Concussion And Thiamine Deficiency

tonto

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Thesis: Concussion causes many symptoms but there are common symptoms that are similar to thiamine deficiency or Wernicke's Encephalopathy, including memory disorder, gait imbalance, and variable eye movement problems. I'll try to explain that the principal problem in concussion is an abrupt thiamine deficiency due to an extreme hypermetabolic state.

Evidence: If you look at the mainstream view of metabolic changes in the brain after concussion as demonstrated in this graph below, you can see the extreme hypermetabolic state by the abrupt rise in glucose use by the brain for several hours or so, followed by 1 week+ of reduced glucose use:

upload_2018-12-15_15-24-10.png


Not surprisingly researchers have jumped on the sugar is bad for concussion band wagon and there are studies showing that glucose administration is harmful during the post-concussive period - these studies tend to suggest Omega-3 fatty acids or Ketosis is preferable. After looking at this problem for some time and reading Peat's work, I've come to the conclusion that the sharp increase in glucose metabolism has depleted the brain of thiamine. Adding glucose to this system IS harmful for that reason. Please note this important point that even a marginal decrease in thiamine can cause mild Beriberi if too much glucose is ingested (see this source) - people that consume large amounts of sugar without nutrient dense foods with thiamine may in fact develop mild Beriberi, the classic thiamine deficiency condition.

In support of a thiamine deficiency being caused NOT by malnutrition BUT by hypermetabolism (which using up of thiamine supplies) I could find only this paper from 1943 - which discusses how the hypermetabolic state of thyrotoxicosis can deplete the body of thiamine (paper is attached).

Conclusion: most athletes with concussion have enough thiamine stores in the body to quickly overcome the abrupt hypermetabolic thiamine depletion in the brain. But, for some athletes or "regular" people that are marginally malnourished, the concussed brain may not get replacement thiamine quickly and longer term symptoms known as post-concussive syndrome, can develop. Thiamine replacement followed by high carbohydrate diet is probably therapeutic if this thesis is correct.

@haidut @aquaman I would be interested in hearing what you and others think of this.
 

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Texon

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Thesis: Concussion causes many symptoms but there are common symptoms that are similar to thiamine deficiency or Wernicke's Encephalopathy, including memory disorder, gait imbalance, and variable eye movement problems. I'll try to explain that the principal problem in concussion is an abrupt thiamine deficiency due to an extreme hypermetabolic state.

Evidence: If you look at the mainstream view of metabolic changes in the brain after concussion as demonstrated in this graph below, you can see the extreme hypermetabolic state by the abrupt rise in glucose use by the brain for several hours or so, followed by 1 week+ of reduced glucose use:

View attachment 11533

Not surprisingly researchers have jumped on the sugar is bad for concussion band wagon and there are studies showing that glucose administration is harmful during the post-concussive period - these studies tend to suggest Omega-3 fatty acids or Ketosis is preferable. After looking at this problem for some time and reading Peat's work, I've come to the conclusion that the sharp increase in glucose metabolism has depleted the brain of thiamine. Adding glucose to this system IS harmful for that reason. Please note this important point that even a marginal decrease in thiamine can cause mild Beriberi if too much glucose is ingested (see this source) - people that consume large amounts of sugar without nutrient dense foods with thiamine may in fact develop mild Beriberi, the classic thiamine deficiency condition.

In support of a thiamine deficiency being caused NOT by malnutrition BUT by hypermetabolism (which using up of thiamine supplies) I could find only this paper from 1943 - which discusses how the hypermetabolic state of thyrotoxicosis can deplete the body of thiamine (paper is attached).

Conclusion: most athletes with concussion have enough thiamine stores in the body to quickly overcome the abrupt hypermetabolic thiamine depletion in the brain. But, for some athletes or "regular" people that are marginally malnourished, the concussed brain may not get replacement thiamine quickly and longer term symptoms known as post-concussive syndrome, can develop. Thiamine replacement followed by high carbohydrate diet is probably therapeutic if this thesis is correct.

