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

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Abstract

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.

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... While in most of the studies that implemented low-fat diet, improvements in some cardiovascular risk factors such as lipid metabolism and oxidative stress were reported, findings that are related to actual vascular measurements have been lacking or conflicting. For example, while Phillips et al. [6] have shown that low-fat diet improved arterial flow-mediated dilation (FMD), contradictory results have been reported by Volek et al. [7], who reported FMD decreases with a low-fat diet and Keogh et al. [8] who demonstrated no effect of low-fat diet on vascular function. Considering these conflicting reports, it is easy to conclude that some additional factors must play a key role in vascular outcomes of the low-fat diet and may reveal contributing mechanisms. ...
... These findings are consistent with the FMD data in medium-sized arteries that have been reported by Phillips et al. [6]. However, they are in contrast to what has been shown by Volek et al. [7] who reported a lack of macrovascular FMD improvements in response to a low-fat diet in overweight individuals with moderate dyslipidemia. The reason for these conflicting data remains unclear especially that the average weight loss in the low-fat fed subjects was very comparable in the two studies (~4-5 kg). ...
... The reason for these conflicting data remains unclear especially that the average weight loss in the low-fat fed subjects was very comparable in the two studies (~4-5 kg). One possible reason for this discrepancy could be related to the different approach that has been used in these studies; while in Phillips et al., [6] meals were prepared by a dietitian and provided to subjects (similar approach has been used in the current study), in Volek et al. [7], only dietary instructions were provided which might have resulted in unsupervised, uncontrolled macronutrient ratios in the meals consumed by the participants. In general, inconsistencies among studies that investigate the effect of diet on vascular function are mostly attributed to lack of control over the macronutrient proportions consumed by study subjects or the inclusion of other macro-or micronutrients that have been reported to modify vascular outcomes such as dietary fiber [42], nitrite-rich green vegetables, and caffeinated beverages. ...
Article
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Obesity is associated with microvascular dysfunction. While low-fat diet improves cardiovascular risk, its contributions on microvascular function, independent of weight loss, is unknown. We tested the hypothesis that nitric oxide (NO)-dependent vasodilation in microvessels is improved by low-fat diets designed for weight loss (LFWL) compared to low-fat weight maintenance (LFWM) diet. Obese adults were randomly assigned to either a LFWL diet (n = 11) or LFWM diet (n = 10) for six weeks. Microvessels were obtained from gluteal subcutaneous fat biopsies before and after the intervention for vascular reactivity measurements to acetylcholine (Ach) and flow, with and without L-NAME or indomethacin. Vascular and serum NO and C-reactive protein (CRP) were also measured. LFWL diet increased flow-induced (FID) and ACh-induced dilation (AChID); an effect that was inhibited by L-NAME. Conversely, LFWM diet did not affect FID or AChID. Indomethacin improved FID and AChID in the baseline and this effect was minimized in response to both diets. Serum NO or CRP did not change in response to either diet. In conclusion, LFWL diet improves microvascular reactivity compared to LFWM diet and increased vascular NO contribution to the improved microvascular dilation. These data suggest that weight reduction on low fat diet is critical for microvascular health.
... Research regarding the effects of long-term macronutrient restriction, with or without weight loss, on postprandial arterial stiffness is scarce. When comparing a 12-week CRD (% total energy from carbohydrate:fat, 12:59) and FRD (% total energy from carbohydrate:fat, 56:24), Volek et al. 41 reported an improvement in peak FMD following a high-fat meal in those prescribed the CRD. Postprandial FMD decreased following the FRD. ...
... Coefficient of variable values reported for FMD measurements were 10.6%, 33,36 2.9%, 42 8.4%, 30 and 2.2%. 41 Coefficient of variance values reported for AIx obtained via applanation tonometry were 16.5% 33 and 16.8%. 36 In addition to measurement error, inconsistencies between interventions regarding factors such as subject characteristics, the degree of macronutrient and energy restriction, study duration, and the amount of weight loss and physical activity may hinder comparisons. ...
... Total leukocyte and neutrophil concentrations, as well as serum IL-6 levels, have been demonstrated to increase in overweight/obese subjects in response to a high-fat meal (908 kcal, % carbohydrate:fat-:protein; 13:84:3). 41 The postprandial leukocyte response was reportedly attenuated following 12 weeks of a CRD. Similar results were not induced by 12 weeks of fat restriction. ...
Article
Metabolic syndrome is a condition characterized by a clustering of risk factors for cardiovascular disease. Emerging data suggest vascular integrity is disrupted in metabolic syndrome. Vascular integrity may be determined using several measurements, including pulse wave velocity, augmentation index, and flow-mediated dilation. Arterial stiffness has become an important clinical indicator of cardiovascular disease risk. Several circulating inflammatory peptides also impact vascular integrity. The present review examines the efficacy of nutritional interventions aimed at improving vascular integrity and reducing levels of associated inflammatory peptides in individuals with metabolic syndrome, with a specific focus on the effect of dietary macronutrient redistribution on these factors.
... week low-carbohydrate diet has been shown to improve postprandial vascular function in human brachial arteries. 121 The authors showed a positive effect of dietary carbohydrate restriction (CRD) in comparison to low-fat diet (LFD) on flow-mediated dilation. 121 After 12 ...
... 121 The authors showed a positive effect of dietary carbohydrate restriction (CRD) in comparison to low-fat diet (LFD) on flow-mediated dilation. 121 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. 121 Several other reports indicate that 6 months of weight reduction and exercise improve macrovascular endothelial function and reduce selective markers of endothelial activation and coagulation in obese subjects with metabolic syndrome regardless of the degree of glucose tolerance. 122,123 A recent study showed that weight reduction with very low-calorie diet improved flow-mediated vasodilation in obese individuals and the improvement was related to the reduction in plasma glucose concentration. ...
Article
Overweight and obesity are chronic diseases, which are increasingly affecting children and adolescents, and if not treated immediately then fat children from today will become patients from tomorrow. The objective of this study was to investigate whether dietary fat restriction normalizes body weight, impaired glucose tolerance and endothelium-dependent contractions induced by high dietary fat intake in young rodents. C57BL/6J mice, 4 weeks of age, were divided into Control group, which was fed with standard rodent chow (12% of fat); High-Fat group, which was fed for 30 weeks with the high-fat (HF) diet (41% fat) and Fat Restriction group, which was fed for 15 weeks with the HF diet (41% of fat), followed by standard chow (12% of fat) for 15 weeks. Body weight was monitored and glucose tolerance test was performed. Vascular responses to acetylcholine were investigated in aortic and carotid artery rings ex vivo in the absence or presence of nitric oxide and prostanoids. Body weight was increased in the High-Fat group and was normalized in the Fat Restriction group to similar levels as in the Control group. Impaired glucose tolerance detected in High- Fat group was normalized in the Fat Restriction group. In the High-Fat group, endotheliumdependent contractions were increased in aorta and carotid arteries, and these contractions were attenuated in the Fat Restriction group to the same level as in the Control group. Moreover, the extent and sensitivity of these contractions varied between aorta and carotid arteries in the presence or absence of nitric oxide. In conclusion, intake of high amounts of fat leads to weight gain, glucose intolerance and enhanced endothelium-dependent contractile responses in aorta and carotid artery of young mice. All these effects were normalized after dietary fat restriction. These findings thus suggest that long term reduction in intake of dietary fat improves the metabolic and vascular function in young mice.
... Nevertheless, another study of two low fat diets found that although SBP and PWV reduced significantly, FMD did not change [68]. In a 12-week study [69] of subjects with moderate hypertriglyceridaemia, brachial artery post-prandial peak FMD and weight loss were significantly increased in the carbohydrate-restricted CR group but decreased in the fat-restricted CR group, indicating that carbohydrate restriction improves postprandial vascular function compared to fat restriction. ...
... Similarly, the study duration varied in successful studies from two weeks to 12 weeks. Again, in multivariate regression analysis, weight loss appears not to be correlated with endothelium-dependent FMD improvement and there is also no correlation with changes in BP, body fat, insulin, insulin resistance or lipids [20,33,40,69], despite many studies showing that obesity is associated with decreased vasodilatation and endothelial dysfunction [20]. There may, however, be a correlation with blood glucose, although studies are divided. ...
... Biochemistry studies have shown that in endothelial cells, hyperinsulinaemia and insulin resistance are associated with impairment of the inositol 3-kinase-dependent signalling pathway, which leads to the synthesis of nitric oxide, confirming that insulin resistance is associated with vascular dysfunction [69,72,[78][79][80], while the increase in plasma asymmetric dimethylarginine (ADMA), an inhibitor of eNOS, correlates with elevated BP and insulin resistance [81,82]. This suggests that nitric oxide is at least one of the mediators of vasodilatation, as seen in a study showing a positive association between forearm endothelial NO synthesis and insulin sensitivity in healthy humans, whereas increased insulin resistance impaired endothelial function through disruption of NO production [33]. ...
Article
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Essential hypertension, fast heart rate, low heart rate variability, sympathetic nervous system dominance over parasympathetic, arterial stiffness, endothelial dysfunction and poor flow-mediated arterial dilatation are all associated with cardiovascular mortality and morbidity. This review of randomised controlled trials and other studies demonstrates that caloric restriction (CR) is capable of significantly improving all these parameters, normalising blood pressure (BP) and allowing patients to discontinue antihypertensive medication, while never becoming hypotensive. CR appears to be effective regardless of age, gender, ethnicity, weight, body mass index (BMI) or a diagnosis of metabolic syndrome or type 2 diabetes, but the greatest benefit is usually observed in the sickest subjects and BP may continue to improve during the refeeding period. Exercise enhances the effects of CR only in hypertensive subjects. There is as yet no consensus on the mechanism of effect of CR and it may be multifactorial. Several studies have suggested that improvement in BP is related to improvement in insulin sensitivity, as well as increased nitric oxide production through improved endothelial function. In addition, CR is known to induce SIRT1, a nutrient sensor, which is linked to a number of beneficial effects in the body.
... We previously showed that a CRD, compared with a low-fat diet, ameliorates markers associated with metabolic syndrome and cardiovascular risk, including impairment of postprandial VEF [6]. Furthermore, a CRD reduced several inflammatory and cellular adhesion molecules compared to an isocaloric low-fat diet in overweight individuals with atherogenic dyslipidemia [5]. ...
... Similar to previous studies conducted in our laboratory [5,6], the CRD emphasized a variety of low carbohydrate foods and an overall diet higher in fat and moderate in protein. ...
... Prior work has shown variable effects of a CRD on VEF [25][26][27]. In our previous work we demonstrated that consumption of a CRD for 12 weeks, compared with a low-fat diet, improved FMD assessed postprandially following a highfat meal [6]. In this same study, fasting FMD was unaffected after 12 weeks on a CRD compared to baseline values. ...
Article
Statins positively impact plasma low-density lipoprotein cholesterol, inflammation and vascular endothelial function (VEF). Carbohydrate restricted diets (CRD) improve atherogenic dyslipidemia, and similar to statins, have been shown to favorably affect markers of inflammation and VEF. No studies have examined whether a CRD provides additional benefit beyond that achieved by habitual statin use. We hypothesized that a CRD (<50 g carbohydrate/d) for 6 weeks would improve lipid profiles and insulin sensitivity, reduce blood pressure, decrease cellular adhesion and inflammatory biomarkers, and augment VEF (flow-mediated dilation and forearm blood flow) in statin users. Participants (n = 21; 59.3 ± 9.3 y, 29.5 ± 3.0 kg/m(2)) decreased total caloric intake by approximately 415 kcal at 6 weeks (P < .001). Daily nutrient intakes at baseline (46/36/17% carb/fat/pro) and averaged across the intervention (11/58/28% carb/fat/pro) demonstrated dietary compliance, with carbohydrate intake at baseline nearly 5-fold greater than during the intervention (P < .001). Compared to baseline, both systolic and diastolic blood pressure decreased after 3 and 6 weeks (P < .01). Peak forearm blood flow, but not flow-mediated dilation, increased at week 6 compared to baseline and week 3 (P ≤ .03). Serum triglyceride, insulin, soluble E-Selectin and intracellular adhesion molecule-1 decreased (P < .01) from baseline at week 3, and this effect was maintained at week 6. In conclusion, these findings demonstrate that individuals undergoing statin therapy experience additional improvements in metabolic and vascular health from a 6 weeks CRD as evidenced by increased insulin sensitivity and resistance vessel endothelial function, and decreased blood pressure, triglycerides, and adhesion molecules.
... A low-carbohydrates (LC) diet has been shown to improve glucose control in adults with obesity [9][10][11][12][13][14][15][16]. However, the effect of LC diet on endothelial function in adults with obesity is not clear with conflicting data, showing either no changes [9,10,[12][13][14], increases [17], or even decreases in endothelial function following LC diet [11,15,16]. The conflicting results may be due to the heterogeneity in subject characteristics, LC diet interventions (e.g., % energy restriction, % carbohydrate restriction, fat content, and dietary sources), and experimental designs (e.g., single group or randomized controlled study). ...
