posted
Do you advocate this with lyme, while taking antibiotics? What do you think it helps?
Posts: 69 | From Washington | Registered: Jan 2007
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
I took it when I was having hard time sleeping, the first five days I had herxiemer increase it deffinatley does something.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
Buhner recommends it in his Healing Lyme book, though I forget why, LOL! I started taking it months ago and have continued it through abx. I also take Source Naturals timed-release in the 2mg dosage.
I think it is supposed to clean up neurotoxins, though my LLMD says that's not true. I figure it can't hurt and, when I'm through on abx I plan to do Buhner's protocol anyway, so I'm continuing to take the melatonin.
-------------------- Getting older is when we would rather not have a good time than have to get over it. - Oscar Wilde Posts: 386 | From Radnor, PA - where the ticks run free | Registered: May 2006
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
{{Definition: Cytokines are a group of proteins and peptides that are used in organisms as signaling compounds. These chemical signals are similar to hormones and neurotransmitters and are used to allow one cell to communicate with another.}}}
The body is attacking the foriegn peptides,that are bound up with ours because of the bacteria's like Bb ability to latch on to our peptides and use them as stealthing, hiding, immune evasion technique.
Furthermore, we demonstrated that these effects are reduced and/or reversed by the pineal indoleamine melatonin. A 24-h exposure to 50 mg/L mercury induced significant cell cytotoxicity in neuroblastoma cells.
Treatment of cells with melatonin before administration of mercury greatly reduced the mercury-induced cytotoxicity.Mercury treatment of cells produced another as yet undocumented phenomenon, that of inducing oxidative stress, as measured by the loss of reduced GSH from cells.
This was a rapid process, requiring only 30 min of exposure to mercury. Similarly, pretreating the cells with melatonin or premixing mercury and melatonin before administration protected cells from the mercury-induced oxidative stress. Melatonin's mechanism of action is at present unclear; however, melatonin is known to bind heavy metals (Limson et al., 1998) and to increase intracellular GSH levels through an up-regulation of GSH-synthesizing enzymes (Todoroki et al., 1998).
It is thus possible to speculate on two mechanisms for melatonin's antioxidant action, namely, (a) melatonin as a chelating agent binding mercury, thus eliminating its cytotoxic properties, or (b) melatonin causing production of increased levels of intracellular antioxidants such as GSH(Todoroki et al., 1998). It is further not excluded that both these mechanisms could be operating simultaneously.
The release of both Ab 1-40 and Ab 1-42 into the culture medium was increased by exposure of SHSY5Y cells to mercury. Melatonin preincubation resulted in a significant decrease in Ab release. The mercury induced increase in Ab release may be caused through mercury's deleterious action on essential kinase enzymes involved in the a-secretase pathway of APP metabolism.
The result could be that cells are pushed toward the b-secretase pathway of APP metabolism, resulting in an increase in Ab release. Mercury has previously been shown to be a potent inhibitor of enzymes, especially those containing sulfhydryl groups (Edstrom and Mattsson, 1976).
Protein kinase C activity in vitro and in brain tissue is markedly reduced in a concentration-dependent manner by mercury (Rajanna et al.,1995).Phorbolester binding to protein kinase C is also inhibited by micromolar concentrations of mercury(Rajanna et al., 1995).
It is thus possible that increased levels of mercury reduce protein kinase C-mediated a-secretase activity with the consequence of increased Ab formation because protein kinase C mediates activation of the a-secretase pathway.
Mercury induces both Ab production and oxidative stress; thus, the chelation of mercury by melatonin could shift the APP metabolism back toward the a secretase pathway, reducing Ab production and the concomitant oxidative stress-inducing effects of mercury and Ab.
Ab Fibrillogenesis is also inhibited by melatonin, thereby potentially reducing the toxic buildup of Ab 1-40 and Ab 1-42 fibrils (Pappolla et al.,1998).
Furthermore, melatonin has been shown to reduce the release of soluble APP from cells in culture and to reduce the levels of APP mRNA and other housekeeping protein mRNAs (Song and Lahiri, 1997).
These data suggest that melatonin may be involved in metabolic mechanisms regulating APP and other essential cellular protein production, over and above its antioxidant capacity.
In a similar fashion mercury induced an increase in tau phosphorylation as compared with untreated cells. Melatonin treatment was able to protect cells from the mercury- induced tau hyperphosphorylation.
Mercury's influence on tau phosphorylation remains unclear; however, it may be an indirect effect via oxidative stress and Ab production. Both Ab and oxidative stress have been shown to influence tau phosphorylation (Busciglio et al., 1995; Takashima et al., 1996).
