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  • Bill Sardi answers questions about efforts to increase the human healthspan and lifespan

    December 9, 2014: by Bill Sardi

    Q. Why do you say human aging progress at three different speeds?

    A. I think of all the various theories about why humans age, the antioxidant theory, the hormonal theory, the wear-and-tear theory, the mitochondrial theory, the telomere theory, the immune theory, (there are many more), none of them help explain why humans age at three different speeds.  Whatever theory of aging that is put to the test should consider this fact.

    The 3-speeds of human aging idea springs from studies that measure the rate of deposition of cellular “garbage.” The buildup of “toxic waste” is said to be responsible for the curse of aging. [Science Aging Knowledge & Environment Feb 2, 2005]

    The many hundreds of energy-producing mitochondria within living cells become damaged over time and cellular debris from the mitochondria becomes an aging pigment known as lipofuscin (LIE-po-FUSS-in — how to pronounce). As one research report explained it, this leads “to what has been appropriately named a ‘garbage catastrophe’.” [Science Aging Knowledge Environment Feb 2005]

    It is widely accepted by researchers who study human aging that tissues accumulate lipofuscin at the rate they age. [Science Aging Knowledge & Environment Feb 2, 2005]

    The accumulation of lipofuscin, a fine granular yellow-brown pigment, is an unequivocal hallmark of aging. [Free Radical Biology Medicine Sept 2002]

    When fruit flies are fed lipofuscin this results in significant reduction of health span and life span. [Free Radical Biology Medicine Dec 2013]

    In a premature aging syndrome known as progeria where young children develop cataracts, baldness, wrinkled skin and arthritis, an accumulation of lipofuscin is noted in many organs including the heart, liver, kidneys, eyes, and adrenal glands. []

    If aging is measured by the rate of accumulation of cellular debris (lipofuscin), then there is little or no aging of accumulation of lipofuscin observed under a microscope in living cells during the growing years (the first 18 years of life); there is progressive buildup of lipofuscin in the adult years; and then the rate of aging flattens out in old age. [Mechanisms Ageing & Development March 1, 1990]

    The only theory of aging that explains this three-speed accumulation of cellular debris is the over-mineralization theory of aging.

    The lipofuscin accumulation rate (and therefore the speed of aging) is largely determined by available the amount of iron and copper. During childhood growth there is a tremendous demand for iron to produce red blood cells, copper to make connective tissue and calcium to make bone. But once childhood growth is achieved, these minerals begin to slowly accumulate.

    After childhood growth is completed males accumulate and store 1 excess milligram of iron per day of life. Females lose iron, about 30 milligrams per month or 1 milligram per day via menstrual flow and therefore are protected from iron overload though a significant percentage of young fertile females will be anemic. By age 40 males have double the amount of iron stored in their body compared to an equal-aged female and experience double the rate of diabetes, cancer and heart disease.

    It is iron accumulation within cellular compartments called lysosomes, organelles that are designed to enzymatically clean up cellular debris, that results in deposition of lipofuscin. The use of iron chelators (key-lay-tors) is proposed to reduce lipofuscin formation. [Rejuvenation Research April 2008]

    An interesting finding is that longevity depends upon the self-eating process dubbed autophagy. Defective autophagy results in deposition of lipofuscin. Nutraceuticals like resveratrol enhance autophagy and increase lifespan. [Journal Cellular Molecular Medicine Nov 2010]

    The enzymatic process of cleaning up living cells via small intracellular organs called lysosomes may result in generation of destructive free radicals. This “self eating” process (called autophagy) may be incomplete and degradation of proteins that binds with metals (called metalloproteins) may release iron and copper in a destructive manner. Unbound iron and copper may also fuel cancer cells. Iron and copper binders (chelators) would be the antidote for this problem. [Antioxidants Redox Signaling Aug 15, 2010]

    Some researchers suggest if clean up of cellular debris (lipofuscin) was a perfect process “several age-related diseases would, perhaps, not take place.” [Histochemistry Cellular Biology April 2008]

    What evidence do we have that the over-mineralization theory of aging can be put into practice in humans?

