Glucose loading cures everything?

[Ecstatic_Hamster]

@sneedful said in Glucose loading cures everything?:

apparently the ideal ratio of glucose:fructose for athletes' regenerating glycogen during / after exercise over 1 hr is 66g dextrose to 33g sucrose. this gives the right ratio without having to buy pure fructose powder.

do you have a cite please? This is interesting.

[A Former User]

@Ecstatic_Hamster this is a website marketing a product, it has references https://www.torqfitness.co.uk/news/understanding-glucose-fructose-ratios

I determined the dextrose:sucrose ratio making the equivalent 2:1 glucose:fructose just by doing the math on the glucose:fructose ratio of sugar and confirmed it with chatgpt. simply because it is easier to buy dextrose only and nearly everyone has plain sugar in their pantry. this way you don't have to buy fructose powder if you're making a sport drink.

66g:33g is also per hour of exercise, im assuming it is for steady state cardio or weightlifting or some sports without long rest periods. this is probably not for weightlifting with long rest periods.

in the link and in other references (this is mostly mainstream exercise science) you can see that the ~100g total (the exact number to be ideal is apparently 120g but whatever, it's easier and simpler to communicate 66g:33g) drink is meant to last for an hour and this ratio actually is more effective at replenishing glycogen than dextrose alone.

[CrumblingCookie]

@sneedful said:

this is a website marketing a product, it has references https://www.torqfitness.co.uk/news/understanding-glucose-fructose-ratios

It refers to these papers:
Fructose and Sucrose Intake Increase Exogenous Carbohydrate Oxidation during Exercise
https://www.mdpi.com/2072-6643/9/2/167
Integrative physiology of transcellular and paracellular intestinal absorption
https://pubmed.ncbi.nlm.nih.gov/28724701/
A Step Towards Personalized Sports Nutrition: Carbohydrate Intake During Exercise
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008807/

What emerges from a brief look into these is that there's a performance benefit in sports starting with 22grs/hour of glucose. They found that intestinal glucose resorption happens through SGLT1 and GLUT2 and maxes out at c. 1gr/min. Fructose resorption on the other hand goes through GLUT5, GLUT2, GLUT8, GLUT12. Effectively, when aiming for the endurance sports performance benefits with glucose servings in excess of the max. hourly resorption, there's the additional route of resorption for fructose. This allows for even higher carbohydrate intakes at 1.3-1.8grs/h and higher oxygenation and performance in endurance sports, and allegedly is also more pleasant/less distressing to the intestine than glucose only at >60grs/hour. It seems most of the added fructose converts to circulating lactate. And using sucrose instead of fructose offers a lower dosing thresold, maxing out at c. 1.2-1.3grs/h because the prior splitting of sucrose becomes a limiting factor with these hourly amounts.

Afaik everybody here doing the glucose protocol is way below a dosing of >60grs/h.
The second paper listed above could be interesting about the details of glucose absorption.

@S-Holmes I'd scrounge some of that dextrose icecream off you! Also curious about those future results from your friends. Really cool that you have other people closely around you who are following through with the dextrose.
I'm wondering whether there are other things for you to approach. Perhaps something about closing that gastroesophageal sphincter or increasing your stomach acid so the stomach won't pump as wildly in trying to make up for such a lack. Or maybe lots of iodide with regard to pcos and low stomach acid or overall low glandular activity. Don't know!

[S.Holmes]

@S-Holmes I'd scrounge some of that dextrose icecream off you! Also curious about those future results from your friends. Really cool that you have other people closely around you who are following through with the dextrose.

I'm wondering whether there are other things for you to approach. Perhaps something about closing that gastroesophageal sphincter or increasing your stomach acid so the stomach won't pump as wildly in trying to make up for such a lack. Or maybe lots of iodide with regard to pcos and low stomach acid or overall low glandular activity. Don't know!

