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Title: Melatonin info I found Post by Leggs on Jul 1st, 2005, 8:55pm I noticed that melatonin was not an option for some, and I was reading up on it in a book I have. I won't tell you the name of it, unless you email me, so the papa bears who are watching out for the hoaxes won't think I am trying to sell it to you!!! X my heart, guys, I am not sellling it, it's just a resource I use since I am SO sensitive to prescription meds. Anyway, I found a section called "maintaining your melatonin level naturally," which may help some folks. All you oldtimers probably know most of this, but since everyone has been so great helping me get "off" OTC drugs this week, I wanted to be helpful too. ;;D. From a resource: As darkness falls, melatonin production increases, and when daylight hits the retina, neural impulses cause production to slow. Light and darkness are primary factors in rhythyms of melatonin production. Other ways to help: Regular meals, melatonin production strengthened by regular daily routines, including meals, help your body be in sync with the rhythms of the day Keep your diet light at night. The digestive process is slowed in the evenings, since melatonin production begins at nightfall. Heavy foods at night, can lead to digestive problems, and interfere with sleep <<and we CH sufferers, need all we can get>>, so eat light at night for a better sleep. Avoid stimulants, including coffee, tea and caffiene containing medications because they interfere with your sleep, leading to interfering with melatonin production. Avoid exercising at night, vigorous activity delays melatonin secretion. For the best benefit, exercise outdoors in the morning. Reading this really prompted me to get off the OTC mess with caffiene. It seemed to make the pain bearable, but it was messing up other systems! Luckily, I was already off the coffee after MONTHS, ugh, that was such an addiction, and such a trigger for me. One other thing I heard, is how important it is to get sleep in a DARK room, even just street lights and night lights can intefere with sleep/melatonin production zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz T. |
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Title: Re: Melatonin info I found Post by Bob P on Jul 2nd, 2005, 6:59am But alas. We clusterheads don't get that rise and fall of melatonin levels. We are melatonin flat liners. Quote:
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Title: Re: Melatonin info I found Post by Bob_Johnson on Jul 2nd, 2005, 7:34am Scientists Discover Key to Melatonin Production and Regulation of Circadian Rhythms ImmuneSupport.com 08-17-2001 Neuroscientists at Jefferson Medical College have clarified how the human eye uses light to regulate melatonin production, and in turn, the body’s biological clock. Their observations are published in the August 15 issue of the Journal of Neuroscience. The scientists discovered what appears to be a fifth human “photoreceptor,” which is the main one to regulate the biological – and non-visual – effects of light on the body. They have identified a novel photopigment in the human eye responsible for reacting to light and controlling the production of melatonin, which plays an important role in the body’s circadian rhythms. They also discovered that wavelengths of light in the blue region of the visible spectrum are the most effective in controlling melatonin production. “We have strong evidence for a novel, fifth photoreceptor and it appears to be independent of the classic photoreceptor for vision. It influences the biological effects of light. It regulates circadian rhythms and hormones in the body. We’ve also shown the fingerprint of wavelength sensitivity for the regulation of the hormone melatonin,” said George Brainard, Ph.D., professor of neurology at Jefferson Medical College of Thomas Jefferson University in Philadelphia. “This discovery will have an immediate impact on the therapeutic use of light for treating winter depression and circadian disorders,” he adds. “Some makers of light therapy equipment are developing prototypes with enhanced blue light stimuli. Four cells in the human retina capture light and form the visual system. One type, rod cells, regulates night vision. The other three types, called cone cells, control color vision. It’s known that exposure to light at night can disrupt the body’s production of melatonin, which is produced by the pineal gland in the brain and plays a vital role in resetting the body’s daily biological clock. Earlier this year, Dr. Brainard and his group showed that the combined three-cone system didn’t control the biological effects of light, at least not for melatonin regulation. But subsequent work led to the surprising discovery that a novel receptor was responsible for the effect. “We didn’t anticipate this at all,” he says. In the study, they looked at the effects of different wavelengths of light on 72 healthy volunteers, exposing them to nine different wavelengths, from indigo to orange. Subjects were brought into the laboratory at midnight, when melatonin is highest. The subjects’ pupils were dilated and then they were blindfolded for two hours. Blood samples were drawn. Next, each person was exposed to a specific dose of photons of one light for 90 minutes, and then another blood sample was drawn. Wavelengths of blue light had the highest potency in causing changes in melatonin levels, he explains. In theory, he says, “If a clinician wants to use light therapeutically, the blue wavelengths may be more effective. If you wanted built-in illumination that would enhance circadian regulation, you might want this wavelength region emphasized. In contrast, if you wanted something that doesn’t produce biological stimulation, you might steer the light more toward the red wavelengths.” But controlled clinical trials will be needed, he adds. Next, Dr. Brainard’s team would like to study the next step in how light regulates not just melatonin, but all of the body’s circadian rhythms, including body temperature, cortisol and performance rhythms. The National Institute of Neurological Disorders and Stroke, the National Space Biomedical Research Institute and NASA funded the research. |
