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  • Update: How To Put Your Anti-Aging Pill To The Test

    August 26, 2014: by Bill Sardi

    Despite the fact a Harvard researcher has recently been quoted to say the secret to halting the aging process is much closer than we think and that “there is no limit on the human lifespan,” [Yahoo News Aug 19, 2014], it is difficult if not impossible to conclusively prove so-called anti-aging pills will produce superlongevity because a 100-year study would be required.

    To underscore this dilemma Longevinex® offers a tongue-in-cheek guarantee. If Longevinex® consumers live 100 years they can mail in a copy of their birth certificate and they will receive a complimentary supply for the remainder of their lives. However, if Longevinex ® does not result in a 100-year lifespan consumers can mail in their proof of purchase and receive a full refund :).

    Markers of aging

    Short of conducting decades-long studies that would be impractical and unaffordable, there are biological markers of aging that may suffice to prove bona fide anti-pills are at hand.

    Resveratrol-based dietary supplements are known as molecular mimics of a calorie-restricted diet. Limited calorie diets have been demonstrated to double the lifespan and healthspan of laboratory animals. [Journal Nutrition July 2010] Having been shown to switch 82% of genes altered by a limited calorie diet, Longevinex® is presently the closest proven mimic of a life-prolonging diet. [Experimental Gerontology Sept 2008]

    The overmineralization theory of aging

    However, as has been conclusively shown, it is the rate at which the human body accumulates minerals and not consumption of calories that governs the speed of aging. Two biological experiments reveal this:

    The first is a study where laboratory animals were fed a 40%-reduced calorie diet and compared against animals given a diet rich in oat bran, which contains a mineral controlling molecule called phytic acid (aka phytate or IP6). The oat fiber bran diet decreased the accumulation of aging pigment called lipofuscin almost equally as well as a limited calorie diet. [Investigative Ophthalmology Nov 1993] Accumulation of lipofuscin is considered a hallmark of aging. [Diabetologia Feb 2010]

    The second study demonstrated that calorie restriction did not produce longevity nor reduce the number of aging deposits in the brain but did reduce the number of aging deposits in the brain when a standard calorie diet with low metallic mineral content (iron, copper) was compared against a diet where animals ate a restricted calorie diet with added minerals. [Biogerontology 2004]

    This means longevity seekers may not have to deprive themselves of food and join The Calorie Restriction Society but may be able to mimic such effects with an oral pill.

    The following section of this report further briefly addresses the validity of the overmineralization theory of aging. The Overmineralization Theory of Aging is also more fully described at the Longevinex website. []

    Why does human aging progress at three different speeds?

    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), none of them help explain why humans age at three different speeds.

    If aging is measured by the rate of accumulation of cellular debris (called lipofuscin), an agreed-upon marker of aging, then there is little or no aging 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. If you look through a microscope at young cells you see very little if any lipofuscin. So humans are having birthdays during their growth years but not getting old biologically.

    That is because calcium from the diet is being directed toward growing new bone, iron to make new red blood cells and copper to make connective tissue during the growth years.

    Once growth ceases then these minerals slowly accumulate. Iron accumulates at the rate of 1 milligram per day of life during adulthood in males but young females will lose about 30 mg of iron in their monthly menstrual flow and donate calcium to their babies, and therefore don’t really begin to age (calcify and rust) till the onset of menopause. This explains why females generally live longer than males. [The Iron Time Bomb 1990]

    By age 40 a male has accumulated and stored twice as much iron and four times as much calcium as an equally-aged female and incurs double the rate of diabetes, heart disease and cancer. If a female undergoes early hysterectomy she experiences the same rate of disease as males.

    Consistent with the overmineralization theory of aging, early surgical hysterectomy increased ferritin (iron storage) levels in the brain [Neurobiology of Aging Sept 2012] and other organs.