... Therefore, brachial artery FMD is an important therapeutic target in adults with obesity to prevent cardiovascular disease. Previous studies have examined the effect of LC diet on FMD but their findings are either confounded by the provision of CR [9,10,[12][13][14][15][16][17] or based on a single group design [31]. We found that the 6-week LC diet, regardless of CR, did not change FMD in women with obesity. ...
... In agreement with our findings, previous studies demonstrated no change [9,10,[12][13][14] or even a decrease [11,15,16] in FMD following a LC diet in adults with obesity. On the other hand, one study found that LC diet improved FMD [17]. The heterogeneity in subject characteristics, LC diet interventions (e.g., % energy restriction, % carbohydrate restriction, nutrient component, and dietary sources), and experimental designs among the published studies makes the comparisons difficult to explain the conflicting results. ...
Article
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Obesity impairs both macro- and microvascular endothelial function due to decreased bioavailability of nitric oxide. Current evidence on the effect of low-carbohydrate (LC) diet on endothelial function is conflicting and confounded by the provision of caloric restriction (CR). We tested the hypothesis that LC without CR diet, but not LC with CR diet, would improve macro- and microvascular endothelial function in women with obesity. Twenty-one healthy women with obesity (age: 33 ± 2 years, body mass index: 33.0 ± 0.6 kg/m2; mean ± SEM) were randomly assigned to receive either a LC diet (~10% carbohydrate calories) with CR (n = 12; 500 calorie/day deficit) or a LC diet without CR (n = 9) and completed the 6-week diet intervention. After the intervention, macrovascular endothelial function, measured as brachial artery flow-mediated dilation did not change (7.3 ± 0.9% to 8.0 ± 1.1%, p = 0.7). On the other hand, following the LC diet intervention, regardless of CR, blocking nitric oxide production decreased microvascular endothelial function, measured by arteriolar flow-induced dilation (p ≤ 0.02 for both diets) and the magnitude was more than baseline (p ≤ 0.04). These data suggest improved NO contributions following the intervention. In conclusion, a 6-week LC diet, regardless of CR, may improve microvascular, but not macrovascular endothelial function, via increasing bioavailability of nitric oxide in women with obesity.
... 16,17 For instance, obese patients following a CR-LF diet (25% fat) increased FMD after 8 weeks of weight loss in a study by Khoo et al. 16 Similarly, Phillips et al. 17 report increases in FMD after 6 weeks of a CR-LF diet (25% fat) and decreases in FMD with a CR-HF diet (60% fat). In contrast, Volek et al., 18 reported increases in FMD with a CR-HF (60% fat) diet and decreases with a CR-LF diet (20% fat), while Keogh et al. 19,20 demonstrated no effect of either diet on vascular endothelial function during weight loss. The reason why our findings differ from those of Volek et al. 18 and Keogh et al. 19,20 is not clear. ...
... In contrast, Volek et al., 18 reported increases in FMD with a CR-HF (60% fat) diet and decreases with a CR-LF diet (20% fat), while Keogh et al. 19,20 demonstrated no effect of either diet on vascular endothelial function during weight loss. The reason why our findings differ from those of Volek et al. 18 and Keogh et al. 19,20 is not clear. However, it should be noted that the studies showing beneficial effects of LF diets and deleterious effects of HF diets, 16,17 all provided food to subjects to ensure that the macronutrient composition of the diets were well controlled. ...
... On the other hand, the studies that demonstrate opposite, 18 or no effect, 19,20 did not provide food to subjects. Thus, the lack of diet standardization in the Volek et al. 18 and Keogh et al. 19,20 studies may partly explain these inconsistent findings. The reason why HF diets impair FMD is not clear, but may involve increased intake of saturated fat. ...
Article
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Background: Alternate day fasting (ADF) with a low-fat (LF) diet improves brachial artery flow-mediated dilation (FMD). Whether these beneficial effects can be reproduced with a high-fat (HF) diet remains unclear. Objective: This study compared the effects of ADF-HF to ADF-LF regimens on FMD. The role that adipokines have in mediating this effect was also investigated. Methods: Thirty-two obese subjects were randomized to an ADF-HF (45% fat) or ADF-LF diet (25% fat), consisting of two phases: (1) a 2-week baseline weight maintenance period and (2) an 8-week ADF weight loss period. Food was provided throughout the study. Results: Body weight was reduced (P<0.0001) in the ADF-HF (4.4±1.0 kg) and ADF-LF group (3.7±0.7 kg). FMD decreased (P<0.05) by ADF-HF relative to baseline (7±1 to 5±2%) and increased (P<0.05) by ADF-LF (5±1 to 7±2%). Blood pressure remained unchanged in both groups. Adiponectin increased (P<0.05) in the ADF-HF (43±7%) and ADF-LF group (51±7%). Leptin and resistin decreased (P<0.05) in the ADF-HF (32±5%; 23±5%) and ADF-LF group (30±3%; 27±4%). Increases in adiponectin were associated with augmented FMD in the ADF-LF group only (r=0.34, P=0.03). Conclusion: Thus, improvements in FMD with ADF may only occur with LF diets and not with HF diets, and adipokines may not have a significant role in mediating this effect.
... We previously showed that a CRD, compared with a low-fat diet, ameliorates markers associated with metabolic syndrome and cardiovascular risk, including impairment of postprandial VEF [6]. Furthermore, a CRD reduced several inflammatory and cellular adhesion molecules compared to an isocaloric low-fat diet in overweight individuals with atherogenic dyslipidemia [5]. ...
... Similar to previous studies conducted in our laboratory [5,6], the CRD emphasized a variety of low carbohydrate foods and an overall diet higher in fat and moderate in protein. ...
... Prior work has shown variable effects of a CRD on VEF [25][26][27]. In our previous work we demonstrated that consumption of a CRD for 12 weeks, compared with a low-fat diet, improved FMD assessed postprandially following a highfat meal [6]. In this same study, fasting FMD was unaffected after 12 weeks on a CRD compared to baseline values. ...
... In both overweight and obese patients, carbohydrate restricted diets are more effective than low-fat diets in terms of atherogenic dyslipemia and other metabolic syndrome characteristics such as inflammation, oxidative stress and CV risk markers (i.e., apolipoproteins A-1 and B, LDL particle distribution, and FMD) [92][93][94][95]. Peripheral small artery vascular function is improved with low carbohydrate diets when there is a decrease in BW [96,97]. ...
... However, some authors report that the degree of weight loss in obese patients is not correlated to changes in BP, endothelial function and inflammatory markers [98]. Restricting dietary carbohydrate positively impacts lipid homeostasis and inflammatory markers (i.e., TNF-α, IL-6, PAI-1) even when the saturated fat intake is higher due to the isocaloric replacement of carbohydrates [92][93][94][95]. Dysregulation of PAI-1 is involved in enhanced inflammation, vascular damage and subsequent thrombogenicity [99]. ...
Article
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Caloric restriction (CR) has proved to be the most effective and reproducible dietary intervention to increase healthy lifespan and aging. A reduction in cardiovascular disease (CVD) risk in obese subjects can be already achieved by a moderate and sustainable weight loss. Since pharmacological approaches for body weight reduction have, at present, a poor long-term efficacy, CR is of great interest in the prevention and/or reduction of CVD associated with obesity. Other dietary strategies changing specific macronutrients, such as altering carbohydrates, protein content or diet glycemic index have been also shown to decrease the progression of CVD in obese patients. In this review, we will focus on the positive effects and possible mechanisms of action of these strategies on vascular dysfunction.
... In a study of 40 overweight adults with high triglycerides, half consumed a hypocaloric (1500 calories) low-carbohydrate diet (12% C, 59% F, 28% P) while the other half consumed a hypocaloric low-fat diet (56% C, 24% F, 20% P). IL-6 levels increased in both diet groups after 3 months, but there was less of a change in the low-carbohydrate group, the group that lost more weight [128]. Finally, a 4-week study involving 29 overweight women found that those on either a low-carbohydrate diet (24% C, 59% F, 18% P) or a low-fat diet (58% C, 12% F, 30% P) increased their IL-6 levels, despite losing weight [129]. ...
... FMD has been observed to increase following 12 weeks of a hypocaloric low-carbohydrate diet (12% C, 59% F, 28% P) in overweight hypertriglyceridemic men and women. Those in this study that followed a hypocaloric low-fat diet (56% C, 24% F, 20% P) for 12 weeks experienced a decrease in FMD [128]. In a 6-week study with 30 overweight or obese women, both a high-carbohydrate diet (60% C, 20% F, 18% P) and a moderate-carbohydrate diet (45% C, 37% F, 18% P) decreased E-selectin levels [125]. ...
Article
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Every year, increasing numbers of children and adolescents are diagnosed with type 2 diabetes. Compared to older adults with type 2 diabetes, youth have more difficulty controlling their glycemia and are faced with a much greater risk for cardiovascular disease. Although pharmaceutical options for management of diabetes and its co-morbidities are limited for youth, studies in adults as well as adolescents indicate that a low-carbohydrate diet may be an alternative way to reduce body weight and control blood sugar levels. To assess whether low-carbohydrate diets can also reduce the cardiovascular disease risk that accompanies type 2 diabetes in youth, we discuss the impact of both ketogenic and non-ketogenic low-carbohydrate diets on indicators of cardiovascular disease. This discussion includes not only traditional cardiovascular disease risk markers such as dyslipidemia, but also other factors that are associated with obesity and type 2 diabetes in adolescents such as interleukin-6, C-reactive protein and endothelial dysfunction. We also explore the practicalities involved in adopting and adhering to a low-carbohydrate diet such as the ketogenic diet, discussing its effects on satiety, its cultural adaptability and the types of foods that it emphasizes. The proficiency with which low-carbohydrate diets can reduce excess body weight, improve lipid profiles and attenuate inflammation without restricting calories or decreasing satiety, suggests that they may be an effective tool to reduce cardiovascular disease risk in youth with type 2 diabetes.
... It is well established that obese subjects underreport intake [20], but we do not believe this differed between diet groups as similar percent weight loss was achieved. Subjects in the both the HFLC and LFHC group consumed close to the recommended proportions of protein, carbohydrate and fat and these levels were similar to some, but not all previous studies [6,7,[21][22][23][24][25]. Overall, the participants' compliance to the recommended dietary intake was good and was most likely the result of the bi-weekly consultation with the study dietitian. ...
... Previous intervention studies have reported comparable reductions in body weight when subjects consumed hypocaloric LF or LC diets for 6 weeks to one year [24][25][26][27]. But several studies (4-24 week interventions) have also reported greater weight loss in overweight/obese subjects consuming hypocaloric HFLC diets compared to LFHC diets [4][5][6][7]21,22,[28][29][30]. We also observed similar losses in lean and fat mass between LFHC and HFLC groups, which is supported by other interventions when similar weight loss was achieved between groups [23,24,27]. ...
Article
High fat, low carbohydrate (HFLC) diets have become popular tools for weight management. We sought to determine the effects of a HFLC diet compared to a low fat high carbohydrate (LFHC) diet on the change in weight loss, cardiovascular risk factors and inflammation in subjects with obesity. Obese subjects (29.0-44.6kg/m(2)) recruited from Boston Medical Center were randomized to a hypocaloric LFHC (n=26) or HFLC (n=29) diet for 12weeks. The age range of subjects was 21-62years. As a percentage of daily calories, the HFLC group consumed 33.5% protein, 56.0% fat and 9.6% carbohydrate and the LFHC group consumed 22.0% protein, 25.0% fat and 55.7% carbohydrate. The change in percent body weight, lean and fat mass, blood pressure, flow mediated dilation, hip:waist ratio, hemoglobin A1C, fasting insulin and glucose, and glucose and insulin response to a 2h oral glucose tolerance test did not differ (P>0.05) between diets after 12weeks. The HFLC group had greater mean decreases in serum triglyceride (P=0.07), and hs-CRP (P=0.03), and greater mean increases in HDL cholesterol (P=0.004), and total adiponectin (P=0.045) relative to the LFHC. Secreted adipose tissue adiponectin or TNF-α did not differ after weight loss for either diet. Relative to the LFHC group, the HFLC group had greater improvements in blood lipids and systemic inflammation with similar changes in body weight and composition. This small-scale study suggests that HFLC diets may be more beneficial to cardiovascular health and inflammation in free-living obese adults compared to LFHC diets.
... These particles have been shown to be the most effective in delivering cholesterol from the bloodstream back to the liver, enhancing reverse cholesterol transport (Zannis et al., 2006). Individuals with CVD, obesity, type 2 diabetes and/or metabolic syndrome commonly have abnormal HDL metabolism (Filippatos and Elisaf, 2013;Kim et al., 2014;Rosenson et al., 2013;Russo et al., 2014), including reduced levels of large HDL, and our data strengthen the evidence that carbohydrate restriction and weight loss help normalize HDL metabolism and atherogenic dyslipidaemia (Lee et al., 2015;Mascarenhas-Melo et al., 2013;Tay et al. 2014;Volek et al., 2009;Zhang et al., 2015). Relative improvements in large HDL levels were much more pronounced than improvements in HDL cholesterol levels, which were modest and not highly correlated with improvements in large HDL. ...
