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High dose vitamin E supplementation extends median and maximum lifespan in mouse study

September 3, 2005 Printer Friendly
In this issue
 

Life Extension Update Exclusive

   

High dose vitamin E supplementation extends median and maximum lifespan in mouse study

 

Protocol

   

Age-associated mental impairment

 

Featured Products

   

Vitamin E Capsules

   

Mitochondrial Energy Optimizer with SODzyme

 

Life Extension Magazine

   

September 2005 issue now online!

Life Extension Update Exclusive

High dose vitamin E supplementation extends median and maximum lifespan in mouse study

Photograph courtesy of University of Cadiz.

A report published online in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (http://ajpregu.physiology.org) revealed the findings of researchers from the University of Cadiz in Spain and the University of Buenos Aires in Argentina that feeding mice high doses of vitamin E increased lifespan and improved neurological performance.

Professor Alberto Boveris of the University of Buenos Aires and colleagues used a senescence accelerated strain of mice whose median lifespan is 60 to 70 weeks and whose maximum lifespan is 100 to 120 weeks. (Maximum lifespan is the greatest amount of weeks, months or years a species has been observed to survive, while median lifespan is a middle value determined from the range of survival times.) Starting at 28 weeks of age, the researchers supplemented the diets of male and female mice with doses of alpha-tocopherol comparable to the 1200 to 2000 milligram doses taken without adverse effects in studies involving Alzheimer’s disease patients. A control group received diets that contained the standard amount of vitamin E.

Male mice received the greatest benefit from high dose vitamin E supplementation, with a 40 percent increase in median lifespan and a 17 percent increase in maximum lifespan. Supplemented male mice also showed greater neuromuscular performance and cognitive exploratory activity than unsupplemented mice over the course of the study, and this difference increased with age.

Female mice, whose median lifespan was improved by only 14 percent, were not tested for neurological performance. Although the female mice did not experience an increase in maximum lifespan associated with vitamin E, maximum lifespan for both supplemented and unsupplemented females was greater than that of males, which has been explained by lower mitochondrial oxidant production and the effect of estrogen on down-regulating oxidant production.

The team also found that the increased mitochondrial content of lipid and protein oxidation products in the brains and livers of older mice was partly prevented by vitamin E. Vitamin E also helped reduce the age-associated decline in mitochondrial enzymatic activity in the brain and liver.

Professor Boveris explained that the results "are in line with the free radical theory of aging put forward by Gerschman and Harman in the 1950s. Our results show a significant negative correlation between the mitochondrial content of the oxidation products of free-radical mediated reactions and mitochondrial enzymatic activities. Moreover, brain mitochondrial enzymatic activities were linearly related to mice success in the tests of neuromuscular function and of exploratory and cognitive activity and to the maximal mice life span.”

The authors conclude that further studies are needed “to suggest a threshold for the vitamin E doses that provide beneficial effects in the neurological function in aging mammals, an effect that is likely mediated by the antioxidant properties of alpha-tocopherol.”

Protocol

Age-associated mental impairment

Numerous published studies indicate that brain aging can be controlled, at least in part. Some of these research findings demonstrate a preventive effect, whereas others show a benefit in reversing the neurological impairment caused by normal aging or by an age-related condition such as having had a stroke.

Free radicals are atoms with unpaired electrons that can cause damage to cells by a process known as oxidation. Brain cells are particularly vulnerable to the effects of oxidation because of their high-energy production. The more energy a cell produces, the greater the number of damaging free radicals. The destructive effects of excess free radical activity have been implicated in many disease processes, including Alzheimer's disease and Parkinson's disease. Antioxidants neutralize free radicals and help prevent some of the damage associated with normal brain aging.

A study in the Journal of the American Geriatric Society compared groups of older people over time and at a given time with regard to antioxidant intake and memory performance. The study found that free recall, recognition, and vocabulary were significantly related to vitamin C and beta-carotene levels. The levels of these antioxidants were found to be significant predictors of cognitive function even after adjusting for possible confounding variables (Perrig et al. 1997).

For protection from the many types of free radicals to which it is vulnerable, the brain needs a wide variety of antioxidants.

Featured Products

Vitamin E Capsules

One or more members of the vitamin E family may:

  • Maintain cell membrane integrity and reduce cellular aging
  • Act as a free radical scavenger of lipids
  • Maintain healthy platelet aggregation
  • Protect nervous system and retina
  • Delay cognitive decline
  • Enhance immune function

Mitochondrial Energy Optimizer with SODzyme

Mitochondrial Energy Optimizer incorporates the tremendous advances in our knowledge about the importance of maintaining mitochondrial integrity as we age. Scientists now know that mitochondrial decay in aging is a major driving force behind the aging process.

As the mitochondria burn fatty acids to produce cellular energy, it generates a host of free radicals in the process. That is why a mitochondrial antioxidant like lipoic acid is so critical. This comprehensive formula provides a much more potent form of lipoic acid (called R-lipoic acid) than its predecessor, ChronoForte, along with a more effective form of carnitine, called acetyl-L-carnitine-arginate.

Life Extension Magazine

September 2005 issue now online!

Reports

 

On the cover: Protecting your DNA from lethal mutations, by Dave Tuttle

 

Why lutein and zeaxanthin are becoming so popular, by Heather S Oliff, PhD

 

Futurist Ray Kurzweil on building bridges to immortality, by Jon VanZile

 

Prescription for Disaster, by Gary Null

 

Vitamin-less vegetables, by Terri Mitchell

Departments

 

As we see it
How many Americans are magnesium deficient?
by William Faloon

 

In the news
Drugmakers abuse FDA approval process, Vitamin B6 protects women from colorectal cancer, Green tea compound mimics anticancer drug, Melatonin lessens pain from irritable bowel syndrome, Magnesium may help obese children avoid diabetes, Vitamin D cuts fracture risk in elderly, Dietary vitamin E may protect against Parkinson’s disease, Grapes guard against atherosclerosis in animal study, Dietary antioxidants may mitigate stroke damage, Sigmoidoscopy overlooks colon cancer in women, Selenium may aid in treating prostate cancer

 

All about supplements
Flaxseed: Potent source of beneficial phytoestrogens, fiber, and omega-3 fatty acids
, by Dale Kiefer

 

Ask the doctor
Topical treatments for rosacea
, by Gary Goldfaden, MD

 

Profile
Daniel Tucker MD, A pioneering practitioner of antiaging medicine
, by Sue Kovach

 

September abstracts
Antimutagenics, zeaxanthin, flaxseed

Questions? Comments? Send them to ddye@lifeextension.com or call 1-800-678-8989.

For longer life,

Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
954 766 8433 extension 7716

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