has anyones stopped their tremor with b 1 or reduced it significantly without any prescription drugs? I'm new here.
tremor: has anyones stopped their tremor... - Cure Parkinson's
tremor
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It reduced my tremor if adjust the dose of B1 accordingly (1 to 2g/day); too much B1 amplifies the tremor.
with no prescription drugs?
yes, with no drugs
What does that equal to in mg
1g = 1000mg
Yes but my tremors are minor. I dont take any rx meds, just b1 and amino acids.
What are amino acid in terms of supplements?
What type specifically do you take? Where do you buy from
Thanks
Dr Marty Hinz Amino Acid Protocol. See my many previous posts on the subject.
Can't be tracking your many posts, ...hours of reading through stuff. If the 20 seconds it takes to write the type amino supplements and where is too much for you, you could as well just say so
sorry Grumpy. I was at work at the time I read your request and didnt have the time to type it all up. The basic supplements are Cysteine for sulfur amino acid support, Mucuna for L-Dopa support, and 5HTP with co factors for serotonin support and neurotransmitter metabolism. You can get them from CHK Nutrition or search the web for them. For dosages, everyone is different so I dont recommend going at it without a practitioner that is trained in their usage.
I want to add that I find there are 2 ways to combat our disease. One is let a Neurolgist or movement disorder specialist give you the traditional drugs.This is the easy way out. I didnt find this method suitable, personally, because it doesnt address the underlying cause but only masks the symptoms. You will probably not stop the progression and will probably develop side effects and co morbidities using this method. And I didnt find that these people, in my experience, had enough empathy to spend the time getting to the root of things or educating the patient.
The other method is a lot more difficult. It requires poring over research, seeking information and educating yourself on the very nature of this disease and its core. This is the kind of people, motivated to heal themselves, that I find making great contributions to this website. People like Retry, Sunvox, Silvestro, Royprop, Giocas, Kia, JohnPepper, ParkBear, P-oui, weareparky, easily, surfdivinity and many others. You should follow all these people. You will learn a lot. We have slowed or stopped our progression and are in some cases better off than when we started this journey.
My advice to you is spend the hours.
Many thanks for the details
Actually I have to apologise because I was a bit blind "Dr Marty Hinz Amino Acid Protocol" was also part of the answer I was looking for and I should have googled the rest
But then your further info and advice is additional bonus, thanks
Grumpy i have to apologize too for my grumpy reply. Take care, my friend!
Do you know where to find b1 with hcl ? I see plenty vitamin b1 without the hcl on the end
Walmart, amazon or vitacost. Thiamine hcl.
No.Only Sinemet works for tremors.
Sinemet or any other prescription drugs which I have tried did not have any effect on my tremors and I have tremor dominant Parkinson’s disease. Is this the case for you, do you have tremors and sinemet controlled your tremors????
Yes, my PD is tremors dominant and Sinemet completely control it. But not at ones. Maybe you need to give yourself a little time , about couple weeks.And it depends also on dosages
Maybe you need to increase it.
Yes mucuna pruriens reduces my tremor significantly. I take half a teaspoon in a squeeze of lemon because the vitamin C helps the absorption and started out with lower dosage because you have to experiment with what works for you.
This is the link nutrivitashop.com/
There seems to be lots of different strengths. Wondering what you started with. Only once a day? Thanks for your help. Sinement has not helped me with anything.
Me neither
Nutrivita sells 99% pure or something to that effect. I do twice a day sometimes once. As needed I've discovered that Parkinson's disease is a roller coaster ride somedays are better than others.
How many mg?
Don't know. Have done lots of experimenting and have settled at 1/8 teaspoon scoop. It's different for everyone so you must start slow.
I've been taking mucuna puriens since October 16th it is now November 2nd I have a terrible terrible tremor I don't take any RX . have I given it long enough to make a difference
What's the purity measurement of the Mucuna pruriens. It should work in an hour if it is the 100% pure L-dopa. But the tremor is one of the most difficult symptoms to control with Parkinson's. Keep trying👍.
Tremor, unlike other motor symptoms in PD, does not correlate well with dopamine cell loss.
If you want to know, more the following article explains in more detail what may cause tremor. See : ncbi.nlm.nih.gov/pmc/articl...
