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| | From:  taka00381 (Original Message) | Sent: 4/18/2007 3:29 AM |
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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I read some interesting stuff like this from Peat, though some of these essays may no longer be on the internet. Have you done searches for "ray peat" on a search engine for this kind of thing? |
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I couldn't find any full Peat's essay on the Pineal gland or melatonin except this:
SOURCE:
http://www.keelynet.com/interact/Arc_7_98-12_98/00001190.htm
QUOTE: from: Using Sunlight to Sustain Life
by Raymond Peat, Ph.D., Ray Peat's Newsletter
Townsend Letter for Doctors & Patients, June 1996, Page 83 - 85
Many health food stores are now selling melatonin, to reduce sleep
and "prevent cancer". They have taken some information out of
context, and don't realize how dangerous melatonin is. It makes
the brain sluggish, causes the sex organs to shrink, and damages
immunity by shrinking the thymus gland. It is the hormone of
darkness and winter, and is produced in the pineal gland by any
stress which increases adrenalin. Adequate sun light suppresses
the formation of melatonin.
Melatonin, or pineal hormone: the pineal gland in the brain
responds to an absence of light (or to any stress which increases
the adrenalin systems) by secreting a hormone called melatonin,
which lightens the skin, makes the brain sluggish, turns off
thyroid and progesterone production, and suppresses immunity and
fertility. UNQUOTE.
This taken together with his warnings about tryptophan and serotonin (precursors of melatonin) seems a bit controversial to me.
SOURCE:
http://raypeat.com/articles/aging/tryptophan-serotonin-aging.shtml
QUOTE: The polyunsaturated oils interact closely with serotonin and tryptophan, and the short and medium chain saturated fatty acids have antihistamine and antiserotonin actions. Serotonin liberates free fatty acids from the tissues, especially the polyunsaturated fats, and these in turn liberate serotonin from cells such as the platelets, and liberate tryptophan from serum albumin, increasing its uptake and the formation of serotonin in the brain. Saturated fats don’t liberate serotonin, and some of them, such as capric acid found in coconut oil, relax blood vessels, while linoleic acid constricts blood vessels and promotes hypertension. Stress, exercise, and darkness, increase the release of free fatty acids, and so promote the liberation of tryptophan and formation of serotonin. Increased serum linoleic acid is specifically associated with serotonin-dependent disorders such as migraine. UNQUOTE.
He also talks about sleep promoting estrogen and inflammation in his free essays recommending long day/light in the night.
Perhaps it all depends on the dose, too much sleep induces estrogen but just the right amount of high quality sleep with melatonin spike is needed for synchronizing the body systems for proper functioning. Also localization may be important, tryptophan may be dangerous in other parts of the body but brain like the PUFAs (DHA) are also concentrated in the brain. Even in EFAD state I guess DHA is still present in the brain. Also more tryptophan may be needed in the growing child or in a bodybuilder but not in a sedentary old adult.
I have seen some recommendations to consume banana or bread with milk and cheese 2 hours before sleep to deliver enough tryptophan to the brain for night melatonin production. When I tried this it felt good but when I tried the whey protein which is "superrich" in tryptophan my feeling was opposite. Coincidentally I have an IgG "allergy" to the globular/albumin proteins like whey and egg white which are rich in tryptophan. It may be wise to consume only low tryptophan protein like gelatin during the day and some cheese with carbohydrates in the evening. |
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One point I make to a lot of people is that there is a balance that needs to be maintained, and so if you go on a vegan diet, you may be low in tryptophan, whereas most people in nations like the USA are probably eating more than they need.
I've debated people on the DHA in the brain claim. The claim is that there is "rapid" DHA turnover in the brain, but this does not explain how my great grandparents could have lived so long, with no apparent loss of cognitive function, and yet had no source of omega 3s beyond the tiniest of trace amounts. My guess is that they had Mead acid in their brains. DHA is too dangerous, especially for the eyes and brain, for them to have lived so long and well, though as I said, since they had no source of omega |
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One point I make to a lot of people is that there is a balance that needs to be maintained, and so if you go on a vegan diet, you may be low in tryptophan, whereas most people in nations like the USA are probably eating more than they need.
I've debated people on the DHA in the brain claim. The claim is that there is "rapid" DHA turnover in the brain, but this does not explain how my great grandparents could have lived so long, with no apparent loss of cognitive function, and yet had no source of omega 3s beyond the tiniest of trace amounts. My guess is that they had Mead acid in their brains. DHA is too dangerous, especially for the eyes and brain, for them to have lived so long and well, though as I said, since they had no source of omega 3s, there could not have been much turnover of DHA even if they were born with it in their brains. |
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I wonder why the brain would need more fluidity at the temperature of 37oC when all normal SFAs are liquid. Perhaps there is some signaling function of DHA in the brain?
