Annie Sawyer, Ph. D.
(Round Table Discussion)
At a symposium that took place at the International Association of Gerontology and Geriatrics 19th World Congress, held in Paris, (July 5-9, 2009), the father of the oxidative theory of aging, Dr. Leonard Hayflick, stated, ”Aging occurs because the complex biological molecules of which we are all composed –mitochondria- become dysfunctional over time as the energy necessary to keep them structurally sound diminishes, thus our molecules must be repaired or replaced frequently by our own extensive repair systems”. The repair body systems, which are also composed of complex molecules, eventually suffer the same molecular dysfunction. The time when the balance shifts in favor of the accumulation of dysfunctional “ waste “ molecules is determined by natural selection — and leads to the manifestation of age changes that we recognize are characteristic of an old person or animal. These fundamental molecular dysfunctional events lead to an increase in vulnerability to age-associated chronic degenerative diseases.
Aging is explained as a waste-full process. In youth, autophagy (a controlled “self-destruction” or “self-eating”) removes and recycles cellular waste that would otherwise compromise cellular function and regeneration of replacement structures. In the mitochondria, which are easily damaged due to their role as the main energy factories in cells and can themselves become a key source of cellular damage, adequate “autophagic” waste recycling is critical for rejuvenation but diminishes in aging cells. Wulf Dröge and other researchers have postulated that the aging-associated decline of mitochondrial autophagy or “mitophagy” may be the first most limiting mechanism that determines maximum life span in most animal species, including man.
Obviously, the key point made by Hayflick, about the theory of “biological aging” is no longer an unsolved problem. It means that the body's “repair and maintenance” systems are the primary determinants of longevity. These repair systems, which are also composed of complex molecules, eventually suffer the same molecular dysfunction. The time when the balance shifts in favor of the accumulation of dysfunctional molecules is determined by natural selection — and leads to the manifestation of age changes that we recognize are characteristic of an old person or animal. It must occur after both reach reproductive maturity, otherwise the species would vanish. These fundamental molecular dysfunctional events lead to an increase in vulnerability to age-associated disease therefore, the study, and even the resolution of age-associated diseases, will tell us little about the fundamental processes of aging.
The question then becomes, “What causes these systems to lose their ability to outpace the damage of daily life?” Hayflick believes that the shift is determined by natural selection, suggesting little can be done to extend lifespan. Dröge has proposed an alternate, much more optimistic, explanation: the shift from a homeostasis of repair to one of snowballing damage is due to the age-related onset of aberrant insulin signaling, which prevents autophagic recycling. Aging occurs because the complex biological molecules of which we are all composed become dysfunctional over time as the energy necessary to keep them structurally sound diminishes, thus our molecules must be repaired or replaced frequently by our own extensive repair systems.
Mitochondrial decay resulting from oxidative damage accumulates with age and is universally recognized as a major contributing factor to the whole range of functional decline and tissue deterioration associated with aging.Aging-associated increases in oxidative damage to key enzymes results in their structural deformation and decreased binding affinity for the co-enzyme, causing a decrease in enzyme function. Ames’ research has demonstrated that increasing the availability of acetyl L-carnitine and α-lipoic acid, two nutrients that serve as mitochondrial enzyme co-factors, restores the velocity of the reactions (KM) in the related enzymes, and thus restores aging mitochondria’s ability to produce youthful levels of ATP. His study also focused on the inter-relationships among the folate, methylation and transsulfuration pathways, whose dysfunction results in increased free radical production coupled with disruption of glutathione (GSH) synthesis, thus accelerating mitochondrial decay and aging.
Ensuring adequacy of the entire nutrient co-factors portfolio, necessary to restore KM in these pathways, as well as in mitochondrial oxidative phosphorylation, is first line therapy for promoting healthy and graceful anti-aging. However, a protocol whose end goal is restoration of KM, while certainly helpful in delaying mitochondrial decay, does not address the more fundamental issue – why does human physiology shift from a homeostasic state that repairs and balances itself to one that allows decay to accumulate? Dröge has called this shift “the first cause of death,” and his insight into its likely causes may both explain why calorie restriction increases longevity and provide a much less onerous way to opt out of the vicious cycle responsible for the age-associated transition from a state of youthful homeostatic repair to one that promotes mitochondrial decay.
