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We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (~1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.

Abnormal distribution of plasma fatty acids and increased inflammation are prominent features of metabolic syndrome. We tested whether these components of metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly attributed to a marked increase in arachidonate (20:4n-6), while its biosynthetic metabolic intermediates were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD. Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-α, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.

We recently showed that a hypocaloric carbohydrate restricted diet (CRD) had two striking effects: (1) a reduction in plasma saturated fatty acids (SFA) despite higher intake than a low fat diet, and (2) a decrease in inflammation despite a significant increase in arachidonic acid (ARA). Here we extend these findings in 8 weight stable men who were fed two 6-week CRD (12%en carbohydrate) varying in quality of fat. One CRD emphasized SFA (CRD-SFA, 86 g/d SFA) and the other, unsaturated fat (CRD-UFA, 47 g SFA/d). All foods were provided to subjects. Both CRD decreased serum triacylglycerol (TAG) and insulin, and increased LDL-C particle size. The CRD-UFA significantly decreased plasma TAG SFA (27.48 ± 2.89 mol%) compared to baseline (31.06 ± 4.26 mol%). Plasma TAG SFA, however, remained unchanged in the CRD-SFA (33.14 ± 3.49 mol%) despite a doubling in SFA intake. Both CRD significantly reduced plasma palmitoleic acid (16:1n-7) indicating decreased de novo lipogenesis. CRD-SFA significantly increased plasma phospholipid ARA content, while CRD-UFA significantly increased EPA and DHA. Urine 8-iso PGF₂α, a free radical-catalyzed product of ARA, was significantly lower than baseline following CRD-UFA (−32%). There was a significant inverse correlation between changes in urine 8-iso PGF₂α and PL ARA on both CRD (r = −0.82 CRD-SFA; r = −0.62 CRD-UFA). These findings are consistent with the concept that dietary saturated fat is efficiently metabolized in the presence of low carbohydrate, and that a CRD results in better preservation of plasma ARA.

A PRIMARY CONCERN WITH CONVENTIONAL WEIGHT LOSS APPROACHES IS THE LOSS OF LEAN BODY MASS THAT OCCURS WHEN FAT MASS IS DECREASED. CONSUMING MODERATE PROTEIN, WHILE RESTRICTING CARBOHYDRATE, ALLOWS FOR GREATER PRESERVATION OF LEAN BODY MASS. A LOW-CARBOHYDRATE DIET IN CONJUNCTION WITH PERIODIZED RESISTANCE TRAINING PROMOTES GREATER FAT LOSS WHILE PRESERVING LEAN BODY MASS AND PROMOTING ROBUST IMPROVEMENTS IN METABOLIC HEALTH. [PUBLICATION ABSTRACT]

The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynex™, Imagenetix, Inc., San Diego, CA 92127, USA) on adipocytokine and regional body composition responses to a weight loss program was examined. Twenty-two women (Supplement group (S) ( n  = 11): age = 36.8 ± 7.2 years; weight = 87.1 ± 6.2 kg; % body fat = 43.4 ± 4.1; Placebo group (P) ( n  = 11): age = 38.3 ± 6.8 years; weight = 86.9 ± 4.7 kg; % body fat = 44.3 ± 2.0) completed an 8-week placebo-controlled, double-blind study consisting of a caloric restricted diet and cardiovascular exercise. Body composition and serum insulin, leptin, and adiponectin were assessed at pre-, mid-, and post-intervention. From pre- to post-intervention, significant decreases ( P  < 0.05) were observed for body weight (S: 87.1 ± 6.2–77.9 ± 5.1 kg; P: 86.9 ± 4.7–82.7 ± 3.8 kg) ( P  < 0.05 S vs. P), % body fat (S: 43.4 ± 4.1–36.1 ± 3.6; P: 44.3 ± 2.0–40.6 ± 1.2) ( P  < 0.05 S vs. P), leptin (S: 28.3 ± 3.5–16.2 ± 2.6 ng ml −1 ; P: 29.4 ± 3.2–19.9 ± 1.1 ng ml −1 ) ( P  < 0.05 S vs. P), and insulin (S: 7.3 ± 0.8–5.1 ± 0.2 mU l −1 ; P: 7.7 ± 0.9–5.1 ± 0.3 mU l −1 ). Serum adiponectin increased ( P  < 0.05) (S: 12.2 ± 2.4–26.3 ± 3.0 μg ml −1 : 12.6 ± 2.0–21.8 ± 3.1 μg ml −1 ) ( P  < 0.05 for S vs. P). Supplementation with a proprietary blend of modified cellulose and cetylated fatty acids during an 8-week weight loss program exhibited favorable effects on adipocytokines and regional body composition.

