Ray Peat does a great job by explaining many diseases of aging by the hormonal imbalances such as estrogen dominance or hypothyroid. His assays and this forum could provide a "manual" how to minimize the body damage caused by aging. However, he doesn't explain what triggers these hormonal imbalances, only what accelerates them. Here I gathered some abstracts related to the topic what is and where in the body we can find the master aging clock which triggers the changes such as puberty or climaterium or the ultimate body destruction what can be greatly postponed but not completely eliminated by the low PUFA diet. Maybe we could find some other nutritional/life style interventions which affect the pineal gland in a more direct way? The work of Pierpaoli is instrumental in this respect. Also Olovnikov, the man who predicted telomeres, describes the hypothetical lunasensor. If he is right (and he already was in the case of telomeres) we could postpone aging by "dancing whole nights" (i.e. shaking head) on the new moon nights ...
Ann N Y Acad Sci. 2005 Dec;1057:112-32.
Lunasensor, infradian rhythms, telomeres, and the chronomere program of aging.
Olovnikov A.
Institute of Biochemical Physics of RAS, Chernyakhovskogo, 5-94, Moscow 125319, Russia. [email protected]
According to the redusome hypothesis, the aging of an organism is determined by the shortening of chronomeres (small perichromosomal linear DNA molecules). In this paper, a presumptive role for infradian hormonal rhythms is considered. Endogenous infradian rhythms are supposed to actively interact with those hormonal shifts which are governed by an exogenous infradian gravitational lunar rhythm. As a result of this interaction, the so-called T-rhythm is formed. Peaks of T-rhythms are used as the pacemaker signals to keep the life-long "clockwork" of the brain running. The "ticking" of this clock is realized by the periodically repeated shortening of chronomeres in postmitotic neuroendocrine cells, which occurs just at the maxima of T-rhythms. Shortening of telomeres in mitotic cells in vivo is a witness of the aging of the organism, but not the cause of aging. The primary cause of aging is shortening of chronomeres, the material carriers of a temporal program of development and aging. To recognize exogenous gravitational infradian rhythms, a special physiological system--the "lunasensor" system--evolved. It is assumed that it is a necessity to have a lunasensor as a particular variant of sensors of gravitation.
Ann N Y Acad Sci. 1998 May 1;840:491-7.
Neuroimmunomodulation of aging. A program in the pineal gland.
Pierpaoli W.
INTERBION Foundation for Basic Biomedical Research, Bellinzona, Switzerland.
We have investigated for 35 years the relationship between the neuroendocrine and the thymo-lymphatic, immune system. In the last decade we have shown that the pineal gland is a main adapter and fine synchronizer of environmental variables and endogenous messages into physiological modifications of basic functions. In particular the pineal gland itself seems to regulate, via circadian, night secretion of melatonin, all basic hormonal functions and also immunity. We have shown with several in vivo models that this fundamental role of the pineal gland decays during aging. Aging itself seems to be a strictly pineal-programmed event similar to growth and puberty. The continuation of our interventions with melatonin against the typical degenerative diseases of aging must be based on an accurate evaluation of its mechanisms of action. Melatonin being a ubiquitous molecule in nature, we suggest that it has acquired during evolution of the species numerous levels of activities. In fact, melatonin can be found in a large variety of cells and tissues, and bindings sites and "receptors" have been identified in many tissues and cells of the neuroendocrine and immune system. Therefore, the progressive understanding of the aging-programming role of the pineal gland also depends on studies of melatonin and its basic regulatory function. Our present studies will be described.
Ann N Y Acad Sci. 2005 Dec;1057:133-44.
The pineal aging and death program: life prolongation in pre-aging pinealectomized mice.
Pierpaoli W, Bulian D.
Walter Pierpaoli Foundation of Life Sciences, Orvieto, Italy. [email protected]
A precise temporal program for growth, fertility, aging, and death exists in the "pineal complex" of the brain. It tracks, like a "clock," the ontogenetic phases of our life program. Transplantation of a very old pineal gland into the thymus or under the kidney capsule of a young mouse produces acceleration of aging and early death. We investigated the existence of such an inner biological clock on the assumption that a time exists in the pineal program when the pineal gland actively starts to deliver aging and death "signals" to the body, thus accomplishing its genetically inscribed sequence. Groups of BALB/c male or female mice were surgically pinealectomized (PX) at the age of 3, 5, 7, 9, 14, and 18 months, and their life span was evaluated. Periodical measurements of blood and hormonal and metabolic parameters were taken. Results showed that while PX at the age of 3 and 5 months promotes acceleration of aging, no relevant effect of PX is observed in mice PX at 7 or 9 months of age. On the contrary, a remarkable life prolongation was observed when mice were PX at the age of 14 months. No effects were seen when the mice were PX at 18 months of age. The same aging-promoting or -delaying effects were confirmed in the hematological and hormonal-metabolic values measured. The findings demonstrate the existence of an evolutionary-developmental role for the pineal complex during growth, fertility, and aging. The dominant role of the pineal in the initiation and progression of aging as a death signal is clear, but its nature and mechanism are totally unknown. In fact new experiments showed that an additional pineal gland from a young donor, when grafted into a young mouse, induces acceleration of aging. The significance of these intriguing findings is discussed.
J Neuroimmunol. 2000 Aug 1;108(1-2):131-5.
The pineal gland and cancer. I. Pinealectomy corrects congenital hormonal dysfunctions and prolongs life of cancer-prone C3H/He mice.
Bulian D, Pierpaoli W.
