Your body is constantly renewing, rebuilding and repairing itself through our life times. It seems that with all this constant renewal we’d be able to stay young forever….unfortunately, that’s not what’s happening. Scientists have observed that even when an individual of, let’s say, 80 years young, produces new cells, they are aged cells that look and act older, not new ones as in someone age 40.
We hear alot about theories of aging such as free-radical damage, glycosylation, collagen cross-linking or other biological mechanisms. In light of new emerging findings, those contributors are important in the aging processes but they are not the root cause. A theory that emerged in the early 1990s was published in Nature, calling attention to telomeres, which changed our methodologies of aging forever.
Dr. Al Sears gives a great example of why our previous theories of, lets say, radical damage is so inaccurate. “Aging because of free-radical damage is analogous to the FAA announcing that the cause of a plane crash was gravity. Clearly, the force of gravity pulled the plane to the ground. But gravity exerts equal force on every plane in the sky, most of which safely reach their destination.”
Dr. Sears continues by saying, “…our bodies are assaulted by free-radicals from the day we are born. We have mechanisms that effectively quench free-radicals and correct the damage.” What we need to now understand is why they stop correcting damage.
Research now understands why our cells stop dividing after about 80 times, known as the “Hayflick Limit” named after it’s discoverer Leonard Hayflick. There is a mechanism built into each cell, kind of a hard drive clock that literally limits the number of times a cell can divide. This happens as a result of telomere’s controlling the stretch of DNA at the end of each and every chromosome.
First of all, we need to understand the importance of homocysteine levels; an amino acid. If you have high levels of this dangerous substance in your blood, you greatly increase your risk of heart disease, Alzheimer’s disease, Parkinson’s disease, impotence, and premature aging of your cells.
Homocysteine has been scientifically connected with the most common degenerative diseases of aging. Researchers discovered that high levels tripled the amount of telomere lenth that was lost during cell division; this triples the speed at which your body ages – levels can easily be measured through a simple blood test. The following nutrients are recommended to correct high homocysteine levels.
Connecting Vitamin B’s, Homocysteine, Aging, and Heart Disease
Your body needs Vitamin B’s to make hemoglobin to carry and increase oxygen within red blood cells to tissues. Tufts University researchers confirm that Vitamin B’s are vital to a healthy immune system, normal brain activity, and assist in preventing or slowing onset of diseases like Alzheimer’s, Dementia, and Parkinson’s. In women of childbearing age, especially those taking oral contraceptives, adequate amounts of Vitamin B’s are essential for healthy estrogen metabolism because the Pill adds more estrogen to your body and estrogen-dominance is a potentially serious condition we should do all we can to avoid.
Recent studies show those over age 60 with low Vitamin B levels were three to six times more likely to lose brain volume than those who had the highest levels of B’s. Oh great! We’re losing alot of “other” things in the aging process, we sure don’t need a shrinking brain.
A term “Vitamin B Complex” (1) actually refers to a family of eight distinct vitamins in one complex: thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7), folate (B9), and cobalamin (B12).
A deficiency of Vitamin B’s and folic acid, may increase your level of homocysteine, the amino acid normally found in your blood. Evidence shows that an elevated homocystein level is an independent risk factor for diseases of aging, including heart disease and stroke. In addition. high homocysteine may damage arteries or make it easier for blood clotting (platelets) to clump together and form a clot.
In future articles I’ll discuss other nutrients important to slow the aging processes, naturally.
(1) Vitamin B Complex is not expensive. It’s one of those anti-aging “tools” that should be included in everyone’s “health tool box” as well as for those who are under excessive stress…and who isn’t these days? Each tablet contains 100 mg. of each of the B’s along with 400 mcg of folic acid. One with each meal is usually adequate for adults over 50 and those under excessive stress. Under age 50, or those with low body weight, one a day is generally adequate unless diagnosed with an autoimmune disorder or a chronic illness.
Your Health Detective:
Uncovering Clues to Add LIFE to Your Years…NOT Merely Years to Your Life, Naturally
Dr. Gloria Gilbère (aka Dr. G), N.D., D.A.Hom., Ph.D.,
EcoErgonomist, Wholistic Rejuvenist
Creator of certificated courses to become a Wholistic Rejuvenist™ (CWR) and for post-graduate education for health professionals. Go to www.gloriagilbere.com and click on Wholistic Skin & Body Rejuvenation (WSBR™) for course outline. Available on-site at worldwide locations, and via distance-learning at your convenience globally.
Dr. Gilbère is renowned worldwide for her work in identifying and finding natural solutions to chemically-induced and inflammatory disorders, multiple chemical sensitivities, fibromyalgia, chronic fatigue, Gulf War Syndrome, and digestive disorders that defy conventional diagnosis and treatment. She consults worldwide via telephone and at her Institute in north Idaho. Visit her website at www.gloriagilbere.com for details about consulting with her
Fossel M “Telomerase and the aging cell: implications for human health” Journal of the American Medical Association June 3, 1998, pp. 1732-5
Sears A, Anti-aging; Wellness Research Foundation, Royal Palm Beach, FL
Xu et al. “Homocysteine accelerates endothelial cell senescence,” FEBS Letters 2000, vol 470, pp. 20-24.
Zglinicki T, “Telomeres
influencing the rate of aging.” Annals of the New York Academy of Science Nov 20, 1998, vol 854, pp. 318-27