... It is plausible that excess dietary intake of refined carbohydrates upregulates CETP activity, perhaps via postprandial and/or chronic elevations of glucose, insulin, triglyceride, and/or VLDL (Kontush et al., 2013;Miller, 2015;Scharnagl et al., 2014;Sprandel et al. 2015), and carbohydrate restriction plausibly reverses this hyperactivity, especially in the setting of insulin resistance and atherogenic dyslipidaemia. This hypothesized mechanism is compatible with other data showing that carbohydrate restriction and weight loss each improve levels of small dense LDL particles (Siri-Tarino et al., 2009;Tay et al. 2014;Volek et al., 2009), and the strong correlation between improvements in large HDL and small-dense LDL particles is consistent with a common underlying mechanism (Mascarenhas-Melo et al., 2013;Shoji et al., 2009). ...
Article
Depressed levels of atheroprotective large HDL particles are common in obesity and cardiovascular disease (CVD). Increases in large HDL particles are favourably associated with reduced CVD event risk and coronary plaque burden. The objective of the study is to compare the effectiveness of low-carbohydrate diets and weight loss for increasing blood levels of large HDL particles at 1 year. This study was performed by screening for body mass index (BMI) and metabolic syndrome in 160 consecutive subjects referred to our out-patient Metabolic Unit in South Italy. We administered dietary advice to four small groups rather than individually. A single team comprised of a dietitian and physician administered diet-specific advice to each group. Large HDL particles at baseline and 1 year were measured using two-dimensional gel electrophoresis. Dietary intake was assessed via 3-day diet records. Although 1-year weight loss did not differ between diet groups (mean 4.4 %), increases in large HDL particles paralleled the degree of carbohydrate restriction across the four diets (p<0.001 for trend). Regression analysis indicated that magnitude of carbohydrate restriction (percentage of calories as carbohydrate at 1 year) and weight loss were each independent predictors of 1-year increases in large HDL concentration. Changes in HDL cholesterol concentration were modestly correlated with changes in large HDL particle concentration (r=0.47, p=.001). In conclusion, reduction of excess dietary carbohydrate and body weight improved large HDL levels. Comparison trials with cardiovascular outcomes are needed to more fully evaluate these findings.
... For example, in a randomized, parallel trial comparing the effects of a low-carbohydrate diet to a low-fat diet in obese adults, the low-carbohydrate diet after 1-year resulted in greater weight and fat loss, a larger increase in HDL-cholesterol, and greater decreases in triglycerides and C-reactive protein as well as other markers of inflammation and endothelial dysfunction [113,114]. In another trial comparing a calorie-unrestricted lowcarbohydrate diet to a reduced-calorie, low-fat diet in obese individuals with metabolic syndrome, the low-carbohydrate KD diet after 3-months resulted in a significant reduction in fasting and postprandial triglycerides, increased HDL-cholesterol, decreased small LDL particles, decreased glucose and insulin, improved vascular functioning as assessed by flow-mediated dilation of the brachial artery, decreased circulating saturated fatty acids, and lower concentrations of several pro-inflammatory meditators [12,64,115]. After 1-year, a group of participants with T2D following a KD showed a small increase in LDLcholesterol (LDL-C), but robust improvement in the vast majority of CVD risk markers including decreases in triglycerides, small LDL particles, blood pressure, antihypertensive medications, C-reactive protein, white blood cell count, and the 10-year atherosclerotic cardiovascular risk score [107]. ...
... These examples are further supported by results from a meta-analysis concluding that low-carbohydrate diets significantly lowered the predicted risk of developing atherosclerotic CVD [57]. Although decreased body mass often accompanies low-carbohydrate diets, the broad-spectrum effects of low-carbohydrate diets on these CVD risk factors, including significant improvement in insulin sensitivity [31], are mostly independent of weight loss [31,32,40,[115][116][117]. ...
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The decades-long dietary experiment embodied in the Dietary Guidelines for Americans (DGA) focused on limiting fat, especially saturated fat, and higher carbohydrate intake has coincided with rapidly escalating epidemics of obesity and type 2 diabetes (T2D) that are contributing to the progression of cardiovascular disease (CVD) and other diet-related chronic diseases. Moreover, the lack of flexibility in the DGA as it pertains to low carbohydrate approaches does not align with the contemporary trend toward precision nutrition. We argue that personalizing the level of dietary carbohydrate should be a high priority based on evidence that Americans have a wide spectrum of metabolic variability in their tolerance to high carbohydrate loads. Obesity, metabolic syndrome, and T2D are conditions strongly associated with insulin resistance, a condition exacerbated by increased dietary carbohydrate and improved by restricting carbohydrate. Low-carbohydrate diets are grounded across the time-span of human evolution, have well-established biochemical principles, and are now supported by multiple clinical trials in humans that demonstrate consistent improvements in multiple established risk factors associated with insulin resistance and cardiovascular disease. The American Diabetes Association (ADA) recently recognized a low carbohydrate eating pattern as an effective approach for patients with diabetes. Despite this evidence base, low-carbohydrate diets are not reflected in the DGA. As the DGA Dietary Patterns have not been demonstrated to be universally effective in addressing the needs of many Americans and recognizing the lack of widely available treatments for obesity, metabolic syndrome, and T2D that are safe, effective, and sustainable, the argument for an alternative, low-carbohydrate Dietary Pattern is all the more compelling.
... We have previously reported that postprandial hyperinsulinemia also induces attenuation of FMD in persons with normal glucose tolerance [12]. Several studies have evaluated differences in FMD attenuation after meals with different carbohydrate contents [13][14][15][16][17]. Although these studies have found that the attenuation of postprandial FMD is affected by postprandial lipid metabolism [14][15][16][17], how it is affected by glucose metabolism after meals with different carbohydrate contents remains unclear. ...
... Several studies have evaluated differences in FMD attenuation after meals with different carbohydrate contents [13][14][15][16][17]. Although these studies have found that the attenuation of postprandial FMD is affected by postprandial lipid metabolism [14][15][16][17], how it is affected by glucose metabolism after meals with different carbohydrate contents remains unclear. ...
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Background: Previous studies have demonstrated that postprandial hyperglycemia attenuates brachial artery flow-mediated dilation (FMD) in prediabetic patients, in diabetic patients, and even in normal subjects. We have previously reported that postprandial hyperinsulinemia also attenuates FMD. In the present study we evaluated the relationship between different degrees of postprandial attenuation of FMD induced by postprandial hyperglycemia and hyperinsulinemia and differences in ingested carbohydrate content in non-diabetic individuals. Methods: Thirty-seven healthy subjects with no family history of diabetes were divided into 3 groups: a 75-g oral glucose loading group (OG group) (n = 14), a test meal group (TM group) (n = 12; 400 kcal, carbohydrate content 40.7 g), and a control group (n = 11). The FMD was measured at preload (FMD0) and at 60 minutes (FMD60) and 120 (FMD120) minutes after loading. Plasma glucose (PG) and immunoreactive insulin (IRI) levels were determined at preload (PG0, IRI0) and at 30 (PG30, IRI30), 60 (PG60, IRI60), and 120 (PG120, IRI120) minutes after loading. Result: Percentage decreases from FMD0 to FMD60 were significantly greater in the TM group (-21.19% ± 17.90%; P < 0.001) and the OG group (-17.59% ± 26.64%) than in the control group (6.46% ± 9.17%; P < 0.01), whereas no significant difference was observed between the TM and OG groups. In contrast, the percentage decrease from FMD0 to FMD120 was significantly greater in the OG group (-18.91% ± 16.58%) than in the control group (6.78% ± 11.43%; P < 0.001) or the TM group (5.22% ± 37.22%; P < 0.05), but no significant difference was observed between the control and TM groups. The FMD60 was significantly correlated with HOMA-IR (r = -0.389; P < 0.05). In contrast, FMD120 was significantly correlated with IRI60 (r = -0.462; P < 0.05) and the AUC of IRI (r = -0.468; P < 0.05). Furthermore, the percentage change from FMD0 to FMD120 was significantly correlated with the CV of PG (r = 0.404; P < 0.05), IRI60 (r = 0.401; p < 0.05) and the AUC of IRI (r = 0.427; P < 0.05). No significant correlation was observed between any other FMDs and glucose metabolic variables. Conclusion: Differences in the attenuation of postprandial FMD induced by different postprandial insulin levels may occur a long time postprandially but not shortly after a meal.
... However, additional markers of MetS, cardiovascular disease (CVD), and inflammation did not differ between quartiles of carbohydrate intake [36]. Additionally, a 12week hypocaloric CRD (12 % carbohydrate, 59 % fat, 28 % protein) increased postprandial flow-mediated dilation when compared to a hypocaloric low-fat diet (56 % carbohydrate, 24 % fat, 20 % protein) in overweight men with moderate hypertriglyceridemia [37], thereby suggesting that CRD improves endothelial function. ...
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Metabolic syndrome (MetS) is a cluster of metabolic abnormalities characterized by central obesity, dyslipidemias, hypertension, high fasting glucose, chronic low-grade inflammation and oxidative stress. This condition has become an increasing problem in our society where about 34 % of adults are diagnosed with MetS. In parallel with the adult situation, a significant number of children present lipid abnormalities and insulin resistance, which can be used as markers of MetS in the pediatric population. Changes in lifestyle including healthy dietary regimens and increased physical activity should be the first lines of therapy to decrease MetS. In this article, we present the most recent information on successful dietary modifications that can reduce the parameters associated with MetS. Successful dietary strategies include energy restriction and weight loss, manipulation of dietary macronutrients-either through restriction of carbohydrates, fat, or enrichment in beneficial fatty acids, incorporation of functional foods and bioactive nutrients, and adherence to dietary and lifestyle patterns such the Mediterranean diet and diet/exercise regimens. Together, the recent findings presented in this review serve as evidence to support the therapeutic treatment of MetS through diet.
... An inflammatory reaction might be at the basis of the observed relation between the abnormal bacterial species in both our oral cavity and intestine and our serum HDL-and LDL-cholesterol [106]. Saturated fats may cause an inflammatory reaction especially when they are combined with a carbohydrate-rich diet, notably carbohydrates with a high glycemic index, and especially in subjects with the insulin resistance syndrome124125126127128. ...
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In this review, we focus on lifestyle changes, especially dietary habits, that are at the basis of chronic systemic low grade inflammation, insulin resistance and Western diseases. Our sensitivity to develop insulin resistance traces back to our rapid brain growth in the past 2.5 million years. An inflammatory reaction jeopardizes the high glucose needs of our brain, causing various adaptations, including insulin resistance, functional reallocation of energy-rich nutrients and changing serum lipoprotein composition. The latter aims at redistribution of lipids, modulation of the immune reaction, and active inhibition of reverse cholesterol transport for damage repair. With the advent of the agricultural and industrial revolutions, we have introduced numerous false inflammatory triggers in our lifestyle, driving us to a state of chronic systemic low grade inflammation that eventually leads to typically Western diseases via an evolutionary conserved interaction between our immune system and metabolism. The underlying triggers are an abnormal dietary composition and microbial flora, insufficient physical activity and sleep, chronic stress and environmental pollution. The disturbance of our inflammatory/anti-inflammatory balance is illustrated by dietary fatty acids and antioxidants. The current decrease in years without chronic disease is rather due to "nurture" than "nature," since less than 5% of the typically Western diseases are primary attributable to genetic factors. Resolution of the conflict between environment and our ancient genome might be the only effective manner for "healthy aging," and to achieve this we might have to return to the lifestyle of the Paleolithic era as translated to the 21st century culture.
... In general, EDV in MetS can be improved by low-fat [142,143] and low-carbohydrate diet [142]. Interestingly, low-carbohydrate diet improved, while low-fat diet decreased postprandial EDV in 40 overweight and obese patients with hypertriglyceridemia [144]. Highfibre diet may also improve EDV [145]. ...
Article
Metabolic syndrome (MetS) is associated with increased risk of both atherothrombotic cardiovascular events and venous thromboembolism. The pro-thrombotic potential of MetS, may explain this association. In this review we discuss the relationship of MetS with hemostasis focusing on endothelial function, platelet activity, coagulation, fibrinolysis and hemorheologic markers. Endothelial-dependent vasodilatation is impaired in MetS. This is mostly mediated by a reduced expression of vasodilators (nitric oxide and prostacyclin) with a concomitant increase of vasoconstrictors (endothelin-1, angiotensin II and thromboxane A2). Platelet activity is enhanced in MetS. A cross-talk between activated endothelium and platelets results in a pro-thrombotic vicious cycle. Enhanced coagulation together with impaired fibrinolysis is also present in MetS. This is mirrored by high fibrinogen and plasminogen activator inhibitor-1 levels. Endothelial dysfunction, expressed by high von Willebrand factor and tissue plasminogen factor levels, also contributes to this abnormality. Whole blood and plasma viscosity is increased in MetS. Lifestyle intervention can improve the MetS-related pro-thrombotic state. These measures include weight reduction and improved composition of the diet. A Mediterranean-style diet rich in olive oil, as a source of monounsaturated fat, and low saturated fat consumption may also be beneficial.