It's interesting that you mention iodine. I use it both orally (Lugols) and topically (povidone). My sister (deceased) had throat cancer so I'm likely a good candidate for that as well. I've had throat issues all my life, usually strep. Remember Dr Peat said everyone over 50 has cancer cells which are usually (hopefully) dealt with by their immune system. Drs. Brownstein and Sircus recommend iodine at high doses for people with cancer. So I use several alternative cancer "treatments" (aspirin, Georgi's B vitamin protocol, iodine, chlorine dioxide, fenbendazole and ivermectin occasionally). My thinking about what was going on with the high dose glucose was that it was trying to heal my throat, causing swelling and inflammation. It stopped when I reduced glucose. Dr. Stephens would say I need MORE glucose. But I have to try and drop some weight before doing high doses again.

[Ecstatic_Hamster]

@S-Holmes I can tell you that Dr. Peat never wanted me to use iodine. He was a convert to the Wolff-Chaikoff suppression effect.

I am not worried about cancer because I've seen how hundreds of people get rid of it in a month or two often (not always) with high dose THC suppositories. See CannabisHealthRadio.com. I have many many stories I've gathered on this too.

[S.Holmes]

@Ecstatic_Hamster said in Glucose loading cures everything?:

@S-Holmes I can tell you that Dr. Peat never wanted me to use iodine. He was a convert to the Wolff-Chaikoff suppression effect.

I am not worried about cancer because I've seen how hundreds of people get rid of it in a month or two often (not always) with high dose THC suppositories. See CannabisHealthRadio.com. I have many many stories I've gathered on this too.

I took iodine for a few years, then found Dr Peat and stopped using it for at least a decade. Then I decided to take another look and found that the Wolff-Chaikov effect had been debunked, so I'm back on it again.

https://www.optimox.com/content/Iodine Research Resources/IOD08.pdf

[Ecstatic_Hamster]

@S-Holmes far from clear. I would not say Peat was wrong.

[S.Holmes]

@Ecstatic_Hamster said in Glucose loading cures everything?:

@S-Holmes far from clear. I would not say Peat was wrong.

Did you read the Optimox article? They were using radioactive iodine. Lugols and radioiodine are not the same.

[Ecstatic_Hamster]

@S-Holmes said in Glucose loading cures everything?:

@Ecstatic_Hamster said in Glucose loading cures everything?:

@S-Holmes far from clear. I would not say Peat was wrong.

Did you read the Optimox article? They were using radioactive iodine. Lugols and radioiodine are not the same.

Yes I did.

There are lots of other studies that say iodine supplementation is harmful. Today the keto bros have been relentlessly pushing iodine as a fad.

This was on .5mg per day — and iodine at this dose resulted in anti thyroid antibody activity. There are a number of similar studies.

They compared T4 with iodine only, to shrink a goiter. Iodine resulted in lymphocyte infiltration and antibody activity in the thyroid gland. I don’t think that’s a good thing.

https://academic.oup.com/ejendo/article-abstract/139/3/290/6748302
At 6 months, markedly increased urinary values of iodine were found in patients receiving iodine (36 microg/24 h at baseline, 415 microg/24 h at 6 months) compared with those receiving T4 (47 microg/ 24 h at baseline, 165 microg/24 h at 6 months; P < 0.0001 compared with iodine group). T4 administration engendered a greater (P < 0.01) decrease in thyroid volume (from 32 ml to 17 ml, P < 0.0001) than did intake of iodine (3 3 ml to 21 ml. P < 0.005). High microsomal and thyroglobulin autoantibody titres were present in six of 31 patients (19%) receiving iodine, and iodine-induced hypo- and hyperthyroidism developed in four and two of them, respectively. Fine-needle biopsy revealed marked lymphocyte infiltration in all six. After withdrawal of iodine thyroid dysfunction remitted spontaneously and antibody titres and lymphocyte infiltration decreased markedly. Follow-up of these six patients for an additional 3 years showed normalisation of antibody titres in four of them.
Conclusion
Although nearly comparable results were obtained with both treatment regimens regarding thyroid size, partly reversible iodine-induced thyroid dysfunction and autoimmunity were observed among patients with endemic goitre.

