Fibromyalgia (FM) is slightly more common in people with PD and FM can cause all over body pain that moves around and can affect tissues, joints and muscles. This group of people with PD and FM are more likely to get dementia and have worse symptoms. FM can cause painful flare-ups at random times, but are often related to stress.
>>> ' This pilot study suggests that transdermal magnesium chloride applied on upper and lower limbs may be beneficial to patients with fibromyalgia. ' <<<
Here is a link to a typical product that you spray on and rub in:
Moving your vitamin D level higher into the reference range may be useful in alleviating some of the pain from fibromyalgia. The vitamin D test required is a "25 OH d " test and the reference range for this test is 30 - 100 ng/ml. Getting this level into the upper half of this range may be useful. The following multi study review confirms the usefulness of vitamin d for Fibromyalgia. It is also worth noting that vitamin D level is usually low in both PwP and Fibromyalgia.
>>> ' Results 2651 studies were retrieved, with 12 studies fulfilling the inclusion criteria. 11 out of these 12 studies were of high quality and showed low risk of bias. 11 of these also demonstrated definitive improvement in clinical status and various outcome measures following supplementation with Vitamin D. Conclusions Our study emphasis an association between supplementation of vitamin D and improvement of the clinical condition fibromyalgia through a systematic review of high-quality studies. ' <<<
Vitamin D also lowers multiple inflammatory mediators that are elevated in PD and Fibromyalgia as I discussed previously here :
Some people report benefit from higher dose oral magnesium in the forms that are considered to be more bioavailable such as magnesium glycinate. Magnesium blood testing is not accurate for determining tissue magnesium levels because the blood only accounts for .08% of body magnesium with the rest being in the bones, muscles and soft tissues, with these last two being where many FM symptoms are felt. You can have a normal serum level while having low tissue levels. Testing higher than recommended magnesium dosing under a doctor's care and guidance to see if you can obtain significant relief that way is one way to test magnesium to see if it can be beneficial in a particular case.
>>> ' Moderate quality of evidence supports acupuncture in reducing pain in patients with FM. Therefore, acupuncture is recommended as a treatment for FM. ' <<<
Fish oil can also offer some benefit through its anti inflammatory effects:
>>> ' This first-ever reported case series suggests that omega-3 fatty acids may be of benefit in the management of patients with neuropathic pain. ' <<<
These are just a few suggestions to consider if his doctor confirms a diagnosis of Fibromyalgia. There are more supplements that have shown benefit for Fibromyalgia, but the ones I mentioned above have also shown benefit for PD.
Art
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Wow thank you! My HWP has similar pain, but it does not match up to the Fibro pain points, it could be central pain. I wish there was more information on preventing dementia in PD. 🙏
Interesting, thank you. I have a Fibro diagnosis, although not PD, and suspect that in my case COMT is involved, as well as MAO and others, with an imbalance of neurotransmitters. I don't think that the imbalance or cause is necessarily the same in all those with Fibro, and we don't all respond to the same types of treatment
Magnesium speeds up a low activity COMT variant and has made a vast difference to my pain and functioning. COMT is a methyl function and impacts the common methylation issues which I believe some have linked to PD, as well as most other chronic conditions, through the folate cycle and homocysteine. I also have a small fibre neuropathy diagnosis, which some consider to underlie many Fibro diagnoses and I understand has also been linked to PD ncbi.nlm.nih.gov/labs/pmc/a...
Thank you for the feedback on the usefulness of magnesium usage in your case! If you don't mind, could you give the brand and type of magnesium as well as the dosage that is effective for you? How much pain reduction, on a scale of 1 to 10 do you feel it offers you after compared to before magnesium?
Thank you also for the new information and links. Fish oil at higher dosing is generally useful for lowering inflammation in general and FM seems to have both inflammation and oxidative stress as two major driving forces. Similarly with vitamin D.
Hi, I started with Epsom salts in the bath or a foot bath, but was advised that mag chloride was better than sulphate so started using Better You, again the flakes in a foot bath of warm/hot (not too hot) water for about 20 minutes. Very sensitive so always start low and go up as body tells me. Now usually use the sensitive oil spray (betteryou.com/collections/m..., at night and during the day if needed, but rarely more than 5 or 6 sprays daily, which seems to suit me. Don't always have the time or energy to use a footbath but do use some form of mag every night. I have changed a lot of other things and pain is lower than years ago, but condition has deteriorated and others have appeared so other pain and neuro issues have developed. Not trying to avoid the pain reduction question but it isn't quite so straightforward (when is it ever?). I was taking tramadol, gabapentin, amitriptylene and venlafaxine or citalopram for approx 15 years. I feel better now, off all of those for 7 years, and using diet, meditation/tapping/vagus exercises, vitamins and minerals. I credit magnesium with a respectable chunk of my personal improvement. For the nerve pain that I've had for 20+ years I'd say it was about half as bad for most of the time. Never tried oral mag as gut is a weak point and absorption poor.