... However, these data were collected postprandially and cannot be directly extrapolated to basal conditions (30) . The present results therefore reinforce the known negative impact of very low-carbohydrate diets on vascular function assessed by FMD under fasting conditions, using the PAT technique. ...
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Low carbohydrate diets have become increasingly popular for weight loss. Although they may improve some metabolic markers, particularly in type 2 diabetes mellitus (T2D) or metabolic syndrome (MS), their net effect on vascular function remains unclear. Evaluate the relation between dietary macronutrient composition and the small artery reactive hyperaemia index (saRHI), a marker of small artery vascular function, in a cohort of MS patients. This cross-sectional study included 160 MS patients. Diet was evaluated by a 3-day food-intake register and reduced to a novel low-carbohydrate diet score (LCDS). Physical examination, demographic, biochemical and anthropometry parameters were recorded, and saRHI was measured in each patient. Individuals in the lowest LCDS quartile (Q1; 45% carbohydrate, 19% protein, 31% fat) had higher saRHI values than those in the top quartile (Q4; 30% carbohydrate, 25% protein, 43% fat) (1.84±0.42 vs. 1.55±0.25, P=.012). These results were similar in T2D patients (Q1=1.779±0.311 vs. Q4=1.618±0.352, P=.011) and also in all of the MS components, except for low HDLc. Multivariate analysis demonstrated that individuals in the highest LCDS quartile, that is, consuming less carbohydrates, had a significantly negative coefficient of saRHI which was independent of confounders (HR: -0.747; 95%CI: 0.201, 0.882; P=.029). These data suggest that a dietary pattern characterized by a low amount of carbohydrate, but reciprocally higher amounts of fat and protein, is associated with poorer vascular reactivity in patients with MS and T2D.
... FMD assessed via upper arm occlusion, which is only partially reduced by NO blockade (Doshi et al., 2009), predicts future cardiovascular events as effectively as FMD following distal cuff occlusion (Green, Jones, Thijssen, Cable, & Atkinson, 2011). Previous studies in our laboratory reported reliable coefficients of variation (2.2%) using the same technique and equipment (Volek et al., 2009; Ballard et al., 2009). FITNESS ASSESSMENT Following FMD assessment, participants consumed a light breakfast which included whole grain bread (one serving), fruit, and a protein/fat spread. ...
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Compared to their physically active peers overweight sedentary postmenopausal women demonstrate impaired vascular endothelial function (VEF), substantially increasing the risk for cardiovascular disease (CVD). Habitual exercise is associated with improved VEF and reduced CVD risk. The purpose of this study was to compare brachial artery flow mediated dilation (FMD), a measure of VEF, in overweight, postmenopausal women who were physically active (EX: n=17, BMI: 29.3±3.11 kg/m2) or sedentary (CON: n=8, BMI: 30.3±3.6 kg/m2). Anthropomorphic measures were similar in both groups (p>0.05). FMD was significantly greater in EX (10.24±2.36%) versus CON (6.60±2.18%) (p<0.002). FMD was not significantly correlated with estimated VO2max (EX: r=0.17, p=0.52; CON: r=0.20, p=0.60) but was negatively associated with percent body fat in EX group (EX: r=-0.48, p=0.05; CON: r=0.41, p=0.31). These results are consistent with the positive effects of habitual exercise on VEF in overweight postmenopausal women.
... Not a randomised controlled trial 4 [71][72][73][74] Duration of the intervention ,12 weeks 40 All three macronutrients not prescribed (or cannot be calculated as proportions of the total energy intake) 20 [115][116][117][118][119][120][121][122][123][124][125][126][127][128][129][130][131][132][133][134] Non-English language 1 [135] Test meal response measured 1 [136] Meal replacement 2 [137,138] Combined interventions were involved 3 [139][140][141] Treatment and control both low carbohydrate -not an eligible comparison 3 [142][143][144] Comparison not meaningful (carbohydrate content of treatment and controls differ ,5% of TE) 2 [145,146] No eligible balanced carbohydrate control 1 [147] Crossover trial where first period data cannot be extracted: 1 1 [148] Substantial disparity in energy intake between prescribed intervention diets 13 [49,51,[149][150][151][152][153][154][155][156][157][158][159] Treatment diet is not low in carbohydrates 26 Control diet is not within balanced macronutrient range 4 [186][187][188][189] Duplicate and/or complimentary 24 Energy intake ad libitum 8 [214][215][216][217][218][219][220][221] Ineligible low carbohydrate diet variant 6 [222][223][224][225][226][227] Less than 10 participants randomised per group 1 [228] RCT = randomised controlled trial; CHO = carbohydrate. doi:10.1371/journal.pone.0100652.t007 ...
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Background Some popular weight loss diets restricting carbohydrates (CHO) claim to be more effective, and have additional health benefits in preventing cardiovascular disease compared to balanced weight loss diets. Methods and Findings We compared the effects of low CHO and isoenergetic balanced weight loss diets in overweight and obese adults assessed in randomised controlled trials (minimum follow-up of 12 weeks), and summarised the effects on weight, as well as cardiovascular and diabetes risk. Dietary criteria were derived from existing macronutrient recommendations. We searched Medline, EMBASE and CENTRAL (19 March 2014). Analysis was stratified by outcomes at 3–6 months and 1–2 years, and participants with diabetes were analysed separately. We evaluated dietary adherence and used GRADE to assess the quality of evidence. We calculated mean differences (MD) and performed random-effects meta-analysis. Nineteen trials were included (n = 3209); 3 had adequate allocation concealment. In non-diabetic participants, our analysis showed little or no difference in mean weight loss in the two groups at 3–6 months (MD 0.74 kg, 95%CI −1.49 to 0.01 kg; I2 = 53%; n = 1745, 14 trials; moderate quality evidence) and 1–2 years (MD 0.48 kg, 95%CI −1.44 kg to 0.49 kg; I2 = 12%; n = 1025; 7 trials, moderate quality evidence). Furthermore, little or no difference was detected at 3–6 months and 1–2 years for blood pressure, LDL, HDL and total cholesterol, triglycerides and fasting blood glucose (>914 participants). In diabetic participants, findings showed a similar pattern. Conclusions Trials show weight loss in the short-term irrespective of whether the diet is low CHO or balanced. There is probably little or no difference in weight loss and changes in cardiovascular risk factors up to two years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomised to low CHO diets and isoenergetic balanced weight loss diets.
... Moreover, the link between dietary fat and inflammation is often made on the grounds that high-fat meals promote a pro-inflammatory state (Herieka & Erridge, 2014), but these studies involve ingestion of a single fat-rich meal by individuals not habitually accustomed to eating the majority of calories from fat and who are definitely not keto-adapted. Volek et al. (2009;Sharman, Gómez, Kraemer, & Volek, 2004) have repeatedly shown that keto-adaptation is associated with significantly enhanced postprandial processing of dietary fat and improved metabolic-risk markers including those relating to vascular function and flow-mediated dilation of the brachial artery. ...
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Abstract A key element contributing to deteriorating exercise capacity during physically demanding sport appears to be reduced carbohydrate availability coupled with an inability to effectively utilize alternative lipid fuel sources. Paradoxically, cognitive and physical decline associated with glycogen depletion occurs in the presence of an over-abundance of fuel stored as body fat that the athlete is apparently unable to access effectively. Current fuelling tactics that emphasize high-carbohydrate intakes before and during exercise inhibit fat utilization. The most efficient approach to accelerate the body's ability to oxidize fat is to lower dietary carbohydrate intake to a level that results in nutritional ketosis (i.e., circulating ketone levels >0.5 mmol/L) while increasing fat intake for a period of several weeks. The coordinated set of metabolic adaptations that ensures proper interorgan fuel supply in the face of low-carbohydrate availability is referred to as keto-adaptation. Beyond simply providing a stable source of fuel for the brain, the major circulating ketone body, beta-hydroxybutyrate, has recently been shown to act as a signalling molecule capable of altering gene expression, eliciting complementary effects of keto-adaptation that could extend human physical and mental performance beyond current expectation. In this paper, we review these new findings and propose that the shift to fatty acids and ketones as primary fuels when dietary carbohydrate is restricted could be of benefit for some athletes.
... However, these data were collected postprandially and cannot be directly extrapolated to basal conditions (30) . The present results therefore reinforce the known negative impact of very low-carbohydrate diets on vascular function assessed by FMD under fasting conditions, using the PAT technique. ...
Article
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Low-carbohydrate diets have become increasingly popular for weight loss. Although they may improve some metabolic markers, particularly in type 2 diabetes mellitus (T2D) or the metabolic syndrome (MS), their net effect on arterial wall function remains unclear. The objective was to evaluate the relation between dietary macronutrient composition and the small artery reactive hyperaemia index (saRHI), a marker of small artery endothelial function, in a cohort of patients at increased cardiovascular (CV) risk. The present cross-sectional study included 247 patients. Diet was evaluated by a 3-d food-intake register and reduced to a novel low-carbohydrate diet score (LCDS). Physical examination, demographic, biochemical and anthropometry parameters were recorded, and the saRHI was measured in each patient. Individuals in the lowest LCDS quartile (Q1, 45 % carbohydrate; 20 % protein; 32 % fat) had higher saRHI values than those in the top quartile (Q4, 29 % carbohydrate, 24 % protein, 40 % fat; 1·66 (sd 0·41) v. 1·52 (sd 0·22), P = 0·037). These results were particularly strong in patients with the MS (Q1 = 1·82 (sd 0·32) v. Q4 = 1·61 (sd 027); P = 0·021) and T2D (Q1 = 1·78 (sd 0·31) v. Q4 = 1·62 (sd 0·35); P = 0·011). Multivariate analysis demonstrated that individuals in the highest LCDS quartile had a significantly negative coefficient of saRHI, which was independent of confounders (OR - 0·85; 95 % CI 0·19, 0·92; P = 0·031). These findings suggest that a dietary pattern characterised by a low amount of carbohydrate, but high amounts of protein and fat, is associated with a poorer small artery vascular reactivity in patients with increased CV risk.
... Under these conditions, dietary SAFA are preserved, while the surplus of the consumed CHO is converted to SAFA by hepatic de novo fatty acid synthesis. Although the conservation of SAFA during excessive intake of CHO with a high glycaemic index is well known, [73][74][75][76] the synthesis of SAFA from (surplus) CHO may not have received sufficient attention. Contrary to widespread belief, de novo fatty acid synthesis is not restricted to hypercaloric conditions or to excessive intake of CHO, but also depends on the type of ingested CHO. ...
Article
The dietary intake of saturated fatty acids (SAFA) is associated with a modest increase in serum total cholesterol, but not with cardiovascular disease (CVD). Replacing dietary SAFA with carbohydrates (CHO), notably those with a high glycaemic index, is associated with an increase in CVD risk in observational cohorts, while replacing SAFA with polyunsaturated fatty acids (PUFA) is associated with reduced CVD risk. However, replacing a combination of SAFA and trans-fatty acids with n-6 PUFA (notably linoleic acid) in controlled trials showed no indication of benefit and a signal toward increased coronary heart disease risk, suggesting that n-3 PUFA may be responsible for the protective association between total PUFA and CVD. High CHO intakes stimulate hepatic SAFA synthesis and conservation of dietary SAFA . Hepatic de novo lipogenesis from CHO is also stimulated during eucaloric dietary substitution of SAFA by CHO with high glycaemic index in normo-insulinaemic subjects and during hypocaloric high-CHO/low-fat diets in subjects with the metabolic syndrome. The accumulation of SAFA stimulates chronic systemic low-grade inflammation through its mimicking of bacterial lipopolysaccharides and÷or the induction of other pro-inflammatory stimuli. The resulting systemic low-grade inflammation promotes insulin resistance, reallocation of energy-rich substrates and atherogenic dyslipidaemia that concertedly give rise to increased CVD risk. We conclude that avoidance of SAFA accumulation by reducing the intake of CHO with high glycaemic index is more effective in the prevention of CVD than reducing SAFA intake per se.
... The beneficial effects of low-carbohydrate diets have been confirmed in randomized long-term studies [66, 67]. Noteworthy, beneficial effects of carbohydrate restriction on postmeal endothelial dysfunction were demonstrated in individuals with abdominal obesity and in those with atherogenic dyslipidemia [68, 69]. ...
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Diabetes mellitus, the metabolic syndrome, and the underlying insulin resistance are increasingly associated with diastolic dysfunction and reduced stress tolerance. The poor prognosis associated with heart failure in patients with diabetes after myocardial infarction is likely attributable to many factors, important among which is the metabolic impact from insulin resistance and hyperglycemia on the regulation of microvascular perfusion and energy generation in the cardiac myocyte. This review summarizes epidemiologic, pathophysiologic, diagnostic, and therapeutic data related to diabetes and heart failure in acute myocardial infarction and discusses novel perceptions and strategies that hold promise for the future and deserve further investigation.