    Overmineralization drives the speed of aging. Mineral chelators (key-lay-tors) prolong life. So does blood-letting (blood donation) to reduce iron stores. [Journal Cancer Epidemiology Dec 2013]

    Human population studies validate this. Countries where there is water and grassland to feed cattle (Scandinavia, Ireland, North America, New Zealand) consume more iron-rich red meat and calcium-rich dairy and have the highest rates of heart disease and cancer.

    What valid markers are there for aging that can be used today?   

    Since it is both impractical and too expensive to conduct a life-long (80-90 year) human longevity study, biologists are left to assess biological markers of aging.  There are a number of valid markers of aging.  These include but are not limited to (1) lipofuscin accumulation (cellular debris), (2) iron accumulation (measured as ferritin), and (3) red blood cell width.

    Lipofuscin and aging

    Lipofuscin aging pigment is a recognized hallmark of aging and the rate of its accumulation correlates with longevity. (For a view of its appearance under the microscope click here.)

    It is formed when compartments within living cells called lysosomes begin to accumulate metals and no longer efficiently clean up cellular debris via enzymatic processes. [Redox Reports 2001] Lipofuscin begins to accumulate in mammals upon full sexual maturation and physical growth is achieved [Mechanisms Ageing Development March 1990] which correlates with the overmineralization theory of aging.

    Lipofuscin can be experimentally increased by exposing cells to greater oxidation and reduced by iron-chelating antioxidants. Lipofuscin can generate free radicals and gene mutations. Once formed lipofuscin is believed to be non-degradable though exceptions are noted. [Free Radical Biology Medicine Sept 2002] For example, elimination of lipofuscin from the human retina has been previously demonstrated. [Neurobiology Aging Oct 2012]

    Certainly lipofuscin generates free radicals (oxidation) and cell senescence (cells don’t duplicate any more). Metal chelators such as resveratrol have been demonstrated to prolong the life of killfish and reduce lipofuscin. [Experimental Gerontology Dec 2012]

    Quantifying the accumulation of lipofuscin in living tissues poses practical problems. However, while lipofuscin would generally require a tissue biopsy to quantify, there may be a non-invasive way to measure it.

    Dr. Stuart Richer OD, PhD with the Rosalyn Franklin School of Preventive Medicine and the North Chicago Veterans Hospital, using direct images of the back of the eyes, has demonstrated that lipofuscin deposits can be reversed via use of oral mineral chelators. His work started with an 80-year old male with failing night vision who was given a nutraceutical (Longevinex®) for 5 months. The patient experienced dramatically improved vision and lipofuscin deposits were measurably reduced as visualized with retinal photography. This approach awaits technology that will quantify rather than just guesstimate the degree of lipofuscin deposits in the human eye. [Optometry Dec 2009]

    Iron accumulation (ferritin) and aging

    Another way individuals taking anti-aging pills can test the effectiveness of these anti-aging pill is to obtain a ferritin blood test.

    Ferritin, the iron storage protein, can also be used as a measure of aging though it is sometimes elevated due to chronic infection, inflammation or malignancy which can skew its interpretation. Since iron promotes inflammation and the growth of germs and cancer cells, the body binds up iron in the ferritin molecule to counter the spread of disease.

    More than three decades ago it was reported that there is a tendency for iron-stores to increase with advancing age and that iron storage levels (ferritin) were generally higher in males than females, which helps to explain why men have shorter lifespans than women. Ferritin is a protein the binds and stores iron in the body as excesses accumulate. [Age Ageing May 1981]

    One study showed that the average ferritin level was found to be 108.0 in males and 26.4 in females among adults over various ages. Ferritin numbers remained low for women into their 40s which was attributed monthly iron losses in menstrual flow whereas ferritin levels rose for males between age 20 and 50. Low ferritin levels were rarely found among women over age 50. [Japanese Journal Clinical Pathology May 1991] Other studies also confirm that blood serum ferritin levels rise in the late teens in men and after menopause in women. [American Heart Journal 2012]

    Healthy ferritin levels should fall between 20-70 nanograms per milliliter of blood. [Journal Molecular Biology Sept 2004]