@haidut @aquaman I would be interested in hearing what you and others think of this.
I also for the following reasons and the fact that I had a severe head injury after a t-bone car crash several years ago.
@haidut @Rafael Lao Wai I have come to find that I am experiencing intermittent to increasing brain toxicity exacerbated by impaired cyp450...see link...https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888527/...for the smoking gun. I took 2 doses of doxycycline a few weeks ago and thought I was losing my mind. I am at a loss as to what to do about the increasing brain symptoms but am glad I was able to link the severe doxy reaction to my bad mental state. I am thinking about hyperbaric oxygen or the niacin/sauna detox by Dr. Yu. Also homocysteine is an issue at levels between 11-14. I started IM 1000 mcgs hydroxocobalamin per week last week which can reduce homocysteine 33% in 8 weeks per PubMed study. Please reply if you guys have any thoughts about any of this. Dr. Mark Gordon, MD is a pioneer using hormone treatment for TBI which a bigger problem than most of us know don't you think? Could high dose thiamine help with these issues?
 

haidut

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I also for the following reasons and the fact that I had a severe head injury after a t-bone car crash several years ago.
@haidut @Rafael Lao Wai I have come to find that I am experiencing intermittent to increasing brain toxicity exacerbated by impaired cyp450...see link...https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888527/...for the smoking gun. I took 2 doses of doxycycline a few weeks ago and thought I was losing my mind. I am at a loss as to what to do about the increasing brain symptoms but am glad I was able to link the severe doxy reaction to my bad mental state. I am thinking about hyperbaric oxygen or the niacin/sauna detox by Dr. Yu. Also homocysteine is an issue at levels between 11-14. I started IM 1000 mcgs hydroxocobalamin per week last week which can reduce homocysteine 33% in 8 weeks per PubMed study. Please reply if you guys have any thoughts about any of this. Dr. Mark Gordon, MD is a pioneer using hormone treatment for TBI which a bigger problem than most of us know don't you think? Could high dose thiamine help with these issues?

Higher dose niacinamide greatly upregulates CYP450. The HED from animal studies is in the 1g-1.5g daily and the maximum effect was seen after about 24 hours. So, you may want to try some niacinamide with the doxycycline.
 

Texon

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Higher dose niacinamide greatly upregulates CYP450. The HED from animal studies is in the 1g-1.5g daily and the maximum effect was seen after about 24 hours. So, you may want to try some niacinamide with the doxycycline.
Thanks Haidut. This is valuable info. I have trouble balancing the homocysteine issue with the obvious benefits of niacinamide. So maybe I will try an idea from Chris Kesser to take some TMG at the same time as the niacinamide.
 

Texon

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Higher dose niacinamide greatly upregulates CYP450. The HED from animal studies is in the 1g-1.5g daily and the maximum effect was seen after about 24 hours. So, you may want to try some niacinamide with the doxycycline.
In your opinion, would plain niacin do the same thing? Or any of the other analogs?
 

haidut

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In your opinion, would plain niacin do the same thing? Or any of the other analogs?

As far as I remember, niacin did not have these effects. I will post the niacinamide studies tomorrow or early next week. The studies were quite impressive, showing that niacinamide was even more potent than phenobarbital, which is the most potent known inducer of CYP450. Hans Selye noted phenobarbital and pregnenolone-16-carbonitrile were the most potent "catatoxic" chemicals he ever experimented with.
Phenobarbital - Wikipedia
"...Phenobarbital is a cytochrome P450 inducer, and is used to reduce the toxicity of some drugs."
"...Phenobarbital is a cytochrome P450 hepatic enzyme inducer. It binds transcription factor receptors that activate cytochrome P450 transcription, thereby increasing its amount and thus its activity. Due to this higher amount of CYP450, drugs that are metabolized by the CYP450 enzyme system will have decreased effectiveness. This is because the increased CYP450 activity increases the clearance of the drug, reducing the amount of time they have to work.[30] Caution is to be used with children. Among anticonvulsant drugs, behavioural disturbances occur most frequently with clonazepam and phenobarbital.[31]"
Protection by catatoxic steroids, phenobarbital and diphenylhydantoin against methaqualone intoxication. - PubMed - NCBI
 

Sheila

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Dear Tonto
Thank you for a most interesting theory. I have a dog that suffered catastrophic brain damage at 1 yr, but I suspect was damaged in utero first, leading to susceptibility. Meaning no disrespect, his symptomatology in general and especially with excitement is very similar to children suffering from cerebral palsy, especially the spastic nature of contractions (they remind me of lactic acid cramping). The reason I tell you this is that when he gets over-excited he can become ataxic, has a very high heart rate and exhibits all signs of a minor concussion again, without any external assault. If I catch this state before he becomes too over-excited, he responds well to honey which I carry with me - and will lick the small jar clean; but if the situation is more advanced, he will not touch honey at all, and it could indeed be that there is a vitamin deficiency at that point that will not allow it to be used. I have him on some modest b-vitamins via Bragg's yeast but am thinking to trial increased b1 for a period and watch him closely. Now that I know there may be potential here, I will have a scout around the literature for b1 and any use in brain damaged conditions generally.
I could not access the Brown University link, but the CAM paper was most interesting indeed.
Thank you again and Happy New Year to you,
Sheila
 

Texon

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Thesis: Concussion causes many symptoms but there are common symptoms that are similar to thiamine deficiency or Wernicke's Encephalopathy, including memory disorder, gait imbalance, and variable eye movement problems. I'll try to explain that the principal problem in concussion is an abrupt thiamine deficiency due to an extreme hypermetabolic state.

