MS Nutrition-summary pts 1st post, p.1

Tell us what you are using to treat your MS-- and how you are doing.

Postby jimmylegs » Tue Jul 31, 2007 7:31 am

sonofabitch! i just lost the saga i had written but somehow hit this back button when i meant to hit it in my other browser window.

short answer: yes, typically i still take D3, and yes i think it could be helping, but it is certainly not the only thing that the immune system needs to function properly.

longer answer:
what D3 is reported to do is reduce relapse rate, and i haven't had a relapse, but it's only been a year and a half since i was diagnosed. also i exercise and take a lot of other stuff that i think all works together, the body is such a complex system.

vitamin D3 is important to the immune system but so are these examples:
vitamin e - immune function, dna repair
zinc - healthy immune system, wound healing
magnesium - muscle and nerve function,heart rhythm, immune system, bones, regulate blood sugar, pressure, energy metabolism, protein synthesis
iron - oxygen delivery to cells (energy, immunity)
and more

i'm also not saying i don't have any symptoms. i don't think D3 is supposed to do anything to repair pre-existing damage to nerves. i think my best nerve repair involved that short regimen of klenner protocol supplements within weeks of my first attack. my hands are still always kind of numb and get worse when i exert myself. when i really overdo it, i can screw up my whole body and start walking funny again and all.
***orig post aug 1/07, update oct 12/07: had an appt with the neuro yesterday, and apparently part of the problem in my hands is because i have carpal tunnel syndrome. more detail further on in this topic.***

right now i am taking a break from D3 because i increased my calcium and magnesium intake. then i had some lower back pain. at first i thought it could be some new way that my cycle was trying to bother me but it didn't go away for weeks. for the last week and a bit, i dropped back to only vitamin B100 complex, C, E, acidophilus, multimineral, and zinc, and the pain has subsided.

so it's complicated but i hope that helped a little :oops:

[2012 comment: fixing D3 wouldn't really help all on its own. i've gotten to a place where i see it not just as a problem nutrient for certain regions of the world - not to downplay its importance in its own right of course - but also as an indicator of poor status of still other nutrients. we all know about the calcium thing, but the relationships with magnesium and zinc have gotten much clearer at this point. cases in point, the TIMS members who have had chronic trouble budging low levels, who have success once adding the right mineral mix into the equation, or have had success raising levels without megadosing, due to proper blending.
hmm, wonder what the 2017 update will be like??]
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Postby Kasuku » Tue Jul 31, 2007 10:53 am

Hi Jimmylegs,

I am curious about your statement of back problem and D3. I would appreciate it if you could expand on it. Thank you

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Postby jimmylegs » Tue Jul 31, 2007 12:48 pm

ha sorry yea looking back over that it is very vague isn't it!

again, short story: to clarify i didn't mean to imply i had too much D3 and got back pain (actually i have found studies to indicate that low D3 can cause muscle pain if not specifically back pain)
i thought my back pain could have been related to excess calcium which i had recently increased to try to match my daily 4000IU of D3.

longer story: for a long time as part of my daily regimen i was taking 4x 1000IU D, plus a combination calcium magnesium and D3 pill. sometimes i find those pills with some zinc added, or some enzyme to help everything absorb properly, but the basics are the cal mag and D3.

the pill was in a ratio, but my daily extra vitamin D3 was not balanced with calcium and mg. recently (i'd say within the last month) i found a cal-mag-D3 where the D3 was 1000IU. i started to think if i took 4 of those each day, my 4000IU of D3 would be nicely balanced.

a few weeks into that regimen, my back started to ache, lower down. after waiting for a while to see if it went away on its own, i looked into it and noted that excess calcium can cause lower back pain, what with the kidneys and all. so i backed off on the whole cal-mag-D3 combo and it seems to have solved the problem. i still feel a little tender but it's not constantly making me nuts!!!

at this stage i am not sure when to start up with my cal-mag-d3 routine again but maybe another week or so? anyway hope that cleared it up!
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Postby Kasuku » Tue Jul 31, 2007 7:06 pm

