Their injections contain other vitamins as well as thiamine, but I just noticed the b12 is cyanocobalamin. Is anyone else taking thiamine injections using this or is it normally just pure thiamine? I thought cyanocobalamin would be best avoided. Is that why Dr Constantine recommended taking b1 only without other vitamins as these mixtures contain the synthetic b12?
I just noticed a Facebook post from someo... - Cure Parkinson's
I just noticed a Facebook post from someone on neurobione (thiamine injections)
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Neurobione has a mega dose of B6 which is not good. I don’t take Thiamine injection but guess other people in HTD use B1 injection alone.
I just wondered if the reason some people respond and others don’t is because some people are taking this neurobione with lots of other things in it.
Vitamin B-6 is absolutely necessary for your overall health. I believe I addressed this complete fallacy previously.
Sharon
I think it’s good in the correct doses but doesn’t too much cause neuropathy? However carbidopa in sinemet uses it up so most people are probably in more danger of having too little I would have thought if taking sinemet.
Hi Lyn. My husband took neurobion before. It has thiamine mononitrate. It had no effect and had large amounts of B6 and B12. I also read that too much B6 causes neuropathy and the B12 is the wrong type. Trust these pharma to produce poor products and you take it thinking it helps
Yu might want to spend some time, when you have time, to read the mid-1970s CTs on L-Dopa and B-6. Interesting in the sense that two major CTs came to completely different conclusions about B-6 with L-Dopa (and more importantly, with or without cardopa, aromatic L-amino acid decarboxylase inhibitor). The PI in one of the CTs completely missed the issue, yet his conclusions have been regurgitated endlessly. It all comes down to the use (or lack thereof) of a Aromatic L-amino acid decarboxylase inhibitor.
Dieticians are not the experts here. I realize that some on this forum have quoted Kholden as the guru when ti comes to b-6 and b-12. Is she? Doubtful.
Neuropathy? B-6? ...do yourself a favor, when you have time of course, and read the Phase III....A Randomized Phase III Study of Vitamins B6 and B12 to Prevent Chemotherapy-Induced Neuropathy in Cancer Patients. Wonder why they chose these B vitamins?
Most neuropathy involves diabetics, (about 50% of the diabetic population) which is no surprise, or it shouldn't be. IOW, if you have PN, you are likely a diabetic whether you know it or not.
Meta analysis indicates that b-6 intake was linked to protection against inflammation. No wonder, It acts as a cofactor for as many as 300 enzymes in macromolecular metabolism, etc. etc. etc. In plain English, low B-6 status and age-related diseases are positively correlated.
In the appropriate context, Among the B complex vitamins, B1, B6, B9 and B12 are proven to help in neuropathy.
Thanks, that’s good to know. Can you please put a list of acronyms and what they mean as I don’t recognise some of them.
hi again, , I had a look at the paper but can’t seem to find the results, only what they were going to do. What was the outcome?
Also all these people were on chemo drugs that possibly depleted b6. Do you know if there are studies on high doses on b6 with people who are not taking pharmaceutical. So if someone reading this who is just on supplements not drugs takes the same amount do you think that would be safe too?
This CT was as of yet unpublished. Could be for several reasons.
Studies on vitamin supplements are not a common occurrence especially when they don't involve a disease (or prevention, i.e. cardiovascular disease especially for b-6) or interaction with or replacement of a drug.
The 2017 study on LCIG (l-dopa by infusion gel) (yikes!) showed minimal B-6 implications for PN....about 20% of the participants had some signs but nothing significant, even though 9 of the 30 had chronic PN before the study even began! Seriously!
Many commentaries on b-6 possibly causing PN but nothing I could find that would substantiate this regurgitation that I would classify as acceptable science.
Multiple sources are available for identifying minimum daily requirements by gender and age without taking into consideration the declining bioavailability of oral b-6 if taken by the elderly or those with intestinal absorption problems. Anecdotal (sometimes worthwhile; sometimes not) commentary suggests 100 milligrams as a daily maximum.
Ok thanks
Yes, cyanocobalamin is the synthetic form of b-12, but it isn't highly toxic (as some suggest and claim) and it ultimately converts in 4 steps to the methyl form of b-12. Tedious but it does convert. They probably use it because presumably it is more stable than the methyl and much cheaper.
