The metabolic effects of low‐carbohydrate diets and incorporation into a biochemistry course

Pogozelski, Wendy; Arpaia, Nicholas; Priore, Salvatore F.

doi:10.1002/bmb.2005.494033022445

Cited by 28 publications

(19 citation statements)

References 60 publications

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“…In addition, the AHA/NHLBI report [90] presents the rationale for low CHO as the effect on appetite. Whereas this may be a component, it has been stated many times, and is part of basic biochemical education [16,93-96], that the rationale of CHO restriction is the control of metabolism by insulin regulation. The effects described above clearly support this.…”

Section: Discussionmentioning

confidence: 99%

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction

2005

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Metabolic Syndrome (MetS) represents a constellation of markers that indicates a predisposition to diabetes, cardiovascular disease and other pathologic states. The definition and treatment are a matter of current debate and there is not general agreement on a precise definition or, to some extent, whether the designation provides more information than the individual components. We consider here five indicators that are central to most definitions and we provide evidence from the literature that these are precisely the symptoms that respond to reduction in dietary carbohydrate (CHO). Carbohydrate restriction is one of several strategies for reducing body mass but even in the absence of weight loss or in comparison with low fat alternatives, CHO restriction is effective at ameliorating high fasting glucose and insulin, high plasma triglycerides (TAG), low HDL and high blood pressure. In addition, low fat, high CHO diets have long been known to raise TAG, lower HDL and, in the absence of weight loss, may worsen glycemic control. Thus, whereas there are numerous strategies for weight loss, a patient with high BMI and high TAG is likely to benefit most from a regimen that reduces CHO intake. Reviewing the literature, benefits of CHO restriction are seen in normal or overweight individuals, in normal patients who meet the criteria for MetS or in patients with frank diabetes. Moreover, in low fat studies that ameliorate LDL and total cholesterol, controls may do better on the symptoms of MetS. On this basis, we feel that MetS is a meaningful, useful phenomenon and may, in fact, be operationally defined as the set of markers that responds to CHO restriction. Insofar as this is an accurate characterization it is likely the result of the effect of dietary CHO on insulin metabolism. Glucose is the major insulin secretagogue and insulin resistance has been tied to the hyperinsulinemic state or the effect of such a state on lipid metabolism. The conclusion is probably not surprising but has not been explicitly stated before. The known effects of CHO-induced hypertriglyceridemia, the HDL-lowering effect of low fat, high CHO interventions and the obvious improvement in glucose and insulin from CHO restriction should have made this evident. In addition, recent studies suggest that a subset of MetS, the ratio of TAG/HDL, is a good marker for insulin resistance and risk of CVD, and this indicator is reliably reduced by CHO restriction and exacerbated by high CHO intake. Inability to make this connection in the past has probably been due to the fact that individual responses have been studied in isolation as well as to the emphasis of traditional therapeutic approaches on low fat rather than low CHO.We emphasize that MetS is not a disease but a collection of markers. Individual physicians must decide whether high LDL, or other risk factors are more important than the features of MetS in any individual case but if MetS is to be considered it should be recognized that reducing CHO will bring improvement. Response of symptoms to CHO ...

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Section: Discussionmentioning

confidence: 99%

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction

2005

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“…It is important to note that there is no singular definition of what constitutes a LCHO diet, although a CHO content comprising <26% of calories (or <130 g CHO) has been suggested as a cut‐off . Variations of the LCHO diet differ in their permitted levels of macronutrients, such as the low‐carbohydrate, high‐fat diet, which emphasises the importance of increasing fat consumption , whereas others increase protein to a greater degree . Absolute intakes (i.e.…”

Section: Introductionmentioning

confidence: 99%

Dietary intake in people consuming a low‐carbohydrate diet in the UK Biobank

Shafique

Russell

Murdoch

et al. 2017

J Human Nutrition Diet

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“…These results are in agreement with our findings of decreased G6PDH and aldolase activities and increased citrate synthase activity in LC-control group. Pogozelski, Arpaia, and Priore (2005) suggested that increased proteins at the expense of carbohydrate in diet leads to decreased glycolysis, which is compensated by an increase in fat breakdown to satisfy body needs of energy via formation of ketone bodies from fatty acids. Amino acids formed from protein catabolism together with fatty acids were utilized in gluconeogenesis.…”

Section: Discussionmentioning

confidence: 99%

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

El-Bahrawy¹,

El-Ashmawy²,

Shamloula³

et al. 2014

IJB

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Incidence of hepatocellular carcinoma (HCC) has increased sharply in the last 10 years, with an especially high incidence in Egypt. This study was conducted to evaluate the impact of unbalanced diets on liver tumor through investigation of some biochemical mediators/pathways implicated in the pathogenesis of HCC. Male albino mice were divided into two major groups: Control group and Hepatocellular carcinoma (HCC) group; each group was further divided into four subgroups according to received diet: high fat (HF), low fat (LF), high carbohydrate (HC), and low carbohydrate (LC) groups. The results indicated that induction of HCC in mice showed marked body weight loss. Liver sections of HCC groups showed malignant giant cells and strong expression of p53. HCC mice groups kept on HF and LC diets showed the lowest survival rate, a significant increase in glucose-6-phosphate dehydrogenase (G6PDH), aldolase, and citrate synthase activities, a significant increase in serum E-cadherin as well as a significant decrease in insulin-like growth factor-1 (IGF-1) compared with LF diet. These results suggest that the molecular pathogenesis of HCC in mice correlates reduction of serum IGF-1 and elevated serum E-cadherin accompanied by reprogrammed metabolic profile shifted towards increased glycolysis and lipogenesis. These pathogenic changes were enhanced by over-consumption of carbohydrates, fats, and proteins, whereas dietary fat restriction could have a protective/ameliorative effect against the incidence of HCC.

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The metabolic effects of low‐carbohydrate diets and incorporation into a biochemistry course

Cited by 28 publications

References 60 publications

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction

Dietary intake in people consuming a low‐carbohydrate diet in the UK Biobank

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

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