Hi Jimmylegs,

Thank you for the clarification; it makes sense.
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Postby jimmylegs » Wed Aug 01, 2007 6:57 am

no probs K
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Postby jimmylegs » Wed Aug 08, 2007 6:46 am

kasuku, i just ran across something related to zinc and thought of your comment some time back:

also would like to attract your attention to the paper on vit. D in the latest posts. The paper described that people with depression did better if they were located in the side of the hospital with sun exposure as well as people recovering from surgery. I assume that the exposure is mostly sunlight filtered by windows so in theory no UVB exposure. Light itself stimulates the pituitary gland resulting in hormone secretions and that could explain quicker recovery from depression as opposed to people kept in darker rooms. Perhaps light itself plays a role in addition to vit D. from UVB exposure. I guess my understanding is that UVB are filtered by glass. Am I right on this? What do you think Jimmylegs?
K


i have the feeling i have made this connection before but in case i didn't post it:

i was just reading these bits and pieces which reminded me of the light exposure sans D3 production element:

Med Hypotheses. 2000 Sep;55(3):239-41.

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.
Johnson S.

Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 microg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.


also found this...
Melatonin: Where It Comes From
Melatonin is a naturally occuring hormone that is synthesized from the neurotransmitter serotonin which in turn is synthesized from the amino acid tryptophan. This synthesis or production occurs primarily in a gland located at the center of the brain called the pineal gland. The pineal gland is light-activated, i.e., it is controlled by the amount of light seen by the eyes each day. This light activation gives rise to the belief that the pineal gland functions as the body's internal clock, regulating functions that are time-related such as sleep and the ageing process. Melatonin production via serotonin synthesis occurs at its peak during the dark hours around 2:00 a.m. Inversely, during daylight hours, melatonin production is low. It is for this reason that melatonin is believed to aid in regulating our sleep cycle and help stimulate sleep. Also, evidence exists that the pineal gland not only controls our 24 hour clock but our "life clock", meaning that it appears to be a major controller regarding our ageig process. As we age, several things happen to our pineal gland that result in it producing less melatonin. Since the pineal gland is derived from nerve tissue, the gland's cells do not replicate when damaged or lost. This loss of pineal gland cells may result from chemical or biological injury to the gland, or for a myriad of other reasons. Therefore, as we age, the pineal gland literally decreases in size or atrophies which has a direct effect on the amount of melatonin it is capable of synthesizing. Additionally, the gland itself is susceptible to the ageing processes that occur, such as calcium deposits and a decreased blood supply due to atherosclerosis. These in conjunction with other ageing processes interfere with the pineal gland’s melatonin-producing activities.


i am working on finding some info on pineal gland nutrition and support, i found one 2001 rat study but will keep looking
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Postby Kasuku » Thu Aug 09, 2007 7:29 pm

Hi Jimmylegs,

Very interesting! Do you recall the work coming out of Stanford where they found that tryptophan giving to mice in the EAE model not only stopped the progression of the disease, but also improved the clinical signs. The connection between tryptophan, melatonin and light is definitely interesting. I wonder if there are ways to stimulate the pineal gland other than with light. Taking melatonin may have the opposite effect due to biofeedback. What do you think?

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Postby jimmylegs » Fri Aug 10, 2007 7:04 am

Hi K, yes I remember the tryptophan connection too. so the question of the moment is, if we need zinc, and absorption is impaired with lower melatonin, and melatonin comes from tryptophan via the pineal gland, we can 1) throw more tryptophan at the gland and 2) make sure that gland is workin.

that rat study i mentioned was definitely indicating that in rats, diet appeared to modify the output of the pineal gland so i'm heading down that road for sure. the question is, did the diet change the functioning in the pineal gland, or just provide it with more ingredients for its usual capability for melatonin secretion?

here's something i got when i put melatonin tryptophan and zinc in google:

The interaction of melatonin and its precursors with aluminium, cadmium, copper, iron, lead, and zinc : An adsorptive voltammetric study
Auteur(s) / Author(s)
LIMSON J. (1) ; NYOKONG T. (1) ; DAYA S. (2) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Chemistry, Rhodes University, Grahamstown 6140, AFRIQUE DU SUD
(2) Department of Biochemistry and Microbiology, Rhodes University, Grahamstown 6140, AFRIQUE DU SUD

Résumé / Abstract
Melatonin, a pineal secretory product, and its precursors, tryptophan and serotonin, were examined for their metal binding affinities for both essential and toxic metals: aluminium, cadmium, copper, iron, lead, and zinc. An electrochemical technique, adsorptive stripping voltammetry, showed the varying abilities of melatonin and its precursors to bind the metals in situ. The results show that the following metal complexes were formed: aluminium with melatonin, tryptophan, and serotonin; cadmium with melatonin and tryptophan; copper with melatonin and serotonin; iron(III) with melatonin and serotonin; lead with melatonin, tryptophan, and serotonin; and zinc with melatonin and tryptophan. Iron(II) showed the formation of an in situ complex with tryptophan only. These studies suggest a further role for melatonin in the reduction of free radical generation and metal detoxification, and they may explain the accumulation of aluminium in Alzheimer's disease.
Revue / Journal Title
Journal of pineal research (J. pineal res.) ISSN 0742-3098 CODEN JPRSE9
Source / Source
1998, vol. 24, no1, pp. 15-21 (25 ref.)


anyway i most definitely am in the camp that thinks you have to give the body's parts the ingredients they need to do their jobs, not sub in their outputs so they can get even more lazy!!
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Postby jimmylegs » Fri Aug 10, 2007 7:18 am

debate seems to be open as to whether ms is related to too much melatonin or not enough!

Located in the third ventricle of the brain, the pineal gland secretes melatonin, a potent antioxidant and modulatory hormone that mediates the body's response to light/dark cycles, immune dysfunction, stress, and a variety of other physiological and emotional factors. Recently, pineal gland dysfunction has been strongly implicated in the pathogenesis and clinical course of MS. Interestingly, independent research has cited both abnormally high and abnormally low levels as possible triggers for the disease.

MS is more prevalent in northern regions of the globe. One possible explanation is that reduced exposure to sunlight in higher latitudes results in chronic oversecretion of melatonin by the pineal gland. This in turn promotes hypertrophy of the thymus, eventually resulting in the inability of the thymus to entrain T-lymphocytes to distinguish between foreign antigens and cells normally found in the body. Indeed, experimental models show that constant darkness exacerbates the symptoms of autoimmune disease. Based on these findings, one researcher proposed that "intercurrent virus infection and higher melatonin levels in winter could be interactive or synergistic risk factors for the development of MS."1

Another model for the etiology of MS focuses on the potential immune vulnerability posed by a melatonin deficiency. MS rarely strikes an individual before age 15--and one researcher has suggested that this age of onset corresponds with rapidly declining levels of melatonin just before puberty--producing heightened immunological susceptibility. A small study of MS patients with onset of the disease immediately before or after puberty revealed significantly lowered nocturnal levels of melatonin.2


http://www.gdx.net/home/assessments/fin ... tonin.html
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Postby Kasuku » Fri Aug 10, 2007 10:39 am

Hi Jimmylegs,


[One possible explanation is that reduced exposure to sunlight in higher latitudes results in chronic oversecretion of melatonin by the pineal gland.]

My understanding was the opposite of the statement above. I thought with increased exposure to sunlight you get oversecretion of melatonin by the pineal gland. Isn't it why we get a tan (melatonin pigmentation in the skin) during exposure to sunlight? I guess the tan comes from exposure to UVB light not sunlight, but I still had the impression that melatonin increases with light exposure. I also remember a study where the pineal glands from autopsies of people with MS were compared with the pineal glands from people without MS (age and sex matched), and the pineal glands from people with MS were significantly more calcified indicating a reduced production of melatonin.