    Experimentally the non-disruptive removal of lipofuscin from the brain has been demonstrated in animal experiments. [Neurobiology Aging Jan 2005] Despite claims that lipofuscin is not dissolvable at least we know it is experimentally possible to remove lipofuscin and slow or even reverse biological aging.

    In a real life situation, the traditional diet of the Japanese compared to natives of Japan who live in Hawaii produces different rates of aging as evidenced by lipofuscin deposition. Lipofuscin accumulation was greatest among Hawaii-based Japanese compared to natives. [Mechanisms Ageing Development Feb 1980]

    Of course it is widely known that calorie restricted diets inhibit the formation of lipofuscin in animals. [Rejuvenation Research Feb 2010] So we could all deprive ourselves of food to live longer. However calorie restriction is not expected to be widely adopted by even the most ardent longevity seekers.

    One of the most striking and yet overlooked studies conducted in the anti-aging arena is University of Washington researchers in Missouri compared an ad libitum (eat as much as you like) diet with a 40% calorie restricted diet and a third group of lab animals who ate an ad libitum diet + oat bran. Thhe oat fiber diet fed ad libitum was almost as effective as restriction of total food intake in slowing lipofuscin accumulation (a marker of aging). [Investigative Ophthalmology Vision Science Nov 1993]

    This study means that selection of foods that contain mineral controlling molecules rather than overall food deprivation may produce the same effect.

    The female advantage

    As baby carriers for the human species females are protected from disease and aging by estrogen. In fact, estrogen is known as a youth molecule.

    Animal lab studies show that estrogen replacement reverses and prevents some of the changes associated with aging. [Journal Aging Research 2011]

    It is interesting to note that menopausal women taking estrogen replacement experience decreased deposition of lipofuscin. [Biogerontology 2005]

    Estrogen reverses some of the aging changes in the brain (lipofuscin deposition). [Neuroscience Letters Sept 8, 2011]

    Lipofuscin and the nervous system

    One of the difficult realities of growing old is that critical organs needed to maintain independence, such as the eyes and brain, may aged faster than the rest of the body. Anti-aging strategies need to focus on these critical organs of the nervous system such as the braina and eyes.

    Lipofuscin-like deposits are found in red blood cells of patients with Alzheimer’s disease, which suggests a disease specific marker in the blood that could be used for early detection. [Experimental Gerontology Jan 2011]

    The accumulation of lipofuscin in the human retina is the first sign of retinal aging and contributes to the disease known as macular degeneration. [Journal Biological Chemistry Sept 2008] Accumulation of retinal lipofuscin begins in the first decades of life but a more toxic form of lipofuscin known as A2E rapidly accumulates later in life that coincides with the geriatric onset of the disease.

    Formation of lipofuscin is a result of the process of autophagy releasing iron and copper that can result in cell death in the retina, the thin film that processes light images at the back of the eyes. In the example of macular degeneration, an age-related disease, a critically important single-cell layer known as the retinal pigment epithelium resists this aging process (flawed autophagy) till late in life. Severe release of worn out parts of light receptor cells doesn’t occur till late in life. [Experimental Eye Research Nov 2013]

    The accumulation of toxic lipofuscin, known as A2E, then sensitizes the retina to solar blue-light damage. [International Journal Biochemistry Cell Biology Aug 2004]

    The human eye provides a non-invasive visual pathway to observe and measure the accumulation of lipofuscin. Dissipation of lipofuscin in the eye would provide evidence that age-reversing strategies are at work.

    Dr. Stuart Richer at the Veterans Health Center in North Chicago has had opportunity to test a commercially available resveratrol pill and reports that it reduces visible lipofuscin from the human retina that correlates with visual improvement. [Optometry Dec 2009; Nutrients June 4, 2013; Nutrients Oct 2014] We have entered a new era of reversing biological time. – ©2014 Bill Sardi,

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