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Title: Re: Melatonin info I found Post by Leggs on Jul 2nd, 2005, 8:19am on 07/02/05 at 06:59:04, Bob P wrote:
So from that last section there, is it saying that the melatonim production is just messed up all together in the group of CH sufferers? EVEN when they were not having a headache, ie: some of these anomalies are independent of the pain? I am starting to wonder, for me, it kind of becomes a matter of what happened first here, I know I have issues with garbage sleep, and the OTC stuff with caffiene did not help, not to mention severe addiction to regular Joe. Did CH sufferers have a messed up control center for melatonin to begin with, leading to CH or did what ever caused the CH mess up the control center? I suppose that's what the research was addressing. I took 1/2 of a melatonin last night, and ALMOST slept through the night.zzzzzzzzzzzzzzzz :-/zzzzzzzzzzzzzz |
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Title: Re: Melatonin info I found Post by ben_uk on Jul 2nd, 2005, 9:59am The master clock in mammals, the suprachiasmatic nuclei (SCN). Receives its retinal projections from the retinohyophalamic tract (RHT), which is formed from a small number of distinct ganglion cells. These ganglion cells (around 1 per cent of the total) tend to be distributed evenly over the entire retina and send an unmapped or random projection to the SCN. Glutamate, a common neurotransmitter, carries the light information signal to individual SCN neurons. By contrast, the ganglion cells of the visual system send a highly mapped projection to the visual centers of the brain, such that a point on the retina maps precisely to a group of cells in the visual cortex. The visual system is thus able to deduce both how much light there is and where it occurs in specific regions of the environment, whereas the SCN receives only information about the general brightness of environmental light. So the mammalian eye has parallel outputs, providing both image and brightness information. Mammals use their eyes to detect all light; if the eyes are lost, a mammal is both visually and circadian blind. It will be unable to entrain to light and will free-run for the rest of its days. However, if the eyes of birds, reptiles, amphibians and fish are removed they can still maintain an entrained circadian rhythm. They have several light-sensing "extra ocular" photoreceptor organs other than the eyes. Mammals lost these extra ocular photoreceptors during their unique evolutionary history. All modern mammals are derived from nocturnal, burrowing insectivorous or omnivorous animals that were living about 100 million years ago. Primitive mammals would have spent their days in burrows and then emerged at dusk (Young, 1962). Extra ocular photoreceptors, are located under the skull, may not have been sufficiently sensitive to discriminate twilight changes. Despite the fact that eye loss results in free-running rhythms in mammals, claims have been made from time to time that they have non-ocular photoreceptors. There was even a recent suggestion that human had photoreceptors behind the knee, as bright light shone there apparently shifted human circadian rhythms. It was a charming thought but unfortunately nobody could replicate the findings. All the experimental evidence points to light entrainment of the circadian system of mammals occurring exclusively via photoreceptors within the eye. Eye loss in every mammal ever studied, including humans, results in free running circadian rhythm. The sensory task of generating an image for the visual system is very different from the sensory task of collecting light for the regulation and entrainment of the clock. The previously reasonable assumption that retinal rods and cones detect light for both these forms of light sensing was a gross oversimplification. Although the entraining photoreceptors of mammals are clearly located in the eye, neither the rods nor the cones are required for this task, and there exists another photoreceptor within the eye. The identification of the non-rod, non-cone photoreceptor resulted from a series of experiments over 10 years in Russell Foster's laboratory. The group started out by looking at mice with naturally occurring genetic disorders of the rods and cones of the eye. The experimental plan was to correlate rod and cone photoreceptor loss with a loss in sensitivity of the circadian system to light. The first mutant mice studied lacked all rods and most of the cones. This mutant strain of mice, known as the retinal degeneration or rd/rd mouse, is visually blind. But but despite the massive (though not complete) loss of their rods and cones, these animals had apparently normal circadian responses to light. These surprising and unexpected findings were met with either polite lack of interest or hostile rejection. The eye has been the subject of serious study for some 200 years, and in broad terms its function was thought to be understood. The conventional understanding was light-sensitive rods and cones of the outer retina transduce light, and the cells of the inner retina provide the initial stages of signal processing before topographically mapped signals travel down the optic nerve to specific sites in the brain for advanced visual processing. Even though there was clear evidence of different visual and circadian pathways from the retina, including the side-shoot that linked into the SCN, there was a strong belief among many biologists that there was a single photoreception apparatus. It seemed inconceivable that something as important as an unrecognized ocular photoreceptor could have been missed. The feeling was that there was no need to upset the neat story of vision, and its evolutionary origins, with new photoreceptors. |
