Comprehensive Library Of Resveratrol News

Scientific dogma lays blame on chronic imperceptible low-grade inflammation as the cause of aging.  No, but inflammation IS a universal feature of aging.

Aiming at inflammation is akin to directing a fire extinguisher at the smoke rather than the fire.  What causes the inflammation?  The answer is not genes either, which are also involved but not causal.  Genes are not expressed (activated) or silence (switched off) on their own, but are influenced by minerals, largely iron, which is the most abundant metallic mineral in the human body.

The proper answer as to what causes inflammation is over-mineralization (iron, copper, calcium), which has been explained in the Overmineralization Theory of Aging.

When does inflamm-aging begin?

The term inflamm-aging was first coined in 2000 (Annals New York Academy Science, Volume 908: pages 244-54, 2000)  Since then, 227 reports have been published at the National Library of Medicine that refer to inflamm-aging.  Anatomically, inflamm-aging is largely going on in the gut bacteria and functionally in the immune system.

Human eye is observation post for aging

The human eye serves as the only internal organ that can be visualized directly to reveal aging changes, namely inflamm-aging.

Why don’t humans being to age biologically till after childhood growth is achieved?

There has to be an explanation as to why humans do not exhibit evidence of aging, as measured by accumulation of cellular debris called lipofuscin, during childhood growth years, then progressive deposition of lipofuscin in tissues (skin, brain, heart, etc.) with advancing age, and then finally somewhat static deposition of lipofuscin in the latter years of life.  The progressive deposition of lipofuscin and drusen in the human retina can be used as a biological clock.

During childhood growth iron is directed to the bone marrow to produce hemoglobin, the red pigment in blood cells.  Over 200 billion new red blood cells are produced per day.

The accumulation of iron in the body after full childhood growth is achieved (~age 18), first in males and later in females with cessation of menstrual blood losses, and the successful use of iron-binders, suggests aging of the retina and the entire body can be slowed, even reversed.

Cellular debris called lipofuscin is hallmark of aging

Lipofuscin is the hallmark sign of aging in the human retina.  Greater consumption of iron-rich red meat compared to white meat (chicken) is associated with early onset of retinal disease and vision loss.

Employment of iron chelators (key-lay-tors) or binders is proposed to delay or eradicate existing lipofuscin in the retina, thus reversing aging.  Oral iron chelators have been shown to protect the eyes from aging degeneration, but sadly chelation therapy is not practiced.

Older eyes exhibit greater deposition of lipofuscin and cholesterol deposits called drusen as well as used-up vitamin A (bis-retinoids) that is shed from night-vision rod cells every morning.

The appearance of these aging deposits is usually observed during an eye exam after age 50.  Drusen being the earliest sign of retinal aging, earlier appearance of drusen suggests premature aging.

Iron deposits in the retina hasten the onset of retinal drusen and lipofuscin.  Food restriction, which would result in less iron intake, has been shown to reduce lipofuscin accumulation, as has the use of bran which binds to iron.

Mineral chelators demonstrated

The successful use of oral mineral chelators (resveratrol/ copper; quercetin/iron; rice bran IP6/ calcium/iron/copper in Longevinex) was reported to clear visible lipofuscin from the retina with concomitant improvement in visual function in an 80-year old subject by researchers Stuart Richer and William Stiles in 2009.

The use of metal chelators (Longevinex®) was successfully demonstrated in the eyes of a middle-aged male with progressive drusen (cholesterol) in the retina beginning at age 44 with accompanying decline in vision in his only functional eye (the other eye being blind from birth).  Statin drugs were ineffective.

Dietary changes accompanied by use of oral metal chelators (Longevinex®) eradicated the drusen deposits, almost doubling the drusen-free area of his retina and improving his functional vision, as documented below (Eureka Alert, American Academy Advancement of Science, Oct 8, 2018)

Destructive macrophages are iron overloaded

When Dr. Claudio Franceschi and colleagues first used the term inflammaging, they also “proposed to return macrophages to their rightful place as central actor not only in the inflammatory response and immunity, but also in stress response.”

Macrophages are large white blood cells that engulf or devour foreign matter, bacteria, viruses, dead red blood cells, cellular debris and loose destructive minerals (namely iron and copper).   In the human retina, cells called glia are another name for macrophages.  When macrophages are over-responsive, they bang into each other, induce inflammation, and release iron.

Macrophages (glia) in the retina and elsewhere in the body accumulate and release iron, becoming a destructive form of macrophage called M1.  Excess unbound iron, delivered by macrophages (glia in the retina), orchestrates inflammation.  Again, chelation (iron removal) is the antidote to prevent age-related vision loss and aging in general.  Humans age because they rust.  Therefore, anti-rusting agents (metal chelators) are appropriate to prolong healthspan and lifespan.