Industry Opportunity: Vitamin E May Benefit Patients with Metabolic Syndrome
30 Mar 2017 --- An increased vitamin E supplementation may have a beneficial effect on patients with Metabolic Syndrome, as characterized by obesity, hyperlidimeia, chronic low-grade inflammation and more.
The study results may highlight opportunity to manufacturers and formulators looking for value in using vitamin E-boosting custom nutrient premixes for people at risk for cardiovascular disease.
The study from Ohio State University found that Metabolic Syndrome patients had decreased vitamin E catabolism, likely due to them having lower vitamin E status.
Metabolic Syndrome (MetS) is characterized by obesity, hyperlipidemia, chronic low-grade inflammation, insulin insensitivity, hyperinsulinemia, and hypertension and is a common condition among many people. It increases the risk of developing Type 2 diabetes and nonalcoholic fatty liver disease.
Nonalcoholic steatohepatitis (NASH) is common in people with MetS and is characterized by fatty infiltration into hepatocytes, inflammation, oxidative stress, and hepatic cellular injury. NASH can progress to cirrhosis, hepatocellular carcinoma, and eventually death.
It is known that peroxidative damage to lipids is increased in NASH patients, suggesting that their vitamin E requirement may be increased.
In order to determine to what extent vitamin E bioavailability may be altered by MetS, investigators from Ohio State University measured plasma and urinary concentrations of α-CEHC and α-CMBHC in 10 MetS patients and 10 healthy controls after administering a stable isotope (deuterium)-labelled dose of α-tocopherol in 4 different forms of milk in a crossover design study.
The subjects consumed 5 mg α-tocopherol for 3 days before the test day and received 15 mg labeled α-tocopherol with breakfast. The Ohio State researchers found that patients with MetS excreted 41% less unlabeled α-CEHC in their urine, 63% less of the labelled α-CEHC and 58% less of labelled α-CMBHC.
Measuring the area under the curve (AUC) for several hours after the acute dose of 15 mg labeled vitamin E also indicated that the labeled α-CEHC breakdown product was lower (52%) in MetS patients compared to healthy controls.
The lower response to supplementation in the MetS group compared to the healthy control group indicated that the MetS patients had decreased vitamin E catabolism, which the authors speculate was due to MetS patients having lower vitamin E status than healthy controls, despite the fact that they had similar plasma α-tocopherol concentrations.
The results also suggested that the lower vitamin E turnover in MetS patient may be caused by increased oxidative and inflammatory stressors.
It was also suggested that the fatty liver in MetS patients may have prevented normal hepatic α-tocopherol and α-CEHC trafficking.
Alternatively, there may have been increased fecal loss of vitamin E metabolites that were not measured in this study.
Regardless of the cause, the authors of the study say that the findings indicate that patients with MetS have lower vitamin E status than healthy controls based on their lower excretion of both labeled and unlabeled vitamin E catabolites.
