF n=10). We found significant group changes from baseline to three– months follow–up in apoB, apoA–I and apoA–I between LFHC–AC and LFHC–C, where the LFHC–C group significantly reduced these apolipoproteins compared to the LFHC–AC group (apoB p=0.048, apoA–I and apoA–II p=0.001). For apoA–II the LCHF group also had a significant reduction from baseline to three–months follow–up compared to the LFHC–AC group (p=0.039), and a significant reduction in apoA–I compared to the LFHC–C group (p=0.015). In addition, the LFHC–C group significantly reduced in all single apolipoproteins from baseline to three–months (p<0.01), the LCHF group significantly reduced in apoA–II, apoC–II, apoC–III and apoE (p<0.05), and LFHC–AC group significantly reduced in apoE (p<0.05). Average weight loss was about 5–6 kg all three diet groups, and they all significantly decreased body weight, BMI, waist circumference (WC) and waist–to–height ratio (WHtR) at three months compared to baseline (all p<0.001), and there were no differences in the changes from baseline to three months for any of these variables between the groups. Conclusions After three months of intervention, LFHC–AC, LFHC–C and LCHF diets, designed to be isocaloric, isoproteinic and normo–caloric, resulted in overall similar changes in markers of atherogenic dyslipidaemia and other lipid–related cardiovascular disease (CVD) risk markers, and similar reductions in body weight, BMI, WC and WHtR, but differential effects in some apolipoproteins.
PublisherThe University of Bergen
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