Regardless, best not to use anything with cyanocobalamin; stick with the methyl.
I’ve read numerous places some people with the mthfr gene can’t convert it and some say it crowds out the natural methyl form from food sources. Do you think that is correct?
The key here: MTHFR is an enzyme. Which B vitamin exerts enormous control of most of the body's enzymes? Is it B-6? Without this B vitamin, you are in big trouble.
Specifically, most people don't know if they have one of the 50 or so variants of the mthfr gene mutation/deficiency. Are the estimates (some as high as 60%!) realistic? I doubt it. Pure guess work. Make it up as they go along.
I realize that people "claim" they have this gene mutation/deficiency (or that gene mutation, or that one, whatever they dream up), but it's a guess for most unless they have had a definitive test, which most haven't. Even then, the testing is often suspiciously random,and they can't do anything about it anyway.
Furthermore, what if someone has one of the many variants? Do they all act the same way? Very doubtful. No one really knows.
Remember, This gene mutation issue "wraps around" back to B-6 and its importance in controlling homocysteine levels. If you are unfortunate enough to actually have this deficiency, and on top of it, you think intake of B-6 is BAD, BAD, BAD=NO GOOD like so many on this forum think, you are at serious cardiovascular risk. Unfortunately, they haven't a clue.
B-6 is critical in so many ways; the L-Dopa/B-6 fallacy or not.
S
Interesting that a recent Japanese study found that the MTHFR mutation decreased with age! Or was it that those who lived to old age didn't have the variant in the first place...for the most part.
I think before prenatal vitamins might have prevented some dying before birth who may have not survived otherwise so there may not be as many people in previous generations who survived. Medical advances mean more people survive things that previously would have died in previous generations. They probably have children with the genes too so you would expect the number with these SNPs would increase at each generation.
When you have time, read the 2012 study on MTHFR (which is supposedly a "snips") and one variant C677T. What I found fascinating as a biochemist was the implication of mild cognitive impairment in two very different cohorts which (in my way of thinking) wraps around back to the unwillingness or inability to use B-6 in PD therapy. Does this unwillingness to take even a small amount of B-6 daily lead to cognitive failure in many PD patients who don't have this variant? I would think so.
I don’t think people are unwilling to take it. My husband takes Hardy’s daily essential nutrients which have 23.3 mg x3 per day. I think the worry is people might take too much of it or too close to their sinemet. If he takes them closer than about an hour apart it makes him shudder violently so he just never takes them together.
Interesting results for pediatric and adult ADHD patients using Hardy's formula. I would like to see a real CT run for 12 months on PD patients in a US PD Center of Excellence. Won't happen, but I can wish.
"Too close to their sinemet"
Are you repeating KHolden? or someone else?
--- give me a clue on how you came up with that.
Totally contrary to Heinz,
--- but what does he know compared to Holden?
--- he is simply one of the best PD researchers.
If he takes the sinemet and vitamins together he suffers a violent shuddering. This is from experience. We had to look it up to try and find out what is was and assume it is the b6 in the Hardy’s. Might be something else in it however.
How many Sinemet doses per day? How many Hardy's? Simultaneously or delayed?
If he is on 4 doses of Sin+Har per day, he is already at the max theoretically for B-6.
I am not going to play doctor like some do on this forum, but Hardy's mixture (DEN) contains some 25 minerals and vitamins, one of which is B-6 (23.2 mgs per scoop) as you pointed out earlier, and a PROPRIETARY mix of additional amino acids, etc. So, don't dismiss the prop mix as a possible culprit. Face it, you are confronted by a host of variables.
The only way to assess if it is truly B-6 (as the independent variable) that is causing his "shuddering" is to eliminate the Hardy's and use P5P with his typical dose of sinemet (l-dopa/carbidopa).
To verify if it is B-6, You should begin the dose of P5P (ONE PER DAY; simultaneously with his 1st Sinemet!) ) at no more than 5 mgs. (use a 10-15 mg. micro scoop or a scale is even better) and work your way up monitoring his "shuddering". If only one dose of 5mgs. of P5P kicks it in, you know what the problem is.