[LetTheRedeemed]

@Ecstatic_Hamster

I never went deep into the literature, when Pro-iodine group produced two results:

1.) it worked after my TSH rode the rollercoaster.

2.) IT DIDN’T WORK AND IM STUCK (I don’t believe this I has to be permanent)

So, Thanks for the counter-counter argument.
I’ve been tempted several times to do the protocol — but I’m contented to stick with food sourced iodine

[CrumblingCookie]

@Ecstatic_Hamster said:

https://academic.oup.com/ejendo/article-abstract/139/3/290/6748302
"Iodine is essential for normal thyroid function and the majority of individuals tolerate a wide range of dietary levels. However, a subset of individuals, on exposure to iodine, develop thyroid dysfunction."

This is simply the typical age-old and to-be-expected observation from raising iodide supply without a concurrent raise in selenium. Thyroid hormone synthesis is highly oxidative and selenium is needed for its protective effects. Thyroid cells bursting open will surely cause autoantibodies as a reaction.
An aching thyroid gland is actually very easily and reliably reproducible when doing high-dose iodide and improves within days of supplying enough selenium if one had forgotten to preventively do so.

I'm tempted to think that high-dose-iodide could match up very well and become much more tolerable with glucose loading.

[S.Holmes]

@CrumblingCookie said in Glucose loading cures everything?:

@Ecstatic_Hamster said:

https://academic.oup.com/ejendo/article-abstract/139/3/290/6748302
"Iodine is essential for normal thyroid function and the majority of individuals tolerate a wide range of dietary levels. However, a subset of individuals, on exposure to iodine, develop thyroid dysfunction."

This is simply the typical age-old and to-be-expected observation from raising iodide supply without a concurrent raise in selenium. Thyroid hormone synthesis is highly oxidative and selenium is needed for its protective effects. Thyroid cells bursting open will surely cause autoantibodies as a reaction.
An aching thyroid gland is actually very easily and reliably reproducible when doing high-dose iodide and improves within days of supplying enough selenium if one had forgotten to preventively do so.

I'm tempted to think that high-dose-iodide could match up very well and become much more tolerable with glucose loading.

100% agree. "Peating" for more than 10 years sans iodine did not seem to help my thyroid status. High dose glucose over a 4 month period, and 35 grams of iodine a day and my temp is still doing great even though I've now cut back on glucose. I still take 5 drops of Lugols a day and use povidone topically in problem areas. I also take 100 mcg of selenium daily...required with iodine supplementation.

[S.Holmes]

Dr. Stephens' new book:
Restored Hope: A Neuroscience Guide to Optimal Brain and Human Function

slktxt.io/11pKR/11458429

[CrumblingCookie]

I've been looking into vitamin B6, the crucial differences in its vitamers, and their impact on liver.
It looks very worthwhile to what dextrose protocol people, myself included, are struggling with.

First off, for closing in on the topic:
Not only vitamin B1 (Thiamin) is much reduced in alcoholics, but to an equal extent also vitamin B6!
So whenever raising the topic of Thiamin, and high-dose thiamin therapy (HDT), and Costantini, I think we also need to include awareness for B6, especially in its active vitamer of pyridoxal-5-phosphate (PLP, P5P).
Vitamin B6 is also reported to be much reduced in many hospitalized people especially, and in folks over 64years of age.
Especially in the latter group, there's an association between sarcopenia with B6-deficiency, with B6 proving to be an exercise-mimetic!
There appears to be a general association between B6-deficiency and inflammatory responses/diseases, too.
Then, there are mixed and both very tissue and time -specific (sometime opposing) effects of vitamin-B6 deficiency on glycogen stores across the body (heart, skeletal muscles, liver).
As for the liver, the glycogen stores seem to be about equal before exercise, but during and after exercise (or (emotional) stress?) the liver glycogen stores deplete much quicker in B6-deficiency, pointing towards a greater all-body glycogen store and utilization in B6-sufficiency.
That's something in the general direction of what we want to achieve, right?