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Postby jimmylegs » Fri Aug 10, 2007 11:14 am

yea me too!

that bit of info is a contradictory little item because it also says

[Another model for the etiology of MS focuses on the potential immune vulnerability posed by a melatonin deficiency.]

so how does that jive with the low light levels at northern latitudes causing overproduction of melatonin?

ewwwwwwwwww i don't want any calcified pineal autopsy thank you! let's work this one out k!

okay here we go

Hokkaido Igaku Zasshi. 1994 Jan;69(1):46-64.Links
[Regulation mechanism of melatonin rhythm in the pineal gland by light: experimental studies by in vivo microdialysis][Article in Japanese]


Kanematsu N.
Department of Physiology, Hokkaido University School of Medicine, Sapporo, Japan.

Light has dual effects on the pineal melatonin; one is the entrainment of the circadian rhythm and the other is suppression of the melatonin synthesis. It is not known whether the entraining and suppressing effects of light are mediated by the same pathway or not. To elucidate the mechanism of the dual effects of light, (1) the sensitivity of the retina, (2) effects of acetylcholine agonist and, (3) the arrhythmicity induced by longterm continuous light, were studied by measuring melatonin continuously from a single rat by means of in vivo microdialysis. Pineal melatonin was suppressed by light more strongly at the late dark phase than at midnight, and by green light (520nm) than by red light (660nm). Pineal melatonin measured by microdialysis was decreased rapidly by a short light exposure and the melatonin rhythm was shifted on the following days. Microinjection of cholinergic agonist, carbachol, into the suprachiasmatic nucleus neither suppressed nor entrained the pineal melatonin rhythm. Immediately after the blinding, rats showed the circadian rhythm in pineal melatonin which had been abolished under long-term continuous light. While, it took several days for the locomotor rhythm to reappear. It is concluded that, (1) suppression of the pineal melatonin by light depends on the circadian phase and on the wavelength of light, (2) the threshold for light suppression is lower than that for phase-shift, (3) the melatonin rhythm starts to phase-shift on the following day of light pulse. (4) Acetylcholine is unlikely to be involved in the photic transmission both to the circadian clock and to the pineal, (5) arrhythmicity induced by long-term continuous light seems to be due to masking for the melatonin rhythm, and to uncoupling from the clock for the locomotor rhythm.


an aside from the authoritative wikipedia:
Production
In higher animals melatonin is produced by pinealocytes in the pineal gland (located in the brain) and also by the retina, lens and GI tract. It is naturally synthesized from the amino acid tryptophan (via synthesis of serotonin) by the enzyme 5-hydroxyindole-O-methyltransferase.

Production of melatonin by the pineal gland is under the influence of the suprachiasmatic nucleus of the hypothalamus (SCN) which receives information from the retina about the daily pattern of light and darkness.

Melatonin is also synthesized by various plants, such as rice, and ingested melatonin has been shown to be capable of reaching and binding to melatonin binding sites in the brains of mammals.[6][7]


okay and some more...
The trigger for melatonin secretion each evening is decreased light exposure; at the end of the day, when our sunlight exposure decreases, melatonin begins to switch on.


so yes, i guess the light stops it from being secreted, and when it gets dark out it comes, but the pineal gland still has to be happy and healthy to make enough when it gets dark?

so maybe, depending on whether UV is involved, there is not enough contrast from the light to dark phase in the more northern latitudes, because we hang around in artificial lighting so much of the time, then we turn out the lights and the pineal has this half assed response to the change? i dunno need to read lots more on this, just a newbie in the pineal dept.
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Postby jimmylegs » Fri Aug 10, 2007 11:16 am

ah yes here we go

Melatonin and the Immune System
It is thought that much repair of the immune system occurs at night, therefore interacting with melatonin. When people are exposed to frequent artificial light and they do not get enough sleep melatonin levels are suppressed. Some forms of cancer are thought to be related to melatonin levels. ôMelatonin levels of breast and prostate patients are reduced to half the normal levels.ö (http://www.liberty.com/home/appaloosa/mel.htm). In two cases of sarcoidosis, which were not responding to long term treatments, melatonin was used. In between four to five months of being treated with 20mg daily, the symptoms were alleviated

http://www.vanderbilt.edu/AnS/psychology/health_psychology/melatonin.htm#Melatonin%20and%20the%20Immune%20System

i apologize i am not going fully into journal refs here, just quick scans...
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Postby jimmylegs » Fri Aug 10, 2007 11:34 am

again, not from a journal

Up until the 1990s, no research had ever been conducted to determine the impact of fluoride on the pineal gland - a small gland located between the two hemispheres of the brain that regulates the production of the hormone melatonin. Melatonin is a hormone that helps regulate the onset of puberty and helps protect the body from cell damage caused by free radicals.

