The bioavailability of vitamin E is lower in people with metabolic syndrome

A new study has shown that people with metabolic syndrome are less able to process vitamin E than the normal population. As this population suffers from a high visceral lipid burden, any reduction in the levels of this potent fat-soluble antioxidant is of concern and suggests that dietary recommendations of vitamin E intake for this group should be revised upward. Metabolic syndrome is extremely common in the Western world and is closely associated with the development of atherosclerosis and type 2 diabetes.

Metabolic syndrome (MetS) is a metabolic dysfunction that can be characterized by the following grouping of symptoms: impaired glucose and insulin metabolism, overweight and abdominal fat distribution, dyslipidemia, and hypertension (2). In recent years, MetS has been in the spotlight because it is directly correlated with the development and progression of atherosclerotic cardiovascular disease, and with type 2 diabetes (T2D).

Metabolic syndrome (MetS) is found ubiquitously in populations that follow a Westernized diet. Indeed, the condition is thought to affect 34.7% of Americans (3). Sufferers of MetS are usually advised to limit their consumption of fats, but this results in a reduction of dietary fat-soluble vitamins. Alpha-Tocopherol is an important antioxidant, able to mop up destructive reactive oxygen species (ROS) formed during lipid metabolism. Less than 92% of Americans meet the Estimated Average Requirement (EAR) for α-Tocopherol of 12 mg per day. In fact, obese individuals have intakes even less than that of the rest of the US population (4).

Bruno et al. (5) showed that individuals who subjected their bodies to high levels of oxidative stress through smoking were less able to retain α-Tocopherol in their bodies than non-smokers. Sufferers of MetS are also subject to high levels of oxidative stress.

In a new study, Mah et al. (1) fed ten MetS patients and ten normal individuals with 240 mL of milk (skimmed, semi-skimmed and full-fat types) containing 15 mg of deuterium labelled RRR-α-Tocopherol. Biochemical analysis of blood samples was carried out on samples taken at regular intervals up to 72 hours after consumption of the milk. The fat content of the milk had no effect on the α-Tocopherol levels in the blood, but there was a considerable difference between the MetS and normal participants, with average maximal α-Tocopherol concentrations (Cmax) over the three days of 2.04 and 2.73 μmol/L respectively. The study provides strong evidence that sufferers of MetS have an impaired ability to retain α-Tocopherol in their tissues.

1. Mah E, Sapper T N, Chitchumroonchokchai C, Failla M L, et al. “α -Tocopherol bioavailability is lower in adults with metabolic syndrome regardless of dairy fat co-ingestion : a randomized , double-blind crossover trial”, AJCN 2015 (published ahead of print). doi.org/10.3945/ajcn.115.118570.
2. Tousoulis D, Plastiras A, Siasos G, Oikonomou E, et al.; “Omega-3 PUFAs improved endothelial function and arterial stiffness with a parallel anti-inflammatory effect in adults with metabolic syndrome”. Atherosclerosis 2014, 232(1): 10–16. doi.org/10.1016/j.atherosclerosis.2013.10.014.
3. Aguilar M, Bhuket T, Torres S, Liu B and Wong R J; “Prevalence of the metabolic syndrome in the United States, 2003-2012”; JAMA 2015; 313:1973–4.
4. Agarwal S, Reider C, Brooks J R and Fulgoni V L; “Comparison of prevalence of inadequate nutrient intake based on body weight status of adults in the United States: an analysis of NHANES 2001-2008”; J Am Coll Nutr 2015; 34: 126–34.
5. Bruno R S, Ramakrishnan R, Montine T J, Bray T M and Traber M G; “α –Tocopherol disappearance is faster in cigarette smokers and is inversely related to their ascorbic acid status”; Am J Clin Nutr 2005; 81: 95–103.