... Pre-to post-intervention changes in FMD were also not statistically significant, as previously reported after six weeks to two years of eight weeks of CRD [6][7][8]28,29 . Conversely, Phillips et al. 5 observed significant reductions in FMD in CRD dieters (-1.4±0.6%) and significant increases in that of conventional dieters (+1.9±0.8%) ...
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Objective: To compare the effects of either a carbohydrate-restrictive diets or a conventional hypoenergetic diet combined with resistance training. Methods: Twenty-one overweight and obese adults participated in an eight-week program consisting of progressive resistance training combined with carbohydrate-restrictive diets (initially set at <30 g carbohydrate; n=12) or conventional hypoenergetic diet (30% energetic restriction; carbohydrate/protein/lipid: 51/18/31% of total energy consumption; n=9). It was hypothesized that the carbohydrate-restrictive diets would induce greater weight loss but that both diets would elicit similar effects on selected health markers. Body mass, and body composition, blood variables and flow-mediated brachial artery dilation (flow-mediated brachial artery dilation; by ultrasound) were used to assess changes due to the interventions. Results: Significant within-group reductions in body mass (-5.4±3.5%; p=0.001 versus -3.7±3.0%; p=0.015) and body fat (body fat; -10.2±7.0%; p=0.005 versus -9.6±8.8%; p=0.017) were identified for carbohydrate-restrictive diets and conventional hypoenergetic diet, respectively, but there were no significant differences between groups as the result of the interventions. Fat free mass, blood variables and flow-mediated brachial artery dilation did not significantly change, except for the total cholesterol/high-density lipoprotein ratio, which was reduced 10.4±16.9% in carbohydrate-restrictive diets (p=0.037) and 0.5±11.3% in conventional hypoenergetic diet (p=0.398). Conclusion: Carbohydrate-restrictive diets associated with resistance training was as effective as conventional hypoenergetic diet in decreasing body mass and body fat, as well as maintaining fat free mass, blood variables and flow-mediated brachial artery dilation, however it was more effective at lowering the total cholesterol/low density lipoprotein ratio.
... For many years, a high-fat diet was considered to elicit an extended cardiovascular risk profile [76]. In contrast, recent studies of carbohydrate-restricted diets have shown improvements in markers of cardiovascular health in adults and revealed no negative effect on measures of subclinical disease despite dyslipidemia [77][78][79]. The protective efficacy of long-term adherence to the LCDs in our subjects against a cardiovascular risk profile is seen in some plasma lipid measures. ...
Article
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The objective of this research was to determine whether chronic (average 3.58 ± 1.56 years) deliberate adherence to low carbohydrate diets (LCDs) is associated with selected markers of metabolism, risk factors of cardiovascular disease (CVD), body mass and physical performance in apparently healthy middle-aged men (n = 12). The control group comprised age, body mass and height matched men using mixed diets (MDs). The diets used were registered for 7 days and analyzed in terms of the energy, carbohydrate, fat and protein contents. It was found that the diets used were isoenergetic, yet varied considerably in carbohydrate and fat content. The LCDs significantly intensified the ketogenesis process, increased resting blood total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and heart rate, (HR) and decreased respiratory exchange ratio (RER) in relation to MD subjects. An exercise trial revealed significant impairment of exercise in subjects following the LCDs. The results showed that in the case where the subjects of two investigated groups did not differ in their somatic variables, long-term adherence to the LCDs was associated with substantially reduced exercise performance in apparently healthy subjects, along with an association with a small unfavorable effect on their lipid profile.
... They found continued improvement in blood glucose levels and blood lipids along with weight loss in both groups, although changes in total cholesterol, triglycerides and glucose were more significant in subjects with high blood glucose levels compared to those with normal blood glucose levels. In addition, low-carbohydrate diets have a more favourable effect on alternative indicators of cardiovascular risk in overweight subjects, including postprandial lipaemia, low-density lipoprotein particle distribution [61] and vascular function [62]. ...
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Obstructive sleep apnoea (OSA) is associated with increased cardiovascular disease (CVD) morbidity and mortality. It is accepted that OSA and obesity commonly coexist. The American Academy of Sleep Medicine recommends dietary-induced weight loss and exercise as lifestyle treatment options for OSA. However, most clinical trials upon which this recommendation is based have focused on establishing the effectiveness of calorie-restricted, often low-fat diets for improving OSA severity, whereas less attention has been given to the means through which weight loss is achieved (e.g. altered dietary quality) or whether diet or exercise mediates the associations between reduced weight, improved OSA severity and the CVD substrate. The current evidence suggests that the benefits of a low-carbohydrate or Mediterranean diet in overweight and obese individuals go beyond the recognised benefits of weight reduction. In addition, exercise has an independent protective effect on vascular health, which may counter the increased oxidative stress, inflammation and sympathetic activation that occur in OSA patients. This review aims to expand our understanding of the effects of diet and exercise on OSA and associated CVD complications, and sets the stage for continued research designed to explore optimal lifestyle strategies for reducing the CVD burden in OSA patients.
... triglyceride levels (12). Nevertheless, many KD studies have documented improvements in markers of cardiovascular risk, including improvements in vascular function (24) reduction in inflammatory markers (10), and other markers of cardiovascular health (13,20). Methodological issues, such as clear definitions of dietary interventions, may play a significant role in obscuring the underlying principles, however, it is clear that more targeted research is warranted. ...
... Retinol binding protein-4 (RBP4), a major vitamin-A transporting protein from the liver to peripheral tissue, is secreted by visceral adipocytes and hepatocytes (Yang et al., 2006). RBP4 mRNA expression and secretion are increased in obesity and the loss of weight decreases RBP4 levels (Volek et al., 2009). It affects insulin sensitivity and glucose homeostasis (Graham and Kahn, 2007). ...
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BACKGROUND Metabolic and endocrine alterations in women with polycystic ovary syndrome (PCOS) affect adipose tissue mass and distribution. PCOS is characterised by hyperandrogenism, obesity and adipocyte dysfunction. Hyperandrogenism in PCOS drives dysfunctional adipocyte secretion of potentially harmful adipocytokines. Glucocorticoids and sex-steroids modulate adipocyte development and function. For their part, adipocyte products interact with adrenal and ovarian steroidogenic cells. Currently, the relationship between adipocyte and steroidogenic cells is not clear, and for these reasons, it is important to elucidate the interrelationship between these cells in women with and without PCOS. OBJECTIVE AND RATIONALE This comprehensive review aims to assess current knowledge regarding the interrelationship between adipocytes and adrenal and ovarian steroidogenic cells in animal models and humans with or without PCOS. SEARCH METHODS We searched for articles published in English and Portuguese in PubMed. Keywords were as follows: polycystic ovary syndrome, steroidogenesis, adrenal glands, theca cells, granulosa cells, adipocytes, adipocytokines, obesity, enzyme activation, and cytochrome P450 enzymes. We expanded the search into the references from the retrieved articles. OUTCOMES Glucocorticoids and sex-steroids modulate adipocyte differentiation and function. Dysfunctional adipocyte products play important roles in the metabolic and endocrine pathways in animals and women with PCOS. Most adipokines participate in the regulation of the hypothalamic–pituitary–adrenal and ovarian axes. In animal models of PCOS, hyperinsulinemia and poor fertility are common; various adipokines modulate ovarian steroidogenesis, depending on the species. Women with PCOS secrete unbalanced levels of adipocyte products, characterised by higher levels of leptin and lower levels of adiponectin. Leptin expression positively correlates with body mass index, waist/hip ratio and levels of total cholesterol, triglyceride, luteinising hormone, oestradiol and androgens. Leptin inhibits the production of oestradiol and, in granulosa cells, may modulate 17-hydroxylase and aromatase enzyme activities. Adiponectin levels negatively correlate with fat mass, body mass index, waist–hip ratio, glucose, insulin and triglycerides, and decrease androgen production by altering expression of luteinising hormone receptor, steroidogenic acute regulatory protein, cholesterol-side-chain cleavage enzyme and 17-hydroxylase. Resistin expression positively correlates with body mass index and testosterone, and promotes the expression of 17-hydroxylase enzyme in theca cells. The potential benefits of adipokines in the treatment of women with PCOS require more investigation. WIDER IMPLICATIONS The current data regarding the relationship between adipocyte products and steroidogenic cells are conflicting in animals and humans. Polycystic ovary syndrome is an excellent model to investigate the interrelationship among adipocyte and steroidogenic cells. Women with PCOS manifest some pathological conditions associated with hyperandrogenism and adipocyte products. In animals, cross-talk between cells may vary according to species, and the current review suggests opportunities to test new medications to prevent or even reverse several harmful sequelae of PCOS in humans. Further studies are required to investigate the possible therapeutic application of adipokines in women with obese and non-obese PCOS. Meanwhile, when appropriate, metformin use alone, or associated with flutamide, may be considered for therapeutic purposes.
... 53 Another mechanism might be through its effect on vascular function by lowering nitric oxide, 54 which was a potent vasodilator critical for vascular endothelial function and BP control via an increase in urate synthesis. 55 In addition, higher total carbohydrate intake might be associated with impaired microvascular function by elevating oxidative stress and inflammation 56 and elevating cellular adhesion molecules. 57 Other research pointed out that its adverse effect might be related to elevated cytosolic free calcium and peripheral vascular resistance. ...
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Background The association between dietary carbohydrate consumption and blood pressure (BP) is controversial. The present study aimed to evaluate the possible gender-specific association of carbohydrate across the whole BP distribution. Method Cross-sectional survey including 2241 rural adults was conducted in northwestern China in 2010. BP was measured by trained medical personnel. Dietary information was collected by semiquantitative Food-Frequency Questionnaire. Multivariate quantile regression model was used to estimate the association between total carbohydrates consumption and systolic BP (SBP) and diastolic BP (DBP) at different quantiles. Gender-specific β coefficient and its 95% CI was calculated. Results The average carbohydrate intake was 267.4 (SD 112.0) g/day in males and 204.9 (SD 90.7) g/day in females, with only 10.6% of males and 6.5% females consumed at least 65% of total energy from carbohydrates. And more than 80% carbohydrates were derived from refined grains. In females, increased total carbohydrates intake was associated with adverse SBP and DBP. An additional 50 g carbohydrates per day was positively associated with SBP at low and high quantiles (10th–20th and 60th–80th) and with DBP almost across whole distribution (30th–90th), after adjusting for age, fortune index, family history of hypertension, body mass index, physical activity level, alcohol intake and smoke, energy, two nutrient principal components, protein and sodium intake. Both relatively low and high carbohydrate intake were associated with increased SBP, with minimum level observed at 130–150 g carbohydrate intake per day from restricted cubic splines. However, no significant associations were observed in males. Conclusions Higher total carbohydrates consumption might have an adverse impact on both SBP and DBP in Chinese females but not males. Additionally, the positive association varies across distribution of BP quantiles. Further research is warranted to validate these findings and clarify the causality.
... Changes in lifestyle, dietary regimens and increases in physical activity can be the first line of therapy in decreasing obesity and its complications 7 . Various studies show that there are nutritional factors that can modulate the immune system, including caloric intake 8 , types of fats 9-11 , carbohydrates 12,13 and the amount of proteins 12 , which have a positive impact on inflammatory markers, body composition modifications and biochemical markers reduction. ...
... Moreover, a study by Jonavoskli et al 15 also stated that a low-carbohydrate diet of <5% might reduce FMD. However, a short-term trial by Volek et al 16 showed an contrasting result; they found that lowcarbohydrate diet was better in maintaining the FMD. Therefore, further studies are needed to address this issue. ...
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Introduction Obesity is a nutritional disease which is still a health burden particularly in Jakarta. The main treatment for obesity is nutritional intervention. Nowadays, several dietary approaches have been developed, including ketogenic diet, which is still controversial. Methods Literature search had been done within 4 databases including PubMed®, Cochrane®, Google® Scholar, and Science Direct®, using keywords: obesity, ketogenic diet, low-fat diet, and weight loss. Then, Medical Sub Heading (MeSH) was used. The search resulted in two articles which were appraised according to aspects of validity, importance, and applicability Results A randomized-controlled trial study showed similar effect of weight loss with ketogenic diet compared to low-fat diet. On the other hand, a meta-analysis study showed ketogenic diet caused more weight loss than low-fat diet. Both studies showed an increased risk of cardiovascular disease from the ketogenic diet group, which were shown by a decrease of flow-mediated dilatation and an increase of LDL-C. Conclusion Ketogenic diet shows a better long-term effect for weight loss in obese patients than low-fat diet. However, ketogenic diet may increase the cardiovascular event risk significantly.
