Eddie Vedder
2011-09-21, 13:39
En ny artikel som diskuterar HDL-kolesterolet och dess potentiella roll i hjärt- kärlsjukdom. Annars brukar ju LDL-kolesterol få mer fokus men den här ser på det ur ett annat perspektiv. Och tittar på studier om livsstilsmönster som förefaller höja HDL-kolesterolet. Något som då brukar anses vara en fördel. HDL och LDL är alltså lipoproteinpartiklar i kroppen som transporterar, bland annat, kolesterol. Det är alltså inte två olika sorters kolesterol som det kanske kan låta. Kolesterolet är detsamma, det är partikeln som transporterar det som skiljer.
Abstract
Multiple dietary factors have been shown to increase high-density lipoprotein cholesterol (HDL-C) concentrations, and HDL-C has been inversely associated with coronary heart disease (CHD) risk. Replacement of dietary carbohydrate with polyunsaturated, monounsaturated and saturated fat has been associated with progressively greater increases in HDL-C (7–12%) in addition to other lipid changes. Added sugars, but not high glycemic carbohydrates, have been associated with decreased HDL-C. Alcohol consumption has been associated with increased HDL-C (9.2%) independent of changes in other measured lipids. Modest effects on HDL-C (~4–5%) among other lipid and non-lipid CHD risk factors have also been observed with weight loss by dieting, omega-3 fatty acids, and a Mediterranean diet pattern. The CHD benefit of increasing HDL-C is unclear given the inconsistent evidence from HDL-raising pharmacologic trials. Furthermore, pleiotropic effects of diet preclude attribution of CHD benefit specifically to HDL-C. Investigation into functional or other properties of HDL may lend further insight.
http://www.springerlink.com/content/l84n07gp3899135j/fulltext.pdf
Siri-Tarino PW. Effects of Diet on High-Density Lipoprotein Cholesterol. Curr Atheroscler Rep. 2011 Sep 8.
Kolhydratrestriktion och kolesterol är ju på tapeten så jag tänkte citera just den delen plus konklusionen:
Dietary Carbohydrate Restriction
As with insulin resistance, dietary carbohydrate, particularly refined carbohydrates, can exacerbate atherogenic dyslipidemia through the stimulation of hepatic lipogenesis and the secretion of triglyceride-enriched apoB-containing lipoprotein particles from the liver [26]. Moderate carbohydrate restriction (26% vs 54% of total energy) has been shown to improve lipid profiles independently of weight loss, such that triglyceride, total cholesterol, apoB, and small, dense LDL concentrations were significantly decreased [27]. Although HDL-C concentrations were not changed, the total cholesterol to HDL (TC:HDL) ratio, as a more powerful predictor of CHD risk than LDL-C [28], was decreased [27].
Studies of very low carbohydrate diets (< 10% or 50 g/d of carbohydrate) have generally been conducted with concomitant weight loss and have shown decreases in triglyceride and increases in total, LDL-C, and HDL-C, along with improved or similar magnitudes of weight loss relative to low-fat diets [29]. The mean increase in HDL-C was 11% for very low carbohydrate diets compared to low-fat diets [29]. In the few studies that have evaluated very low carbohydrate diets independent of weight loss, improvements in triglyceride concentrations and post-prandial lipemia have been observed [30, 31]. Increases in total cholesterol, LDL-C, and HDL-C were also observed, with men and women showing differences in the magnitude of increases (5%, 4%, and 12% vs 16%, 15%, and 44% percent, respectively) [30, 31]. Variation in the magnitude of effect may have been due to differences in diets (ie, enrichment with monounsaturated fat in the study in women [31]) or study population.
Overall, carbohydrate restriction improves atherogenic dyslipidemia, with the effects being greatest and most consistent for triglyceride. Increases in HDL-C may or may not be significant, but because these increases are generally greater than increases in total cholesterol, the TC:HDL-C ratio is decreased. Whether reduction in the TC:HDL ratio offsets the CHD risk imposed by increases in LDL cholesterol remains to be definitively established, although it has been suggested that in the setting of insulin resistance and obesity, modulation of atherogenic dyslipidemia may be of primary importance [32, 33•]. Of note, increases in LDL cholesterol observed with carbohydrate restriction and replacement of carbohydrate with fat and/or protein has been shown to be specific to larger and more buoyant LDL particles rather than smaller, more dense and more atherogenic LDL particles [27].
[...]
Although there exist parallel bodies of evidence for the modulation of HDL-C by diet and for associations of these same dietary factors or patterns with CHD risk, a causal chain that links diet with CHD risk through HDL-C has not been established. Diet effects on HDL-C are relatively modest (up to 12%), and concordant effects of diet on other lipid and non-lipid CHD risk factors make attribution of CHD benefit to increases in HDL-C difficult. Of particular relevance, data from pharmacologic interventions designed specifically to increase HDL-C have not consistently demonstrated CHD benefit [11••, 12••]. Finally, given the heterogeneity and complexity of HDL structure and function [14•], continued investigation into properties of HDL beyond its associated cholesterol concentrations may reveal relevant factors modifiable by diet that may independently and more accurately predict CHD risk.