It is speculated that Ab's action is through the activation of glycogen synthase kinase-3 concomitant with an inhibition of phosphatidylinositol 3-hydroxykinase (Busciglio et al., 1995; Takashima et al., 1996). Phosphatidylinositol 3-hydroxykinase has further been shown to regulate glycogen synthase kinase-3 negatively via activation of protein kinase B and its pathway (Burgering and Coffer, 1995; Cross et al., 1995).
Mercury could thus exert an effect within this pathway not unlike that in the a secretase pathway of APP metabolism.
In conclusion, our data suggest that inorganic mercury could be involved in some of the pathophysiological aspects of AD. The pineal indoleamine melatonin is able to counteract, at least in part, these effects and needs further investigation as a potential therapeutic agent.
From: blackwell-synergy
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Melatonin: The pineal hormone that helps to regulate the sleep/wake cycle, melatonin is also an anti-oxidant. It is relatively unique among natural anti-oxidants in that it is a terminal antioxidant: once oxidized, it cannot be reduced36. This characteristic means that melatonin cannot participate in destructive redox cycling, where an oxidized compound is reduced by oxidizing another compound. One study has found that neurons are protected from mercury damage by hormonal levels of melatonin37.
Melatonin is also concentrated in the mitochondria and protects them from oxidative damage.38 Aside from its anti-oxidant properties, melatonin helps to regulate the sleep/wake cycle, which is often seriously deranged in autistic children. Its long-term use in institutionalized children has established its safety39.
Doses of up to 0.1 mg/kg at bedtime should be adequate to help with sleep disturbances. Some clinicians have noted that smaller doses of melatonin (0.3 mg in adults) are just as effective for sleep and may cause fewer problems with nightmares and/or night terrors. A sustained release form of melatonin is currently under development and should help with those children who awaken four to six hours after the dose of melatonin. 13
From: Mercury Detoxification of Autistic Children: Consensus Position Paper - Part 3Mercola
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8) Heavy Metals Can Disrupt Sleep The Cycle The Melatonin hormone controls the sleep/no sleep states. If Melatonin is on in the day, one will feels tired. If it is off at night, one cannot sleep (it should be the other way around).
Too much noradrenaline (NA) at night can also inhibit the sleep state. A chemical called SAMe reduces the level of NA at night; yet mercury, lead, arsenic, cadmium and a variety of other chemicals can bind to SAMe and make it less affective at reducing the night-time NA. If this is the case, supplementing with SAMe, available from health food stores, can help one sleep.
In our example case, George's Melatonin was off at night, and on during the day, which is the opposite of what one would want.
Those with mercury induced autoimmune problems can worsen from Melatonin supplements, and therefore Melatonin supplementation is not recommended for people with mercury issues.
ME> Problems get worse because of ??? just mercury getting out or is this a herx??? From: How Mercury Can Cause CFS/FMS
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These results provide strong experimental evidence that mercury toxicity may be involved in Alzheimer's development, the authors suggested. Melatonin, on the other hand, shows a marked potential to neutralize this toxic-induced pathology, by boosting antioxidant defense and binding to heavy metals. From:
MERCURY, MELATONIN, AND ALZHEIMER'S DISEASE
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FIGHTS FREE RADICAL DAMAGE INDUCED BY LEAD EXPOSURE
At first glance, you wouldn't think there was a connection between a hormone that modulates your sleep patterns and your body's natural defense against the effects of lead toxicity. But melatonin, secreted by the pineal gland in the brain, may actually act as a type of natural "antidote" against some of the damaging effects of lead poisoning mediated by oxidative stress.
"One of the major concepts on the mechanisms of Pb (lead) toxicity is its ability to generate reactive oxygen species," notes a new study appearing in the Journal of Biochemical Molecular Toxicology.
In response to lead exposure, free radicals quickly multiply and break down the cell's natural antioxidant defenses, eventually damaging cell membranes, proteins, and DNA. Stores of zinc and copper inside the cell, crucial components of this antioxidant system, may also plunge. At the same time, the body's ability to synthesize hemoglobin - the blood's life-giving "porter" that carries its precious cargo of oxygen to surrounding tissues - becomes significantly stymied.
Researchers conducted an experiment to see if melatonin could help to block this destructive toxic cascade. They found that in laboratory rodents exposed to lead, melatonin reduced lipid peroxidation - free radical damage to fats that serve as critical structural components of the cell membrane - by over one-third, as evidenced in liver tissue. Melatonin also reduced the lead-induced drop in levels of the powerful antioxidant glutathione by over 65%.