Then, it's also widely accepted that supplementing PLP even in normal=healthy subjects raises AST and ALT, which are PLP-dependent liver enzymes. Now, raised liver enzymes in the serum are usually a bad sign. But what we are seeing with PLP supplementation is probably more a reversal of falsely low serum liver aminotransferase levels as in: The same amounts of hepatocytes are being damaged and releasing their enzymes into circulation, but the low quantity of those enzymes in this case is reflective of the low cytosolic content of these enzymes within the perishing hepatocytes.
On the other hand, some few long-term PLP users indeed progress into cirrhosis or carcinoma of the liver for which "The cause remains uncertain; possibilities included aldehyde stress from PLP and pyridoxal, or toxicity of PLP photodegradation [especially from liquid PLP suspensions prepared in pediatrics] products" and so the jury's still out.

Now, to the glucose loading, brain restoration, concussions, the impress of trauma, and especially of early-life trauma of nutritional, physical and emotional kinds.
As we all know, early life trauma messes up things for life, especially so with regard to the rate of metabolism and the predominance of serotonin, a high-stress basal state, conditions of literally freezing-up in conditions of stress as the impaired third way of response instead of fight-or-flight, the helplessness etc., as retold by dozens of cited studies and findings by haidut and even mainstream psychology.
There seems to be a helpful connection with PLP:
There are lots of studies titled similar to
Pyrithioxine in the prevention of late consequences of intrauterine and postnatal hypoxia and malnutrition in new-born babies. Act Nerv Super (Praha). 1978 Feb;20(1):85-6.
(that's a Czech one), which unfortunately I cannot source the full texts of. Indeed, there are lots of studies particularly from the former Eastern Block which looked into B6 with regard to autism, epilepsy, learning difficulties, hypoxia, concussion, low protein (LP) or low calorie (LC) malnutrition, e.g.
[Developmental dysphasia: assessment of the drug treatment efficacy],
Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova, 2012, Volume: 112, Issue:7 Pt 2:

    To assess the efficacy of treatment with encephabol, we examined 40 children, 
aged from 3 to 5 years, with developmental dysphasia. All patients were randomized into two equal groups: 
group 1 received encephabol (suspension form, daily dosage 200-250 mg, or 12-15 mg/kg) during 2 months; 
group 2 did not receive this medication. 
In the first group, there was a significant improvement of expressive and impressive speech and speech attention; 
the active vocabulary and a number of phrases in colloquial speech increased by a factor of 3 versus 1.5 in the control group. 
After the treatment with encephabol, the parents reported the decrease in motor disturbances, psychosomatic disorders, 
the improvement of attention and the emotional state of the children.

Let me elucidate what "encephabol" is. It's also called pyritinol or pyrithioxine and a semi-synthetic vitamin B6 analog, bonding 2 compounds of pyridoxine together with a disulfide bridge.
Quoting off wikipedia: "It is approved for "symptomatic treatment of chronically impaired brain function in dementia syndromes" and for "supportive treatment of sequelae of craniocerebral trauma" in various European countries".
Craniocerebral trauma. Chronically impaired brain functions regardless of origin. hmm!

According to this study in rats, Pyrithioxine is much more selectively effective yet with its benefits much less extensive than ordinary pyridoxine. And what's really important to know is that pyridoxine is still very crap in comparison to PLP.
This study
The effect of pyrithioxine and pyridoxine on individual behavior, social interactions, and learning in rats malnourished in early postnatal life
Psychopharmacologia. January 1976Volume 46, pages 325–332, (1976)

showed that those early life brain insults of protein or caloric restrictions could be significantly alleviated by a proper form of B6!

The treatment with pyrithioxine reduced significantly behavioral disturbances in adult LP rats
 except the increase of intersignal reactions which was even potentiated. 
Pyridoxine was less effective but normalized the increased number of intersignal reactions both in LP and LC rats. 
The effect of pyridoxine treatment in early life on learning and dyadic interaction of adult LC rats was interesting. 
There was significant improvement in all registered parameters of avoidance learning and a significant increase of sexual acts was recorded.