It is now known - thanks to the meticulous research of Dr. Jennifer Luke from the University of Surrey in England - that the pineal gland is the primary target of fluoride accumulation within the body.

The soft tissue of the adult pineal gland contains more fluoride than any other soft tissue in the body - a level of fluoride (~300 ppm) capable of inhibiting enzymes.

The pineal gland also contains hard tissue (hyroxyapatite crystals), and this hard tissue accumulates more fluoride (up to 21,000 ppm) than any other hard tissue in the body (e.g. teeth and bone).

After finding that the pineal gland is a major target for fluoride accumulation in humans, Dr. Luke conducted animal experiments to determine if the accumulated fluoride could impact the functioning of the gland - particulalry the gland's regulation of melatonin.

Luke found that animals treated with fluoride had lower levels of circulating melatonin, as reflected by reduced levels of melatonin metabolites in the animals' urine. This reduced level of circulating melatonin was accompanied - as might be expected - by an earlier onset of puberty in the fluoride-treated female animals.

Luke summarized her human and animal findings as follows:

"In conclusion, the human pineal gland contains the highest concentration of fluoride in the body. Fluoride is associated with depressed pineal melatonin synthesis by prepubertal gerbils and an accelerated onset of sexual maturation in the female gerbil. The results strengthen the hypothesis that the pineal has a role in the timing of the onset of puberty. Whether or not fluoride interferes with pineal function in humans requires further investigation."


here's something journalesque about fluoride...
http://star.tau.ac.il/~eshel/Bio_complexity/8.Human%20Brain/Autism-Mitochondria-mercury.pdf

et voila, i like it when i can find nutrition involvement, even if it's just birds:
Comp Biochem Physiol A Mol Integr Physiol. 1998 Feb;119(2):593-8. Related Articles, Links


Vitamin A deficiency reduces the responsiveness of pineal gland to light in Japanese quail (Coturnix japonica).

Fu Z, Kato H, Sugahara K, Kubo T.

Faculty of Agriculture, Utsunomiya University, Japan.

Synthesis of melatonin in pineal gland is under the control of light environment. The recent finding of the presence of rhodopsin-like photopigment (pinopsin) and retinal in the avian pinealocytes has led to a hypothesis that vitamin A is involved in photoresponses of the pineal gland. We have thus analyzed the effect of vitamin A deficiency on the regulatory system of melatonin synthesis in the pineal gland of Japanese quail. Depletion of vitamin A from Japanese quails was attained by feeding them with a vitamin A-free diet supplemented with retinoic acid. In the vitamin A-deficient birds, diurnal rhythm in melatonin production persisted such that the phase of the wave was similar to that seen in the control birds. However, the amplitude of the nighttime surge of pineal melatonin was damped by vitamin A deficiency. When the control birds were briefly exposed to light at night, pineal melatonin dropped to the daytime level. In contrast, only slight decrease was observed in the vitamin A-deficient quails. The light responsiveness was restored after feeding the vitamin A-deficient quails with the control diet for 1 week. These results indicate that vitamin A plays essential roles in maintaining sufficient responsiveness of the avian pineal gland to photic input.


jus rollin thru the alphabet now...