Jean Choay Institute for Biomedical Research, INTERBION Foundation for Basic Biomedical Research and CHRONOLIFE Inc., Via Industria, 16, CH-6826, Riva San Vitale, Switzerland. [email protected]
Hormonal derangements almost invariably anticipate and signal the onset of tumors. Chronic, nocturnal melatonin administration delays aging in normal strains of mice. On the contrary it promotes and accelerates the onset of tumors in the cancer-prone strain of C3H/He mice. Grafting of a young pineal gland into aging mice prolongs their longevity and maintains juvenile circadian hormonal functions while pinealectomy (Px) does the opposite. We investigated if Px in C3H/He mice would modify their congenitally deranged pituitary function and affect their longevity. It was found that contrarily to Px in normal mice, Px in C3H/He mice remarkably maintains juvenile night levels of thyroid hormones and lipids, preserves a cell-mediated immune response and significantly prolongs their life. The pineal gland and its pathology may be the key for understanding, not only the causes of metabolic aging, but also the origin of those congenital or progressive aging-related hormonal alterations preceding onset of all tumors and thus allow preventive corrective interventions with pineal-derived agents.
Ann N Y Acad Sci. 2005 Dec;1057:319-26.
Neurodegenerative diseases: a common etiology and a common therapy.
Pierpaoli W.
Walter Pierpaoli Foundation of Life Sciences, Orvieto, Italy. [email protected]
The variety of names of neurodegenerative diseases (NDDs) does not indicate that there is a wide variety of causes and a multiple number of cures. In fact NDDs derive from a common and repetitive, almost monotonous multicausal origin. NDDs are initiated invariably by a sudden or silent insidious decrease in immunologic resistance of the T cell-dependent or delayed type, produced by a large variety of psychological-emotional and/or environmental "stressors" (e.g., social, family-domestic, economic, alimentary, traumatic, and professional). These stressors increase the vulnerability of tissues (in this case, a section of the central or peripheral nervous system) to attack by a common virus (e.g., adenoviruses and herpesviruses). This attack creates a vicious circle leading to emergence of virus-generated tissue autoantigens and then to formation of autoantibodies. Use of corticosteroids and immunosuppressive drugs dramatically worsen and "eternalize" the diseases with further immunosuppression. Invariably, onset of NDDs is anticipated by a clear-cut alteration of the hormonal cyclicity, which closely controls immunity. My experience with patients in the last five years indicates a new approach to prevent and cure NDDs, based on a system totally divergent from present therapies. In fact "resetting the hormonal cyclicity clock" results in restoration of hormone-dependent antiviral immunity, arrest of disease progression, and at least partial recovery of neural functions, whatever the origin, anatomic location, and course of pathology.
Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):787-91.
Pineal control of aging: effect of melatonin and pineal grafting on aging mice.
Pierpaoli W, Regelson W.
Biancalana-Masera Foundation for the Aged (Convention I.N.R.C.A. and University of Ancona), Neuroimmunomodulation Laboratory, Italy.
Dark-cycle, night administration of the pineal hormone melatonin in drinking water to aging mice (15 months of age) prolongs survival of BALB/c females from 23.8 to 28.1 months and preserves aspects of their youthful state. Similar results were seen in New Zealand Black females beginning at 5 months and C57BL/6 males beginning at 19 months. As melatonin is produced in circadian fashion from the pineal, we grafted pineals from young 3- to 4-month-old donors into the thymus of 20-month-old syngeneic C57BL/6 male recipients, and a 12% increase in survival was induced. Prolongation of survival was also seen on pineal transplant to the thymus in C57BL/6, BALB/cJ, and hybrid female mice at 16, 19, and 22 months. In all studies, the endogenous pineal of grafted mice was left in situ. Pineal grafted aged mice display a remarkable maintenance of thymic structure and cellularity. Preservation of T-cell-mediated function, despite age, as measured by response to oxazolone is seen. Other evidence suggests that melatonin and/or pineal-related factors could produce their effects through an influence on thyroid function. These data indicate that pineal influences have a place in the physiologic regulation of aging.
Journal of Anti-Aging Medicine, Mar 2001, Vol. 4, No. 1 : 31 -37
The Pineal Aging and Death Program. I. Grafting of Old Pineals in Young Mice Accelerates Their Aging
Walter Pierpaoli, Daniele Bulian
Experimental work initiated in 1985 progressively demonstrated the aging-delaying and/or life-prolonging effects of circadian, nocturnal administration of the pineal indoleamine melatonin in old rodents, and the even more pronounced aging-delaying effects of young-to-old pineal grafting. Another model, in which young pinealectomized mice were transplanted with pineal glands from older donors, showed a remarkable aging-accelerating effect produced in the younger mice by the "old" pineal. More work showed that, not only the course of aging can be modified, but even reversed. Apparently, aging is an evolutionary and developmental program similar to growth, onset of puberty and maintenance of fertility, and is amenable to be modified. The novel observation is reported here that implantation of pineal glands from very old donors into the thymus of normal, non-pinealectomized young hosts, accelerates their aging and induces an earlier death. No effect on aging and longevity can be seen when the young mice are transplanted with a pineal gland from young donors. It thus seems that the grafted pineal gland from a very old donor delivers active "aging and death messages" that cannot be permanently antagonized by the existing own "young" pineal gland in the host. This new observation also suggests that the "program of aging," even in a disease-free individual, may be different from the "program of death." In fact, a very old pineal gland seems to dominate on a young pineal and thus produce an earlier death at a time when the genetically determined neuroendocrine program of growth, fertility and aging in the engrafted old pineal has expired. The mechanism for the explication of these aging-promoting mechanisms in the "pineal network" is under investigation. |
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