Beatus, qui prodest, quibus potest
An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women.
Volek JS, Sharman MJ, Gomez AL, Scheett TP, Kraemer WJ.
Department of Kinesiology, University of Connecticut, Storrs, CT 06269-1110, USA. [email protected]
Very low carbohydrate diets are popular, yet little is known about their effects on blood lipids and other cardiovascular disease risk factors. We reported previously that a very low carbohydrate diet favorably affected fasting and postprandial triacylglycerols, LDL subclasses and HDL cholesterol (HDL-C) in men but the effects in women are unclear. We compared the effects of a very low carbohydrate and a low fat diet on fasting lipids, postprandial lipemia and markers of inflammation in women. We conducted a balanced, randomized, two-period, crossover study in 10 healthy normolipidemic women who consumed both a low fat (<30% fat) and a very low carbohydrate (<10% carbohydrate) diet for 4 wk each. Two blood draws were performed on separate days at 0, 2 and 4 wk and an oral fat tolerance test was performed at baseline and after each diet period. Compared with the low fat diet, the very low carbohydrate diet increased (P <or= 0.05) fasting serum total cholesterol (16%), LDL cholesterol (LDL-C) (15%) and HDL-C (33%) and decreased serum triacylglycerols (-30%), the total cholesterol to HDL ratio (-13%) and the area under the 8-h postprandial triacylglycerol curve (-31%). There were no significant changes in LDL size or markers of inflammation (C-reactive protein, interleukin-6, tumor necrosis factor-alpha) after the very low carbohydrate diet. In normal weight, normolipidemic women, a short-term very low carbohydrate diet modestly increased LDL-C, yet there were favorable effects on cardiovascular disease risk status by virtue of a relatively larger increase in HDL-C and a decrease in fasting and postprandial triaclyglycerols.
A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men.
Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gomez AL, Scheett TP, Volek JS.
Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs 06269-1110, USA.
Very low-carbohydrate (ketogenic) diets are popular yet little is known regarding the effects on serum biomarkers for cardiovascular disease (CVD). This study examined the effects of a 6-wk ketogenic diet on fasting and postprandial serum biomarkers in 20 normal-weight, normolipidemic men. Twelve men switched from their habitual diet (17% protein, 47% carbohydrate and 32% fat) to a ketogenic diet (30% protein, 8% carbohydrate and 61% fat) and eight control subjects consumed their habitual diet for 6 wk. Fasting blood lipids, insulin, LDL particle size, oxidized LDL and postprandial triacylglycerol (TAG) and insulin responses to a fat-rich meal were determined before and after treatment. There were significant decreases in fasting serum TAG (-33%), postprandial lipemia after a fat-rich meal (-29%), and fasting serum insulin concentrations (-34%) after men consumed the ketogenic diet. Fasting serum total and LDL cholesterol and oxidized LDL were unaffected and HDL cholesterol tended to increase with the ketogenic diet (+11.5%; P = 0.066). In subjects with a predominance of small LDL particles pattern B, there were significant increases in mean and peak LDL particle diameter and the percentage of LDL-1 after the ketogenic diet. There were no significant changes in blood lipids in the control group. To our knowledge this is the first study to document the effects of a ketogenic diet on fasting and postprandial CVD biomarkers independent of weight loss. The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia.
Dodatkowo podczas kilku badań zaobserwowano dalszą poprawę profilu lipidowego, gdy już nie było utraty wagi
ale to nie zmienia faktu, że lepiej jak jest ta utrata tkanki tłuszczowej
Beatus, qui prodest, quibus potest
co do badan coz sugeruja ze dieta nisko ww posiada pewna przewage metaboliczna w stosunku do diet ww

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http://www.sfd.pl/Zdrowie_bez_tluszczu_nie_mozliwe!!!-t164189.html#post0
zresztą każdy aby wytrzymać dłużej na tej diecie musi używać wspomagaczy , pobudzaczy itp
wcale nie chce przez to powiedzieć ze dieta powinna zawierać np 600 gram wegli ale te 3gramy na kilogram masy ciała powinny być
pozdrawiam i śledze ciekawy POST
Zmieniony przez - Rothen w dniu 2006-05-16 20:46:40
Ja swoje poglądy mam, ale teraz czasy takie, że na wszelki wypadek się z nimi nie zgadzam.