Abstract
Multiple dietary factors have been shown to increase high-density lipoprotein cholesterol (HDL-C) concentrations, and HDL-C has been inversely associated with coronary heart disease (CHD) risk. Replacement of dietary carbohydrate with polyunsaturated, monounsaturated and saturated fat has been associated with progressively greater increases in HDL-C (7–12%) in addition to other lipid changes. Added sugars, but not high glycemic carbohydrates, have been associated with decreased HDL-C. Alcohol consumption has been associated with increased HDL-C (9.2%) independent of changes in other measured lipids. Modest effects on HDL-C (~4–5%) among other lipid and non-lipid CHD risk factors have also been observed with weight loss by dieting, omega-3 fatty acids, and a Mediterranean diet pattern. The CHD benefit of increasing HDL-C is unclear given the inconsistent evidence from HDL-raising pharmacologic trials. Furthermore, pleiotropic effects of diet preclude attribution of CHD benefit specifically to HDL-C. Investigation into functional or other properties of HDL may lend further insight.
http://www.springerlink.com/content/l84n07gp3899135j/fulltext.pdf
Siri-Tarino PW. Effects of Diet on High-Density Lipoprotein Cholesterol. Curr Atheroscler Rep. 2011 Sep 8.
Kolhydratrestriktion och kolesterol är ju på tapeten så jag tänkte citera just den delen plus konklusionen:
Dietary Carbohydrate Restriction
As with insulin resistance, dietary carbohydrate, particularly refined carbohydrates, can exacerbate atherogenic dyslipidemia through the stimulation of hepatic lipogenesis and the secretion of triglyceride-enriched apoB-containing lipoprotein particles from the liver [26]. Moderate carbohydrate restriction (26% vs 54% of total energy) has been shown to improve lipid profiles independently of weight loss, such that triglyceride, total cholesterol, apoB, and small, dense LDL concentrations were significantly decreased [27]. Although HDL-C concentrations were not changed, the total cholesterol to HDL (TC:HDL) ratio, as a more powerful predictor of CHD risk than LDL-C [28], was decreased [27].
Studies of very low carbohydrate diets (< 10% or 50 g/d of carbohydrate) have generally been conducted with concomitant weight loss and have shown decreases in triglyceride and increases in total, LDL-C, and HDL-C, along with improved or similar magnitudes of weight loss relative to low-fat diets [29]. The mean increase in HDL-C was 11% for very low carbohydrate diets compared to low-fat diets [29]. In the few studies that have evaluated very low carbohydrate diets independent of weight loss, improvements in triglyceride concentrations and post-prandial lipemia have been observed [30, 31]. Increases in total cholesterol, LDL-C, and HDL-C were also observed, with men and women showing differences in the magnitude of increases (5%, 4%, and 12% vs 16%, 15%, and 44% percent, respectively) [30, 31]. Variation in the magnitude of effect may have been due to differences in diets (ie, enrichment with monounsaturated fat in the study in women [31]) or study population.
Overall, carbohydrate restriction improves atherogenic dyslipidemia, with the effects being greatest and most consistent for triglyceride. Increases in HDL-C may or may not be significant, but because these increases are generally greater than increases in total cholesterol, the TC:HDL-C ratio is decreased. Whether reduction in the TC:HDL ratio offsets the CHD risk imposed by increases in LDL cholesterol remains to be definitively established, although it has been suggested that in the setting of insulin resistance and obesity, modulation of atherogenic dyslipidemia may be of primary importance [32, 33•]. Of note, increases in LDL cholesterol observed with carbohydrate restriction and replacement of carbohydrate with fat and/or protein has been shown to be specific to larger and more buoyant LDL particles rather than smaller, more dense and more atherogenic LDL particles [27].
[...]
Although there exist parallel bodies of evidence for the modulation of HDL-C by diet and for associations of these same dietary factors or patterns with CHD risk, a causal chain that links diet with CHD risk through HDL-C has not been established. Diet effects on HDL-C are relatively modest (up to 12%), and concordant effects of diet on other lipid and non-lipid CHD risk factors make attribution of CHD benefit to increases in HDL-C difficult. Of particular relevance, data from pharmacologic interventions designed specifically to increase HDL-C have not consistently demonstrated CHD benefit [11••, 12••]. Finally, given the heterogeneity and complexity of HDL structure and function [14•], continued investigation into properties of HDL beyond its associated cholesterol concentrations may reveal relevant factors modifiable by diet that may independently and more accurately predict CHD risk.