Increased brain oxidation, cognitive dysfunction associated with vitamin E deficiency

Tuesday, January 5, 2016

An article appearing in the Journal of Nutritional Science and Vitaminology in 2015 reports the outcome of a study conducted at Japan's Shibaura Institute of Technology of an increase in cognitive dysfunction in vitamin E deficient mice. Animals that experienced long term deficiency exhibited an increase in brain lipid peroxidation, indicating that a continual lack of vitamin E, a well-known antioxidant, may accelerate brain oxidation.

"It is well known that the elevation of oxidative products in living tissues accelerates the risk of the development and progression of serious diseases such as neurodegenerative disorders, liver disease, and heart disease," write authors Koji Fukui and colleagues. "In order to prevent the risk of the development or progression of free radical diseases in the senescence process, it is necessary to attenuate reactive oxygen species production or oxidative damage . . . Vitamin E (alpha-tocopherol), which is a natural lipophilic vitamin, possesses a powerful antioxidant function."

The study included mice given a vitamin E-deficient or standard diet beginning at one month of age and continuing until the age of three or six months, followed by cognitive testing.  Lipid peroxidation was measured in the cerebral cortex, cerebellum and hippocampus, and serum cholesterol levels were assessed.

Deficient animals in both age groups showed impairments in cognitive function compared to mice that received a standard diet. They also had higher serum cholesterol levels in comparison with their age-matched controls. While brain lipid peroxidation was similar between deficient and nondeficient three-month-old mice, six-month-old deficient mice exhibited a greater amount of peroxidation in the cortex and cerebellum in comparison with nondeficient mice of the same age, indicating a significant effect in association with long-term deficiency.

The authors remark that only a few weeks of vitamin E deficiency—in this case, eight weeks--has the potential to cause cognitive dysfunction.

"These results indicate that chronic vitamin E deficiency may slowly accelerate brain oxidation," they conclude. "Thus, vitamin E concentrates may need to be monitored in order to prevent the risk of cognitive dysfunction, even under normal conditions."

What's Hot
JAMA reports reduced functional decline in Alzheimer's patients given vitamin E
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The January 1, 2014 issue of the Journal of the American Medical Association (JAMA) reports the outcome of a double-blinded trial involving mild to moderate Alzheimer's disease patients which found a reduction in the rate of functional decline in comparison with a placebo among those who received a daily vitamin E supplement.

The trial included 613 predominantly male patients at fourteen Veterans Affairs medical centers. Participants were divided to receive 2,000 international units (IU) vitamin E, 20 milligrams of the drug memantine, both treatments, or a placebo daily over a follow-up period that averaged 2.3 years. The subjects were assessed on their ability to perform activities of daily living, cognitive function, memory and language, psychological and behavioral problems, and time necessitating caregiver assistance at the beginning of the study and every six months thereafter.

While memantine as well as memantine plus vitamin E were not associated with a benefit, functional decline was slowed in patients who received vitamin E, translating into a delay in clinical progression of approximately 6.2 months over follow-up. Those who received the vitamin also needed less caregiver assistance in comparison with the placebo group.

"The current study is one of the largest and longest treatment trials in patients with mild to moderate Alzheimer's disease," Maurice W. Dysken, MD, and colleagues announce. "It is the first large scale clinical trial to assess not only the effectiveness of alpha tocopherol in patients with mild to moderate Alzheimer's disease, but also the combination of alpha tocopherol and memantine."

"In contrast to the conclusion drawn from a 2005 meta-analysis of vitamin E, which showed that high-dose vitamin E may increase the risk of all-cause mortality, we found no significant increase in mortality with vitamin E," they observed. "The annual mortality rate was 7.3 percent in the alpha tocopherol group vs. 9.4 percent for the placebo group."

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Health Concern

Age-related cognitive decline

Many factors contribute to age-related cognitive decline:

  • Oxidative stress and free radical damage
  • Chronic low-level inflammation
  • Declining hormone levels like estrogen, testosterone, DHEA, pregnenolone
  • Inner arterial lining (endothelium) dysfunction
  • Insulin resistance
  • Excess body weight
  • Suboptimal nutrition
  • Loneliness, lack of social network, and high stress

The brain is particularly susceptible to oxidative damage since it consumes roughly 20% of the oxygen used by the entire body, and because it contains high concentrations of phospholipids, which are especially prone to oxidative damage in the context of high metabolic rate. As we age, there is a significant and progressive increase in the level of oxidatively damaged DNA and lipids in the brain; this is true even for healthy individuals. Over time, this free radical damage leads to the death of neurons.

Numerous studies have implicated oxidative stress in the pathology of mild cognitive impairment and Alzheimer's disease alike.

In a study of 338 individuals, researchers analyzed blood samples from patients with various neurodegenerative diseases and found that the antioxidant capacity of their blood was reduced by as much as 28%, relative to healthy controls.


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