The provision of dietary nutrients is a powerful method by which to alter plasma substrate and hormone concentrations, and to impact cell signalling and protein balance positively in skeletal muscle. Growth hormone, insulin-like growth factor I, testosterone, cortisol and insulin are each uniquely affected by dietary nutrients and exercise. This article summarizes some of the work that has been conducted to assess how diet affects these hormones, in particular the exercise-induced hormone response, with an emphasis on skeletal muscle as a target tissue. Clearly, certain combinations of nutrients, such as carbohydrate combined with protein, can be used to alter nutrient and hormone availability to augment skeletal muscle protein balance. There is a need to link acute diet-induced hormonal responses with chronic muscle adaptations to training, and to determine how chronic manipulations in diet affect training adaptations specific to skeletal muscle.

Background. Carbohydrate-restricted diets (CRD) consistently improve risk factors associated with Metabolic Syndrome (MetSyn). Recently, we showed that a saturated-fat rich hypocaloric CRD significantly reduced serum content of saturated fatty acids (SFA) and significantly increased arachidonic acid (AA) and the omega-6/omega-3 polyunsaturated (PUFA) ratio while significantly decreasing inflammation compared to a low-fat diet. This disconnect between dietary and circulating lipid lead us to explore how varying the fat composition of a CRD affects these variables, in addition to oxidative stress. Methods. Eight healthy weight-stable men (age 45 ± 7.9 y, body fat 28.4 ± 6.5%) were fed two eucaloric CRD varying in saturated fat and unsaturated fat with the same macronutrient distribution (12%en carbohydrate, 30%en protein, 58%en fat, 850 mg cholesterol) for 6 weeks each without weight loss. Similar foods were fed but CRD-SFA emphasized dairy fat while CRD-UFA emphasized olive oil, omega-3 fortified eggs, salmon, and walnuts. CRD-SFA provided almost twice as much SFA (86 g vs 47 g) and less monounsaturated fat (MUFA) and omega-6 and omega-3 PUFA than CRD-UFA, confirmed by chemical analysis. Fasting blood and 24 hr urine was analyzed at baseline and following each diet for fasting lipoproteins, insulin, glucose, inflammatory markers, fatty acid composition in plasma triacylglycerides (TAG), phospholipids (PL) and cholesteryl esters (CE), and urine 8-iso PGF2α. Results. Regardless of fat quality, both CRD significantly decreased TAG and insulin, and increased HDL-C and LDL particle size (P < 0.05). Despite increased total-cholesterol (TC) and LDL-cholesterol (LDL-C) after CRD-SFA, the TC/LDL-C ratio was not different between diets. Total plasma SFA in CE, PL, and TAG were unchanged after the CRD-SFA, and plasma PL and CE AA content was significantly increased. CRD-UFA significantly increased PL and CE EPA+DHA content and the PL omega-3 index. Inflammation was not different between diets or compared to baseline, but urinary 8-iso PGFza was significantly lower than baseline following CRD-UFA (-32.4%). PL AA was significantly inversely correlated to 8-iso PGF2α with both diets. Conclusion. Regardless of SFA content, CRD positively influence risk factors associated with MetSyn and do not increase plasma SFA content. Elevated plasma AA following a high-SFA CRD does not have deleterious effects while replacement of some SFA with MUFA and omega-3 PUFA significantly decreased plasma SFA, increased omega-3/omega-6 PUFA ratio and reduced oxidative stress as measured by lower urinary 8-iso PGF2α.