"Pathophysiologically, tremor is linked to altered activity in not one, but two distinct circuits: the basal ganglia, which are primarily affected by dopamine depletion in Parkinson's disease, and the cerebello-thalamo-cortical circuit, which is also involved in many other tremors."
"Patients with tremor-dominant Parkinson's disease have milder cell loss in the substantia nigra pars compacta (particularly in the lateral portion) and in the locus coeruleus than patients with non-tremor Parkinson's disease (Paulus and Jellinger, 1991; Jellinger, 1999). This suggests that patients with tremor-dominant Parkinson's disease have less dopaminergic (and possibly also less nor-adrenergic) dysfunction than non-tremor patients. This could explain some of the clinical advantages that are associated with tremor. On the other hand, patients with tremor-dominant Parkinson's disease have considerably more cell loss in the retrorubral area of the midbrain,"
"The failure [of tremors] to respond to dopaminergic treatment is difficult to reconcile with most models, which assume that tremor is triggered by dopamine depletion. One possibility is that non-dopaminergic neurotransmitters play a role. For example, patients with Parkinson's disease have 27% lower serotonin binding in the raphe than controls, and tremor correlates with the amount of serotonin depletion (Doder et al., 2003). In humans, there are serotonergic projections from the raphe to the basal ganglia, including the pallidum (Wallman et al., 2011). If both serotonergic and dopaminergic changes can produce tremor, then this may explain why some patients fail to respond to dopaminergic therapy.
These authors make the point that for tremor to occur requires good motor neuron function and that when increasing dopamine supply in turn restores motor neuron function, tremor amplitude can increase. Inversely PD patients in the later stages of the disease see their tremors diminished since the motor neuron function continues to diminish.
In the case of Thiamin treatment, it has been suggested that the dopamine-producing nerves in the substantia nigra are revived and begin producing more dopamine since a whole range of other symptoms are considerably improved. This additional domapimine will do nothing to stop tremor if the cause is also elswhere in the midbrain, but may help transmit the tremor more effectivley to the peripheral muscles.
In the longer term, thiamin may also help to correct the midbrain dysfunction, but only time will tell. We should probably look for other medication than dopamine replacement to correct tremor. PD is clearly multicentric and will require multi-functional medication to ccorrect all the symptoms.
You wrote the following: "in the case of Thiamin treatment, we know that the dopamine-producing nerves in the substantia nigra are revived and begin producing more dopamine..."
Could you provide a reference that supports this claim?
Increasing evidence shows that PD is a GABAminergic disease as well. Besides Dopamine & Serotonin denervation, the low response of dopamine in Tremors may be in fact be due to :
1) the decreased activity of GABA ncbi.nlm.nih.gov/pmc/articl... , which principal role is reducing neuronal excitability throughout the nervous system, and
2) the increasing activity of Glutamate, which is the major excitatory neurotransmitter ncbi.nlm.nih.gov/pmc/articl... and excitotoxic on high levels. ncbi.nlm.nih.gov/pubmed/243...
3) The increased activity of the excitatory neurotransmitter Acetylcholine, in non-cholinergic-deficit brain sections. nature.com/articles/npjpark...
Thiamine may increase the activity of the enzyme α-ketoglutarate dehydrogenase (αKGDH) which is implicated in glucose oxidation and in the synthesis of the neurotransmitters Glutamate and GABA. Thiamine also may increase the activity of the enzyme Acetyl CoA, an important component in the synthesis of the neurotransmitter acetylcholine, which is an excitatory neurotransmitter. pdfs.semanticscholar.org/d1...
The increase in GABA may reduce tremors, reduce anxiety and induce relaxation of muscles, but the increase of glutamate beyond normal levels has an excitotoxic effect and may increase tremors and dyskinesia ncbi.nlm.nih.gov/pubmed/213....
Possibly there is a fine line between neuroprotection and neurotoxicity with Thiamine. This may explain why some patients experience increased tremors when on excess dosage of thiamine.
Your question is pertinent Green Day. As far as I know the action of thiamine is still hypothetical. I have edited the text to that effect.