    There is also difficulty in interpreting high ferritin levels because ferritin levels rise even in a state of iron deficiency. Also unbound iron is a source of inflammation and ferritin levels rise in order to limit inflammatory reactions. Since inflammation is regarded as a mechanism of aging (“inflammaging”), it is important to assess ferritin levels. Ferritin levels may be more important in assessing inflammation than other tests such as C-reactive protein. [European Geriatric Medicine Oct 2012]

    Since iron has been called the predominant “malignant spirit” in aging [Ageing Research Reviews Jan 2003] it would serve to know the major sources of iron in the human diet. Iron dietary supplements and red meat are the two primary sources of highly absorbable iron whereas whole grains that provide bran decrease absorption of dietary iron. [American Journal Clinical Nutrition Dec 2002]

    If ferritin levels are deemed to be excessively high there are a variety of ways to limit its intake and/or remove existing stores. These are (1) blood-letting; (2) limiting red meat consumption and iron in multivitamins; (3) avoidance of ascorbic acid (vitamin C) with meals since vitamin C increases iron absorption from the diet; (4) use of iron chelators with meals such as from beverages (tea, coffee), from the diet (bran from whole grains) or from dietary supplements (IP6 rice bran extract, quercetin).

    Don’t be alarmed if you find your ferritin level is unusually high. This may mean you have underlying infection or inflammation and may be a temporary condition.

    Red blood cell width distribution

    Red blood cell width was first recognized as a marker of human mortality in 2009, though it has been known that red blood cell width increases with advancing age since 1972. [British Medical Journal Feb 26, 1972]

    Wider red blood cells indicate accelerated aging and are associated with increased morality rates from all causes. [Archives Internal Medicine March 23, 2009]

    One must ask why the research community is mired in the animal lab attempting to prove or disprove various interventions that slow the rate of ageing? The intriguing aspect of red blood cell width as a marker of human aging is that is a widely available and economical off-the-shelf test performed every day with the aid of a Coulter counter in blood laboratories. [Wallace H Coulter Foundation]

    If red cell width can be deemed to be a valid marker of progressive human aging then lab dish analysis of living cells and laboratory studies involving animals can be skipped over and researchers can go directly to human studies involving red blood cell width.

    Red cell width is associated with all-cause mortality. [Cardiology June 2014; European Journal Preventive Cardiology Jan 8, 2014] And Red cell width is predictive of long-term prognosis for survival. [BMC Cardiovascular Disorders Dec 10, 2013]

    Of particular interest is that red blood cell width has been correlated with telomere length in white blood cells. [PLoS One Dec 4, 2012] It is also widely known that telomere lengths are longer in centenarians (and their offspring). [Experimental Gerontology June 27, 2014] Telomeres are end caps that protect the ends of chromosomes. As a person ages the width of their red blood cells expand and their telomeres shorten.

    Males have significantly shorter telomere lengths than females, [PLoS One Dec 4, 2012] which is again consistent with the overmineralization theory of aging (males are more iron overloaded).

    Human red blood cells usually fall within the range of 6-8 micrometers in diameter. However red cell width measures the deviation of the red blood cell width, not the actual width or size of individual cells. They generally vary in an individual by 11.0 to 15.0%. A high red cell width variation (over 14.5%) means that the red blood cells vary a lot in size. A red cell width variation below 10.2% means that the red cells vary very little in size. To understand more how red blood cell width is defined and calculated, click here.

    Given the unexplained foot dragging by researchers in the field of aging over measurement of red blood cell width variance, a pilot human clinical study has been launched using Longevinex® in a 6-month study to measure red cell width. The study should be completed before the end of 2014 and results reported.

    Serious longevity seekers can go to a local blood testing lab and order up a complete blood count (CBC) that includes measure of red blood cell width variance and test this over time and determine how well their anti-aging regimen is working. It would be wise to have a lab draw an extra tube of blood for a ferritin test at the same time.

    Be aware, some people have been taking resveratrol pills now for more than ten years. Long-time users of anti-aging nutraceuticals may not produce marked differences in ferritin and red cell width variation as new users. ©2014

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