I may have to go back to think about fish oil. I generally use EV olive for inflammation and vit E, plus vit D at a decent level.
Regarding fish oil, in studies the effective dose I have seen is in the 3 to 4 grams of combined EPA and DHA per day, which is a significant amount and FO is known to have blood thinning effects, which is worth keeping in mind in case you are taking other things that are also considered to have blood thinning effects like vitamin E.
Thank you, I'll look into that. I do take the vitamin E precisely for blood thinning, as I struggle to tolerate aspirin and have anti-cardiolipin antibodies.
I use magnesium oil for my cramp-fasciculations. Walmart sells it in their tiny organic personal care section. Attached photo of the products I use for pain and inflammation.
There is a commercial Fibromyalgia test - my test was strongly positive. I am not generally in pain. The test looks for anti-NMDA receptor antibodies.
CCraspberry has posted extensively on the links between NMDA receptor antibodies, neurodegenerative disorders and the underlying pathology of brain inflammation.
How would the standard of care change if PD/AD/ALS were in fact treatable autoimmune conditions?
I'm trying to connect the dots between causation, condition and recovery.
Thank you for your feedback on how you use MO! It is used on this forum for muscle cramping, minor pains in muscles and joints and to relax muscles before exercise such as walking and or stretching. When you do have pain, one of the better topicals that is easy to find at local drug stores and not expensive is this one :
Regarding connecting the dots, that is essentially part of what I try to do. That is why I write so much about the age related decline of melatonin and the inverse relationship it has to the rise of age related diseases like PD. The lower melatonin declines in people the sooner age related diseases begin and their symptoms increase.
Melatonin has shown the ability to work against a multitude of features of PD, not just one or a few. Melatonin has already shown benefit in PwP at 10 and 50 mg/day, but what is needed are higher dose studies to get a better idea of what the optimal dose of melatonin might be for PD and the best way to deliver it to avoid side effects. There are important reasons that melatonin is produced in every cell in the body and our health declines with the age related decline of melatonin.
Thanks you! Do you think the StopPain is more bioavailable that taking a supplement? I know my gut is "leaky" and feel like part of the problem is malabsorption. I look for alternative ways to support my body, like detox baths and topicals. I have the supplies now to make melatonin cocktail suppositories. I don't think 200mg is too much!
Regarding Stopain, to me it makes sense to use a topical pain reliever if the pain is localized to just a few places, beyond that then oral supplements that go systemic make more sense and more practical than applying pain reliever to 5 or more areas of the body.
If you think 200 mg melatonin suppositories is a lot, look at these :
Yes, a 400 mg suppository! Apparently the suppository route does not cause next day drowsiness as noted in the study link below.
Notice the things that they are implying that it "may" help.
I will be very interested to know how your experiment goes. I have never used such a high dose. One of the highest dose schedules I have seen was a 300 mg dose delivered rectally and it was used in ALS patients for up to 2 years.
Too bad that ALS study is behind a pay wall. Art, you turned on a HUGE lightbulb for me!!!!!
I was curious about how the pineal gland is affected by certain toxins and how it might relate to my condition. I found this abstract from the NY Academy of Science:https: //nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1998.tb09920.x?sid=nlm%3Apubmed
Melatonin is a neurohormone of the pineal gland. It is a direct free radical scavenger and indirect antioxidant.
Melatonin has been shown to scavenge the hydroxyl radical, superoxide anion radical, singlet oxygen, peroxyl radical, and the peroxynitrite anion.
This is what got my attention - melatonin's antioxidant actions probably derive from its stimulatory effect on the antioxidant enzymes; superoxide dismutase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase and its inhibitory action on nitric oxide synthase.
[Copper-Zinc] superoxide dismutase (SOD) protein misfolding and accumulation in the CNS is considered the primary mode of parthenogenesis in ALS.
Structurally weakend SOD loses its affinity for binding Zinc.
Zinc-deficient SOD induces apoptosis in motoneurons through a mechanism involving peroxynitrite.
Sounds like melatonin is synergistic with Copper/Zinc to revive SOD production.
As it relates to causation- in models of oxidative stress, melatonin has been shown to resist lipid peroxidation induced by paraquat, lipopolysaccharide, ischemia-reperfusion, L-cysteine, potassium cyanide, cadmium chloride, glutathione depletion, alloxan, and alcohol ingestion. I don't think it's too strong of a statement to say, melatonin is the antidote.