What's more, while rodents exposed to lead showed severely suppressed levels of powerful antioxidant enzymes such as glutathione reductase and superoxide dismutase by over 50%, melatonin treatment effectively restored these protective enzymes to near normal, pre-exposure status. In fact, laboratory rodents that received melatonin while being exposed to lead produced nearly the same amount of hemoglobin as healthy rats that had not been exposed to the toxin.
What gives melatonin its one-two punch against lead toxicity? "The prophylactic action of melatonin against lead-induced changes might be associated with two mechanisms," the study concluded. "First, protection of antioxidant capacity in cells, and second, its ability to scavenge hydroxyl radical directly due to its structural features."
Previous studies have reported that melatonin can quench the highly toxic hydroxyl and peroxyl free radicals even more effectively than powerful antixoxidants like glutathione or Vitamin E.
Source: El-Missiry MA. Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats. J Biochem Molecular Toxicology 2000;14(1):57-62.
From: MELATONIN: A VALIANT GUARDIAN AGAINST HEAVY METAL TOXICITY
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A recent study provides additional clinical evidence that practitioners can achieve improved patient outcomes by working with the body's natural wisdom, rather than against it.
By reestablishing the body's natural circadian rhythm of melatonin, a powerful regulatory "sleep" hormone produced in the pineal gland of the brain, practitioners can help patients free themselves from long-term dependence on benzodiazepines, the potentially addictive prescription drugs commonly used to treat insomnia.
In a double-blind placebo-controlled study appearing in the Archives of Internal Medicine, Tel Aviv University researchers report that elderly patients who receive a nightly dose (2 mg) of controlled-release melatonin are much more successful at weaning themselves off medications such as alprazolam, oxazepam, brotizolam, and lorzepam. After six weeks of melatonin therapy, 14 out of 18 patients were able to completely discontinue their benzodiazepine treatment. Only 4 of 16 patients in the control group were able to do so. When patients from the control group were later provided the same melatonin treatment, however, an additional 6 patients were able to end their dependence on benzodiazepines, raising the success rate to 63%.
Ironically, benzodiazepines themselves seem to cause or worsen the problem they attempt to treat. "Long-term benzodiazepine therapy may impair the endogenous melatonin rhythm, which may in turn induce or aggravate sleep disturbances," the researchers noted.
Patients who had their melatonin natural circadian rhythm improved by therapy also showed improved sleep quality, even after quitting their use of benzodiazepines. A six-month follow-up revealed that 79% of the patients who quit using benzodiazepines with melatonin therapy still remained off the drugs. Other clinical studies have shown that patients taking melatonin do not develop tolerance, and experience no withdrawal when therapy is discontinued, unlike patients treated with benzodiazepines.
In an accompanying editorial, Harold J. Bursztajn, M.D., of Harvard Medical School applauded the study's findings and described melatonin therapy as an alternative that "integrates good clinical care with effective risk management." According to Bursztajn, by avoiding the dream-suppressing effects of sedatives, practitioners can also better approach the affective conditions, such as chronic bereavement, depression, and stress disorders, that can cause or worsen insomia among the elderly.
NOTE: The Melatonin Profile is an important diagnostic tool to help physicians successfully utilize this powerful new clinical approach for treating insomnia and benzodiazepine dependence. This noninvasive salivary analysis evaluates melatonin activity over the complete light-dark cycle, clearly revealing any disrupted secretion patterns and providing practitioners with a sound clinical basis for developing and monitoring treatment protocols. Assessment is an important first step in identifying imbalanced circadian rhythm and for individualiing therapeutic interventions.
Source: Garfinkel D, Zisapel N, Wainstein J, Laudon M. Facilitation of benzodiazepine discontinuation by melatonin: a new clinical approach. Arch Intern Med 1999;159:2456-2460.
Bursztajn HJ. Melatonin therapy: from benzodiazepine-dependent insomnia to authenticity and autonomy [editorial]. Arch Intern Med 1999;159(8):2393-95.
From:
MELATONIN THERAPY HELPS PATIENTS END DEPENDENCE ON BENZODIAZEPINES
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PROTECTS CELL MEMBRANES FROM LIPID PEROXIDATION
Free radicals seem to have a hard time getting over their loss of an electron. In large numbers, these unstable molecules wreak metabolic havoc in the human body, attacking DNA, protein, and lipid components of healthy cells. Eventually this assault can lead to cell breakdown and death, accelerated aging, and degenerative disease.
The human body may have a powerful natural ally against free radical activity, however, in the form of melatonin, a circadian hormone produced by the pineal gland in the brain. Researchers have discovered that by blocking free radical damage, melatonin significantly reduces pancreatic injury in laboratory rodents with experimentally-induced acute pancreatitis. This increased protection was evidenced by lower rates of lipid peroxidation and reduced edema in both the pancreas and stomach.
