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Journal of Endocrinology & Metabolism

Review

Volume 8, Number 2-3, May 2018, pages 27-31

Effects of Energy and Carbohydrate Intake on Serum High-Density Lipoprotein-Cholesterol Levels

High-density lipoprotein (HDL) plays a role in reverse cholesterol transport from the peripheral tissues to liver, suppressing cholesterol accumulation in the peripheral tissue. Therefore, serum low HDL-cholesterol (HDL-C) level was considered to be one of risk factors for coronary artery diseases [1, 2].

We previously studied effects of energy and carbohydrate intake on serum HDL-C levels to make “Dietary Reference Intakes for Japanese 2015”, and reported the results by reviewing papers by 2012 [3]. Here we review articles about the effects of energy and carbohydrate intake on serum HDL-C levels which were published from 2012 to 2018, to make “Dietary Reference Intake for Japanese 2020”.

To make “Dietary Reference Intake for Japanese 2020”, we searched meta-analyses of randomized controlled trials (RCTs) which have the highest evidence level. A search was conducted by using PubMed, Embase and Google Scholar, with the following keywords: high-density lipoprotein-cholesterol (HDL-C) and energy intake and meta-analysis or high-density lipoprotein-cholesterol (HDL-C) and carbohydrate intake and meta-analysis. The search period was comprised between January 2012 and March 2018.

We found three meta-analyses which studied effects of energy intake on HDL-C. Parretti et al conducted a meta-analysis of very-low-energy diets (VLEDs) used to treat obesity, by using RCTs included where the intervention included an VLED and the comparator was no intervention or an intervention that could be given in a general medical setting in adults that were overweight [4]. Compared with a behavioral program alone, VLEDs combined with a behavioral program achieved -3.9 kg (95% confidence interval (CI): -6.7 to -1.1) at 1 year. An increase of HDL-C of 0.06 mmol/L (95% CI: 0.00, 0.13 mmol/L) was obtained.

In the systematic review with meta-analysis which assessed the effect of diet on changes in parameters describing the body size phenotype of metabolically healthy obese subjects, the combined analyzed population consists of 1,827 subjects aged 34.4 to 61.1 with a body mass index (BMI) of > 30 kg/m² [5]. Time of intervention ranged from 8 to 104 weeks. This systematic review revealed a significant association between restricted energy diet and BMI (-2.70 kg/m²; 95% CI: -4.01, -1.39), triglyceride (TG) (-0.11 mmol/L; 95% CI: -0.16, -0.06). However, a significant association between restricted energy diet and HDL-C could not be observed.

A systematic review and meta-analysis of studies that compared energy-restricted, isocaloric, high-protein, low-fat (HP) diets with standard-protein, low-fat (SP) diets on cardiometabolic risk factors was conducted [6]. Compared with an SP diet, an HP diet produced more favorable changes in weighted mean differences for reductions in body weight, fat mass, and TG. However, HDL-C was similar across dietary treatments.

Meta-analyses evaluated effects of carbohydrate intake on HDL-C as shown in Table 1 [7-13]. Seven meta-analyses were eligible. Only one meta-analysis failed to prove that low-carbohydrate diet increases HDL-C. However, six meta-analyses showed that low-carbohydrate diet significantly increased serum HDL-C levels.

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Table 1. Meta-Analyses Evaluated Effects of Carbohydrate Intake on HDL-C

Meta-analyses evaluated effects of sugar intake on HDL-C as shown in Table 2 [14-17]. Four meta-analyses were eligible.

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Table 2. Meta-Analyses Evaluated Effects of Sugar Intake on HDL-C

When free sugars were substituted for complex carbohydrates, a significant increase in HDL was observed [14]. However, in another systematic review and meta-analysis of RCTs that examined effects of the modification of dietary free sugars on lipids, higher compared with lower sugar intakes significantly raised HDL-C [15].

In a meta-analysis which searched through July 7, 2015 for controlled feeding trials with follow-up ≥ 7 days, which investigated the effect of oral fructose compared to a control carbohydrate on lipids, fructose had no effect on HDL-C in isocaloric trials [16]. In a systematic review and meta-analysis of human, controlled, feeding trials involving isocaloric fructose exchange for other carbohydrates to quantify the effects of fructose on serum lipids in adult humans, fructose exerted no effect on HDL-C [17].

