What resveratrol promises Longevinex® delivers



  • A unifying theory of aging

    Jan 03 2007

    Longevinex® is more than resveratrol

    Ingredients in Longevinex® address the many theories of aging.

    While resveratrol has recently gained widespread public and scientific attention for it age prolonging qualities, Longevinex® is a unique multi-ingredient dietary supplement that is more than just resveratrol.

    The ingredients in Longevinex® are designed to address five major theories of aging: the free radical/antioxidant theory, the hormonal theory (estrogen/testosterone), the mitochondrial (cell energy) theory, the cell cleansing or autophagy theory, and the metabolic, calorie restriction/Sirtuin gene activation theory.

    There is another theory of aging, also addressed by the ingredients in Longevinex®, which may supercede and better explain other theories of aging.  It is proposed here.

    Introduction: Why slow aging?

    There are many theories as to why humans age prematurely and what can be done to slow the rate of aging.  Slowing the onset of aging is critically important since most chronic disease is age related.  A recent goal was announced by a consortium of researchers involved in the study of human aging.  The objective is to delay the onset of aging by seven years, thus pushing off the onset of age-related disease and adding more healthy years of life, which would save Medicare from its predicted financial demise.

    The idea of living more youthful years is now at hand since the mapping of the human genome and the knowledge that individual genes control aging.  Increasing the healthspan and lifespan is within reach, as these strategies improve both the quality and quantity of life.

    Despite the fact more Americans are overweight and have diabetes (now coined the diabesity epidemic), more Americans are living longer than ever thought possible.  About one in four 65-year old adults will live to age 92 or beyond. That is a staggering figure.

    In recent times it has become apparent that humans can immediately begin to put into practice certain age-delaying tactics, the most prominent and accepted anti-aging regimen being calorie restriction.  While food deprivation is not likely to be widely practiced, its molecular mimic, resveratrol, is now being touted as a metabolic shortcut to avert the frailties and senility associated with advanced age.  For example, a recent experiment demonstrated that resveratrol-fed mice given a high-fat diet retained their motor skills (balanced and coordination) as well as mice on a lower-calorie diet.

    While resveratrol has broad biological action, it does not fully address all of the major biological pathways to control aging.

    Major theories of aging

    • Antioxidant/free-radical theory
    • Hormonal theory
    • Mitochondrial mutation theory
    • Cell debris/cleansing theory (autophagy)
    • Calorie-restriction or resveratrol mimic theory of aging

    An alternate and unifying theory of aging

    There is another theory of aging, proposed here, which has been overlooked – over-mineralization.  The rate of over-mineralization in the human body parallels the rate of aging.

    The gradual overload of minerals, particularly calcium and iron, which are the predominant minerals in bone and blood, explain a great deal of aging, and partially if not totally explain the free radical, the mitochondrial, the hormonal and the calorie-restriction theories of aging.

    As an oversimplification, the human body rusts and calcifies (turns into a statue) over time.

    Calorie restricted diets and vegetarian diets are known to prolong human life and both obviously limit the amount of calcium and iron consumed.

    When does aging begin?

    During the years of growth, birthdays occur, but aging really doesn’t begin till full growth is achieved, usually around age 18.  Birthdays occur, but aging changes in tissues don’t accelerate till full growth is achieved.


    Lipofuscin aging pigments, seen above, are generated by
    excessive iron and are increasingly found in tissues throughout
    the human body with advancing age.

    For example, the amount of an aging pigment (called lipofuscin) within the cytoplasm of rabbit cells is miniscule, representing only 0.29% of the cytoplasm volume at 12 months of life, whereas it reaches 2% of cytoplasm volume at 79 months (7 times increase).

    During growth years, all of the iron that is ingested is directed toward the production of new red blood cells (millions must be produced every second) and calcium is shuttled to develop bones.  So it is very difficult to develop iron or calcium overload during youth.  In fact, this may explain why the first two decades of life are largely free of disease.

    Even the symptoms of hereditary iron overload (hemochromatosis) do not emanate till age 12-18.

    Accumulation of cellular debris (lipofuscin) at the back of the human eye (retina) does not begin till age 19.

    Retinal lipofuscin deposits, induced by iron and calcification in retinal tissues, are generally not found until the 3rd decade of life, and more advanced cellular garbage deposits in the retina, called drusen, aren’t normally observed during an eye examination till the 5th decade of life.

    Retinal drusen

    Retinal drusen, seen early in child
    with premature aging syndrome.

    Retinal drusen was reported in a young girl with a premature aging syndrome (Bloom syndrome).  The girl was admitted to the hospital for failure to grow.

    Progeria is considered a disease of premature aging.  It is characterized by calcification of arteries and heart valves.  Generally, children with progeria are of short stature (~3 feet in height) and their demand for calcium for bone formation is reduced compared to healthy children.

    When full is growth achieved, the demand for iron and calcium diminishes and excesses can begin to accumulate.

    Gradual iron overload

    Most well-nourished people in developed countries have 3-4 grams (3000-4000 milligrams) of iron in their bodies. Of this, about 2.5 grams (2500 milligrams) is contained in the red blood cell hemoglobin pigment that carries oxygen as blood circulates through arteries and veins.  As red blood cells die, their iron is recycled to bone marrow to make new blood cells.

