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Lipid profile is associated with decreased fatigue in individuals with progressive multiple sclerosis following a diet-based intervention: Results from a pilot study.
Fellows Maxwell, K, Wahls, T, Browne, RW, Rubenstein, L, Bisht, B, Chenard, CA, Snetselaar, L, Weinstock-Guttman, B, Ramanathan, M
PloS one. 2019;14(6):e0218075
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Fatigue is a frequent and debilitating symptom of multiple sclerosis (MS) and is independent of level of disability. The authors previously reported that a 12 months diet and lifestyle intervention was effective at reducing fatigue in patients with progressive MS. The aims of this study were to characterise the changes in lipid and cholesterol biomarkers during the intervention, and to investigate whether these biomarkers were associated with fatigue outcomes. Data of 18 MS patients were analysed. The intervention consisted of a modified Paleolithic diet, supplemented with exercise, neuromuscular electrical stimulation (NMES) and stress reduction techniques (Wahl’s protocol). Fatigue was significantly decreased at 3, 6, 9 and 12 months compared to baseline, and more so in those having more of the recommended foods and less of the excluded foods. The exercise, NMES, and stress reduction components of the intervention were not associated with changes in fatigue. All variables of the lipid profiles improved during the 12 months intervention. These improvements were associated with the changes in nutrient intakes, in particular, with amounts and types of fat, carbohydrates and fibre. Changes in total and HDL cholesterol, but not LDL cholesterol or triglycerides were associated with a decrease in fatigue. The authors hypothesise that the benefits of the changes in lipid profile on fatigue may be mediated by the positive effects of HDL-cholesterol on mitochondrial function (mitochondria are the “power houses” of every cell, i.e. produce energy on the cellular level), in particular those in the muscles. Limitations of the study include the small sample size, lack of control group and randomisation. The authors conclude that diet-induced changes in HDL and total cholesterol may mediate the positive effects of a dietary and lifestyle intervention on fatigue in MS patients.
Abstract
PURPOSE To investigate associations between lipid profiles and fatigue in a cohort of progressive multiple sclerosis (MS) patients on a diet-based multimodal intervention. METHODS This pilot study included 18 progressive MS patients who participated in a prospective longitudinal study of fatigue following a diet-based multimodal intervention that included exercise, neuromuscular electrical stimulation and stress reduction. The diet recommended high intake of vegetables and fruits, encouraged consumption of animal and plant protein and excluded foods with gluten-containing grains, dairy and eggs. Fatigue was measured on the Fatigue Severity Scale (FSS) at baseline and every 3 months for 12 months. A lipid profile consisting of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) and triglycerides (TG) was obtained on fasting blood samples at baseline and 12 months. RESULTS FSS scores decreased from a baseline of 5.51 (95% CI: 4.86, 6.16) to a mean of 3.03 (95% CI: 2.23, 3.82) at 12 months (p < 0.001). At 12 months, increases in HDL-C (mean change: +6.0 mg/dl; 95% CI: 0.3, 12.0; p = 0.049) and decreases in BMI (mean change: -2.6 kg/m2; 95% CI: -3.6, -2.5; p < 0.001), LDL-C (mean change: -10.4 mg/dl; 95% CI:-19.7, -1.2; p = 0.029), TG (mean change: -29.2 mg/dl; 95% CI: -44.3, -14.2; p = 0.001), TG to HDL-C ratio (mean change: -0.6; 95% CI: -1.0, -0.3; p = 0.002) and TC to HDL-C ratio (mean change:-0.6; 95% CI: -1.0, -0.3; p = 0.003) were observed compared to baseline. Improvements in FSS were associated with increases in HDL-C (β = -0.05; 95% CI: -0.1, -0.0004; p = 0.048) and changes in TC (p = 0.005) from baseline to 12 months. CONCLUSIONS Lipid profile variables are associated with improvements in fatigue in progressive MS patients on a diet-based multimodal intervention.
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Fructose metabolism and metabolic disease.
Hannou, SA, Haslam, DE, McKeown, NM, Herman, MA
The Journal of clinical investigation. 2018;128(2):545-555
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Sugar consumption is thought to be a contributing factor in the increase in diabetes and obesity and the associated risk of cardiovascular disease worldwide. Sucrose (table sugar) and high fructose corn syrup contain almost equal amounts of fructose and glucose and are commonly added to processed foods. Whilst long-term studies are lacking, some short-term intervention studies show that fructose can impair lipid metabolism and insulin sensitivity in humans. This article reviews the biochemistry and molecular genetics of fructose metabolism as well as potential mechanisms by which excessive fructose consumption contributes to cardiometabolic disease. Fructose absorption in the human intestine is saturable, and there is a large range in capacity to absorb fructose between individuals, and unabsorbed fructose may contribute to gastrointestinal symptoms including pain and bloating. Fructose concentrations in the blood can increase 10-fold after consumption, but are rapidly cleared, mostly by the liver, where it provides substrate for metabolic processes, but may also be involved in signalling functions. Fructose may enhance glucose uptake by the liver and storage as glycogen and lipids. It may also increase production of uric acid which is implicated with gout. Excessive fructose consumption affects lipid metabolism and may contribute to fat accumulation in the liver and increase circulating triglycerides, a risk factor for heart disease. In animal models it also induces increased insulin levels. Fructose is one of the sweetest sugars which may affect appetite and overeating. It may also induce addiction-like behaviours such as binging and dependence in part by stimulating dopaminergic pathways. It also appears to induce leptin resistance which further increases food intake and obesity.
Abstract
Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.