If 5mgs. of P5P doesn't kick it in, add it simultaneously to every sinemet dose he takes in a day... going from 1 dose to how ever many he takes in a day. Then start all over at 10 mgs. etc. etc. etc.go to 15---20---25.
I think you get the idea. Good luck
Actually before the Hardy’s he was on the vitamins including p5p individually and he did have the shuddering then too but we hadn’t figured out what was doing it back then. He was taking lots of other things too so could have been one of them.
He takes Hardy’s 12 a day, split over 3 times. Sinemet once.
Not keen to go off Hardy’s to experiment as there has been no other thing that so quickly made so much difference to his anxiety which was life threatening. He was on similar amounts of all the vitamins previously as I had tried to mimic the Hardy’s vitamin levels because I couldn’t get the psychiatrist to agree to sign off on them initially and they wouldn’t sell it to me unless he did.
He seems ok keeping them separate so that’s what we’re doing now. He’s currently going through a bad patch despite the Hardy’s and I think it is possibly just winter sapping his seratonin.
I am getting a better picture of your situation; it took awhile.
Just stick with what is working. Too much trouble to define what is causing his "shuddering". If he is genetically defective in one or more genes, it becomes far too complicated and time consuming to figure out what is going on, and more importantly, why ... and what to do about it. Assuming you can do anything about it once you know.
The gene mutations probably (definitely) change the permeability of the BBB as time passes, so what may work one day may not work the next, and no "apparent" reason exists that is so apparent that you can draw a conclusion. An extremely difficult journey to say the least.
I frankly don't understand your situation in NZ vis-vis your psychiatrist, your husband's anxiety, and vitamins/mineral supplementation since I live in the US. We have no such restrictions but we have basically a free-market system for the most part. Almost impossible to understand why you needed a prescription unless unless it has something to do with co-pay. Thank goodness that Hardy's is at least working.
Hi, it isn’t that he needs a prescription, but the Hardy’s supplier here isn’t allowed to sell it to someone under a GP or psychiatrist who has prescribed antidepressants unless the prescribing doctor says they will supervise the gradual withdrawal of medication if he becomes over medicated. And the psychiatrist doesn’t believe nutrients will help and is based at the acute department of the public hospital so is not available as a private specialist. The GP won’t tinker with what the psychiatrist has prescribed. Complicated alright!.
He also has other SNPs that mean vit D and A pathways don’t work well, and his detox ones don’t process toxins or pharmaceuticals well. I’m not sure how common any of these are. Maybe half the population has them, but otherwise it sounds terrible.
He has high dopamine beta hydroxylase activity SNPs which the gene test has labelled “bad”. He doesn’t know this as I don’t want to worry him.
On his catecholamine metabolism flowchart it shows the DDC box before the dopamine box is 3/4 shaded, (possibly why sinemet makes no difference) and from the dopamine box the MAOA is 3/4 shaded and the MAOB is completely shaded, and the TPH2 and TPH1 leading into 5-HTP from Tryptohan are both almost completely shaded amongst other things.
Apparently theseenzymes are bad because they are all running too fast (I thought initially it meant they weren’t working but they are actually working too fast I think?)
I’m not sure where seratonin fits into the diagram. I can’t find it.
I just looked up DDC enzyme and it says carbidopa inhibits it. So that means carbidopa is good then?
The pathway does say b6 on it so you are right! But he already takes 70mg per day so I’m not sure if he could take more.
Does the fact that the pathways in and out of the dopamine box are both very fast compensate for each other? Do you know how to interpret these charts?
I am going to take one thing at a time.
I am a biochemist and not a gene theorist, so I am somewhat skeptical of some of the gene theories.
However, gene mutations and deviation do exist. if your gene(s) are mutated from birth (?) or are somehow mutated by the environment you live in over time (possible?), then the enzymes needed to covert whatever you intake into dopamine (to prevent or minimize PD) don't function very well or at all. Without enzymes, someone is in deep trouble and B-6 is the most "pervasive" and encompassing vitamin in relation to the enzyme complex.