I guess your quote refers to the following animal study with the thiamine derivative Sulbutiamine "Evidence for a modulatory effect of sulbutiamine on glutamatergic and dopaminergic cortical transmissions in the rat brain." ncbi.nlm.nih.gov/pubmed/109... , where an increase of D1 dopaminergic (DA) binding sites was observed.
The hypothesis is whether those results can extrapolate to humans with thiamine treatment. However, based on many thiamine accounts, the improvement in symptoms, as those reported by many patients, such as reduced pain, stiffness, anxiety, and the relaxation of muscles, relate to the increase of GABA activity. The increase of dopamine would result in the reduction of dopamine drugs such as in the citicoline studies researchgate.net/publicatio... , this is not commonly reported with thiamine. However, any increase in dopamine may be useful to decrease the activity of glutamate-induced excitotoxicity nature.com/articles/cddis20... . Therefore this effect of thiamine on dopamine neurons cannot be excluded.
Thanks for all these references Greenday, I'll take a look at them all over the next few days. As you will see from my profile, this fascinating subject came into my life less than 2 months ago. From what you write, you're well ahead of me in the learning curve so keep on writing so that I can catch up a bit. Do you have professional experience in this subject and if so are you on Researchgate ?
You don't seem convinced that thiamine boosts the production of dopamine. My personal experience for what it's worth is that thiamine has cleared ALL my PD symptoms except tremor and smell in 4-5 weeks just as well as ropinirole. I now don't need or want the latter. Could this be simply due to the increase in GABA activity ?
in reply to wriga
There is a theory known as the “GABA Collapse hypothesis”
frontiersin.org/articles/10...
Not well supported however!
No hypothesis can negate another one unless proved otherwise.
* It is not just GABA:
Thiamine as disphosphate (TDP) is an important Coenzyme in the glucose and other metabolic pathways. The modulatory effect of TDP on Acetylcholine, Glutamate, GABA, ATP, NADH, and pyruvate, lactic acid build-up, could reduce (or increase on excess dose) the severity of certain symptoms in PD, as those commonly reported by many patients who are on thiamine treatment (explained later).
* It is not just Dopamine:
Dopaminergic, Gabaminergic, Serotonergic & Cholinergic denervation is involved in PD pathology. The Nondopaminergic neurotransmitters involved include: Acetylcholine, GABA, Serotonin, Glutamate, noradrenaline, Adenosine, Histamine ncbi.nlm.nih.gov/pmc/articl...
Patients with early parkinsonism or those not on a levodopa treatment report the most improvements. Thiamine TDP CSF levels are lower in patients who are not on levodopa treatment and higher in those who are receiving levodopa. Therefore thiamine may correct deficient levels in those who are not on a levodopa therapy, which mainly suggests that those early in the disease may see the most improvements. ncbi.nlm.nih.gov/pubmed/104...
Besides a few anecdotal reports, the long-lasting effects of thiamine (>6 months) in Parkinson's are yet to be proved.
A placebo effect cannot be excluded (<3 months), at least on certain improvements reported by some patients. A recent double-blind placebo-controlled study of intranasal glutathione in PD, surprisingly resulted in an overwhelming 100% placebo effect, which lasted 3 months ncbi.nlm.nih.gov/pubmed/284....
Thiamine may have a significant effect on certain genes and proteins and therefore thiamine may exert neuroprotective activity against oxidation in PD. Various cell and animal studies suggest that thiamine may affect the following biomarkers: transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3β, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate, DJ-1 gene . ncbi.nlm.nih.gov/pubmed/234...
For Example：
P53 gene & protein: In CNS P53 serves as a regulator of neuronal cell apoptosis. The activation pf P53 has been reported in animal models of PD and autopsied tissues from patients with PD ncbi.nlm.nih.gov/pubmed/956... and inhibition of P53 was shown to prevent MPTP degeneration of neurons in animal models ncbi.nlm.nih.gov/pubmed/891... Thiamine inhibits intracellular p53 activity; thiamin diphosphate (TDP) inhibits binding.
Luong and Nguyễn have reviewed the literature for studies, which suggest a connection between thiamine and PD pathology, and candidate pathways involved, the complete review is available online for rent or purchase. onlinelibrary.wiley.com/doi... . However, further investigation into the effects of thiamine in PD is needed.
