The full report is available to read. Results are based on lab tests, but still very exciting. Interesting that they took 25 mg at noon and 25 mg 30 minutes before bedtime:
Effect of Melatonin Administration on Mitochondrial Activity and Oxidative Stress Markers in Patients with Parkinson’s Disease hindawi.com/journals/omcl/2...
"Abstract
Mitochondrial dysfunction and oxidative stress are extensively linked to Parkinson’s disease (PD) pathogenesis. Melatonin is a pleiotropic molecule with antioxidant and neuroprotective effects. The aim of this study was to evaluate the effect of melatonin on oxidative stress markers, mitochondrial complex 1 activity, and mitochondrial respiratory control ratio in patients with PD. A double-blind, cross-over, placebo-controlled randomized clinical trial study was conducted in 26 patients who received either 25 mg of melatonin or placebo at noon and 30 min before bedtime for three months. At the end of the trial, in patients who received melatonin, we detected a significant diminution of lipoperoxides, nitric oxide metabolites, and carbonyl groups in plasma samples from PD patients compared with the placebo group. Conversely, catalase activity was increased significantly in comparison with the placebo group. Compared with the placebo group, the melatonin group showed significant increases of mitochondrial complex 1 activity and respiratory control ratio. The fluidity of the membranes was similar in the melatonin group and the placebo group at baseline and after three months of treatment. In conclusion, melatonin administration was effective in reducing the levels of oxidative stress markers and restoring the rate of complex I activity and respiratory control ratio without modifying membrane fluidity. This suggests that melatonin could play a role in the treatment of PD."
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Bolt_Upright
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"Taken together, our data showed that melatonin supplementation recovers mitochondrial function and diminishes oxidative stress. Thus, this indolamine could play a role as an adjuvant in the treatment of PD."
Sorry. From my original post: Effect of Melatonin Administration on Mitochondrial Activity and Oxidative Stress Markers in Patients with Parkinson’s Disease hindawi.com/journals/omcl/2...
Tryptophan converts to 5HTP which converts to Seratonin which converts to Melatonin. Im looking in to Tryptophans effect on dopamine to hopefully better understand Dr. Bernstein’s theory. I have read in a couple places that Melatonin decreases dopamine. But it helps Parkinson’s?
“ Dopamine reduces the impact of melatonin on your mind and body. But does melatonin decrease dopamine? It seems it does.”
Is Dr. Sackner Bernstein on to something? I think he might be.
If melatonin helps reduce (for lack of a better term) PD then what do it’s precursors (tryptophan, 5HTP, seratonin do? Could they be neuro protective?
Is dopamine neuro toxic?
in reply to
“Dopamine, due to metabolism by monoamine oxidase or autoxidation, can generate toxic products such as hydrogen peroxide, oxygen-derived radicals, semiquinones, and quinones and thus exert its neurotoxic effects. ““
“ The iron chelator desferrioxamine completely protected against dopamine-induced mortality. “
sounds pretty wonderful. On the flip side, what might be, or are, any negative effects of having so much melatonin, and doing so chronically (chronic treatment with this level of melatonin is probably what is implied to have to do)? There must be trade-offs I for anything, so a magic panacea is a country in phantasy land usually... Is it all that safe to take large doses? Really there should be, and will need to be, knowledge in some evidence accumulated about taking large doses. There is never only one side to a story and ignoring the other side may be highly dangerous and irresponsible, so it will have to be researched and studied and established. Now if somebody has any knowledge, knowledge and not speculation, genuine evidence not "it worked for me and I'm fine" amateur sales or religious anecdotes, it's not at all my field and I really would like to know... In fact, we are all going to need to know.
For instance, the Best way to impose horrifying psychosis and terrifying physical side effects is to excessively suppress dopamine production globally... Using known d1, and D2 dopamine receptor suppressants like the well known antipsychotic class of medications and substances... And if you want some real horror stories look up geodon. I've seen them in action when someone shouldn't have had them, or their degree of problems weren't properly matched to the particular treatments chosen. Pretty horrible when it goes bad. If you're not psychotic and don't need that level of psychiatric help with excess dopamine production, to reduce your excess dopamine production, well, to use a metaphor to illustrate, suppose you are a person with good eyesight and somebody gave you something that it's side effect made you totally blind... Well that is what dopamine shut down does to your sensorium and even to your physical mobility and for example, side effect of geodon is freezing your neck muscles...these are very powerful global dopamine shutdown mechanisms. So we want to and badly need to know what trade-offs, if any, exist and that means thorough research to find out.
I share the same questions and concerns. Melatonin decreases dopamine release but I have not read that it decreases it’s production. I would like to know that. Excess dopamine is toxic. (Not speculation, fact) Melatonin increases GABA. But does this GABA convert to glutamate increasing glutamate Excitotoxicity?