    About 1 milligram of excess iron accumulates daily in males after full growth is achieved, which results in about 5000-8000 excess milligrams of stored iron in a male by age 40.  A 45-year old male has as much iron in his blood circulation as a 70-year old female.  At age 45 a male has four times as much iron stored in his body as females at this age, and has a heart attack rate four times that of women.

    A female however will dump excess iron via monthly menstruation (about 30 milligrams) and have half the iron load of a male at age 40.  Iron overload results in middle age males having twice the iron load as an equal-aged female and twice the rate of diabetes, cancer and heart disease.  If females undergo early hysterectomy, then they will develop the same disease rates as males.  In females iron overload begins much later, with menopause, and women live on average about 5-8 years longer than men.


    FEMALES: High demand for calcium and iron
    during growth and reproductive years

    Proof of the theory of over-mineralization and aging


    Calcium is the most abundant mineral in the body.  Of the two to three pounds of calcium contained in the human body, 99% is located in the bones and teeth.

    There are inborn ways to limit calcification in nature.  For example, elk avoid over-calcification by periodically shedding its antlers.  Female mammals avoid over-calcification by donating calcium to their offspring.  Later in life, as estrogen production wanes, calcium is released from women’s bones and enters the blood circulation where it clogs and hardens arteries (arteriosclerosis), the gallbladder (gallstones), heart valves (mitral valve), and kidneys (kidney stones).  The main source of the calcium deposits is the bones.  Over time, there is loss of calcium from bones, which become brittle and fracture (osteoporosis).

    Artery with small amount of calcified plaque

    Artery with small amount of calcified plaque

    Many studies confirm the problem of over-calcification in humans.  In a study of 582 aortas from humans (the aorta is the first blood vessel outside of the heart), it was shown that only 4% of patients aged 20–30 years had significant aortic calcification, which increased to 98% in individuals above 50 years.

    It is suggested that the calcium content of arteries may increase 30 to 40 times in a lifespan.

    Calcification of the aorta (first blood vessel outside of the heart) is greater and progresses faster among women who experience calcium/bone loss with the onset of menopause.

    The Klotho gene is involved in longevity.  Activation of the klotho gene extends the life of mice by 19-31%.
    It is interesting to note that a defect in the expression (activation of proteins) of the Klotho gene in the mouse, which results in extensive calcification and loss of elasticity of the aorta, produces a syndrome that mimics human aging. Furthermore, iron overload switches off the Klotho gene, while iron chelation re-activates the production of Klotho gene proteins.

    Calcification of the pineal gland

    The body’s clock or synchronizer is the pineal gland, located at the base of the brain.  At night, when the eyes are closed, the pineal gland secretes a strong antioxidant hormone, melatonin, which also induces sleep.  Melatonin has drawn great attention as an anti-aging hormone. With calcification of the pineal gland comes reduced production of melatonin. Calcification of melatonin-producing cells in the pineal gland is more prevalent in old versus young animals.

    Over a decade ago it was demonstrated that the replacement of the pineal gland of an old mouse with the pineal from a young, donor mouse, remarkably prolongs its life and, conversely, the “old” pineal gland transplanted into a younger mouse will considerably shorten its life span.

    The pineal gland, located at the base of the brain, secretes melatonin during sleep.  This hormone has strong reparative and antioxidant properties and also controls sleep.  Melatonin levels decline gradually over the life-span and are related to sleep problems, very often associated with advancing age.

    The increasing degree of pineal calcification may result in a decrease in melatonin secretion by the pineal gland, which subsequently may lead to a disturbed sleep-wake cycle, with the principal symptom being daytime tiredness, often experienced among older adults.

    A theory was presented in 1990 that the pineal gland is a centralized clock that controls aging, and that the calcification process occurring within the pineal gland “provides a highly accurate bio-inorganic timing mechanism.”

    Researchers indicate melatonin is a prime candidate for slowing the aging process. Melatonin is described as having profound “gerontoprotective” and antioxidant activities.  Supplementation with melatonin “may become a promising, safe, and effective intervention strategy to slow aging and the initiation and progression of age-related disorders.”

    In postmortem examination of 33 human subjects (age range 3 months to 65 years), calcium deposits in the pineal gland correlated with advancing age and calcium levels correlated with a decline in melatonin content.

    Even though oral melatonin supplementation has proven to help with sleep problems, low melatonin levels are not related to sleep disturbances, nor does it predict response to melatonin replacement therapy.  Researchers theorize individual differences in body and glandular size confounds an accurate understanding of melatonin biology.  In Germany a method was devised to measure the degree of pineal gland calcification using computed tomography.  The size of the pineal gland and its uncalcified volume was estimated and was correlated with melatonin levels.  Researchers concluded that the decline in melatonin secretion with advancing age “can be sufficiently explained by an increase in pineal calcification.”

    Of great interest is the discovery, that while some calcification of the pineal gland occurs in the first six years of life, there is a steep rise in the incidence of pineal calcification during the second decade of life, which coincides with slower body growth rates. A study shows that the frequency of pineal calcification is 3% in the first 12 months of life rising gradually to 7.1% in children at 10 years of age. From 10 years onwards, there is a marked increase of frequency of calcifications of the pineal gland up to 33% in the group of children of 18 years of age.