As I said previously, to me it is all about whether someone's enzyme complex, and in PD their specific enzymes related to dopamine, is functioning at a level necessary to prevent the minimization of dopamine absorption by the brain.
So we are left with a couple of questions about your husband...
#1 Why all the gene mutations?
#2 Were these mutations existent at birth from his mother?
#3 Are these mutations increasing?
#4 Do some of the mutations cease to exist to be supplanted by others?
DBH (high dopamine beta hydroxylase activity SNPs) is the key enzyme (probably) in the conversion of dopamine. If that pathway is screwed up, only so much sinemet will be converted to dopamine regardless of how much sinemet you give him. So, I assume your chart is signalling that.
Whether you chose to call it "blocked", and I chose to call it "converted" it amounts to the same thing.
DBH abnormalities (if they actually exist in an individual) lead to a host of problems which drugs and supplements can only mitigate and will over time fail because the enzyme(s) can't convert what it needs to convert to sustain health. It is like running your care with a blocked oil filter due to slug because you have never changed the filter.
So to me (and I am not truly sure about this) the key gene mutation for PD is the DBH gene mutation (and naturally, DBH is also called an enzyme). Other gene mutations can play a part, but this one is the big dog.
Complex.
Yes, I did chemistry but it’s not much help with this stuff. I had initially thought the shaded boxes on the chart meant the enzymes were blocked and didn’t work. But now rereading it it seems they are running too fast. So is that better? At least you can slow them down?
In answer to your questions I don’t know. I thought genes exist from birth and can’t change, but methylation ( and other things?) can alter their function switching them off(?) through epigenetics.
Does the following seem right to you:
So if his DBH is too fast dopamine is being converted to norepinephrine too fast.
It looks like mao breaks it down so maoi would stop it being broken down. Bad
Caffeine increases norepinephrine. Bad
EGCG in green tea reduces it. Good
Blackcurrant juice is a maoi and he has been taking that. Bad
5htp increases mao Activity so decreases norepinephrine, but also dopamine. .? Is that good or bad?
Yet this suggestsincreasing seratonin and using SSRI decreases dopamine and norepinephrine :
“ This is because unilateral support of serotonin leads to a compensatory decrease in dopamine and norepinephrine. That’s right, most of the most commonly prescribed medications in the world cause fatigue, apathy, emotional numbness, and other low-dopamine/norepinephrine symptoms”
integrativepsychiatry.net/b...
So maybe his sertraline SSRI is overcompensating and the problem is too little norepinephrine in which case his blackcurrant is good. I certainly thought he seemed better initially on it.
Complex alright.
I’m pretty annoyed that all these pharmaceuticals may have actually made it all worse and I don’t know how to reverse out of it. I had to promise the psych that I wouldn’t reduce his meds except under consultation but he isn’t available to consult so he is stuck on them unless I reduce it myself. I’m not going to do that as he has been suicidal before so don’t want to go there again!
I was in the dark about the fact he was on Zoloft. Frankly, what is he on that you haven't told me?
Zoloft, or any SSRI for that matter, is serious, serious business, especially when you are combining it with other meds and with an older male (how old? I don't know). Suicidal behavior, major depression, extreme anxiety are the usual reasons for it.
I'm just being honest here. SSRI drugs are in no-mans land when it comes to impacting and balancing certain chemicals in the brain that PRESUMABLY are out of balance.
Is it contrary indicated with Sinemet (or its generics)?
--- a very, very good question....
--- certainly with any MAO-I
Serious stuff IMO.
I am sure you understand that Zoloft and other SSRI drugs dramatically increase mortality. Tampering with the brain is dangerous business. The trade off has to be weighed.
As you can tell I am not a fan of SSRI drugs. I am not saying"never" because I don't have an answer. But the statistics from meta analysis speak for themselves.
Yes well he was put on them years ago by go before the diagnosis and before I had read anything about all of this. His full list is on my profile. Sorry I should have directed you there first.
He was first on Prozac/ fluoxetine. That made him suicidal after a while. Then mirtazapine and fluoxetine made him hyper, risk taking, speeding, gampbling but on the upside more outgoing and fun briefly until he became suicidal again. Then they dropped the fluoxetine and left mirtazapine. That made him dopey and lethargic and I couldn’t get him out of bed, and he started with more of the Pd symptoms like funny walk and blank face. That’s when he was diagnosed with Pd as his hands weren’t working properly.