Interesting reading about how exposure to artificial light affects obesity, diabetes, hypertension, depression, MS and more. at the following URL:
http://photoperiodeffect.com/
Also taken from Wikipedia:
SOURCE:
http://en.wikipedia.org/wiki/Darkness_therapy
QUOTE: But there are other, less transcendental, reasons for the impact of darkness therapy. In the biochemistry of the brain, the neurotransmitter, serotonin, is produced by the body in reaction to light, and enables us to inhabit normal waking consciousness - to see "reality" as it is normally experienced. In darkness, however, melatonin is produced instead and is then converted into pinoline, which is involved in dreaming and new states of consciousness, so that we see reality in a wholly uncommon way.
Once pinoline is released into the brain, the production of another biochemical, DMT, is stimulated. DMT represents the body's natural ability to create any reality we choose and, interestingly, is also one of the main active ingredients within many psychotropic plants, and is present in some versions of the visionary Amazonian brew, ayahuasca, which is believed to create telepathic states among those who take it, as well as communion with the spirits of the dead. Simply being in darkness, therefore, will lead naturally to a new sense of reality. (Edit: It should be stated that there is no proof that endogenous DMT reaches the relevant receptors in the brain, even if it is a plausible theory. See Strassman , DMT: The Spirit Molecule) UNQUOTE. |
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| If there is a crucial "signaling" function of DHA in the brain, there would have to be rapid turnover, as most seem to believe, but then the "EFAD" people would have severe cognitive and/or other dysfunctions. I don't see evidence for this supposed function, assuming Mead acid is there instead. There may be tiny amounts of DHA in eyes or brain, which could explain strange cravings by pregnant women, but if significant amounts are needed, I would have experienced some problems by now (and my great grandparents wouldn't have lived so long and/or so well). |
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This article shows that melatonin protects against breast cancer and inhibits linoleic acid (omega-6) uptake and metabolism to 13-HODE by cancer cells. I think that enough sleep may also decrease the AA incorporation into cells in the people immune to the omega-6 overload syndromes ...
Cancer Res. 2005 Dec 1;65(23):11174-84.
Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats.
Blask DE, Brainard GC, Dauchy RT, Hanifin JP, Davidson LK, Krause JA, Sauer LA, Rivera-Bermudez MA, Dubocovich ML, Jasser SA, Lynch DT, Rollag MD, Zalatan F.
Laboratory of Chrono-Neuroendocrine Oncology, Bassett Research Institute, The Mary Imogene Bassett Hospital, Cooperstown, New York 13326, USA. [email protected]
The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 microW/cm2) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 microW/cm2 (i.e., 2,800 lx). Compared with tumors perfused with daytime-collected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers.
PMID: 16322268
QUOTE: The suppression of
circadian melatonin production by ocular exposure to bright white
light at night, leading to augmented nocturnal tumor uptake of
dietary linoleic acid and its conversion to mitogenically active 13-
HODE, can now be afforded serious consideration as a new risk
factor for human breast cancer (4, 5) and a significant public health
issue (55). The high nocturnal dietary intake of fat, particularly
linoleic acid, reported for night shift workers (56, 57), coupled with
melatonin suppression by exposure to light at night provide a firm
mechanistic basis upon which to explain, in part, the increased risk
of breast cancer in some women who work night shifts for many
years (9�?1). Thus, strategies to preserve the integrity of the
circadian melatonin signal (i.e., avoidance of bright light at night,
intelligent lighting design, circadian-timed physiologic melatonin
supplementation) coupled with modifications in nocturnal dietary
fat intake may offer a unique approach to the prevention of breast
cancer, and perhaps other melatonin-sensitive cancers, in our
increasingly 24-hour society. UNQUOTE. |
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"...people immune to the omega-6 overload syndromes..."
Who are these people? Where is the evidence that there are such people? If you don't get enough sleep, you will release AA, as it acts as a stressor, and stressors release AA. This can be measured - one could measure the AA metabolites in those who got at least 9 hours sleep versus those who got 5 or so hours of sleep. |
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SOURCE:
http://news.yahoo.com/s/ap/20071129/ap_on_he_me/night_shift_cancer
Graveyard shift work linked to cancer By MARIA CHENG, AP Medical Writer
Like UV rays and diesel exhaust fumes, working the graveyard shift will soon be listed as a "probable" cause of cancer. It is a surprising step validating a concept once considered wacky. And it is based on research that finds higher rates of breast and prostate cancer among women and men whose work day starts after dark.