Improvement is seen in the absence of weight loss
Since it is known that weight loss generally improves MetS, it is important to ask whether beneficial metabolic responses to low CHO diets are dependent on weight loss. The question was specifically addressed by Volek's group [42,43] in normal-weight men and women encouraged to maintain their weight and by Allick and colleagues in patients with diabetes mellitus type 2 [44] (Table 3). The studies in normal weight women [43] and type 2 diabetics [44], in particular, used a cross-over experimental design removing the confounding effect of group differences. These studies were also well-controlled. In the case of Allick, formula was used and, in the studies by Volek, compliance was documented by measuring elevation of serum and urine ketones, thereby eliminating dietary reporting errors as a confounding factor. Improvement in the TAG/HDL ratio ranged from 40 to 55%. In summary, a low CHO regimen clearly improves MetS relative to low fat diets even in the absence of weight loss.
In addition to studies in which weight maintenance was a feature of experimental design it is important to consider data reported by Foster [45] (Figure 1, (Table 4), who compared low CHO and LF diets. It is widely quoted that the low CHO diet is better at 6 months but that there is no difference in the diets at 12 months. However, it has been pointed out [12] that the particular form of low CHO diet used (Atkins diet) allowed increases in CHO consumption as the trial progressed indicating that it is likely this reintroduction of CHO that predisposes to long-term regain in weight. Most notable in this study, is that the improvement in lipid profile persisted (Figure 1, (Table 4) even after the effect on weight loss disappeared.

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Redukujesz tkankę tłuszczową - http://www.sfd.pl/10_wskazówek_żywieniowych-t315293.html
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http://www.sfd.pl/Zdrowie_bez_tluszczu_nie_mozliwe!!!-t164189.html#post0
Od małego jak widziałem mięso to mi ślinka leciała.
Druga sprawa kiedyś nie było ryżu, ziemniaków, mąki, chleba - mówie o naszych początkach.
Wyłączmy nasz abstrakcyjny sposób myślenia i popatrzmy "dzikimi" instynktami. Jesteśmy zwierzętami - inteligentnymi zwierzętami.
A natura wie jak nas dostosować i jest nieomylna. Jedyne źródło węglowodanów - owoce, które od czasu do czasu jak koczowaliśmy znaleźliśmy gdzieś na drzewie no i orzechy. Tamci ludzie nie mieli raka, zawałów, miażdżycy i innych chorób jak we współczesnej, węglowodanowej i zdrowej cywilizacji, gdzie nawet osoby szczupłe ograniczające tłuszcz dostają zawałów z niewyjaśnionych przyczyn. Ale myśle, że to z tego względu, że często nie było łatwo o jedzenie i organizm był raczej przyzwyczajony do niedostatku niż nadmiaru. Do tego dochodzi ciągła aktywność fizyczna. Praczłowiek nie siedział przed komputerem, czy telewizorem i nie dłubał w nosie. Koczowniczy tryb życia, walka o przetrwanie i zdobywanie jedzenia dla populacji. Patrząc na to z tej strony można dużo zrozumieć i przynajmniej starać się symulować nasz Pra-sposób bycia.
"Life is full of compromises."
to by miało sens , ale wydaje mi się że troche się mylisz że organizm człowieka nie ewoluował i się nie zmienił od czasu kiedy biegaliśmy za antylopami czy jakimiś mamutamiJa swoje poglądy mam, ale teraz czasy takie, że na wszelki wypadek się z nimi nie zgadzam.