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IntroductionCarbohydrate-restricted diets are one of the most effective dietary interventions for weight loss. However, the optimum carbohydrate intake for implementing the most effective weight-loss interventions is still being discussed. We aimed to determine the optimum carbohydrate intake for short- and long-term weight loss in adults with overweight and obesity.MethodsWe searched PubMed, Scopus, Web of Science, and CENTRAL from inception to May 2021 for randomized controlled trials examining the effect of a carbohydrate-restricted diet (≤45% of energy intake) as compared to a control diet (carbohydrate intake >45% of energy intake) on body weight in adults with overweight/obesity. A random-effects dose–response meta-analysis was conducted to calculate the mean difference for each 10% decrease in carbohydrate intake at the 6-month follow-up (1 to 6 months), 12-month follow-up (6 to 12 months), and follow-up longer than 12 months. The shape of the dose-dependent effects was also evaluated. The certainty of the evidence was rated using the GRADE approach. The minimal clinically important difference (MCID) threshold was defined as 5% weight loss (equal to 4.39 kg).ResultsA total of 110 trials were selected for the present meta-analysis. In the linear dose–response meta-analysis, each 10% decrease in carbohydrate intake reduced body weight by 0.64 kg (95% CI: −0.79 to −0.49; n = 101 trials with 4,135 participants, high-certainty evidence) at the 6-month follow-up and by 1.15 kg (95% CI: −1.61 to −0.69; 42 trials with 2,657 participants, moderate-certainty evidence) at the 12-month follow-up. Non-linear dose–response meta-analyses indicated a monotonic reduction in body weight with the decrease in carbohydrate intake, with the greatest reduction at 5% at the 6-month follow-up (mean difference 5%: −3.96 kg, 95% CI: −4.92 to −3.00) and 10% at the 12-month follow-up (mean difference 10%: −6.26 kg, 95% CI: −10.42 to −2.10). At follow-up longer than 12 months, dose–response analyses suggested a non-linear effect, wherein carbohydrate intakes higher than 40% and lower than 30% were not effective for weight loss.DiscussionCarbohydrate restriction is an effective dietary strategy for important weight loss in adults with overweight and obesity. At 6-month and 12-month follow-ups, body weight decreased proportionally, more than the MCID threshold, along with the decrease in carbohydrate intake. At follow-up longer than 12 months, there was a non-linear effect, with the greatest reduction at 30% carbohydrate intake.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42022315042.

BackgroundCarbohydrate restriction may benefit β-cell function and glucose metabolism in type 2 diabetes (T2D) but also leads to weight loss which in itself is beneficial.MethodsIn order to determine the additional effect of carbohydrate restriction in addition to a fixed body weight loss, we randomly assigned 72 adults with T2D and obesity (mean ± SD HbA1c 7.4 ± 0.7%, BMI 33 ± 5 kg/m2) to a carbohydrate-reduced high-protein diet (CRHP; energy percent from carbohydrate/protein/fat: 30/30/40) or an isocaloric conventional diabetes diet (CD; 50/17/33) for 6 weeks. All foods were provided free of charge and total energy intake was tailored individually, so both groups lost 6% of baseline body weight.ResultsDespite significantly greater reductions in HbA1c (mean [95% CI] −1.9 [−3.5, −0.3] mmol/mol) after 6 weeks, the CRHP diet neither improved glucose tolerance, β-cell response to glucose, insulin sensitivity, during a 4-h oral glucose tolerance test, nor basal proinsulin secretion when compared to the CD diet, but increased C-peptide concentration and insulin secretion rate (area under the curve [AUC] and peak) significantly more (~10%, P ≤ 0.03 for all). Furthermore, compared with the CD diet, the CRHP diet borderline increased basal glucagon concentration (16 [−0.1, 34]%, P = 0.05), but decreased glucagon net AUC (−2.0 [−3.4, −0.6] mmol/L ×240 min, P < 0.01), decreased basal triglyceride and total AUC (~20%, P < 0.01 for both), and increased gastric inhibitory polypeptide total AUC (14%, P = 0.01).ConclusionA moderately carbohydrate-restricted diet for 6 weeks decreased HbA1c but did not improve β-cell function or glucose tolerance beyond the effects of weight loss when compared with a conventional diabetes diet in people with T2D.Clinical trials registrationwww.Clinicaltrials.gov, Identifier: NCT02472951.