What if one were to increase melatonin production more naturally via supplementing with the precursor tryptophan?
Well one way or another if you shut down dopamine production or block its effect, your net effect is the same isn't it? Actually the horrible side effects come from blocking dopamine, I'm not sure that it stops dopamine production but they certainly are well established to block dopamine, in fact that blockade is the basis for their desired clinical main effect in psychiatry.
“Using known d1, and D2 dopamine receptor suppressants” I understand regarding suppressing dopamine receptors. What happens when suppressing dopamine production?
Is there validity to Dr. Sackner-Bernsteins hypothesis that there is an excess of dopamine production?
Is the PD dopamine problem not a lack of dopamine but a lack of functioning dopamine receptors?
I understand that you don’t like speculation but it is required in the learning process to direct oneself towards what is worth learning and I must learn.
All your questions are reasonable questions, the problem is that they have to be actually answered by legitimate experimentation. There is no such thing as a valid hypothesis, which is a GUESS about the FUTURE... "valid" refers to a attribute, construct, conclusion (or interpretation), about a PAST event, a part of actual history, of data created as a result of experimentation.
Speculation is more akin to: "it's okay to stick your finger in a light socket." Or "it is not okay to stick your finger in a light socket." Valid conclusion would be that we estimate with some amount of empiric evidence that it is or is not ok, because when we have the results of 10 different persons each sticking a finger one time in (the 1 same socket or 10 different sockets, take your pick because eventually to be valid we'll have to do both experiments) 10 different light sockets, the number of resulting electrocutions could be a fair approximation of the number of times you will be electrocuted when doing so, and as we continue doing more such trials we will eventually be able to generate a roughly VALID conclusion as to the number of times people must stick their finger in electric socket in order to kill half of the group of persons doing so, which we will call LD50 (lethal dose of 50%, ie the shock dose that kills 50% of those who stick a finger in a light socket). (In my example, even the example is a variable, because the shock dose is a function of time, the longer contact the more electricity is dosed, which means there can be many different doses to investigate).
Note that valid does not apply to the value good or bad, only the degree of confidence of the description and liklihood of the result, or outcome. An example would be "it's BAD because it will kill you half the time" or the same result "is GOOD, because half the time you will survive." (How could we say both? Well consider if we were talking about a cancer treatment. So it very much "depends.") But either way, it's VALID to say that half the people will die and half the people will not die.
So I guess the reasonableness of your question about whether we should really go about speculating might have to do with what's at risk in doing so. At some point we're going to have to find out. So asking me, so a trial has to follow eventually. How would you feel if I answered you "sure it's a valid speculation or a reasonable speculation or reasonable hypothesis. After all we don't know anything yet we don't know the answer. The proposed action is to dose x amount of (oral, IM, IV, surgical site delivery) melatonin to detante dopamine production or blockade at D1/D2 receptors. So next, we get to go find out. You first."
Repeating my questions: “What happens when suppressing dopamine production?
Is there validity to Dr. Sackner-Bernsteins hypothesis that there is an excess of dopamine production?
Is the PD dopamine problem not a lack of dopamine but a lack of functioning dopamine receptors?”
You like to critique semantics even when the intent is obvious which derails the subject and gets us no where. Well, you get to display your intelligence and superior command of English but we get no where as far as increasing our knowledge of PD.
Obviously there has to be “legitimate experimentation.”
Is there? Maybe there is.
Is there a better way of phrasing “suppressing dopamine production” that could help my search?
There are neurological problems that benefit from decreased dopamine receptors but is suppressing production ever sought?
You have the scientific background that could help guide how to seek out this info.
Answer: I don't have the foggiest, and I don't have a lot of faith in the whole line of inquiry Plus I'm tired and I want some hot chocolate now, so I will let somebody else do the work of finding out the answer to that question, assuming they accept your commission. My guess is it is an unknown and that means the only way to answer responsibly just to see some research done first. Legitimate research costs a ton it takes a long time and an entire research community, not just one investigator and not just one pot of dollars. Anything less is just casual and small and haphazard, thus very limited value. That's my guess as to the state of the knowledge on the questions you set, and yes, they are good questions worth asking.
Well yes one must critique. Somebody has to do it or the needle they stick in you will have poison. You really should be thankful about somebody willing to do that at the cost of your fire for asking and criticizing that which must be criticized in order to reasonably get to the truth... That's part of how it's done, that's part of what it takes to actually get the knowledge. Effective critiquing is a skill.... It doesn't mean doing the investigation or other things is also bestowed upon the one who is good at critiquing. It takes a village. For instance, not everyone can be a doctor, how good are you at enjoying looking at a human body whose skin has been removed? Doctors can, so you don't have to. What if that had to be left to you?
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