~ Multinutrient Supplement Extends Lifespan in Mouse Model of Aging

Researchers at McMaster University in Ontario, Canada, reported in the March 2005 issue of the Journals of Gerontology Series A—Biological Sciences and Medical Sciences (http://biomed.gerontologyjournals.org/) that a complex dietary supplement extended lifespan and prevented or delayed some of the signs of aging in mice bred to experience accelerated aging.

Jennifer Lemon of McMaster's department of biology and her colleagues used mice bred to overexpress growth hormone. Overexpression of growth hormone had been found in previous research with mice to accelerate aging and reduce lifespan. One hundred twenty of these transgenic mice were supplemented beginning at the age of 2 months with a formula designed to address key factors of aging by reducing oxidative stress and inflammation, promoting membrane and mitochondrial integrity and increasing insulin sensitivity. The formula consisted of vitamins B1, B3, B6, B12, C, D and E, acetyl-L-carnitine, alpha-lipoic acid, acetylsalicylic acid, beta-carotene, bioflavonoids, chromium picolinate, cod liver oil, coenzyme Q10, DHEA, flax seed oil, folic acid, garlic, ginger, ginkgo, ginseng, green tea extracts, L-glutathione, magnesium, melatonin, N-acetyl-cysteine, potassium, rutin, selenium and zinc. Two hundred five of the transgenic mice served as controls. The supplement was also given to 25 normal mice who did not overexpress growth hormone, while 75 normal mice did not receive the supplement.

The researchers found that the supplemented transgenic mice had increased survivorship at all ages compared to transgenic mice who did not receive the formula, and that they experienced a 28 percent increase in mean longevity compared to untreated mice. Twenty percent of untreated mice died before any of the supplemented transgenic mice had expired. When the normal mice were compared, the supplemented group also lived longer than those who did not receive the supplement, with an 11 percent increase in mean longevity found in treated compared to untreated mice.

When the mice were evaluated at 12 months of age, 14 percent of the untreated transgenic mice and 6 percent of the normal untreated mice had cataracts, while none of the supplemented transgenic mice and only 4 percent of the normal supplemented mice had the condition. The loss of body weight that normally occurs at this age was completely absent in the normal supplemented mice compared to 10.9 percent of the unsupplemented normal mice, and was also lower in the supplemented transgenic mice than in those that were not supplemented. Arthritis was also significantly reduced and coat quality improved in supplemented mice. The main cause of death of the mice in all groups was determined to be kidney and liver degeneration, which was apparently delayed in the supplemented mice.

The authors write that "Simultaneous treatment for multiple processes contributing to aging may benefit strongly by acting synergistically on these interdependent processes. Our results confirm that complex formulations can indeed obtain remarkable results."

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