In addition to decreased HDL-C, elevation of TG is commonly observed in an insulin-resistant state such as obesity, metabolic syndrome and type 2 diabetes [18]. Reduction of body weight increases HDL-C and decreases TG. Therefore, we evaluated effects of energy, carbohydrate and sugar intake on body weight and other serum lipids in addition to HDL-C.

One meta-analysis showed a significant association between energy restriction and body weight and TG, however, failed to show a significant association between energy restriction and HDL-C in metabolically healthy obese subjects [5]. Another meta-analysis using overweight adults who were not always defined as metabolically healthy, showed significant improvement of body weight and HDL-C [4]. Energy-restricted, isocaloric, high-protein, low-fat diets did not make a difference in HDL-C as compared with standard-protein, low-fat diets [6]. Effects of energy restriction on HDL-C may vary by backgrounds of subjects, the ratio of carbohydrate, protein and fat intake.

The low carbohydrate diet, in which carbohydrates are replaced by greater intake of fat and/or protein, is a popular weight-loss option compared with the conventional low-fat diet. However, concerns have been raised with regard to the macronutrient shift with an extreme carbohydrate restriction and the liberal intakes of fats, which may present detrimental effects on cardiovascular risk factors [19].

In present review, although six meta-analyses showed that low-carbohydrate diet significantly increased HDL-C, only one meta-analysis did not show beneficial effect of low-carbohydrate diet on HDL-C.

Naude et al compared the effects of low carbohydrate and isoenergetic balanced weight loss diets on overweight and obese adults assessed in RCTs [8]. In non-diabetic and diabetic participants, little or no difference was detected at 3 - 6 months and 1 - 2 years for HDL-C. They suggested that there is probably little or no difference in weight loss and changes in cardiovascular risk factors up to 2 years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomized to low-carbohydrate diets and isoenergetic balanced weight loss diets.

Four of six studies which showed an increase of HDL-C by low-carbohydrate diet demonstrated a significant reduction of both body weight and TG. In the meta-analysis by Ajala et al, reduction of body weight was observed; however, data about TG were not available [10]. The meta-analysis by Huntriss et al showed statistical significance in favor of the low-carbohydrate intervention arm for TG; however, body weight did not demonstrate a statistically significant difference between interventions [11]. Low-carbohydrate diet may increase HDL-C, which may be due to body weight reduction and/or improvement of insulin resistance.

In a meta-analysis of RCTs to compare diets that provide a given amount of energy from free sugars with a control diet that provides the same amount of energy from complex carbohydrates, a significant increase in HDL-C was observed; however, significant increases in LDL-C and TG were also observed [14]. In another meta-analysis, higher compared with lower sugar intakes significantly raised HDL-C, TG and LDL-C [15]. Regarding the effect of free sugar intake on HDL-C, two meta-analyses showed the opposite result. However, both studies showed that free sugar intake was significantly associated with an increase of TG and LDL-C. Further studies including effects of free sugar on other risk factors in addition to HDL-C should be performed in the future.

Two meta-analyses showed no effect of fructose intake on HDL-C [16, 17]. There were no effects of fructose intake on LDL-C, non-HDL-C, apolipoprotein B, and TG in isocaloric trials. However, in hypercaloric trials, fructose increased apolipoprotein B and TG [16]. Isocaloric fructose exchange for carbohydrates increased LDL-C at > 100 g fructose/day [17]. However, no effect was shown on LDL-C when the fructose intake was ≤ 100 g/day. Fructose intake may exert no effect on HDL-C; however, the fructose intake ≤ 100 g/day may be recommended considering unfavorable effects of fructose on LDL-C and TG.

Effects of energy restriction on HDL-C may depend on backgrounds of subjects studied and the ratio of macronutrients. Low-carbohydrate diet may increase HDL-C, which may be due to reduction of body weight and/or amelioration of insulin resistance. Further studies including effects of free sugar on other risk factors in addition to HDL-C should be performed in the future. Fructose intake may exert no effect on HDL-C; however, the fructose intake ≤ 100 g/day may be recommended considering unfavorable effects of fructose on other risk factors.

Conflict of Interest

The authors declare that they have no conflict of interest.

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