Evidence: If you look at the mainstream view of metabolic changes in the brain after concussion as demonstrated in this graph below, you can see the extreme hypermetabolic state by the abrupt rise in glucose use by the brain for several hours or so, followed by 1 week+ of reduced glucose use:

View attachment 11533

Not surprisingly researchers have jumped on the sugar is bad for concussion band wagon and there are studies showing that glucose administration is harmful during the post-concussive period - these studies tend to suggest Omega-3 fatty acids or Ketosis is preferable. After looking at this problem for some time and reading Peat's work, I've come to the conclusion that the sharp increase in glucose metabolism has depleted the brain of thiamine. Adding glucose to this system IS harmful for that reason. Please note this important point that even a marginal decrease in thiamine can cause mild Beriberi if too much glucose is ingested (see this source) - people that consume large amounts of sugar without nutrient dense foods with thiamine may in fact develop mild Beriberi, the classic thiamine deficiency condition.

In support of a thiamine deficiency being caused NOT by malnutrition BUT by hypermetabolism (which using up of thiamine supplies) I could find only this paper from 1943 - which discusses how the hypermetabolic state of thyrotoxicosis can deplete the body of thiamine (paper is attached).

Conclusion: most athletes with concussion have enough thiamine stores in the body to quickly overcome the abrupt hypermetabolic thiamine depletion in the brain. But, for some athletes or "regular" people that are marginally malnourished, the concussed brain may not get replacement thiamine quickly and longer term symptoms known as post-concussive syndrome, can develop. Thiamine replacement followed by high carbohydrate diet is probably therapeutic if this thesis is correct.

@haidut @aquaman I would be interested in hearing what you and others think of this.
This is really important info since Ray is a proponent of significant sugar intake don't you think.
 

LeeLemonoil

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I also for the following reasons and the fact that I had a severe head injury after a t-bone car crash several years ago.
@haidut @Rafael Lao Wai I have come to find that I am experiencing intermittent to increasing brain toxicity exacerbated by impaired cyp450...see link...https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888527/...for the smoking gun. I took 2 doses of doxycycline a few weeks ago and thought I was losing my mind. I am at a loss as to what to do about the increasing brain symptoms but am glad I was able to link the severe doxy reaction to my bad mental state. I am thinking about hyperbaric oxygen or the niacin/sauna detox by Dr. Yu. Also homocysteine is an issue at levels between 11-14. I started IM 1000 mcgs hydroxocobalamin per week last week which can reduce homocysteine 33% in 8 weeks per PubMed study. Please reply if you guys have any thoughts about any of this. Dr. Mark Gordon, MD is a pioneer using hormone treatment for TBI which a bigger problem than most of us know don't you think? Could high dose thiamine help with these issues?

The link doesn’t work because you linked up „for“ too.

Does doxy impair brain-cyp450?
 
OP
tonto

tonto

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@Shiela @Texon @LeeLemonoil

Sorry here is this interesting paper attached and summary here (my emphasis):
Thiamin(e), also known as vitamin B1, is now known to play a fundamental role in energy metabolism.
Its discovery followed from the original early research on the ‘anti-beriberi factor’ found in rice polishings.
After its synthesis in 1936, it led to many years of research to find its action in treating beriberi, a
lethal scourge known for thousands of years, particularly in cultures dependent on rice as a staple. This
paper refers to the previously described symptomatology of beriberi, emphasizing that it differs from
that in pure, experimentally induced thiamine deficiency in human subjects. Emphasis is placed on
some of the more unusual manifestations of thiamine deficiency and its potential role in modern nutrition.
Its biochemistry and pathophysiology are discussed and some of the less common conditions associated
with thiamine deficiency are reviewed. An understanding of the role of thiamine in modern
nutrition is crucial in the rapidly advancing knowledge applicable to Complementary Alternative Medicine.
References are given that provide insight into the use of this vitamin in clinical conditions that are
not usually associated with nutritional deficiency. The role of allithiamine and its synthetic derivatives is
discussed. Thiamine plays a vital role in metabolism of glucose. Thus, emphasis is placed on the fact that
ingestion of excessive simple carbohydrates automatically increases the need for this vitamin. This is
referred to as high calorie malnutrition
.
 

