The Ketogenic Diet Reverses Indicators of Heart Disease. The Ketogenic Diet Reverses Indicators of Heart Disease. The Ketogenic Diet Reverses Indicators of Heart Disease. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. Samaha, M.D., Nayyar Iqbal, M.D., Prakash Seshadri, M.D., Kathryn. By adopting a ketogenic diet high in protein with minimal carbohydrates, you'll be able to take advantage of the diet's anti-inflammatory effects. Amber January 1, 2013. I just made the suggestion that a ketogenic diet might plausibly enhance muscular growth as well as recovery (http://www.ketotic.org/2012/12. MEMRI bridges the language gap which exists between the West and the Middle East, providing timely translations of Arabic, Persian, Urdu-Pashtu, and Turkish media, as. Cardiovascular disease (CVD) is the leading cause of death worldwide. Furthermore, if an LDL- C/HDL- C ratio > 5 was combined with hypertriglyceridaemia (> or = 2. The association between hypertriglyceridaemia and CHD events may be related to the presence of atherogenic, triglyceride- rich particles in plasma, such as LDL and very low density lipoproteins. Read more about a ketogenic diet & the paleo diet. Browse The Paleo DietThe low-carbohydrate diet produced a greater weight loss (absolute difference, approximately 4 percent) than did the conventional diet for the first six. Cardiovascular disease (CVD) is the leading cause of death worldwide 1. Because of its prevalence and life-threatening nature, and because it appears that a keto diet. High triglyceride levels may also predispose to thrombosis.''. The multivariate analysis by logistic regression OR gave 1. Analysis of receiver operating characteristic curves showed that only TG/HDL- c and HDL- c were useful for detecting extensive coronary disease, with the former more strongly associated with disease. One was a very low- carbohydrate (< 1. Blood was drawn from fasting subjects on separate days and an oral fat tolerance test was performed at baseline, after the very low- carbohydrate diet period, and after the low- fat diet period. Both diets had the same effect on serum total cholesterol, serum insulin, and homeostasis model analysis- insulin resistance (HOMA- IR). Neither diet affected serum HDL cholesterol (HDL- C) or oxidized LDL (ox. LDL) concentrations. Serum LDL cholesterol (LDL- C) was reduced (P < 0. Fasting serum triacylglycerol (TAG), the TAG/HDL- C ratio, and glucose were significantly reduced only by the very low- carbohydrate diet (. Postprandial lipemia was significantly reduced when the men consumed both diets compared with baseline, but the reduction was significantly greater after intake of the very low- carbohydrate diet. Mean and peak LDL particle size increased only after the very low- carbohydrate diet. The short- term hypoenergetic low- fat diet was more effective at lowering serum LDL- C, but the very low- carbohydrate diet was more effective at improving characteristics of the metabolic syndrome as shown by a decrease in fasting serum TAG, the TAG/HDL- C ratio, postprandial lipemia, serum glucose, an increase in LDL particle size, and also greater weight loss (P < 0. A cutoff point of 1. TG- to- HDL cholesterol ratio distinguishes between patients having small LDL values better than TG cutoff of 1. It may be suitable for the selection of patients needing an earlier and aggressive treatment of lipid abnormalities.''. Of these deaths, an estimated 7. Low- and middle- income countries are disproportionally affected: over 8. CVD deaths take place in low- and middle- income countries and occur almost equally in men and women. By 2. 03. 0, almost 2. CVDs, mainly from heart disease and stroke. These are projected to remain the single leading causes of death. Evidence type: observational. Role of lipid and lipoprotein profiles in risk assessment and therapy. Aug; 1. 46(2): 2. Green, MD, Kathleen Reagan, MD, Charles E. Total cholesterol level alone is a poor predictor of CAD, particularly in older patients in whom the major lipid risk factor is the HDL cholesterol level. Jul; 1. 24 Suppl: S1- 9. TC levels measured were useless (by themselves) for predicting risk of CHD . Indeed, twice as many individuals who had a lifetime TC level of less than 2. CHD compared with those who had a TC level greater than 3. Fig. Because of the extensive overlap between levels, it was impossible to differentiate the patients with CAD from the control subjects. Ordovas, Ph. D, Jennifer L. Jenner, BSc, Steven R. Silberman, Ph. D, Keaven M. Anderson, Ph. D, Peter W. F. Salem, MD, FACC, Ernst J. However, as more recent research has expanded our understanding of lipoprotein function and metabolism, it has become apparent that LDL- C is not the only lipoprotein species involved in atherogenesis. A considerable proportion of patients with atherosclerotic disease have levels of LDL- C and total cholesterol (TC) within the recommended range . Newschaffer, MS; Michael J. Klag, MD, MPH; Trudy L. Multivariate analysis was performed to provide RR estimates adjusted for other CVD risk factors. High- density lipoprotein and triglyceride levels were strong predictors of CVD death in age- adjusted and multivariate analyses. Low- density lipoprotein and total cholesterol levels were poorer predictors of CVD mortality. After adjustment for other CVD risk factors, HDL levels less than 1. L (5. 0 mg/d. L) were strongly associated with cardiovascular mortality (RR = 1. Triglyceride levels were associated with increased CVD mortality at levels of 2. L (2. 