Hannah L Mayr1, Catherine Itsiopoulos2, Audrey C Tierney3, Teagan Kucianski4, Jessica Radcliffe4, Manohar Garg5, Jane Willcox2, Colleen J Thomas6. 1. School of Allied Health, Human Services and Sport, La Trobe University, Melbourne, Victoria, 3086, Australia; Nutrition and Dietetics Department, Princess Alexandra Hospital, Brisbane, Queensland, 4102, Australia; Bond University Nutrition and Dietetics Research Group, Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Queensland, 4226, Australia. Electronic address: H.Mayr@latrobe.edu.au. 2. School of Allied Health, Human Services and Sport, La Trobe University, Melbourne, Victoria, 3086, Australia. 3. School of Allied Health, University of Limerick, Castletroy, Limerick, V94 T9PX, Ireland; Department of Dietetics, Nutrition and Sport, School of Allied Health, Human Services and Sport, La Trobe University, Melbourne, Victoria, 3086, Australia. 4. Department of Dietetics, Nutrition and Sport, School of Allied Health, Human Services and Sport, La Trobe University, Melbourne, Victoria, 3086, Australia. 5. Nutraceuticals Research Program, School of Biomedical Sciences & Pharmacy, University of Newcastle, New South Wales, 2308, Australia. 6. Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, Victoria, 3086, Australia.
Abstract
BACKGROUND & AIMS: The Mediterranean diet (MedDiet) is recognised to reduce risk of coronary heart disease (CHD), in part, via its anti-inflammatory and antioxidant properties, which may be mediated via effects on body fat distribution. Diet efficacy via these mechanisms is however unclear in patients with diagnosed CHD. This study aimed to determine: (1) the effect of ad libitum MedDiet versus low-fat diet intervention on adiposity, anti-inflammatory marker adiponectin, oxidative stress marker malondialdehyde (MDA) and traditional CVD risk markers, and (2) whether improvement in MedDiet adherence score in the pooled cohort was associated with these risk markers, in a pilot cohort of Australian patients post coronary event. METHODS:Participants (62 ± 9 years, 83% male) were randomised to 6-month ad libitumMedDiet (n = 34) or low-fat diet (n = 31). Pre- and post-intervention, dietary adherence, anthropometry, body composition (Dual-energy X-ray Absorptiometry) and venepuncture measures were conducted. RESULTS: The MedDiet group reduced subcutaneous adipose tissue (SAT) area compared to the low-fat diet group (12.5 cm2 more, p = 0.04) but not visceral adipose tissue or other body composition measures. In the pooled cohort, participants with greatest improvement in MedDiet adherence score had significantly lower waist circumference (-2.81 cm, p = 0.01) and SAT area (-27.1 cm2, p = 0.04) compared to participants with no improvement in score at 6-months. There were no changes in adiponectin, MDA or other risk markers in the MedDiet compared to low-fat diet group, and no differences in 6-month levels between categories of improvement in MedDiet score (p > 0.05). Within the MedDiet group only, the proportion of participants taking beta-blocker medication reduced from baseline to 6-months (71% vs. 56%, p-trend = 0.007). CONCLUSIONS: Adherence to 6-month ad libitum MedDiet reduced subcutaneous fat and waist circumference which discounts the misconception that this healthy but high fat diet leads to body fat gain. The effect of MedDiet on body fat distribution and consequent anti-inflammatory and antioxidant effects, as well as need for medications, in patients with CHD warrants exploration in larger studies. Clinically significant effects on these markers may require adjunct exercise and/or caloric restriction. TRIAL REGISTRATION: ACTRN12616000156482.
RCT Entities:
BACKGROUND & AIMS: The Mediterranean diet (MedDiet) is recognised to reduce risk of coronary heart disease (CHD), in part, via its anti-inflammatory and antioxidant properties, which may be mediated via effects on body fat distribution. Diet efficacy via these mechanisms is however unclear in patients with diagnosed CHD. This study aimed to determine: (1) the effect of ad libitum MedDiet versus low-fat diet intervention on adiposity, anti-inflammatory marker adiponectin, oxidative stress marker malondialdehyde (MDA) and traditional CVD risk markers, and (2) whether improvement in MedDiet adherence score in the pooled cohort was associated with these risk markers, in a pilot cohort of Australian patients post coronary event. METHODS:Participants (62 ± 9 years, 83% male) were randomised to 6-month ad libitum MedDiet (n = 34) or low-fat diet (n = 31). Pre- and post-intervention, dietary adherence, anthropometry, body composition (Dual-energy X-ray Absorptiometry) and venepuncture measures were conducted. RESULTS: The MedDiet group reduced subcutaneous adipose tissue (SAT) area compared to the low-fat diet group (12.5 cm2 more, p = 0.04) but not visceral adipose tissue or other body composition measures. In the pooled cohort, participants with greatest improvement in MedDiet adherence score had significantly lower waist circumference (-2.81 cm, p = 0.01) and SAT area (-27.1 cm2, p = 0.04) compared to participants with no improvement in score at 6-months. There were no changes in adiponectin, MDA or other risk markers in the MedDiet compared to low-fat diet group, and no differences in 6-month levels between categories of improvement in MedDiet score (p > 0.05). Within the MedDiet group only, the proportion of participants taking beta-blocker medication reduced from baseline to 6-months (71% vs. 56%, p-trend = 0.007). CONCLUSIONS: Adherence to 6-month ad libitum MedDiet reduced subcutaneous fat and waist circumference which discounts the misconception that this healthy but high fat diet leads to body fat gain. The effect of MedDiet on body fat distribution and consequent anti-inflammatory and antioxidant effects, as well as need for medications, in patients with CHD warrants exploration in larger studies. Clinically significant effects on these markers may require adjunct exercise and/or caloric restriction. TRIAL REGISTRATION: ACTRN12616000156482.