Low Carbohydrate and Low-Fat Diets: What We Don't Know and Why we Should Know It

Heather Seid, Michael Rosenbaum, Heather Seid, Michael Rosenbaum

Abstract

In the 1940s, the diet-heart hypothesis proposed that high dietary saturated fat and cholesterol intake promoted coronary heart disease in "at-risk" individuals. This hypothesis prompted federal recommendations for a low-fat diet for "high risk" patients and as a preventive health measure for everyone except infants. The low carbohydrate diet, first used to treat type 1 diabetes, became a popular obesity therapy with the Atkins diet in the 1970s. Its predicted effectiveness was based largely on the hypothesis that insulin is the causa prima of weight gain and regain via hyperphagia and hypometabolism during and after weight reduction, and therefore reduced carbohydrate intake would promote and sustain weight loss. Based on literature reviews, there are insufficient randomized controlled inpatient studies examining the physiological significance of the mechanisms proposed to support one over the other. Outpatient studies can be confounded by poor diet compliance such that the quality and quantity of the energy intake cannot be ascertained. Many studies also fail to separate macronutrient quantity from quality. Overall, there is no conclusive evidence that the degree of weight loss or the duration of reduced weight maintenance are significantly affected by dietary macronutrient quantity beyond effects attributable to caloric intake. Further work is needed.

Keywords: carbohydrate; diet; fat; macronutrient; obesity; weight gain; weight loss.

Conflict of interest statement

: The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Possible mechanisms associated with the intake of high fat diet and obesity. (A) A high fat diet causes an alteration in intestinal microbiota from low to high Firmicutes and high to low Bifidobacterium. (B) The low expression of adenosine monophosphate kinase (AMPK) leads to decreased fatty acid oxidation. (C) Fasting induce adipose factor (FIAF) expression causes activation of lipoprotein lipase (LPL) that leads to triglyceride (TG) accumulation. (D) Low glucagon-like peptide 1 (GLP-1) leads to increased insulin resistance and decreased bile acid secretion from liver. (E) Decreased peptide YY (PYY) causes low satiety in obese host. (F) Increased lipogenesis via upregulated acetyl-CoA carboxylase (Acc1) and fatty acid synthase (Fas) enzymes. (G) The activation of endo cannabinoid loop via release of lipopolysaccharide (LPS) due to damages intestinal epithelium. (H) The modulation of intestinal immune response via toll-like receptor 5 (TLR-5) downstream signaling. (I) The systemic inflammation caused by inflammatory cytokines and bacterial. (Reprinted from Dahiya et al. [23]). Cpt-1 - carnitine palmitoyltransferase, GPR – G-protein coupled receptors, FXR – Farnesoid X Receptor.
Figure 2
Figure 2
Schematic of the insulin-carbohydrate model. Increased carbohydrate intake promotes increased insulin secretion resulting in depletion of circulating concentrations of metabolic fuels that are used in lipogenesis. The decreased circulating glucose and lipids results in adaptive thermogenesis and hyperphagia which promote weight gain or regain (Based on Ludwig [6]).
Figure 3
Figure 3
Meta-analysis of the effects of diet low in fat or carbohydrate on energy expenditure in isocaloric studies. Overall, energy expenditure is significantly higher on the low-fat diet (p < 0.0001) but the actual value is only 26 Kcal/day. (Reprinted from Hall and Guo [32]).

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Source: PubMed

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