In addition to thiamine and free thiamine, there are several derivatives such as Thiamin diphosphate (ThDP), thiamine monophosphate (ThMP), thiamine triphosphate (ThTP), adenosine thiamine triphosphate (AThTP) and adenosine thiamine diphosphate (AThDP) . Each of those has different biological function and their role is not clearly understood. L Bettendorff suggests that thiamine may have a non-coenzyme role. oapublishinglondon.com/arti... . This coenzyme-independent form may have an important neuroprotective effect in Parkinson's. The non-coenzyme action of Thiamine is supported by other studies as well omicsonline.org/open-access... , however, there is still no direct evidence.
Reports on thiamine improvement are not consistent in symptoms and duration
Most of the reported benefits are attributed to the effect of Thiamin diphosphate (ThDP/TDP) as a Coenzyme factor in different metabolic pathways
Common improvements with thiamine treatment include the following :
1) Increased Energy & Reduced Fatigue:
Thiamin diphosphate may increase the excitatory neurotransmitters Acetylcholine & Glutamate and increase the production of ATP, NADH by increasing the activity of Pyruvate. Pyruvate affinity for TPP reduces the build-up of lactic acid
2) Reduced Pain and stiffness, Calming effect, Relaxation of muscles:
Thiamin diphosphate upregulates the enzyme OGDC/AKGDH which modulates the neurotransmitter GABA. Thiamine reverses the lactic acidosis.
3) Mild reduction of Tremors
Thiamin diphosphate increases the activity of AKGDH which modulates the levels of GABA. Correcting deficient levels of GABA or upregulating GABA receptors may decrease the severity of tremors. GABA also exerts antianxiety effect and can help reduce tremors.
The severity of tremor correlated with the abnormalities found in GABA receptor binding, suggesting a primary gabaergic deficiency or a functional abnormality at the level of GABA(A) receptor subtypes ncbi.nlm.nih.gov/pubmed/225...
Thiamin diphosphate (ThDP) is well-known as a coenzyme of the enzymes of central metabolism, such as A) cytosolic transketolase, B) mitochondrial pyruvate and C) 2-oxoglutarate dehydrogenases (OGDC) or α-ketoglutarate dehydrogenase complex (AKGDH). Pyruvate dehydrogenase produces acetyl-CoA for acetylcholine synthesis.
The enzyme OGDH/AKGDH oxidizes the glutamate precursor 2-oxoglutarate. As a result, inhibition of pyruvate dehydrogenase decreased synaptosomal synthesis of acetylcholine. Inhibition of OGDC/AKGDH changed Glutamate and GABA levels in different systems including cultured primary neurons and rat brain. omicsonline.org/open-access... .
In the absence of thiamine, pyruvate cannot enter the citric cycle and, instead, is converted to lactic acid. Thiamine can reverse the high levels of lactic acid ncbi.nlm.nih.gov/pmc/articl... . The mitochondrial pyruvate and OGDH/AKGDH are part of biochemical pathways that result in the generation of ATP, which is a major form of energy for the cell. en.wikipedia.org/wiki/Pyruv...
Most patients in medium and advanced stages don't report a reduction in levodopa drugs.
Increased improvements are reported by newly diagnosed patients with mild Parkinsonism, who are usually are not on levodopa treatment or they are on low dose levodopa.
A study showed that PD patients under levodopa therapy had significantly higher CSF thiamine diphosphate (ThDP) and total thiamine than those not treated with levodopa. ncbi.nlm.nih.gov/pubmed/104... . Therefore newly diagnosed patients who are not on levodopa therapy may correspond better to thiamine treatment. Free thiamine was low in both groups; however thiamine diphosphate (ThDP) appears as a major biomarker in Parkinson's.
A rat study showed that Intrastriatal administration of thiamine triphosphate (TTP) or thiamin diphosphate (TDP) induced DA release, but thiamine monophosphate (TMP) or thiamin did not show any change. These findings suggest that, in contrast to TMP and thiamin, TTP and TDP may play a specific role in DA release from nerve terminals. ncbi.nlm.nih.gov/pubmed/823...
The questions remain:
- If and why thiamine deficiency does exist in parts of the brain in Parkinson's patients with normal and high thiamine levels in the blood plasma.