... Moreover, a study by Jonavoskli et al 15 also stated that a low-carbohydrate diet of <5% might reduce FMD. However, a short-term trial by Volek et al 16 showed an contrasting result; they found that lowcarbohydrate diet was better in maintaining the FMD. Therefore, further studies are needed to address this issue. ...
Article
Full-text available
Introduction Obesity is a nutritional disease which is still a health burden particularly in Jakarta. The main treatment for obesity is nutritional intervention. Nowadays, several dietary approaches have been developed, including ketogenic diet, which is still controversial. Methods Literature search had been done within 4 databases including PubMed®, Cochrane®, Google® Scholar, and Science Direct®, using keywords: obesity, ketogenic diet, low-fat diet, and weight loss. Then, Medical Sub Heading (MeSH) was used. The search resulted in two articles which were appraised according to aspects of validity, importance, and applicability Results A randomized-controlled trial study showed similar effect of weight loss with ketogenic diet compared to low-fat diet. On the other hand, a meta-analysis study showed ketogenic diet caused more weight loss than low-fat diet. Both studies showed an increased risk of cardiovascular disease from the ketogenic diet group, which were shown by a decrease of flow-mediated dilatation and an increase of LDL-C. Conclusion Ketogenic diet shows a better long-term effect for weight loss in obese patients than low-fat diet. However, ketogenic diet may increase the cardiovascular event risk significantly.
... However, effects of weight loss on postprandial vascular function markers have hardly been studied. Results, however, are difficult to interpret as no-weight loss control groups were missing [10,11]. Effects of weight loss are of particular interest, as abdominally obese adults have disturbed postprandial cardiometabolic responses that may contribute to the development of CVD [12]. ...
Article
Background: Effects of weight loss on postprandial vascular function have not been studied so far. We therefore examined (i) effects of diet-induced weight loss on postprandial changes in various vascular function markers after consumption of a mixed meal and (ii) differences between normal-weight and abdominally obese men of comparable age at baseline and after weight loss. Methods: Fifty-four apparently healthy abdominally obese (waist circumference: 102-110 cm) and 25 normal-weight men (waist circumference: <94 cm) participated. The abdominally obese men were randomly allocated to a diet-induced weight-loss program or a no-weight loss control group. Men assigned to the weight-loss program followed a calorie-restricted diet for six weeks targeting a waist circumference of less than 102 cm, followed by a weight-maintenance period for two weeks. The control group maintained their habitual diet and physical activity levels. Measurements were performed before and two hours after consumption of the test meal consisting of two muffins (containing 56.6 g fat) and 300 mL low-fat milk. Results: The mean weight loss was 10.3 kg in the weight-loss compared with the control group. The postprandial change in flow-mediated vasodilation of the brachial artery (FMD) was significantly higher at baseline in normal-weight as compared with the postprandial change in abdominally obese men (1.89 ± 2.52 versus 0.48 ± 2.50 percentage points; P = 0.027). However, no differences in postprandial changes were observed in the abdominally obese men after weight loss compared with the control treatment. Also, weight reduction did not affect postprandial changes in carotid-to-femoral pulse wave velocity, retinal microvascular caliber properties, or plasma markers of microvascular endothelial function. Even though postprandial increases in triacylglycerol (P = 0.028), insulin (P = 0.029) and C-peptide concentrations (P < 0.001) were reduced in the abdominally obese men following weight loss, postprandial changes in FMD at the end of the weight-loss treatment were still more unfavorable as compared with those observed in normal-weight individuals. Conclusion: In this trial with abdominally obese men, we did not find effects of diet-induced weight loss on postprandial changes in vascular endothelial function, arterial stiffness and markers of microvascular function. This trial was registered on ClinicalTrials.gov under study number NCT01675401.
... FMD assessed via upper arm occlusion, which is only partially reduced by nitric oxide blockade (Doshi et al., 2001), predicts future cardiovascular events as effectively as FMD following distal cuff occlusion (Green, Jones, Thijssen, Cable, & Atkinson, 2011 ). Previous studies in our laboratory reported reliable coefficients of variation (2.2%) using the same technique and equipment (Volek et al., 2009; Ballard et al., 2009). ...
... However, research examining FMD following short-term low-carbohydrate high-fat diet interventions in young healthy human populations is lacking. Longer duration low-carbohydrate high-fat diet interventions have demonstrated increases [32], reductions [33], and no change [34] in FMD, but these studies contain confounding factors, most importantly co-existing weight loss and caloric restriction. This inconsistency in the literature makes it difficult to interpret the effect of repeated high-fat feeding on FMD in the absence of weight loss. ...
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Postprandial hyperglycemia has been linked to elevated risk of cardiovascular disease. Endothelial dysfunction and/or damage may be one of the mechanisms through which this occurs. In this exploratory study, we determined whether acute glucose ingestion would increase markers of endothelial damage/activation and impair endothelial function before and after a short-term low-carbohydrate high-fat diet (HFD) designed to induce relative glucose intolerance. Nine healthy young males (body mass index 23.2 ± 2 kg/m2) consumed a 75 g glucose drink before and <24 hours after consuming seven days of an iso-energetic HFD consisting of ~70% energy from fat, ~10% energy from carbohydrates, and ~20% energy from protein. CD31+/CD42b- and CD62E+ endothelial microparticles (EMPs) were enumerated at fasting, 1 hour (1 h), and 2 hours (2 h) post-consumption of the glucose drink. Flow-mediated dilation (FMD), arterial stiffness, and diameter, velocity, and flow of the common and internal carotid, and vertebral arteries were assessed in the fasting state and 1 h post glucose consumption. After the HFD, CD31+/CD42b- EMPs were elevated at 1 h compared to 2 h (p = 0.037), with a tendency for an increase above fasting (p = 0.06) only post-HFD. CD62E EMPs followed the same pattern with increased concentration at 1 h compared to 2 h (p = 0.005) post-HFD, with a tendency to be increased above fasting levels (p = 0.078). FMD was reduced at 1 h post glucose consumption both pre- (p = 0.01) and post-HFD (p = 0.005). There was also a reduction in FMD in the fasting state following the HFD (p = 0.02). In conclusion, one week of low-carbohydrate high-fat feeding that leads to a relative impairment in glucose homeostasis in healthy young adults may predispose the endothelium to hyperglycemia-induced damage.
... Low carbohydrate or very low carbohydrate/relatively low protein ketogenic diets may also reduce circulating insulin levels. At least two clinical trials have tested insulin sensitivity while comparing very low carbohydrate with low fat diets, and both showed superior improvements in insulin sensitivity in the low-carbohydrate arms [51,52] . Furthermore, the most recent meta-analysis of low-carbohydrate clinical trials, with low carbohydrate intake correctly defined as less than 20% of caloric intake, showed a higher net weight loss with low-carbohydrate interventions [53] . ...
Article
Purpose of review: This overview examines the rationale for dietary interventions for prostate cancer by summarizing the current evidence base and biological mechanisms for the involvement of diet in disease incidence and progression. Recent findings: Recent data have further solidified the association between insulin resistance and prostate cancer with the homeostatic model assessment of insulin resistance. Data also show that periprostatic adipocytes promote extracapsular extension of prostate cancer through chemokines, thereby providing a mechanistic explanation for the association observed between obesity and high-grade cancer. Regarding therapeutics, hyperinsulinemia may be the cause of resistance to phosphatidylinositol-3 kinase inhibitors in the treatment of prostate cancer, leading to new investigations combining these drugs with ketogenic diets. Summary: Given the recently available data regarding insulin resistance and adipokine influence on prostate cancer, dietary strategies targeting metabolic syndrome, diabetes, and obesity should be further explored. In macronutrient-focused therapies, low carbohydrate/ketogenic diets should be favored in such interventions because of their superior impact on weight loss and metabolic parameters and encouraging clinical data. Micronutrients, including the carotenoid lycopene which is found in highest concentrations in tomatoes, may also play a role in prostate cancer prevention and prognosis through complementary metabolic mechanisms. The interplay between genetics, diet, and prostate cancer is an area of emerging focus that might help optimize therapeutic dietary response in the future through personalization.
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Objective To determine the relative effectiveness of dietary macronutrient patterns and popular named diet programmes for weight loss and cardiovascular risk factor improvement among adults who are overweight or obese. Design Systematic review and network meta-analysis of randomised trials. Data sources Medline, Embase, CINAHL, AMED, and CENTRAL from database inception until September 2018, reference lists of eligible trials, and related reviews. Study selection Randomised trials that enrolled adults (≥18 years) who were overweight (body mass index 25-29) or obese (≥30) to a popular named diet or an alternative diet. Outcomes and measures Change in body weight, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, systolic blood pressure, diastolic blood pressure, and C reactive protein at the six and 12 month follow-up. Review methods Two reviewers independently extracted data on study participants, interventions, and outcomes and assessed risk of bias, and the certainty of evidence using the GRADE (grading of recommendations, assessment, development, and evaluation) approach. A bayesian framework informed a series of random effects network meta-analyses to estimate the relative effectiveness of the diets. Results 121 eligible trials with 21 942 patients were included and reported on 14 named diets and three control diets. Compared with usual diet, low carbohydrate and low fat diets had a similar effect at six months on weight loss (4.63 v 4.37 kg, both moderate certainty) and reduction in systolic blood pressure (5.14 mm Hg, moderate certainty v 5.05 mm Hg, low certainty) and diastolic blood pressure (3.21 v 2.85 mm Hg, both low certainty). Moderate macronutrient diets resulted in slightly less weight loss and blood pressure reductions. Low carbohydrate diets had less effect than low fat diets and moderate macronutrient diets on reduction in LDL cholesterol (1.01 mg/dL, low certainty v 7.08 mg/dL, moderate certainty v 5.22 mg/dL, moderate certainty, respectively) but an increase in HDL cholesterol (2.31 mg/dL, low certainty), whereas low fat (−1.88 mg/dL, moderate certainty) and moderate macronutrient (−0.89 mg/dL, moderate certainty) did not. Among popular named diets, those with the largest effect on weight reduction and blood pressure in comparison with usual diet were Atkins (weight 5.5 kg, systolic blood pressure 5.1 mm Hg, diastolic blood pressure 3.3 mm Hg), DASH (3.6 kg, 4.7 mm Hg, 2.9 mm Hg, respectively), and Zone (4.1 kg, 3.5 mm Hg, 2.3 mm Hg, respectively) at six months (all moderate certainty). No diets significantly improved levels of HDL cholesterol or C reactive protein at six months. Overall, weight loss diminished at 12 months among all macronutrient patterns and popular named diets, while the benefits for cardiovascular risk factors of all interventions, except the Mediterranean diet, essentially disappeared. Conclusions Moderate certainty evidence shows that most macronutrient diets, over six months, result in modest weight loss and substantial improvements in cardiovascular risk factors, particularly blood pressure. At 12 months the effects on weight reduction and improvements in cardiovascular risk factors largely disappear. Systematic review registration PROSPERO CRD42015027929.
Article
Dietary restriction of carbohydrate has been demonstrated to be beneficial for nervous system dysfunction in animal models and may be beneficial for human chronic pain. The purpose of this review is to assess the impact of a low-carbohydrate/ketogenic diet on the adult nervous system function and inflammatory biomarkers to inform nutritional research for chronic pain. An electronic data base search was carried out in May 2021. Publications were screened for prospective research with dietary carbohydrate intake <130g/day and duration of ≥2 weeks. Studies were categorised into those reporting adult neurological outcomes to be extracted for analysis and those reporting other adult research outcomes Both groups were screened again for reported inflammatory biomarkers. From 1548 studies there were 847 studies included. Sixty-four reported neurological outcomes with 83% showing improvement. Five hundred and twenty-three studies had a different research focus (metabolic n=394, sport/performance n=51, cancer n=33, general n=30, neurological with non-neuro outcomes n=12, or gastrointestinal n=4). The second screen identified 63 studies reporting on inflammatory biomarkers with 71% reporting a reduction in inflammation. The overall results suggest a favourable outcome on the nervous system and inflammatory biomarkers from a reduction in dietary carbohydrates. Both nervous system sensitisation and inflammation occur in chronic pain and the results from this review indicate it may be improved by low-carbohydrate nutritional therapy. More clinical trials within this population are required to build on the few human trials that have been done.