Also, reading this article
Malnutrition and the Brain: Changing Concepts, Changing Concerns
The Journal of Nutrition Volume 125, Supplement 8, August 1995, Pages 2212S-2220S

just rings all the bells of what Dr. DS is on about as the authors are making it very clear that it's not even the malnutrition per se doing most of the long-lasting harm but the emotional responses concomitant with such stressful events:

"However, recent neuropharmacological research has revealed long-lasting, if not permanent, 
changes in brain neural receptor function resulting from an early episode of malnutrition. 
These more recent findings indicate that the kinds of behaviors and cognitive functions 
impaired by malnutrition may be more related to emotional responses to stressful events 
than to cognitive deficits per se, the age range of vulnerability to 
these long-term effects of malnutrition may be much greater than we had suspected 
and the minimal amount of malnutrition (hunger) necessary 
to produce these long-term alterations is unknown."

Again, this also reminds me of the extensive findings off the Massachusetts Starvation Experiment (MSE) and the very long-lasting aftereffects on its participants from "a meager" 3-4 months of not even full starvation but a caloric cut to about c. 1800 kcal IIRC (The MSE was a trial run for what came to be applied, intensely and extensively for several years, on the population of the defeated German Reich). Remember that lots of folks actually subsist on such caloric intakes nowadays and that metabolism and body overall body temperatures were much higher a hundred years ago.

[Ecstatic_Hamster]

I did take 13mg of ioderal for several years, and selenium, with no good or bad effects. Not noticeable at all. I took thyroid too. And was cold all the time. It did nothing for me.

Anyhow, glucose continues. I’m up to 260 or 300g per day. Given the glucose, I easily gain body fat so I keep trying to cut down on fats. I weighed a lot today but it’s probably from water weight last few days.

No ill effects really. I’m working on specific issues that I want to fix and the jury is out. I’m about 1 month in.

[S.Holmes]

@Ecstatic_Hamster said in Glucose loading cures everything?:

I did take 13mg of ioderal for several years, and selenium, with no good or bad effects. Not noticeable at all. I took thyroid too. And was cold all the time. It did nothing for me.

Anyhow, glucose continues. I’m up to 260 or 300g per day. Given the glucose, I easily gain body fat so I keep trying to cut down on fats. I weighed a lot today but it’s probably from water weight last few days.

No ill effects really. I’m working on specific issues that I want to fix and the jury is out. I’m about 1 month in.

I hope the glucose helps you! Keep us posted!

[S.Holmes]

@CrumblingCookie said in Glucose loading cures everything?:

I've been looking into vitamin B6, the crucial differences in its vitamers, and their impact on liver.
It looks very worthwhile to what dextrose protocol people, myself included, are struggling with.

First off, for closing in on the topic:
Not only vitamin B1 (Thiamin) is much reduced in alcoholics, but to an equal extent also vitamin B6!
So whenever raising the topic of Thiamin, and high-dose thiamin therapy (HDT), and Costantini, I think we also need to include awareness for B6, especially in its active vitamer of pyridoxal-6-phosphate (PLP, P5P).
Vitamin B6 is also reported to be much reduced in many hospitalized people especially, and in folks over 64years of age.
Especially in the latter group, there's an association between sarcopenia with B6-deficiency, with B6 proving to be an exercise-mimetic!
There appears to be a general association between B6-deficiency and inflammatory responses/diseases, too.
Then, there are mixed and both very tissue and time -specific (sometime opposing) effects of vitamin-B6 deficiency on glycogen stores across the body (heart, skeletal muscles, liver).
As for the liver, the glycogen stores seem to be about equal before exercise, but during and after exercise (or (emotional) stress?) the liver glycogen stores deplete much quicker in B6-deficiency, pointing towards a greater all-body glycogen store and utilization in B6-sufficiency.
That's something in the general direction of what we want to achieve, right?