(Round Table Discussion)
At a symposium that took place at the International Association of Gerontology and Geriatrics 19th World Congress, held in Paris, (July 5-9, 2009), the father of the oxidative theory of aging, Dr. Leonard Hayflick, stated, ”Aging occurs because the complex biological molecules of which we are all composed –mitochondria- become dysfunctional over time as the energy necessary to keep them structurally sound diminishes, thus our molecules must be repaired or replaced frequently by our own extensive repair systems”. The repair body systems, which are also composed of complex molecules, eventually suffer the same molecular dysfunction. The time when the balance shifts in favor of the accumulation of dysfunctional “ waste “ molecules is determined by natural selection — and leads to the manifestation of age changes that we recognize are characteristic of an old person or animal. These fundamental molecular dysfunctional events lead to an increase in vulnerability to age-associated chronic degenerative diseases.
Aging is explained as a waste-full process. In youth, autophagy (a controlled “self-destruction” or “self-eating”) removes and recycles cellular waste that would otherwise compromise cellular function and regeneration of replacement structures. In the mitochondria, which are easily damaged due to their role as the main energy factories in cells and can themselves become a key source of cellular damage, adequate “autophagic” waste recycling is critical for rejuvenation but diminishes in aging cells. Wulf Dröge and other researchers have postulated that the aging-associated decline of mitochondrial autophagy or “mitophagy” may be the first most limiting mechanism that determines maximum life span in most animal species, including man.
Obviously, the key point made by Hayflick, about the theory of “biological aging” is no longer an unsolved problem. It means that the body's “repair and maintenance” systems are the primary determinants of longevity. These repair systems, which are also composed of complex molecules, eventually suffer the same molecular dysfunction. The time when the balance shifts in favor of the accumulation of dysfunctional molecules is determined by natural selection — and leads to the manifestation of age changes that we recognize are characteristic of an old person or animal. It must occur after both reach reproductive maturity, otherwise the species would vanish. These fundamental molecular dysfunctional events lead to an increase in vulnerability to age-associated disease therefore, the study, and even the resolution of age-associated diseases, will tell us little about the fundamental processes of aging.
The question then becomes, “What causes these systems to lose their ability to outpace the damage of daily life?” Hayflick believes that the shift is determined by natural selection, suggesting little can be done to extend lifespan. Dröge has proposed an alternate, much more optimistic, explanation: the shift from a homeostasis of repair to one of snowballing damage is due to the age-related onset of aberrant insulin signaling, which prevents autophagic recycling. Aging occurs because the complex biological molecules of which we are all composed become dysfunctional over time as the energy necessary to keep them structurally sound diminishes, thus our molecules must be repaired or replaced frequently by our own extensive repair systems.
Mitochondrial decay resulting from oxidative damage accumulates with age and is universally recognized as a major contributing factor to the whole range of functional decline and tissue deterioration associated with aging.Aging-associated increases in oxidative damage to key enzymes results in their structural deformation and decreased binding affinity for the co-enzyme, causing a decrease in enzyme function. Ames’ research has demonstrated that increasing the availability of acetyl L-carnitine and α-lipoic acid, two nutrients that serve as mitochondrial enzyme co-factors, restores the velocity of the reactions (KM) in the related enzymes, and thus restores aging mitochondria’s ability to produce youthful levels of ATP. His study also focused on the inter-relationships among the folate, methylation and transsulfuration pathways, whose dysfunction results in increased free radical production coupled with disruption of glutathione (GSH) synthesis, thus accelerating mitochondrial decay and aging.
Ensuring adequacy of the entire nutrient co-factors portfolio, necessary to restore KM in these pathways, as well as in mitochondrial oxidative phosphorylation, is first line therapy for promoting healthy and graceful anti-aging. However, a protocol whose end goal is restoration of KM, while certainly helpful in delaying mitochondrial decay, does not address the more fundamental issue – why does human physiology shift from a homeostasic state that repairs and balances itself to one that allows decay to accumulate? Dröge has called this shift “the first cause of death,” and his insight into its likely causes may both explain why calorie restriction increases longevity and provide a much less onerous way to opt out of the vicious cycle responsible for the age-associated transition from a state of youthful homeostatic repair to one that promotes mitochondrial decay.
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These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
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