So then he slowly weaned off mirtazapine over months as it was making his symptoms worse as he would sleep all day and not exercise. He was fine for a few months then became extremely anxious and suicidal again and the public crisis unit got involved and put him back on mirtazapine and Zoloft too. He got even more anxious on Zoloft so they doubled it! And said it takes a while to work. Then I eventually persuaded them to allow him to go onto Hardy’s den and he seemed to come right in 3 days like a miracle. ( he had also been on other nutrients for months too by then) and his mirtazapine is down to 1/8 of a tablet. At least he is not anxious or depressed any more but feels nauseous, fluey, and exhausted all the time.
Believe me if I knew then what I know now I would have tried to stop him going on the fluoxetine in the first place. He also had been on doxycycline for roseacea for years for all of this and I do believe that may have started this all off by unbalancing his microbiome.
I’m not sure now if there is any way to unwind all of this as I think the way the Zoloft eventually works is by clear felling all the excess seratonin receptors so it isn’t flooded and overwhelmed so I am not even sure if it is possible to regrow them. It’s probably why he couldn’t stop mirtazapine completely without suffering severely once the final lot was out of his system. He’s probably got almost no seratonin or dopamine receptors any more.
I might put it this way: "damaged beyond repair".
He is only 59. Apparently Zoloft is the drug of choice to accompany sinemet according to the psych. And his big book of drugs.
When he was first given fluoxetine he was depressed and he has always seemed anxious since I met him at 39. He always gets down in winter. But since the drugs he has been on a roller coaster. I trusted the doctor and left him to manage his own health issues but they have made him a zombie, can’t do anything any more or go anywhere. Won’t shower, do any chores, make his own food or tea even and not interested in anything least of all helping himself so I am stuck.
Sorry to vent. I used to trust doctors now I think they have no idea of what they are playing with.
If you are referring to a psychiatrist in your comment, I find most of them know very little about drug interactions. It simply isn't what their education and clinical practice focuses upon. A few know drugs; most don't.
If you really need help with drug interactions, the best source is your university in NZ which has a Ph.d. program in pharmacology (not your local pharmacist although he might have access to a good computer data base.)
As a biochemist I specialize in cancer drugs, not SSRIs, but I know that SSRI drugs actually have a fairly substantial record (anecdotal documentation) for creating PD symptoms or exacerbating them. Anti psychotic and anti depressant drugs are very toxic (powerful) drugs that can create long lasting, and sometimes irreversible changes in the brain. They may work for awhile; then they may not and may end up damaging the brain.
These 2 genre of drugs are far and away more powerful (therefore also more dangerous) than L-Dopa, which as we know is an amino acid that exists within all of us humans (presumably) via another amino acid, L-Tyrosine.
Light years of difference.
Zolofit and Prozac probably account for more than 50 million prescriptions in the US per year. Mind boggling to say the least. Obviously, the "herd" mentality when it comes to figuring out how to treat depression, particularly in those under 25 or older than 50 (male suicide rates are always higher than females in any age cohort, particularly above 50 where they are substantially higher, much higher in fact).
You may want to read:
Gerber, PE; Lynd, LD. Selective serotonin-reuptake inhibitor-induced movement disorders. Ann Pharmacother, 1998 Jun; 32(6): 692-8.
--- via researchgate.
Old, but still relevant.
Thank you. I will. I feel mirtazapine caused a lot of the initial symptoms by slowing him down so much he wouldn’t do anything or get up. That can’t have been good. He was much better and proactive off it but seems to need the last 1/8 of the tablet to counteract the sertraline agitation and anxiety symptoms
I don’t know who kholden is sorry.
KHolden (who writes a blog on PD) is the nutrionist/dietician who has promoted the idea of waiting 2 hours after Sinemet to take B-6. Since many PD patients take their meds 4-6 times per day, it doesn't make any sense, clinically nor does any study or CT suggest it that I can remember.