Next month, the International Agency for Research on Cancer, the cancer arm of the World Health Organization, will add overnight shift work as a probable carcinogen. The American Cancer Society says it will likely follow. Up to now, the U.S. organization has considered the work-cancer link to be "uncertain, controversial or unproven."
The higher cancer rates don't prove working overnight can cause cancer. There may be other factors common among graveyard shift workers that raise their risk for cancer.
However, scientists suspect that overnight work is dangerous because it disrupts the circadian rhythm, the body's biological clock. The hormone melatonin, which can suppress tumor development, is normally produced at night.
If the graveyard shift theory eventually proves correct, millions of people worldwide could be affected. Experts estimate that nearly 20 percent of the working population in developed countries work night shifts.
Among the first to spot the night shift-cancer connection was Richard Stevens, a cancer epidemiologist and professor at the University of Connecticut Health Center. In 1987, Stevens published a paper suggesting a link between light at night and breast cancer.
Back then, he was trying to figure out why breast cancer incidence suddenly shot up starting in the 1930s in industrialized societies, where nighttime work was considered a hallmark of progress. Most scientists were bewildered by his proposal.
But in recent years, several studies have found that women working at night over many years were indeed more prone to breast cancer. Also, animals that have their light-dark schedules switched develop more cancerous tumors and die earlier.
Some research also suggests that men working at night may have a higher rate of prostate cancer.
Because these studies mostly focused on nurses and airline crews, bigger studies in different populations are needed to confirm or disprove the findings.
There are still plenty of skeptics. And to put the risk in perspective, the "probable carcinogen" tag means that the link between overnight work and cancer is merely plausible.
Among the long list of agents that are listed as "known" carcinogens are alcoholic beverages and birth control pills. Such lists say nothing about exposure amount or length of time or how likely they are to cause cancer. The American Cancer Society Web site notes that carcinogens do not cause cancer at all times.
Still, many doubters of the night shift link may be won over by the IARC's analysis to be published in the December issue of the journal Lancet Oncology.
"The indications are positive," said Vincent Cogliano, who heads up the agency's carcinogen classifications unit. "There was enough of a pattern in people who do shift work to recognize that there's an increase in cancer, but we can't rule out the possibility of other factors."
Scientists believe having lower melatonin levels can raise the risk of developing cancer. Light shuts down melatonin production, so people working in artificial light at night may have lower melatonin levels.
Melatonin can be taken as a supplement, but experts don't recommend it long-term, since that could ruin the body's ability to produce it naturally.
Sleep deprivation may be another factor in cancer risk. People who work at night are not usually able to completely reverse their day and night cycles.
"Night shift people tend to be day shift people who are trying to stay awake at night," said Mark Rea, director of the Light Research Center at Rensselaer Polytechnic Institute in New York, who is not connected with the IARC analysis.
Not getting enough sleep makes your immune system vulnerable to attack, and less able to fight off potentially cancerous cells.
Confusing your body's natural rhythm can also lead to a breakdown of other essential tasks. "Timing is very important," Rea said. Certain processes like cell division and DNA repair happen at regular times.
Even worse than working an overnight shift is flipping between daytime and overnight work.
"The problem is re-setting your body's clock," said Aaron Blair, of the United States' National Cancer Institute, who chaired IARC's recent meeting on shift work. "If you worked at night and stayed on it, that would be less disruptive than constantly changing shifts."
Anyone whose light and dark schedule is often disrupted �?including frequent long-haul travelers or insomniacs �?could theoretically face the same increased cancer risk, Stevens said.
He advises workers to sleep in a darkened room once they get off work. "The balance between light and dark is very important for your body. Just get a dark night's sleep."
Meanwhile, scientists are trying to come up with ways to reduce night workers' cancer risk. And some companies are experimenting with different lighting, seeking a type that doesn't affect melatonin production.
So far, the color that seems to have the least effect on melatonin is one that few people would enjoy working under: red.
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P.S. This is my main stressor I think - erratic sleep/wake cycle and I have yet to install the yellow lights in all living rooms (hard to do if you are not living alone...) Also I feel 8-9 hours of daily regular sleep is ideal for me but now getting hardly 7, rather 6. Also compensating for the stress at work by doing "night research" on the Internet may be a problem ... |
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You should read what Ray Peat has to say about melatonin and sleep.