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Objective: Impairment of flow-mediated dilation of the brachial artery is a marker of endothelial dysfunction and often predisposes atherosclerosis and cardiovascular events. In this study, we propose a user-guided automated approach for monitoring arterial cross-section during hyperemic response to improve reproducibility and sensitivity of flow-mediated dilation. Material and methods: Ultrasound imaging of the brachial artery was performed in 11 volunteers in cross-sectional and in 5 volunteers in longitudinal view. During each examination, images were recorded continuously before and after inducing ischemia. Time-dilation curves of the brachial lumen cross-section were measured by user-guided automated segmentation of brachial images with the feed-forward active contour (FFAC) algorithm. %FMD was determined by the ratio of peak dilation to the baseline value. Each measurement was repeated twice in two sessions 1 h apart on the same arm to evaluate the reproducibility of the measurements. The intra-subject variation in flow-mediated dilation between two sessions (subject-specific) and inter-group variation in flow-mediated dilation with all the subjects within a session grouped together (group-specific) were measured for FFAC. The FFAC measurements were compared with the conventional diameter measurements made using echo tracking in longitudinal views. Results: Flow-mediated dilation values for cross-sectional area were greater than those measured by diameter dilation: 33.1% for cross-sectional area compared to 22.5% for diameter. Group-specific flow-mediated dilation measurements for cross-sectional area were highly reproducible: 33.2% vs. 33.0% (p > 0.05) with coefficient of variation CV of 0.4%. The group-specific flow-mediated dilations measured by echo tracking for the two sessions were 21.1 vs. 23.9% with CV of 9%. Subject-specific CV for cross-sectional area by FFAC was 10% ± 2% versus 24% ± 10% for the conventional approach. Using correlation as a metric of evaluation also showed better performance for cross-sectional imaging: correlation coefficient, R, between two sessions for cross-sectional area was 0.92 versus 0.72 for the conventional approach based on diameter measurements. Conclusion: Peak dilation area measured by continuous automated monitoring of cross-sectional area of the brachial artery provides more reproducible and higher-sensitivity measurement of flow-mediated dilation compared to the conventional approach of using vascular diameter measured using longitudinal imaging.
Article
Objetivo: Comparar la efectividad de un plan de alimentación hipocalórico hiperproteico con otro normoproteico sobre la composición corporal, los parámetros bioquímicos y las citocinas inflamatorias en pacientes obesos precirugía bariátrica sometidos a un tratamiento integral. Método: Se estudiaron 76 pacientes con un índice de masa corporal (IMC) ≥ 40 kg/m² previamente a la cirugía bariátrica. Un grupo fue tratado con una dieta hipocalórica hiperproteica y se comparó con una dieta hipocalórica normoproteica. Se evaluaron parámetros bioquímicos, parámetros antropométricos, composición corporal y valores de citocinas inflamatorias en suero al inicio y después de 4 meses de tratamiento. Resultados: En ambos grupos se observó una disminución de peso, de IMC y de masa grasa, así como un incremento de la masa muscular respecto al momento basal (p < 0.05), sin diferencias entre los grupos estudiados. No se encontraron cambios en los parámetros bioquímicos ni en las concentraciones séricas de factor de necrosis tumoral (TNF) e interleucina (IL)-6 antes y después de 4 meses de tratamiento, ni entre los grupos evaluados (p > 0.05). Las concentraciones séricas de IL-1β disminuyeron únicamente con la dieta hipocalórica normoproteica (p = 0.02). Conclusiones: La dieta hipocalórica hiperproteica no muestra ventajas en la reducción de peso y grasa corporal, ni en la ganancia de masa muscular, en comparación con la dieta hipocalórica normoproteica en pacientes con obesidad mórbida precirugia bariátrica sometidos a un tratamiento integral. Objective: Compare the effectiveness of a hyperproteic hypocaloric feeding plan with a normoproteic on body composition, biochemical parameters and inflammatory cytokines in obese pre-bariatric surgery patients in the integral treatment. Method: Seventy-six pre-bariatric surgery patients with body mass index (BMI) ≥ 40 kg/m² were studied. One group was treated with a hyperproteic hypocaloric diet and compared with a normoproteic hypocaloric diet. Biochemical parameters, anthropometric parameters, body composition and levels of tumor necrosis factor (TNF), interleukin (IL)-6 and IL-1β in serum were evaluated at the initiation of treatment and after 4 months. Results: In both groups studied, a decrease in weight, BMI and fat mass was observed, as well as an increase in muscle mass compared to baseline (p < 0.05), no differences showed between the groups studied. No change was found in the biochemical parameters and serum levels of TNF and IL-6 before and after 4 months of treatment, nor among the groups evaluated (p > 0.05). Serum IL-1β levels decreased after treatment with only a normoprotein hypocaloric diet (p = 0.02). ­. Conclusions: Hyperproteic hypocaloric diet does not show advantages in weight reduction and body fat or in muscle mass gain compared to the normoproteic hypocaloric diet in patients with morbid obesity bariatric pre-surgery in the integral treatment.
Article
There is a significant amount of controversy related to the optimal amount of dietary carbohydrate. This review summarizes the health-related positives and negatives associated with carbohydrate restriction. On the positive side, there is substantive evidence that for many individuals, low-carbohydrate, high-protein diets can effectively promote weight loss. Low-carbohydrate diets (LCDs) also can lead to favorable changes in blood lipids (i.e., decreased triacylglycerols, increased high-density lipoprotein cholesterol) and decrease the severity of hypertension. These positives should be balanced by consideration of the likelihood that LCDs often lead to decreased intakes of phytochemicals (which could increase predisposition to cardiovascular disease and cancer) and nondigestible carbohydrates (which could increase risk for disorders of the lower gastrointestinal tract). Diets restricted in carbohydrates also are likely to lead to decreased glycogen stores, which could compromise an individual's ability to maintain high levels of physical activity. LCDs that are high in saturated fat appear to raise low-density lipoprotein cholesterol and may exacerbate endothelial dysfunction. However, for the significant percentage of the population with insulin resistance or those classified as having metabolic syndrome or prediabetes, there is much experimental support for consumption of a moderately restricted carbohydrate diet (i.e., one providing approximately 26%-44 % of calories from carbohydrate) that emphasizes high-quality carbohydrate sources. This type of dietary pattern would likely lead to favorable changes in the aforementioned cardiovascular disease risk factors, while minimizing the potential negatives associated with consumption of the more restrictive LCDs.
Article
Importance Many claims have been made regarding the superiority of one diet or another for inducing weight loss. Which diet is best remains unclear.Objective To determine weight loss outcomes for popular diets based on diet class (macronutrient composition) and named diet.Data Sources Search of 6 electronic databases: AMED, CDSR, CENTRAL, CINAHL, EMBASE, and MEDLINE from inception of each database to April 2014.Study Selection Overweight or obese adults (body mass index ≥25) randomized to a popular self-administered named diet and reporting weight or body mass index data at 3-month follow-up or longer.Data Extraction and Synthesis Two reviewers independently extracted data on populations, interventions, outcomes, risk of bias, and quality of evidence. A Bayesian framework was used to perform a series of random-effects network meta-analyses with meta-regression to estimate the relative effectiveness of diet classes and programs for change in weight and body mass index from baseline. Our analyses adjusted for behavioral support and exercise.Main Outcomes and Measures Weight loss and body mass index at 6- and 12-month follow-up (±3 months for both periods).Results Among 59 eligible articles reporting 48 unique randomized trials (including 7286 individuals) and compared with no diet, the largest weight loss was associated with low-carbohydrate diets (8.73 kg [95% credible interval {CI}, 7.27 to 10.20 kg] at 6-month follow-up and 7.25 kg [95% CI, 5.33 to 9.25 kg] at 12-month follow-up) and low-fat diets (7.99 kg [95% CI, 6.01 to 9.92 kg] at 6-month follow-up and 7.27 kg [95% CI, 5.26 to 9.34 kg] at 12-month follow-up). Weight loss differences between individual diets were minimal. For example, the Atkins diet resulted in a 1.71 kg greater weight loss than the Zone diet at 6-month follow-up. Between 6- and 12-month follow-up, the influence of behavioral support (3.23 kg [95% CI, 2.23 to 4.23 kg] at 6-month follow-up vs 1.08 kg [95% CI, −1.82 to 3.96 kg] at 12-month follow-up) and exercise (0.64 kg [95% CI, −0.35 to 1.66 kg] vs 2.13 kg [95% CI, 0.43 to 3.85 kg], respectively) on weight loss differed.Conclusions and Relevance Significant weight loss was observed with any low-carbohydrate or low-fat diet. Weight loss differences between individual named diets were small. This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.
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De evolutionaire geneeskunde, ook wel darwinistische geneeskunde, maakt gebruik van kennis van de paleolithische omgeving, genetica, vergelijkende anatomie, bio-geochemie, archeologie, antropologie, (patho)fysiologie en epidemiologie. Het betreft een nog jonge discipline die ziekte en gezondheid tracht te verklaren vanuit onze evolutionaire achtergrond. Deze kennis is belangrijk voor de identificatie van factoren die een rol spelen in onze huidige ongezonde leefstijl. De discipline komt niet zelden in conflict met heersende wetenschappelijke paradigma’s. In de paleolithische tijd (2,5 miljoen tot 10.000 jaar geleden) is ons brein gegroeid van ongeveer 400 naar 1.300–1.400 mL. Deze groei kon slechts plaatsvinden in het land-water ecosysteem, waar overvloedige hoeveelheden ‘hersen-selectieve nutriënten’ samenkomen. Ze omvatten jodium, selenium, ijzer, vitamines A, D en B12, en de visolievetzuren EPA en DHA. Wereldwijd behoren hun tekorten momenteel tot de meest voorkomende deficiënties. Onze uniek grote verhouding tussen hersen- en totaal lichaamsgewicht heeft ons gevoelig gemaakt voor glucosetekorten. Deze dreigen vooral bij hongeren, zwangerschap en infectie. Hiertoe passen we ons energiemetabolisme aan, onder andere door het veroorzaken van insulineresistentie. Onze huidige ongezonde leefstijl wordt gekenmerkt door chronische stress, chronisch slaapgebrek, wanvoeding, onvoldoende fysieke activiteit, abnormale microbiële flora en milieuverontreiniging. Ze brengen ons in een chronische toestand van lage-graad inflammatie, hetgeen leidt tot metabole aanpassingen. Op lange termijn veroorzaken deze aanpassingen het metabool syndroom en de typische welvaartsziekten, zoals diabetes mellitus type 2, hart- en vaatziekten en bepaalde vormen van kanker. Terugkeer naar de paleolithische tijd met behoud van de cultuur van de 21e eeuw is de enige natuurlijke manier om gezond oud te worden.
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A obesidade é uma doença inflamatória crônica caracterizada pelo acúmulo excessivo de gordura no tecido adiposo. Componentes fisiopatológicos decorrentes do excesso de gordura corporal, como alterações no balanço de adipocinas, resistência insulínica e aumento de mediadores inflamatórios, promovem disfunção endotelial, e, consequentemente, maior risco de morbidade e mortalidade de origem cardiovascular. Por outro lado, a adoção de dieta hipocalórica tem sido recomendada como medida não farmacológica para o tratamento da obesidade. Portanto, o objetivo desse artigo foi o de realizar uma revisão de literatura sobre os efeitos da dieta hipocalórica na função endotelial em adultos com obesidade. Foram analisados 26 artigos com os descritores dieta redutora, restrição calórica e perda de peso, combinados com os termos vasodilatação e endotélio, publicados nas bases de dados eletrônicas Medline e Scielo. Foi possível observar que a dieta hipocalórica, quando associada à perda de peso corporal, melhora os parâmetros metabólicos, inflamatórios, hemodinâmicos e neurovasculares, os quais promovem melhora da função endotelial em indivíduos obesos. Entretanto, para que esses benefícios sejam obtidos, a dieta deve ser individualizada, balanceada e com orientação e prescrição de especialistas.
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Postprandial hyperglycemia has deleterious effects on endothelial function. Restricting carbohydrate intake and postmeal walking have each been shown to reduce postprandial hyperglycemia, but their combination and subsequent effects on endothelial function have not been investigated. Here, we sought to examine the effect of blunting postprandial hyperglycemia by following a low-carbohydrate diet, with or without postmeal walking exercise, on markers of vascular health in type 2 diabetes (T2D). In a randomized crossover design, individuals with T2D ( n = 11) completed three 4-day controlled diet interventions consisting of 1) low-carbohydrate diet alone (LC), 2) low-carbohydrate diet with 15-min postmeal walks (LC + Ex), and 3) low-fat control diet (CON). Fasting blood samples and brachial artery flow-mediated dilation (%FMD) were measured before and after each intervention. Total circulating microparticles (MPs), endothelial MPs, platelet MPs, monocyte-platelet aggregates, and adhesion molecules were assessed as biomarkers of vascular health. There was a significant condition × time interaction for %FMD ( P = 0.01), with post hoc tests revealing improved %FMD after LC + Ex (+0.8 ± 1.0%, P = 0.02), with no change after LC or CON. Endothelial MPs were significantly reduced with the LC diet by ~45% (from 99 ± 60 to 44 ± 31 MPs/μl, P = 0.02), with no change after LC + Ex or CON (interaction: P = 0.04). Total MPs were lower (main effect time: P = 0.02), whereas monocyte-platelet aggregates were higher (main effect time: P < 0.01) after all interventions. Plasma adhesion molecules and C-reactive protein were unaltered. Attenuating postprandial hyperglycemic excursions using a low-carbohydrate diet combined with postmeal walking appears to be an effective strategy to improve endothelial function in individuals with T2D. NEW & NOTEWORTHY Carbohydrate restriction and postmeal walking lower postprandial hyperglycemia in individuals with type 2 diabetes. Here, we show that the combination significantly improved endothelial function and that carbohydrate restriction alone reduced circulating endothelial microparticles in individuals with type 2 diabetes. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/low-carb-diet-and-exercise-improve-endothelial-health/ .