Vol. 95, Issue 11, 6097-6102, May 26, 1998


Biochemistry
Vitamin B2-based blue-light photoreceptors in the retinohypothalamic tract as the photoactive pigments for setting the circadian clock in mammals
(cryptochromes / retina / suprachiasmatic nucleus)

Yasuhide Miyamoto and Aziz Sancar*
Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599

Communicated by Johann Deisenhofer, University of Texas Southwestern Medical Center, Dallas, TX, April 1, 1998 (received for review March 9, 1998)

In mammals the retina contains photoactive molecules responsible for both vision and circadian photoresponse systems. Opsins, which are located in rods and cones, are the pigments for vision but it is not known whether they play a role in circadian regulation. A subset of retinal ganglion cells with direct projections to the suprachiasmatic nucleus (SCN) are at the origin of the retinohypothalamic tract that transmits the light signal to the master circadian clock in the SCN. However, the ganglion cells are not known to contain rhodopsin or other opsins that may function as photoreceptors. We have found that the two blue-light photoreceptors, cryptochromes 1 and 2 (CRY1 and CRY2), recently discovered in mammals are specifically expressed in the ganglion cell and inner nuclear layers of the mouse retina. In addition, CRY1 is expressed at high level in the SCN and oscillates in this tissue in a circadian manner. These data, in conjunction with the established role of CRY2 in photoperiodism in plants, lead us to propose that mammals have a vitamin A-based photopigment (opsin) for vision and a vitamin B2-based pigment (cryptochrome) for entrainment of the circadian clock.


Vitamin D3 enhances mood in healthy subjects during winter
Allen T. G. Lansdowne1, S. C. Provost1

Abstract

Mood changes synchronised to the seasons exist on a continuum between individuals, with anxiety and depression increasing during the winter months. An extreme form of seasonality is manifested as the clinical syndrome of seasonal affective disorder (SAD) with carbohydrate craving, hypersomnia, lethargy, and changes in circadian rhythms also evident. It has been suggested that seasonality and the symptoms of SAD may be due to changing levels of vitamin D3, the hormone of sunlight, leading to changes in brain serotonin. Forty-four healthy subjects were given 400rIU, 800rIU, or no vitamin D3 for 5 days during late winter in a random double-blind study. Results on a self-report measure showed that vitamin D3 significantly enhanced positive affect and there was some evidence of a reduction in negative affect. Results are discussed in terms of their implications for seasonality, SAD, serotonin, food preference, sleep, and circadian rhythms.


k i've had enough of this for now, need lunch :) ttfn
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Postby Kasuku » Fri Aug 10, 2007 11:50 am

Wow! this is a lot of information.

I like the idea that perhaps there is some kind of ratio between light/dark cycles and the stimulation of the pineal gland. I know for a fact that in animal breeding light/dark cycles are extremely important for breeding, especially rodent breeding. The reproductive hormones are under the control of the pineal gland. For example, most research rodent facilities keep their animals under 12 hours of light and 12 hours of darkness. Any changes in this cycle have detrimental effects on the breeding of the animals. If there is too much ligth or too much dark the breeding efficiency decreases due to a sluggish pineal gland. Maybe we should adopt the 12/12 hours cycle like at the equator where MS is practically inexistent. I am stretching here but ...

I enjoy the brainstorming sessions and yes no more autopsy studies.

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Postby jimmylegs » Fri Aug 10, 2007 1:46 pm

that 12 and 12 idea is great. check this out too, i had heard about it before but it's making more sense to me now:

http://www.sciencenews.org/articles/20060107/bob9.asp

...He had hypothesized that nighttime illumination, by interrupting the body's mainly nocturnal production of the hormone melatonin, might increase the risk of breast cancer. Animal experiments and surveys of people over the past 2 decades supported that hypothesis without proving it, says Stevens, currently at the University of Connecticut Health Center in Farmington.

"Now, a watershed study has provided the first strong experimental support," Stevens says.

A woman's blood provides better sustenance for breast cancer just after she's been exposed to bright light than when she's been in steady darkness, researchers led by David E. Blask of the Bassett Research Institute in Cooperstown, N.Y., report.

"Light at night is now clearly a risk factor for breast cancer," Blask says. "Breast tumors are awake during the day, and melatonin puts them to sleep at night." Add artificial light to the night environment, and "cancer cells become insomniacs," he says.


doesn't sound like UV is a factor then, unless all those participants had full spectrum lighting everywhere they went!
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