Ok, well he just learned this the hard way. I’ve not read any of Kholden’s stuff. He doesn’t wait that long though. Just up to an hour. Sometimes less. He only takes sinemet once per day though.
Well my husband has a double SNP for it, he had the tests. He has relatives with Spina bifida. They probably have it. I suspect many people who have health problems may have it, possibly that is part of the reason they have have health problems.
I don’t think people think b6 is bad, but even a good thing might be bad if you have too much of it. Obviously it is needed for all those enzymes so it’s not bad.
I hesitate to say this, but most of these "genetic" tests, particularly the on-line ones, are somewhat dubious in terms of their validity. The MTHFR gene mutation is hot-button topic with many medical types, but that doesn't mean they even know what to do if someone has it, or they can send you to a qualified genetic lab for testing.
Just my opinion, but anyone who is seriously interested in gene testing should go to the Mayo Clinic Lab. An outstanding lab.
We’re in New Zealand so it’s difficult.
NZ...that is what I thought if you were using Hardy's.
Then forget what I said about testing for B-6. Your purpose is to help your husband day-to-day; not conduct a mini clinical trial on B-6. If waiting 2 hours after Sinemet to give him Hardy's gives good results, stay with it. We are all somewhat different.
If your husband has the MTHFR gene mutation, way too complicated to figure out exactly what is happening when he goes into violent shuddering. It isn't worth the trouble IMO as long as it doesn't happen under the protocol you are currently using with him. If he changes over time, back to the drawing board.
My prayers are with you.
S
Thanks.
I just remembered about your husband's depression during your winter. Buy your husband 5-6 "light box" units from Amazon.
My older sister lives near the Canadian border and would have serious depression episodes during the winter months (very little natural sunlight in upstate NY during the winter). So I bought her 6 "Verilux" (this brand is very good) units and had her husband hire someone to install them in her office at home where she spent her evenings and where she took her coffee in the morning and read the paper. She was literally surrounded by full spectrum light for several hours.
I believe in this type of light therapy. At least for my sister.
Yes, we have one which he used last winter and as he was going so well up to late May/ June this year I stupidly forgot about it. I have got it out and have set it up on timer next to the bed so it comes on at 7am a few days ago.
It does seem almost certain it is a seratonin/ dopamine unbalance causing his troubles at the moment so it might be able to get him out of it again. I imagine it would be slow to have effect?
I had noticed last year that when he watched football last season and was out under bright skies all day on saturdays he felt sick the next day. Other days he had less light as he was only out for an hour walk. I wonder if a full day of light on top of the Zoloft is overdosing the seratonin then wiping out the dopamine? It might explain why he suddenly got sick as he started going to football all day again on saturdays. Could that be right?
both are biogenic amines and as such are both neurotransmitters doing many of the same things in a slightly different way and at other times doing things very differently...ASSUMING someone has a sufficient and appropriate supply of each transmitter in the brain! A big Assumption for PD patients which is usually erroneous.
And somewhere along the line, day to day, enzymes are needed to facilitate tryptophan and l-tyrosine in doing their essential jobs.
IF somehow (many possibilities!) one or both neurotransmitters get out of whack or kilter, someone can and will have all sorts of problems. The end result is what people normally "see", the psychologist's diagnosis confirms something is wrong, which is NOT the root cause.
So someone freaks out or starts doing things we associate with mental disturbance for no apparent reason, compulsive gambling, suicidal thoughts and actions, etc. yet we know that something disturbed the relationship across and between the brain's neurotransmitters. It isn't his or her fault per se.
Then, you couple that with a possible gene mutation specifically related to the ability of their enzyme complex to convert elements so they can cross the BBB to facilitate the functions of their neurotransmitters, you have something that is extremely if not impossible to completely resolve.
It isn't going to happen. No silver bullet(s) so the caregiver enters the world of "pallative care".
just my background, and contrary to Heinz and some others, I would avoid 5-htp and melatonin supplements if you want to maximize dopamine conversion...of course, assuming his receptors are not completely dysfunctional..
Remember, dopamine can become inhibitory.Then someone has real problems. Their nerve impulses never fire as they should. The car has fouled spark plugs so it won't start regardless if you install a new starter!
Ok thanks.
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