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Background: Chronic low-grade inflammation has been associated with insulin resistance, diabetes, atherosclerosis, obesity and Metabolic Syndrome (MetS). A pro-inflammatory environment contributes to several metabolic disturbances and possibly the development of MetS. Dietary approaches have defined impact on immune function and putative anti-inflammatory effects. Objective: To assess the effects of different dietary approaches on markers of inflammation among patients with metabolic syndrome. Further effects on weight loss and fasting insulin were analysed. Design: MEDLINE/Pubmed, Scopus and the Cochrane Library were screened through September 2014 for randomized controlled trials (RCTs) on different dietary approaches for participants with metabolic syndrome as defined by NCEP ATP III. Primary outcome were markers of immune system. Secondary outcome was body weight and fasting insulin. Standardized mean differences (SMD) and 95% confidence intervals (CI) were calculated. Results: 13 RCTs with a total of 2017 patients were included. Low-fat diets (29±2 % energy from fats) decreased C- reactive protein when compared to control diets (SMD=-0.98, 95% CI -1.6, -0.35, p= 0.002). Low- carbohydrate diets (SMD=-0.33, 95% CI -0.63, -0.03, p=0.004, 23±10% energy from carbohydrates) and multimodal interventions (SMD=-1.02, 95% CI-1.97, -0.07, p=0.04) were able to induce significant weight loss. Low carb diets were able to decrease insulin (SMD: -0.33; 95% CI -0.63, -0.03; p=0.03). Conclusion: Low-fat diets are able to reduce CRP, however this effect is also dependent from weight loss. Further low-carb diets have beneficial effects on insulin and body weight. Dietary approaches should mainly try to reduce macronutrients and enrich functional food components such as vitamins, flavonoids and unsaturated fatty acids. People with metabolic syndrome will benefit most by combining weight loss and anti-inflammatory nutrients.
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A popular diet used for weight reduction is the low-carbohydrate diet, which has most calories derived from fat and protein, but effects of this dietary regimen on coronary vascular function have not been identified. We tested the hypothesis that obesity-induced impairment in coronary endothelial function is reversed by a low-carbohydrate diet. We used four groups of male Zucker rats: lean and obese on normal and low-carbohydrate diets. Rats were fed ad libitum for 3 wk; total caloric intake and weight gain were similar in both diets. To assess endothelial and vascular function, coronary arterioles were cannulated and pressurized for diameter measurements during administration of acetylcholine or sodium nitroprusside or during flow. When compared with lean rats, endothelium-dependent acetylcholine-induced vasodilation was impaired by approximately 50% in obese rats (normal diet), but it was restored to normal by the low-carbohydrate diet. When the normal diet was fed, flow-induced dilation (FID) was impaired by >50% in obese compared with lean rats. Similar to acetylcholine, responses to FID were restored to normal by a low-carbohydrate diet. N(omega)-nitro-L-arginine methyl ester (10 microM), an inhibitor of nitric oxide (NO) synthase, inhibited acetylcholine- and flow-induced dilation in lean rats, but it had no effect on acetylcholine- or flow-induced vasodilation in obese rats on a low-carbohydrate diet. Tetraethylammonium, a nonspecific K(+) channel antagonist, blocked flow-dependent dilation in the obese rats, suggesting that the improvement in function was mediated by a hyperpolarizing factor independent of NO. In conclusion, obesity-induced impairment in endothelium-dependent vasodilation of coronary arterioles can be dramatically improved with a low-carbohydrate diet most likely through the production of a hyperpolarizing factor independent of NO.
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The effects of a very-low-carbohydrate, high-saturated-fat weight-loss diet (LC) on brachial artery flow-mediated dilatation (FMD) and markers of endothelial function are unknown. The effect of an LC on markers of endothelial function and cardiovascular disease (CVD) risk was compared with that of an isocaloric high-carbohydrate, low-saturated-fat diet (HC). FMD and markers of endothelial function (n = 70) and CVD risk were measured before and after 8 wk of weight loss. Ninety-nine subjects aged 50.0 +/- 8.3 y with a body mass index (in kg/m2) of 33.7 +/- 4.1 completed the study. Mean (+/-SD) FMD did not change significantly (P = 0.55) with either diet. Pulse wave velocity improved with both diets (P < 0.01). Endothelial markers, E- and P selectin, intracellular and cellular-adhesion molecule-1, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 decreased (P < 0.001), with no diet effect. Adiponectin did not change significantly. More weight (P = 0.05 for diet x time interaction) and more abdominal fat mass (P = 0.05 for diet x time interaction) were lost with the LC than with the HC. LDL cholesterol decreased more with the HC than with the LC (P < 0.05, time x diet), and C-reactive protein decreased more with the HC than with the LC (P < 0.05 for diet x time interaction). Homocysteine increased more with the LC (P < 0.01 for diet x time interaction). Folate decreased with the LC and increased with the HC (P < 0.05, time; P < 0.001 for diet x time interaction). An LC does not impair FMD. We observed beneficial effects of both diets on most of the CVD risk factors measured. This trial was registered with the Australian Clinical Trials Registry as ACTR N0 12606000203550.
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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 (~1,500kcal): 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.
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Much has been written about the potential role of antioxidants in the prevention of atherosclerosis. To assess the short-term effect of a single high-fat meal with and without pretreatment with antioxidant vitamins on endothelial function in healthy, normocholesterolemic subjects. Observer-blinded randomized trial. University hospital. Twenty healthy, normocholesterolemic (total and low-density lipoprotein cholesterol <5.2 mmol/L and <3.4 mmol/L [<200 mg/dL and <130 mg/ dL], respectively), male (7) and female (13) hospital employee volunteers, aged 24 to 54 years. Three randomly administered breakfasts: (1) a high-fat meal (3766 J [900 calories], 50 g of fat); (2) a low-fat meal (3766 J [900 calories], 0 g of fat); and (3) a high-fat meal and pretreatment with oral administration of vitamins C (1 g) and E (800 IU) (high-fat meal with vitamins). A subgroup of 10 subjects also ate the low-fat meal with the same vitamin pretreatment (low-fat meal with vitamins). High-resolution ultrasound assessed flow-mediated (endothelium-dependent) brachial artery vasodilation measured as percent diameter change before and hourly for 6 hours following each meal. Flow-mediated vasodilation fell from a mean+/-SD of 20%+/-8% before to 12%+/-6%, 10%+/-6%, and 8%+/-9% at 2, 3, and 4 hours, respectively, after the high-fat meal (P<.001). No significant changes in flow-mediated vasodilation occurred after the low-fat meal, high-fat meal with vitamins, or low-fat meal with vitamins. The change in flow-mediated vasodilation after the low-fat and high-fat meals correlated inversely with the 2-hour postprandial change in triglyceride levels (r=-0.54; P<.001). A single high-fat meal transiently reduces endothelial function for up to 4 hours in healthy, normocholesterolemic subjects, probably through the accumulation of triglyceride-rich lipoproteins. This decrease is blocked by pretreatment with antioxidant vitamins C and E, suggesting an oxidative mechanism.
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The purpose of this study was to test the hypothesis that intake of used cooking fat is associated with impaired endothelial function. Diets containing high levels of lipid oxidation products may accelerate atherogenesis, but the effect on endothelial function is unknown. Flow-mediated endothelium-dependent dilation and glyceryl trinitrate-induced endothelium-independent dilation of the brachial artery were investigated in 10 men. Subjects had arterial studies before and 4 h after three test meals: 1) a meal (fat 64.4 g) rich in cooking fat that had been used for deep frying in a fast food restaurant; 2) the same meal (fat 64.4 g) rich in unused cooking fat, and 3) a corresponding low fat meal (fat 18.4 g) without added fat. Endothelium-dependent dilation decreased between fasting and postprandial studies after the used fat meal (5.9 +/- 2.3% vs. 0.8 +/- 2.2%, p = 0.0003), but there was no significant change after the unused fat meal (5.3 +/- 2.1% vs. 6.0 +/- 2.5%) or low fat meal (5.3 +/- 2.3% vs. 5.4 +/- 3.3%). There was no significant difference in endothelium-independent dilation after any of the meals. Plasma free fatty acid concentration did not change significantly during any of the meals. The level of postprandial hypertriglyceridemia was not associated with change in endothelial function. Ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function. These findings suggest that intake of degradation products of heated fat contribute to endothelial dysfunction.
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It has been suggested that a high-fat meal may acutely impair endothelium-dependent vasodilation and that this impairment may be prevented by concomitant intake of antioxidants. Because red wine contains antioxidant polyphenols and may reduce cardiovascular disease, we examined the effect of red wine on postprandial endothelial function. Using a crossover design, 13 healthy volunteers consumed a high-fat meal (0.8 g fat/kg body weight) with red wine (3 ml/kg) or an isocaloric control beverage on 2 separate days, 1 week apart. Flow-mediated dilation of the brachial artery was examined by vascular ultrasound at baseline and at 2, 4, and 6 hours after the meal. At these times, flow-mediated dilation with the high-fat meal and control beverage was 9.5 +/- 5.0%, 7.9 +/- 5.1%, 6.8 +/- 3.6%, and 7.3 +/- 4.6%, respectively (nonsignificant trend). There was also a nonsignificant trend for flow-mediated dilation after the high-fat meal with wine: 8.0 +/- 4.1%, 5.7 +/- 4.7%, 6.4 +/- 3.1%, and 6.9 +/- 3.8%, respectively. There was no difference in the effects between wine and the control beverage (p = 0.77). Triglycerides increased 2- to 2.7-fold over baseline (p = 0.0001) with a peak occurring 5 hours after the high-fat meals. In contrast to previous studies, the present study did not demonstrate a significant effect of a high-fat meal on endothelial vasomotor function in healthy subjects. Under these conditions, we did not demonstrate a beneficial acute effect of red wine on endothelial function.
Article
The effects of a prolonged low-carbohydrate diet rich in n-3 fatty acids on blood lipid profiles have not been addressed in the scientific literature. This study examined the effects of an eight-week ketogenic diet rich in n-3 fatty acids on fasting serum lipoproteins and postprandial triacylglycerol (TG) responses. Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks. Fasting blood samples were collected before and after one week of habitual diet and on two consecutive days after 2, 4, 6 and 8 weeks of the intervention diet. Postprandial TG responses to a fat-rich test meal were measured prior to and after the intervention diet. Compared to the habitual diet, subjects consumed significantly (p < or = 0.05) greater quantities of protein, fat, MUFA and n-3 fatty acids and significantly less total energy, carbohydrate and dietary fiber. Body weight significantly declined over the experimental period (-4.2+/-2.7 kg). Compared to baseline, fasting total cholesterol, LDL cholesterol and HDL cholesterol were not significantly different after the intervention diet (+1.5%, +9.7% and +10.0%, respectively). Fasting TG were significantly reduced after the intervention diet (-55%). There was a significant reduction in peak postprandial TG (-42%) and TG area under the curve (-48%) after the intervention diet. A hypocaloric low-carbohydrate diet rich in MUFA and supplemented with n-3 fatty acids significantly reduced postabsorptive and postprandial TG in men that were not hypertriglyceridemic as a group before the diet. This may be viewed as a clinically significant positive adaptation in terms of cardiovascular risk status. However, transient increases in total cholesterol and LDL cholesterol were also evident and should be examined further in regard to which particular subfractions are elevated.
Article
it appears that hypertriglyceridemia (HTG) is a risk factor of atherosclerosis as demonstrated by recent studies. In this study, we analyzed the effects of acute HTG on endothelial function and oxidative stress, which are important mechanisms in the pathogenesis of atherosclerosis. in a high fat meal group (n = 11), serum triglycerides and PMA-activated leukocyte O(2)(-)* production were significantly (P < 0.005) increased from 146 +/- 69 mg/dl and 4.09 +/- 0.93 nmol/10(6) cells/min preprandially to 198 +/- 88 mg/dl and 5.49 +/- 1.19 nmol/10(6) cells/min, respectively, 2 h after eating a high-fat meal. The flow-mediated endothelium-dependent brachial artery dilation (FMD; high-resolution ultrasound) was decreased from 13.7 +/- 3.3% preprandially to 8.2 +/- 3.7%, 2 h after eating a high-fat meal (P < 0.005). However, following a low-fat meal (n = 9), there were no significant changes in triglycerides, leukocyte O(2)(-)* production and FMD. Changes of serum triglycerides were correlated negatively (r = -0.650, P < 0.005) with changes of FMD, but were correlated positively (r = 0.798, P < 0.001) with changes of leukocyte O(2)(-)* production, which - in turn - were correlated negatively (r = -0.784, P < 0.001) with changes of FMD in all study subjects (mean age: 56 years, n = 20). this study suggests that acute HTG causes endothelial dysfunction via enhanced oxidant stress and this may pave the way for the development of atherosclerosis under chronic conditions.