Free radical damage to DNA induced by ionizing radiation, the chemical carcinogen safrole, lipopolysaccharide, and kainic acid are inhibited by melatonin.
Neurotoxins, Kainic acid and AMPA, are two of the three (the other being NMDA) agonists at ionotropic glutamate receptor binding sites involved in glutamate excitotoxicity and neuroinflammation.
Melatonin is an AMPA/Kainate receptor antagonist, it blocks binding to the glutamate receptors, and inhibits neurotoxicity.
The active ingredient in Roundup is Glyphosate, whose metabolite is AMPA. The glutamate agonist α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), is a potent inhibitor of melatonin synthesis in vitro. In the primate pineal gland, glutamate can act on glial cells via AMPA-gated receptor channels in unusual subunit configurations that likely underly high calcium permeability. This may be a mechanism for glyphosate neurotoxicity.
The protective effects of melatonin against
brain oxidative stress has also been shown in neurodegener-
ative diseases, such as Alzheimer’s and Parkinson’s diseases.
Melatonin can easily cross all physiological barriers, such as the placenta or the blood–brain barrier, and it can enter all cells of the body. Melatonin is not exclusively produced in the pineal gland, but it is also locally synthesized in several cells and tissues, such as the retina, the gastrointestinal tract, and the innate immune system. Studies have proposed that mitochondria are the primary sites of melatonin synthesis. Melatonin has direct access to the CNS because of its presence in cerebrospinal fluid.
So much more to tease out, the take away for me is that melatonin needs to be supplemented at levels higher than the oral 50mg therapeutic dose along with zinc and copper.
I can see that you are focusing in on why I have written so much about melatonin on this forum. It seems it does everything it can to try and maintain homeostasis in the body for as long as it can until the age related decline of melatonin declines to a level where it can no longer fully maintain its protective effects throughout the body and that seems to coincide with the onset of age related diseases. Once melatonin production drops to that level, then age related diseases seem to have an easier time of progressing.
I don't know that oral supplementation is the optimal way to regain melatonin levels that are more optimal for health, but it seems like the easiest way to test. The poor bioavailability of oral melatonin at 3 to 15% requires very high oral dosing for testing. The rectal route is probably a more bioavailable route.
I want to add that NAD declines by 50% by approx age 50 as well. NAD is literally life sustaining. In human trial for precursors for PD and aging in general is ongoing.
Thank you for sharing your knowledge on melatonin. I'm focused on finding a protocol that will help me (and others) recover.
This requires understanding the nuts and bolts of causation. What caused the injury, how did it cause the injury, where is the injury, and how can I help it heal. You don't put a cast on your arm when you have a broken leg. We need to heal our beautiful and complex broken brains.
My lightbulb was the realization that melatonin is the AMPA/Kainate receptor antagonist I was searching for. I knew what I needed to find because I understand causation and Art's post prompted me to look closer at melatonin.
Brain inflammation underlies ALL neurodegenerative illnesses. Brain inflammation is caused by excitotoxicity from a neurotoxin that activates glutamate receptors which stimulates overactivation of our neurons.
General question: do you think a-synuclien plaques are the cause or effect of Alzheimer's; how about Lewy Bodies, cause or effect; loss of dopamine in the substantia nigra, cause or effect; muscle wasting in ALS, cause or effect?
They are the result of our body trying to protect higher processes in the CNS from a toxic cascade. How quickly or slowly this happens depends on multiple factors. In my case it happened very quickly, inhaling a neurotoxic stew of chemicals overwhelmed my detox system and depleted my antioxidants. I didn't know it at the time.
As silly as it sounds, researchers thought ALS was caused by dying back of neurons, only recently has it been recognized as a brain disease. Now they think ALS is more than one disease. If I could just bend their ear about my experiences.
I don't believe we can refer to neurodegenerative illnesses as age related anymore - they are environmental illness. You don't just wake up with ALS at age 52. That's not how the nervous system works. For some people it's chronic neuroinflammation and others it's acute- I'm in the latter group, people with PD can learn from my experience.
I'm gonna put some melatonin in the nether regions along with THC/CBD oil, reduced glutathione and some cu-zn.
You are correct that you don't wake one day with ALS, PD or any other age related disease. The chances of getting an age related disease increases with age and in PD, age is the number one risk factor of getting PD, hence the references to PD as an age related disease.
So by our current medical standards, PD is an age related disease with an average age of onset of 60 years. If 50 years of age is a tipping point for the age related decline of melatonin as it appears to be, it makes sense because it is often related that people likely have PD at least a decade before the symptoms become clear and apparent enough for a diagnosis of PD. Same with other age related diseases which begin to accelerate in frequency around the age of 50 years.
Keep us updated on your testing, it sounds interesting!
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