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Title: Re: Melatonin info I found Post by ben_uk on Jul 2nd, 2005, 10:00am This conventional wisdom was challenged by a few researchers interested in how vertebrate clocks are regulated by light and whose background and training were rooted not in vision research but in fields such as circadian and reproductive physiology and animal behavior. These researchers were not trained as visual scientists, but their naiveté was combined with an acute awareness that the vertebrate central nervous system is packed with "enigmatic" photoreceptors that help adjust circadian rhythms to the local light environment. They were aware that birds, reptiles, amphibians and fish employ specialized photo sensory cells in the basal brain and pineal to regulate their circadian rhythms. Foster's own undergraduate tutor was Alan Roberts, who introduced him to the study of pineal photoreception in frogs. This theme was developed in doctoral studies with Sir Brian Follett on the interplay of light and seasonal reproduction in birds. Michael Menaker, who at the time was on a sabbatical year at Bristol University, took an interest in this work and suggested that it could be developed using mice with hereditary retinal disorders. Circadian Biologists had no problems with organisms having a whole array of photoreceptors performing visual and/or circadian functions. This made it much easier for them to accept the notion of dedicated photoreceptors in the retina separated from the visual system. It seemed perfectly reasonable to ask whether rods, cones, uncharacterized retinal photoreceptors or a combination thereof might regulate the circadian rhythms of mammals, and these questions have radically altered the way in which we think about the eye as a sensory organ. But when you are out to convince the skeptics, or trespass across the disciplinary fields erected by scientists, then the science has to be like Caesar's wife - beyond reproach. Further studies, using different mouse mutants in different laboratories around the world, were able to repeat the Foster laboratory's observations and showed that the loss of visual responses due to retinal disease did not block circadian responses to light. At the very least, these studies in mice, and other rodents such as the "blind mole rat" (David-Grey et al., 1998), showed that the processing of light by the eye for vision was very different from the way in which the eye processed information for the clock. Rodents could be visually blind but not circadian blind. However, suggestive as these early studies were, they did not conclusively demonstrate the existence of a new ocular photoreceptor. Although the rods and cones were massively reduced in these rodents, they were never completely eliminated. There was the possibility that even a small number of rods and cones might still be sufficient to maintain normal circadian responses to light. Rather than wait for the chance discovery of a mutant mammal with absolutely no rods and cones, a new mouse strain was developed, known affectionately if unoriginally as the rd/rd cl mouse. This mouse had no rods whatsoever. Although completely visually blind, such mice still showed the normal circadian responses to light in the laboratory. By blocking the light reaching the eye, the effects of light on the circadian system were abolished, so there had to be a novel photoreceptor. Because these mice lacked an outer retina, the new photoreceptor cells were probably located within the inner retina. The key questions were the nature and location of this photoreceptor, but there were no obvious candidates visible under the microscope. Science rarely proceeds along straight lines. Chance and serendipity are the researcher's bedfellows. A clue to the mammalian photoreceptor came from work on fish. Quite by accident, Bobby Soni, who was working his doctoral thesis, discovered a new gene in the salmon eye that was similar to the genes that code for rod and cone photo pigments, but nevertheless had clear differences. When photons enter a rod or cone, many of them interact with photo pigments. The photo pigments of all animals consist of a form of opsin protein that binds a specific type of vitamin A (11-cis-retinaldehyde) to form a photosensitive complex. The absorption of a photon of light by 11-cis-retinaldehyde converts it to an all-trans form. This change in shape of vitamin A alters the opsin, which in turn triggers the photo transduction cascade. This ultimately causes a change in the electrical activity of the photoreceptor cell that is transmitted by neural pathway and ends with what we know as vision. Soni's key finding was that the new (VA-opsin) gene was not expressed in the salmon's rods and cones. It was found only in certain cells in the inner part of the retina which had not been thought to contain any photoreceptors. This was the first discovery of a photo pigment in the eye that was separate from the rods and the cones (Soni et al 1998). Although Soni had been working with fish, the discovery of the new opsin suggested a possible mechanism for non-rod, non-cone photoreception in vertebrates in general. |