"Recent reports suggest that oxygen-derived free radicals play an important role in the pathogenesis of [acute pancreatitis]," researchers commented. By preventing lipid peroxidation, melatonin may help preserve the integrity of the cell membranes, preventing the "leaks," or increased permeability, that cause tissue edema. It may also cut off free radical-triggered inflammatory mechanisms, such as the leukocyte migration and accumulation in injured tissue that often fuels pancreatitis and its complications.
"...melatonin is highly protective of the gut against a variety of toxic agents," researchers noted. "The implication of these findings is that melatonin may have utility in treating a variety of degenerative gastrointestinal conditions."
These results add to a large body of clinical evidence supporting melatonin's role as a "highly efficient free radical scavenger" that can inactivate potentially destructive agents of oxidative stress, including the highly toxic hydroxyl (OH) and peroxyl (LOO) radicals, investigators point out. "Additionally [melatonin] stimulates several antioxidative enzymes, including SOD [superoxide dismutase], gluthathione peroxidase, and glutathione reductase."
Researchers speculate, in fact, that melatonin may even be more powerful and pervasive than most other antioxidants in the body, since it can be absorbed into both water and fat, allowing it easy access - and thus the ability to protect - virtually all parts of the cell.
NOTE: By evaluating the circadian secretion pattern of this critical antioxidant, the Melatonin Profile reveals deficiencies that may be playing an important contributory role in a variety of degenerative conditions and diseases, especially those associated with aging and free-radical damage.
Source: Qi W, Tan D-X, Reiter RJ, Kim SJ, Manchester LC, Cabrera J, Sainz RM, Mayo JC. Melatonin reduces lipid peroxidation and tissue edema in cerulein-induced acute pancreatitis in rats. Dig Dis Sci 1999;44(11):2257-2262.
From: MELATONIN STEMS FREE RADICAL DAMAGE IN PANCREATITIS
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The cap letters above are from Great Smokie Lab
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
Mg has MANY, MANY functions. It is dropping, spiraling downward, because so much is being used for its many functions.
Every enzyme, every hormone, every protein (including our own antibodies) need Mg to be made.
We need Mg-ATP to control the conversion of ATP -> ADP by raising cAMP. It INactivates PFK...the rate controlling enzyme for glycolysis. Bb is "PFK dependent". And believe me..we are "stuck" in the glycolysis (low levels of ATP) if we have lyme.
Go here (just skim it and you will be blown away):
Thats why I didnt stay on it more than 10 days at a time But Iam still using and the effects have lessend.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
My LLMD told me to take melatonin for my sleep issues. It works for me but I try not to take it unless I really need it. Also gave it to my son who was having trouble falling asleep for awhile. He doesn't have problems sleeping though once he gets to sleep. Anyhow, it works great for us. There don't appear to be any negative effects at all. Actually I just ran out so I need to get more at my next doctor visit. Any suggestions from anyone on a brand?
Posts: 547 | From Maryland | Registered: Mar 2005
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Beverly
Frequent Contributor (5K+ posts)
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posted
I take a timed released and a sublingual by Source Naturals. I think it helps.
Intresting info Tree.
Posts: 6638 | From Michigan | Registered: Jun 2001
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posted
Thanks a trillion billion, going to buy some tomorrow!
Posts: 69 | From Washington | Registered: Jan 2007
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
If it slams you the first time you take it skipp a day or 2 then try again. I aslo dont take it for more than 1or2 weeks at a time.
I always took it 1/2 hr before bedtime stay out of light or it will be used up faster turn off all lights in bedroom quick as possible at bedtime.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
5dana8
Frequent Contributor (1K+ posts)
Member # 7935
posted
I switched over from regular melatonin to the timed release and have been feeling alot worse on most levels for aprox 3/4 days now. Pain, fatigue,brain fog worse,muscle aches... Feels almost like a herx.
Wondering 2 things:
Does the time released lag over into the next day and cause day time sleepiness?
Since melatonin cross's the BB barrior can it also kill bb?...If this is possible might the time released melatonin be keeping higher levels in the system longer?
Thanks for any answers. Have bad brain fog so pretty please try to keep the answers simple
Thanks Dana
-------------------- 5dana8 Posts: 4432 | From some where over the rainbow | Registered: Sep 2005
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posted
I haven't had an issue with residual drowsiness on my timed release 2mg. Sometimes I wake up too early, actually.
Maybe you're detoxing your brain?
It isn't claimed as an actual Bb killer that I know of.
-------------------- Getting older is when we would rather not have a good time than have to get over it. - Oscar Wilde Posts: 386 | From Radnor, PA - where the ticks run free | Registered: May 2006
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
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