- What is the specific biological role of thiamine and each of its numerous phosphorylized and dephosphorylized derivatives in PD
- Which positive effects of thiamine are attributed to its Coenzyme or Coenzyme-independent role or both.
- After initial improvements with thiamine, why positive effects are not consistent and long-lasting (›3 months) as many patients report?
in reply to Greenday
The following study shows that magnesium helps to get the most out of thiamine:
Clin Nutr ESPEN. 2018 Jun;25:8-17. doi: 10.1016/j.clnesp.2018.02.007. Epub 2018 Mar 15.
The role of thiamine dependent enzymes in obesity and obesity related chronic disease states: A systematic review.
Maguire D1, Talwar D2, Shiels PG3, McMillan D4.
Author information
Abstract
The WHO 2016 report indicates that worldwide obesity is rising, with over 600 million people in the obese range (BMI>30). The recommended daily calorie intake for adults is 2000 kcal and 2500 kcal for women and men respectively. The average American consumes 3770 kcal/day and the average person in the UK consumes 3400 kcal/day. With such increased caloric intake, there is an increased load on metabolic pathways, in particular glucose metabolism. Such metabolism requires micronutrients as enzyme co-factors. The recommended daily allowance (RDA) for thiamine is 1.3 mg/day and 0.5 mg thiamine is required to process 1000 kilocalories (kcal). Therefore, despite the appearance of being overfed, there is now increasing evidence that the obese population may nutritionally depleted of essential micronutrients. Thiamine deficiency has been reported to be in the region of 16-47% among patients undergoing bariatric surgery for obesity. Thiamine, in turn, requires magnesium to be in its active form thiamine diphosphate, (TDP). TDP also requires magnesium to achieve activation of TDP dependent enzymes, including transketolase (TK), pyruvate dehydrogenase (PDH) and alpha-keto glutaric acid dehydrogenase (AKGDH), during metabolism of glucose. Thiamine and magnesium therefore play a critical role in glucose metabolism and their deficiency may result in the accumulation of anaerobic metabolites including lactate due to a mismatch between caloric burden and function of thiamine dependent enzymes. It may therefore be postulated that thiamine and magnesium deficiency are under-recognized in obesity and may be important in the progress of obesity and obesity related chronic disease states. The aim of the present systematic review was to examine the role of thiamine dependent enzymes in obesity and obesity related chronic disease states.
PMID: 29779823 DOI: 10.1016/j.clnesp.2018.02.007
Wriga, you haven't posted for a while. How are you doing? Are you still on B1 protocol? Thank you.
Hi Despe,
I'm doing well after more than 7 months on B1 at 3.5g. I think I hit a long term overdose problem two weeks ago when lots of pain came back and tremor became very strong. I have now stopped B1 for 3 days and I have practically no symptoms. Tremor has almost stopped again. I will do a break off B1for a week to see how things go and then decide what dose to use. I seem to observe that others are lowering their dose levels and that 2.5 to 3g seems to be popular after a long period on B1. I hope you're doing ok too.
Wriga, I experienced the same thing at about 6-1/2 months. Symptoms (tremor) slightly worsened and back pain was strong. Still trying to pinpoint the new correct dose, while mitigating the back pain. I went from 2000mg to a 5 day break with little or no symptoms, now 1000mg daily, with some intermittent tremor. Lower back seems to be improving. I'm going to stay on a lower B1 dose for a while with Mucuna. no rx.
Hi Constance (I suppose),
It's good to hear that I'm not alone. I was worried when the tremor got very strong thinking that was a bad progression, but all is now in order and no meds for 3 days.
in reply to wriga
In some people the need for thiamine can decrease after months of use and this decreased need can manifest as a worsening of symptoms because you are essentially mildly overdosing on a dose that has worked for you for months.
Recently Kia17 had a similar event after about a year and a half on B-1 and Dr. C figured out that all Kia needed to do was keep the same dose, but take one day off per week. Problem solved! Having confidence in Dr. C's experience with this HDT protocol can pay dividends or at least make you better!