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tonto

tonto

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@Texon @haidut

Rodent model and human SPECT/PET scan appear to show that concussion results in short period of hyperglycolysis that results in mitochondrial oxidative damage with evidence of:
  • Cytochrome oxidase impairment
  • Reduced NADH/NAD ratios
  • Lactic acid formation
Supplementing with (1) Niacinamide, (2) Red light therapy or Methylene Blue, (3) Thiamine and magnesium, (4) Biotin and chromium, and (5) vitamin E (antioxidant/estrogen) may all be helpful, followed by high carb, adequate protein, low fat intake.
 

Texon

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@Texon @haidut

Rodent model and human SPECT/PET scan appear to show that concussion results in short period of hyperglycolysis that results in mitochondrial oxidative damage with evidence of:
  • Cytochrome oxidase impairment
  • Reduced NADH/NAD ratios
  • Lactic acid formation
Supplementing with (1) Niacinamide, (2) Red light therapy or Methylene Blue, (3) Thiamine and magnesium, (4) Biotin and chromium, and (5) vitamin E (antioxidant/estrogen) may all be helpful, followed by high carb, adequate protein, low fat intake.
I believe your info is very relevant. I am also about to be in touch with Dr. Mark Gordon MD who is apparently the expert at treating TBI with hormones and supps to correct the root cause which he believes to be damage to the HPA.
 

johnsmith

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I believe your info is very relevant. I am also about to be in touch with Dr. Mark Gordon MD who is apparently the expert at treating TBI with hormones and supps to correct the root cause which he believes to be damage to the HPA.
Please let us know how that goes.
 

Sheila

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Messages
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Good day to you @tonto,
Perhaps you have seen the attached already, but I think it supports your theory, emphasis mine.

...As part of acute management of TBI, it is
common for patients with a depressed level of
consciousness, who may also be under the
influence of alcohol, to be rehydrated with
dextrose infusions or given total parenteral nutri-
tion (TPN) which has a high glucose content.
These carbohydrate loads, added to that of any
alcohol ingested prior to injury, could be respon-
sible for further depletion of already low thiamine
stores, and may precipitate Wernicke's encephalo-
pathy
(Vortemeyer et al, 1992; Chataway and
Hardman, 1995).

Their consideration was 200mg thiamine long term.

Best wishes
Sheila
PS Edit. Oh and this one too https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2398086/pdf/postmedj00028-0059a.pdf
 

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haidut

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@Texon @haidut

Rodent model and human SPECT/PET scan appear to show that concussion results in short period of hyperglycolysis that results in mitochondrial oxidative damage with evidence of:
  • Cytochrome oxidase impairment
  • Reduced NADH/NAD ratios
  • Lactic acid formation
Supplementing with (1) Niacinamide, (2) Red light therapy or Methylene Blue, (3) Thiamine and magnesium, (4) Biotin and chromium, and (5) vitamin E (antioxidant/estrogen) may all be helpful, followed by high carb, adequate protein, low fat intake.

Good to know, thanks. I think there are some human studies underway with inosine for TBI and stroke and inosine also restrains excessive glycolysis and lowers lactic acid, while also increasing the NAD/NADH ratio. So, we should know soon if this approach works.
Inosine Increases NAD/NADH Ratio And Reduces Systemic Inflammation
Inosine Powerfully Stimulates Mitochondriogenesis, Oxidative Metabolism & Cell Differentiation
 

Astolfo

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@Texon How is it going?

I was already have been using B complex (50 mg niacinamide- 50 mg thiamin) at the time when I got a concussion. Although, I took my dose a few hours after the incident.

So, I guess I'm lucky at this point.
 

Texon

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Messages
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@Texon How is it going?

I was already have been using B complex (50 mg niacinamide- 50 mg thiamin) at the time when I got a concussion. Although, I took my dose a few hours after the incident.

So, I guess I'm lucky at this point.
Going ok. @haidut tagged you too as you may find an NR product discussed below very interesting...Finding that for whatever reason lack of optimal B12 and or acetaldehyde processing is a very big deal for me. I was actually noticing disturbing neurological symptoms that clearly improve when I take b12 consistently. Currently on 1000 mics injectable hydroxo B12 eod with the intent of going hopefully to once per week for life probably. There may some sort of b vitamin "stealing" phenomenon in play caused by fungal or other pathogen in that taking undecylenic acid, pantethine b5, and molybdenum chelate concurrently seems to be helping in subtle ways. Going to meet with a compounding pharmacist next week to arrange a prescription for a product called Synapsin. It is apparently is being used successfully in treating tbi, various neurological issues. etc.
Synapsin® Nasal Spray | No More Brain Fog - Neurological Health
Synapsin is a nasal spray that includes Nicotinamide Riboside, rg3, a ginseng component, and vitamin b12. Looks extremely interesting.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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