Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate 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 PGF(2α), 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 PGF(2α) 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.

Effects of dietary carbohydrate restriction versus low-fat diet on flow-mediated dilation.

We previously reported that a carbohydrate-restricted diet (CRD) ameliorated many of the traditional markers associated with metabolic syndrome and cardiovascular risk compared with a low-fat diet (LFD). There remains concern how CRD affects vascular function because acute meals high in fat have been shown to impair endothelial function. Here, we extend our work and address these concerns by measuring fasting and postprandial vascular function in 40 overweight men and women with moderate hypertriacylglycerolemia who were randomly assigned to consume hypocaloric diets (approximately 1500 kcal) restricted in carbohydrate (percentage of carbohydrate-fat-protein = 12:59:28) or LFD (56:24:20). Flow-mediated dilation of the brachial artery was assessed before and after ingestion of a high-fat meal (908 kcal, 84% fat) at baseline and after 12 weeks. Compared with the LFD, the CRD resulted in a greater decrease in postprandial triacylglycerol (-47% vs -15%, P = .007), insulin (-51% vs -6%, P = .009), and lymphocyte (-12% vs -1%, P = .050) responses. Postprandial fatty acids were significantly increased by the CRD compared with the LFD (P = .033). Serum interleukin-6 increased significantly over the postprandial period; and the response was augmented in the CRD (46%) compared with the LFD (-13%) group (P = .038). After 12 weeks, peak flow-mediated dilation at 3 hours increased from 5.1% to 6.5% in the CRD group and decreased from 7.9% to 5.2% in the LFD group (P = .004). These findings show that a 12-week low-carbohydrate diet improves postprandial vascular function more than a LFD in individuals with atherogenic dyslipidemia.

Influences of a dietary supplement in combination with an exercise and diet regimen on adipocytokines and adiposity in women who are overweight.

The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynextrade mark, 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 microg ml(-1): 12.6 +/- 2.0-21.8 +/- 3.1 microg 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.

Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet.

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 (approximately 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.

Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation.

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-alpha, 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.

Physiogenomic analysis of weight loss induced by dietary carbohydrate restriction.

BACKGROUND: Diets that restrict carbohydrate (CHO) have proven to be a successful dietary treatment of obesity for many people, but the degree of weight loss varies across individuals. The extent to which genetic factors associate with the magnitude of weight loss induced by CHO restriction is unknown. We examined associations among polymorphisms in candidate genes and weight loss in order to understand the physiological factors influencing body weight responses to CHO restriction. METHODS: We screened for genetic associations with weight loss in 86 healthy adults who were instructed to restrict CHO to a level that induced a small level of ketosis (CHO approximately 10% of total energy). A total of 27 single nucleotide polymorphisms (SNPs) were selected from 15 candidate genes involved in fat digestion/metabolism, intracellular glucose metabolism, lipoprotein remodeling, and appetite regulation. Multiple linear regression was used to rank the SNPs according to probability of association, and the most significant associations were analyzed in greater detail. RESULTS: Mean weight loss was 6.4 kg. SNPs in the gastric lipase (LIPF), hepatic glycogen synthase (GYS2), cholesteryl ester transfer protein (CETP) and galanin (GAL) genes were significantly associated with weight loss. CONCLUSION: A strong association between weight loss induced by dietary CHO restriction and variability in genes regulating fat digestion, hepatic glucose metabolism, intravascular lipoprotein remodeling, and appetite were detected. These discoveries could provide clues to important physiologic adaptations underlying the body mass response to CHO restriction.

Protein and overtraining: potential applications for free-living athletes.

Despite a more than adequate protein intake in the general population, athletes have special needs and situations that bring it to the forefront. Overtraining is one example. Hard-training athletes are different from sedentary persons from the sub-cellular to whole-organism level. Moreover, competitive, "free-living" (less-monitored) athletes often encounter negative energy balance, sub-optimal dietary variety, injuries, endocrine exacerbations and immune depression. These factors, coupled with "two-a-day" practices and in-season demands require that protein not be dismissed as automatically adequate or worse, deleterious to health. When applying research to practice settings, one should consider methodological aspects such as population specificity and control variables such as energy balance. This review will address data pertinent to the topic of athletic protein needs, particularly from a standpoint of overtraining and soft tissue recovery. Research-driven strategies for adjusting nutrition and exercise assessments will be offered for consideration. Potentially helpful nutrition interventions for preventing and treating training complications will also be presented.

Modification of lipoproteins by very low-carbohydrate diets.

Very low-carbohydrate diets (VLCDs) are popular, but remain controversial. This review summarizes the latest studies that have examined the effects of VLCDs on lipoproteins and related risk factors for cardiovascular disease. Prospective studies indicate that VLCDs improve the lipoprotein profile independently of weight loss. Although not as effective at lowering LDL cholesterol (LDL-C), VLCDs consistently improve postabsorptive and postprandial triacylglycerols (TAGs), HDL cholesterol (HDL-C), and the distribution of LDL-C subfractions to a greater extent than low-fat diets. VLCDs also improve proinflammatory markers when associated with weight loss. Studies usually report mean lipid responses, but individual data indicate a large degree of variability in the magnitude and in some cases the direction (e.g., LDL-C) of lipoprotein responses to both low-fat and VLCDs. Such variability makes it hard to defend a single diet recommendation, especially considering the potential for low-fat/high-carbohydrate diets to exacerbate TAG, HDL-C, and other characteristics of the metabolic syndrome. Considering the effectiveness of VLCDs in promoting fat loss and improving the metabolic syndrome, discounting or condemning their use is unjustified. We encourage a more unbiased, balanced appraisal of VLCDs.

Diet and exercise for weight loss: a review of current issues.

Obesity is a fast growing epidemic that is primarily due to environmental influences. Nutrition and exercise represent modifiable factors with a major impact on energy balance. Despite considerable research, there remains continued debate regarding the energy content and the optimal macronutrient distribution for promoting healthy and effective weight loss. Low-fat diets have been advised for many years to reduce obesity. However, their effectiveness has been recently challenged, partly because the prevalence of obesity continues to rise despite reductions in fat intake. There are also concerns regarding the methodology of clinical trials showing benefits of fat reduction on weight loss. Although often viewed as a fad diet, very low-carbohydrate (ketogenic) diets are very popular and several recent clinical trials indicate they are more effective at promoting short-term weight loss and improving characteristics of the metabolic syndrome than low-fat diets. However, there is a need to obtain long-term safety and efficacy data. Clearly, weight loss can be achieved with a variety of diet interventions but the effects on other health-related aspects also need to be considered and studied in more detail. Exercise can have positive effects on weight loss, weight control and overall general health, although debate exists concerning the most effective mode, duration and intensity of exercise required to achieve these effects. Importantly, any effective weight control treatment must consider a life-long plan or there will likely be weight regain. Perhaps the most challenging, but rewarding, question that faces researchers is how to predict individual responses to diet and exercise interventions.