Emerging evidence suggests that "leanness" and good metabolic health markers may predict larger increases in LDL cholesterol (LDL-C) in response to carbohydrate restriction. Specifically, a recent cohort study demonstrated an inverse association between BMI and LDL-C change among individuals on carbohydrate-restricted diets and identified a subgroup of "Lean Mass Hyper-Responders" (LMHR) who exhibit exceptional increases in LDL-C, in the context of low triglycerides and high HDL-C. We present the case of one subject, LM, who adopted a ketogenic diet for management of ulcerative colitis. He subsequently experienced an increase in LDL-C from 95 to 545 mg/dl, at peak, in association with HDL-C >100 mg/dl and triglycerides ~40 mg/dl, typical of the emergent LMHR phenotype. Assessments of LM's dietary intake, lipid panels, and BMI are consistent with prior data and suggest that the LMHR phenomenon is not dependent on saturated fat intake but inversely associates with BMI changes. Finally, computed tomography angiography conducted on LM after over 2 years of hypercholesterolemia revealed no evidence of calcified or non-calcified plaque. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that “leanness” and good metabolic health markers may predict larger increases in LDL cholesterol (LDL-C) in response to carbohydrate restriction. Specifically, a recent cohort study demonstrated an inverse association between BMI and LDL-C change among individuals on carbohydrate-restricted diets and identified a subgroup of “Lean Mass Hyper-Responders” (LMHR) who exhibit exceptional increases in LDL-C, in the context of low triglycerides and high HDL-C. We present the case of one subject, LM, who adopted a ketogenic diet for management of ulcerative colitis. He subsequently experienced an increase in LDL-C from 95 to 545 mg/dl, at peak, in association with HDL-C >100 mg/dl and triglycerides ~40 mg/dl, typical of the emergent LMHR phenotype. Assessments of LM’s dietary intake, lipid panels, and BMI are consistent with prior data and suggest that the LMHR phenomenon is not dependent on saturated fat intake but inversely associates with BMI changes. Finally, computed tomography angiography conducted on LM after over 2 years of hypercholesterolemia revealed no evidence of calcified or non-calcified plaque.

Low carbohydrate diets have a promising mechanistic rationale in the treatment of cancer with favorable preclinical data. The strongest data suggest synergistic effects of dietary interventions with traditional cancer therapies. Recent prospective clinical trials suggest that low carbohydrate diets are safely and feasibly added within a busy oncology clinic, with hopeful additive effects in treatment enhancement.

Although carbohydrate restriction is not a new approach for the management of Type 2 diabetes, interest in its safety and efficacy has increased significantly in recent years. The purpose of the current narrative review is to summarise the key relevant research and practical considerations in this area, as well as to explore some of the common concerns expressed in relation to the use of such approaches. There is a strong physiological rationale supporting the role of carbohydrate restriction for the management of Type 2 diabetes, and available evidence suggests that low carbohydrate dietary approaches (LCDs) are as effective as, or superior to, other dietary approaches for its management. Importantly, LCDs appear to be more effective than other dietary approaches for facilitating a reduction in the requirement for certain medications, which leads to their effects on other health markers being underestimated. LCDs have also been demonstrated to be an effective method for achieving remission of Type 2 diabetes for some people. The available evidence does not support concerns that LCDs increase the risk of cardiovascular disease, that such approaches increase the risk of nutrient deficiencies, or that they are more difficult to adhere to than other dietary approaches. A growing number of organisations support the use of LCDs as a suitable choice for individuals with Type 2 diabetes.