00 to 3. 99 mg/d. L) (RR = 1. 6. 5; 9. CI, 0. 9. 9 to 2. L (4. 00 mg/d. L) or greater (RR = 3. CI, 1. 6. 5 to 7. At total cholesterol levels of 5. L (2. 00 mg/d. L) or greater and at all levels of LDL and triglycerides, women with HDL levels of less than 1. L (< 5. 0 mg/d. L) had CVD death rates that were higher than those of women with HDL levels of 1. L (5. 0 mg/d. L) or greater. Dec; 8. 7(1. 2): 7. LDL particle size decreases with increasing density. Smaller, denser LDL particles seem more atherogenic than the larger, lighter particles, based on the experimental findings that smaller LDL particles are more susceptible for oxidation in vitro, have lower binding affinity for the LDL receptors and lower catabolic rate, have a higher concentration of polyunsaturated fatty acids, and potentially interact more easily with proteoglycans of the arterial wall. Clinical studies have shown that a smaller LDL subfraction profile is associated with an increased risk of heart disease, even when total cholesterol level is only slightly raised. There is a strong inverse association between LDL particle size and triglyceride concentrations. Although LDL particle size is genetically determined, its phenotypic expression may also be affected by environmental factors such as drugs, diet, obesity, exercise or disease. Factors that shift the LDL subfractions profile towards larger particles may reduce the risk of heart disease. Gardner, Ph. D; Stephen P. Fortmann, MD; Ronald M. Controls were matched by sex, 5- year age groups, survey time point, ethnicity, and FCP treatment condition. The sample included 1. The significant case- control difference in LDL size was independent of levels of high- density lipoprotein cholesterol (HDL- C), non—HDL cholesterol (non- HDL- C), triglyceride, smoking, systolic blood pressure, and body mass index, but was not significant after adjusting for the ratio of total cholesterol (TC) to HDL- C (TC: HDL- C). Among all the physiological risk factors, LDL size was the best differentiator of CAD status in conditional logistic regression. However, when added to the physiological parameters above, the TC: HDL- C ratio was found to be a stronger independent predictor of CAD status. Sep; 2. 5(3): 1. 99- 2. Three recent prospective, nested case- control studies have since confirmed that the presence of small, dense LDL particles was associated with more than a three- fold increase in the risk of CHD. The small, dense LDL phenotype rarely occurs as an isolated disorder. It is most frequently accompanied by hypertriglyceridemia, reduced HDL cholesterol levels, abdominal obesity, insulin resistance and by a series of other metabolic alterations predictive of an impaired endothelial function and increased susceptibility to thrombosis. Aug; 1. 7(8): 8. 59- 6. LDL particle size was measured by nondenaturing gradient gel electrophoresis. Men with an LDL particle size less than 2. A had a significant 2. IHD (P< 0. 0. 01) compared with men having an LDL particle size greater than 2. A. Multivariate and subgroup analyses indicated that small, dense LDL particles predicted the rate of IHD independent of LDL cholesterol, triglycerides, high density lipoprotein (HDL) cholesterol, apolipoprotein B and the total cholesterol to HDL cholesterol ratio. Finally, the magnitude of the increase in IHD risk attributed to lipid risk factors was modulated to a significant extent by variations in LDL particle size. LDL size has been accepted as an important predictor of cardiovascular events and progression of coronary artery disease as well as an emerging cardiovascular risk factor by the National Cholesterol Education Program Adult Treatment Panel III. Small, dense LDL, with elevated triglyceride levels and low HDL- cholesterol concentrations, constitute the 'atherogenic lipoprotein phenotype (ALP)', a form of atherogenic dyslipidemia that is a feature of type 2 diabetes and the metabolic syndrome. Dec 1; 3. 70(9. 60. Total cholesterol was weakly positively related to ischaemic and total stroke mortality in early middle age (4. Moreover, a positive relation was seen only in middle age and only in those with below- average blood pressure; at older ages (7. Hg, total cholesterol was negatively related to haemorrhagic and total stroke mortality. The primary outcome measure was the composite of death from any cause or nonfatal myocardial infarction (MI). The independent association between HDL- C levels measured after 6 months on optimal medical therapy (OMT) and the rate of cardiovascular events after 4 years was assessed. Similar analyses were performed separately in subjects with LDL- C levels below 7. L (1. 8 mmol/L). Among subjects with LDL- C levels < 7. L, those in the highest quintile of HDL- C had a 6. MI as compared to the lowest quintile, with HDL- C quintile demonstrating a significant, inverse predictive effect (P=0. This relationship persisted and appeared more prominent even when LDL- C was reduced to optimal levels with intensive dyslipidemic therapy. To insure comparability, only studies reporting the association between fasting triglyceride levels and incident cardiovascular endpoints were included. Using standard meta- analysis calculations, relative risks (RR) and 9. CI) were calculated and standardized with respect to a 1 mmol/l increase in triglyceride. Multivariable- adjusted RRs were determined for the six studies in men and two studies in women that reported adjustments for HDL cholesterol.
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