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Title: Re: Melatonin info I found Post by ben_uk on Jul 2nd, 2005, 10:01am Rods and cones are easy to identify microscopically. Although countless microscopic investigations had revealed a huge range of cell types within the inner retina, no one had seen anything that could be considered a photoreceptor. Soni's work suggested that if the mammalian equivalent of the salmon VA-opsin could be found and localized, there was a strong presumption that this would be the inner retinal photoreceptor. A new opsin was soon found. Melanopsin was discovered by Ignacio Provencio in a range of mammals and localized to the ganglion cells that that form the RHT and project to the SCN (Provencio et al., 2000; Hattar et al., 2003) . Furthermore, in vitro, these cells were directly sensitive to light (Berson et al ., 2002; Sekaran et al ., 2003). It looks as though these cells were the non-rod , non-cone photoreceptors. Unfortunately, there is so little melanopsin in the mammalian eye that it has not been possible to produce enough of the protein to do the biochemistry to prove that melanopsin is the photo pigment. An experimental conundrum soon emerged. When the melanopsin gene in a normal mouse was experimentally "turned off", the melanopsin ganglion cells of the RHT were no longer directly light sensitive, and the circadian response to light was diminished, but critically it was far from abolished. Further, when the melanopsin photosensitive ganglion cells in the rodless-and-coneless mice are "turned off", all circadian responses to light completely disappear (Hattar et al 2003). What has to be explained is how it is that rodless-and-coneless mice nevertheless have an apparently normal circadian entrainment to light and melanopsin-deficient normal mice have an attenuated circadian entrainment to light, but melanopsin-deficient rodless-and-coneless mice have no circadian entrainment to light. Somehow the rods and cones must play a part, but rods and cones are not necessary for apparently normal circadian responses to bright light. Although in the bright light of artificial laboratory conditions the rods and cones are not necessary for the regulation of the circadian system, this does not mean that these photoreceptors play no role in the wild. This could be the answer to the conundrum. Under certain experimental conditions involving dim light/dark cycles that in some ways more closely resemble the light levels encountered in nature, rodless-and-coneless mice entrain but not with the same precision as normal sighted mice. In addition, electrical recordings made from the SCN of rats by Hilmar Meissl and his colleagues in Frankfurt have demonstrated that the rods and cones do send light information to the SCN (Aggelopoulos & Meissl, 2000). It could be that under bright light the contribution of the rods and cones is "swamped" and only becomes apparent in the dimmer light of early dawn and late dusk. Organisms have to be able to extract time-of-day information from dawn and dusk. Dawn and dusk are not single points but transient events, and during them the amount of light, the spectral composition of the light and the source of light (the position of the sun) all change in a systematic way. In theory, all these factors could be used and integrated by the circadian system to detect the phase of the solar cycle. It is possible that the changing color of the sky at dawn and dusk, and the position of the sun with respect to the horizon, might indeed act as a cue for entrainment in some species. Different photoreceptors, sampling slightly different aspects of the twilight scene, may allow a more accurate measure of the phase. They also allow an organism to compensate for sudden, acute changes in light environment when say, a cloud passes over the sun, or an animal moves into the shade. Animals in the wild have to cope with both the reliably predictable daily changes and the unpredictable, moment-to-moment fluctuations. Establishing that ther are photoreceptors other than the classic rods and cones has practical applications. The studies in retinally degenerate mice encouraged studies of circadian functions in blind people. Josephine Arendt and her group at the University of Surry and Charles Czeisler's group at Harvard both identified blind individuals who had eyes but lacked conscious light perception (Czeisler et al. 1995; Lockley et al.,1997). Despite this, some of these individuals were able still to regulate their circadian responses to light. One practical result is that every attempt is now made to preserve an intact eye in people suffering from certain forms of eye disease so that it can perform its circadian function. Taken from;- RHYTHMS OF LIFE. The Biological Clocks that Control the Daily Lives of Every Living Thing Russell Foster & Leon Kreitzman. ISBN 1 86197 235 0. :o |
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Title: Re: Melatonin info I found Post by Karla on Jul 4th, 2005, 9:33pm I noticed that you made no mention not to take meletonin if you are on an antiphycotic either. I found that on a label of a melatonin bottle as I was ready to pick up one and toss it into the cart. I talked to my phyarmacist and dr and they both said the label was correct and I was wise not to mix the two. |
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Title: Re: Melatonin info I found Post by cazman on Jul 4th, 2005, 10:34pm ouch i just got hit reading all that over load my my brain |
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