Art
wriga in reply to
Thanks Art. I started on 2.5g in March 2018 and was much improved after 3 weeks, but Dr C suggested I up the dose. I have been at 3.5g and doing well for 6 months then symptoms came back strong. It seems I don't need so much which is good. I note that Dr Hinz also uses the "pill stop" method to check if the dose is too high. If symptoms improve when you stop, the dose is too high.
in reply to wriga
wriga,
I recently added a link to the "thiamine primer page" for the best price I could find for thiamine 100 mg. capsules for this very reason. Now that some forum members have been on the HDT protocol for months at their optimum dose, it will be more common to see people who's need for thiamine has reduced and the 100 mg capsules will offer one easy way to fine tune the dose to compensate for this change. In some cases, Dr. C may just have you eliminate the lunch time dose just once or twice a week to compensate for this mild overdose condition. As always, it is best to contact him if this occurs and he will get you back on track quickly!
Art
I had an interesting evolution with B1, too. I started in March at 2g/day. I felt good improvement in a week. At certain time I went 3g/day but the things went bad so I went back to 2g. After 5 months I realized my tremor got reduced if went to 1g/day. During last month I noticed a slow increase in my symptoms culminating with full return last week: balance, concentration, foot freezing, increased tremor. I switched back to 2g/day and in a week I feel ok again. Tremor went down like 3 months ago when I switched from 2g to 1g; this time I switched from 1g to 2g. it seems maybe my ideal dose is 1.5g but for now I'll stay on 2g.
Wriga, thanks for replying. I believe my husband is going the same route as you are. Although, he didn't start B1 therapy as back as you did, following Dr. C's recommendation, he originally started 100mg x 2/week, then increased to 250mg/week, then lowered back to original dose (100mg x 2/week) and currently upped to 100mg x 3/week for a month as Dr. C. suggested. He started the upped dose a week ago, but he seems to have back and knee problems, mainly pain, and worse tremor, especially on his "good" hand which he didn't have before. If symptoms worsen, he will probably stop it, and will email Dr. C. again as Dr. C. asked for further dose instructions.
Cannabis
I started using MP whole bean powder back in Feb., 1/4 tsp 3x day, increased to 1/2 tsp 3x day, then tried pure MP extract which made me loopy. Returned to MP powder ,which was working all along, but decided to try it in tablet form for convenience. Banyan now has them. I was always experimenting with doses. I find that if I know I'M going to get stressed for an event, I take 1/2 pill every half hr /45 min starting 2 hrs before and during the event. Generally I take 1 tablet 3 x daily. I'm on 3 B 1 which helps with stiffness, rigdity, anxiousness, and balance. MP helps greatly with tremor, and anxiousness. I take a few other vitamins too...had PD about 10 yrs, got worse 2-3 yrs ago. Have gotten things under control...no meds.
Thanks for sharing. We need more of your testimonies.
1 tsp of whole bean MP powder is too less. Raw bean contains 4 to 5 percent ldopa
I know, but I'm very sensitive. Just 1 Banyan 500 mg tablet 4 to7 % dopa makes me feel drugged, so I take less, but more frequently. I take the tablet because it's so convenient.
I'm also realizing that thiamine together with MP may be reducing my bp too much, most recently 104/67 and I'm not an athlete.
Could you tell me please what MP is? Suffering Socks
Mucuna pruriens
Thanks KERRINGTON - Can you obtain that from a Health Food store?
I haven't looked in the health food stores, but purchase the tablets online from Banyan Botanicals. Most people use the powder form. Make sure you understand the difference between extract, and whole bean powder where you get less dopa. Right now I use the whole bean powder tablet which has only 4 to 7 % dopa . Many use powder with 40% dopa which wd knock me out.
Thiamine has been calming and has reduced the stress induced tremor for me. Interestingly GABA agonists temporarily do the same
Thiamine seems to have reduced my tremor.
Sorry to say for my husband no prescription med helps. He has. Ad tremors in both arms for four years now. We are so frustrated with medication. The side effects are worse then anything.
I'm reminded yet again about how grateful I am for this site and for the thoughtful, scientific discussions in which many of you engage. Wriga, Greenday, and Easilly, I don't understand much of what you are discussing, but I'll follow your leads any time. I would never have known about B1 if not for this site and I appreciate the contributions of everyone who replied to this post and others. We are all in this together. Thank you all!
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