Melatonin is a metabolite of tryptophan which is a highly reactive amino acid.
Also, I am wondering if they controlled for factors such as diet. Think about police who work night shifts, or nurses or doctors who work night shifts. What do they typically eat? Donuts, cake, etc. I don't know if they controlled for this factor or not though. |
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| Ray Peat recommends Red Light, not Yellow. |
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Just to remind you the link I have posted previously:
https://www.lowbluelights.com
The problem is blue light - there is a 530 nm separate receptor for it in human eyes directly connected to the pineal ... Red light is of course even farther from the blue spectrum but as the link above suggests yellow/orange is sufficient and easier to purchase in an electric shop.
As far as I remember Ray Peat was rather against melatonin and suggested more bright illumination to shorten nights. IMO this is same as with the insulin - you want to have strong spikes at the right times but not constantly elevated (SAD). From what I have red the best is to put orange glasses on the face or switch to yellow/red light early evening but get the naked face (and possibly whole body due to VitD) on the sun in the morning (same time everyday if possible).
As for the history - recently the Japanese patent blue light LED diodes appeared in the market - e.g. Christmas house and street illuminations. When used in night they may greatly disrupt the natural melatonin signaling. Let's see if we have them classified as health risk in cup of decades ... |
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Interesting article linking the beneficial and anticancer effects of melatonin to linoleic acid:
QUOTE: Blask's team determined that melatonin blocks cancer cells' metabolism of linoleic acid, a polyunsaturated fat that's abundant in food. The same team had previously shown that 13-hydroxyoctadecadienoic acid, the product of linoleic acid metabolism, spurs cancer cells to divide. UNQUOTE.
QUOTE: Night-shift workers face fundamental challenges, Blask says. "Melatonin works, to a large degree, by inhibiting the cancer cells from taking up linoleic acid," he says. Cravings for fatty foods frequently assail workers in the middle of the night. As a result, many shift workers consume large amounts of linoleic acid just when their melatonin production is suppressed and unable to protect them from the polyunsaturated fat, he says. UNQUOTE.
SOURCE: http://www.sciencenews.org/articles/20060107/bob9.asp
Worth reading it all! |
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I am now reading the following book and it is quite fascinating:
Lights Out
Sleep, Sugar, and Survival
by T. S. Wiley, Bent Formby Ph.D.
http://www.thewileyprotocol.com/content/view/18/71/ |
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An interesting paper showing that the circadian control of hormone secretions is disrupted in the HIV-positive individuals. Now what comes first, HIV or the disruption? The "experts" would certainly blame the "non-existing HIV virus" but stress and bad non-periodic lifestyle can do the same I guess ...
AIDS Res Hum Retroviruses. 1997 Sep 20;13(14):1243-9.
Circadian secretory pattern of growth hormone, insulin-like growth factor type I, cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, and prolactin during HIV infection.
Rondanelli M, Solerte SB, Fioravanti M, Scevola D, Locatelli M, Minoli L, Ferrari E.
Department of Internal Medicine, University of Pavia, Italy.
The circadian rhythms of plasma growth hormone (GH), insulin-like growth factor type I (IGF-I), cortisol, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and prolactin (PRL) were evaluated in 13 HIV-seropositive patients (8 males and 5 females; mean age [+/-SD], 30 +/- 5 years), classified as CDC C2. Sixteen clinically healthy subjects (9 males and 7 females; mean age [+/-SD], 32 +/- 8 years) were chosen as control group. Samples were taken every 4 hr from 04:00 to 20:00 and every 2 hr from 20:00 to 04:00. Plasma GH was evaluated by IRMA procedure, plasma IGF-I by RIA (after separation of soluble IGF-I from IGF-I-binding proteins, using acid-ethanol extraction), plasma cortisol by a solid-phase RIA, plasma ACTH by double-antibody RIA, and serum TSH and serum PRL by a solid-phase two-site fluoroimmunometric assay. Rhythmometric data were analyzed by single and population mean cosinor analysis; the comparison of the parameters of the rhythm between patients and controls was carried out by the mesor test and the amplitude-acrophase Hotelling test. Alterations of the circadian pattern of GH, IGF-I, cortisol, ACTH, TSH, and PRL were demonstrated in HIV-seropositive patients. In fact, the circadian profiles of these hormones were clearly flattened and no statistically significant 24-hr rhythm was detectable (with the exception of cortisol). These results are consistent with the hypothesis that alterations of the circadian temporal structure may already be present in HIV-seropositive patients without wasting and infectious complications.
PMID: 9310292
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