Abstract

The level of high-density lipoprotein is thought to be critical in inhibiting lesion formation as well as reducing the lipid load of preexisting atherosclerotic lesions. With the aim of determining the main determinants of plasma HDL-cholesterol (HDL-c) in free-living adults, 997 individuals (52.3 ± 10 years, 67% females) were selected for a descriptive cross-sectional study. The used data corresponded to the baseline obtained from participants clinically selected for a lifestyle modification program. Covariables of clinical, anthropometry, food intake, aerobic fitness, and plasma biochemistry were analyzed against plasma HDL-c either as continuous or categorized variables. After adjustments for age, gender, and BMI the excess of abdominal fat along with high carbohydrate-energy intake and altered plasma triglycerides were the stronger predictors of reduced plasma HDL-c. In conclusion lifestyle interventions aiming to normalize abdominal fatness and plasma triglycerides are recommended to restore normal levels of HDL-c in these free-living adults.

Highlights

  • It is established that oxidation of LDL constitutes a key event in inflammation and atherogenesis [1]

  • Reduced plasma HDL-c levels were found in individuals with higher BMI, Waist circumference (WC), and body fat, higher plasma concentrations of uric acid, triglycerides, and C-reactive protein (CRP) along with lower values of muscle-mass index, VO2 max and plasma albumin (Table 1)

  • There was no significant correlationship between plasma HDL-c and the variables: body fat (%), muscle-mass index (MMI), the energy contribution of ingested CHO, total and saturated, mono- or polyunsaturated fat, ingested fiber, and servings of grains, fruits, dairy, sugar, and oils, as well as dietary variety and Healthy Eating Index (HEI)

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Summary

Introduction

It is established that oxidation of LDL constitutes a key event in inflammation and atherogenesis [1]. Mechanisms of LDL oxidation in vivo involve concerted modification through oxidation by oxidants produced by arterial wall cells, such as reactive nitrogen species, reactive chlorine species, hydroxyl radicals, and lipid soluble free radicals [2]. Such a spectrum of chemically diverse oxidants implies that any single low-molecular weight antioxidant such as vitamin E or C, even at physiologically relevant doses, may not provide complete oxidative protection of LDL in vivo [1, 2]. The usual protective features of high HDL-c are reverse cholesterol transport, antioxidative, anti-inflammatory, antiapoptotic, antithrombotic, anti-infections, vasodilatation, and so forth [5]

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