Then, it's also widely accepted that supplementing PLP even in normal=healthy subjects raises AST and ALT, which are PLP-dependent liver enzymes. Now, raised liver enzymes in the serum are usually a bad sign. But what we are seeing with PLP supplementation is probably more a reversal of falsely low serum liver aminotransferase levels as in: The same amounts of hepatocytes are being damaged and releasing their enzymes into circulation, but the low quantity of those enzymes in this case is reflective of the low cytosolic content of these enzymes within the perishing hepatocytes.

Now, to the glucose loading, brain restoration, concussions, the impress of trauma, and especially of early-life trauma of nutritional, physical and emotional kinds.
As we all know, early life trauma messes up things for life, especially so with regard to the rate of metabolism and the predominance of serotonin, a high-stress basal state, conditions of literally freezing-up in conditions of stress as the impaired third way of response instead of fight-or-flight, the helplessness etc., as retold by dozens of cited studies and findings by haidut and even mainstream psychology.
There seems to be a helpful connection with PLP:
There are lots of studies titled similar to
Pyrithioxine in the prevention of late consequences of intrauterine and postnatal hypoxia and malnutrition in new-born babies. Act Nerv Super (Praha). 1978 Feb;20(1):85-6.
(that's a Czech one), which unfortunately I cannot source the full texts of. Indeed, there are lots of studies particularly from the former Eastern Block which looked into B6 with regard to autism, epilepsy, learning difficulties, hypoxia, concussion, low protein (LP) or low calorie (LC) malnutrition, e.g.
[Developmental dysphasia: assessment of the drug treatment efficacy],
Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova, 2012, Volume: 112, Issue:7 Pt 2:

    To assess the efficacy of treatment with encephabol, we examined 40 children, 
aged from 3 to 5 years, with developmental dysphasia. All patients were randomized into two equal groups: 
group 1 received encephabol (suspension form, daily dosage 200-250 mg, or 12-15 mg/kg) during 2 months; 
group 2 did not receive this medication. 
In the first group, there was a significant improvement of expressive and impressive speech and speech attention; 
the active vocabulary and a number of phrases in colloquial speech increased by a factor of 3 versus 1.5 in the control group. 
After the treatment with encephabol, the parents reported the decrease in motor disturbances, psychosomatic disorders, 
the improvement of attention and the emotional state of the children.

Let me elucidate what "encephabol" is. It's also called pyritinol or pyrithioxine and a semi-synthetic vitamin B6 analog, bonding 2 compounds of pyridoxine together with a disulfide bridge.
Quoting off wikipedia: "It is approved for "symptomatic treatment of chronically impaired brain function in dementia syndromes" and for "supportive treatment of sequelae of craniocerebral trauma" in various European countries".
Craniocerebral trauma. Chronically impaired brain functions regardless of origin. hmm!

According to this study in rats, Pyrithioxine is much more selectively effective yet with its benefits much less extensive than ordinary pyridoxine. And what's really important to know is that pyridoxine is still very crap in comparison to PLP.
This study
The effect of pyrithioxine and pyridoxine on individual behavior, social interactions, and learning in rats malnourished in early postnatal life
Psychopharmacologia. January 1976Volume 46, pages 325–332, (1976)

showed that those early life brain insults of protein or caloric restrictions could be significantly alleviated by a proper form of B6!

The treatment with pyrithioxine reduced significantly behavioral disturbances in adult LP rats
 except the increase of intersignal reactions which was even potentiated. 
Pyridoxine was less effective but normalized the increased number of intersignal reactions both in LP and LC rats. 
The effect of pyridoxine treatment in early life on learning and dyadic interaction of adult LC rats was interesting. 
There was significant improvement in all registered parameters of avoidance learning and a significant increase of sexual acts was recorded.

Also, reading this article
Malnutrition and the Brain: Changing Concepts, Changing Concerns
The Journal of Nutrition Volume 125, Supplement 8, August 1995, Pages 2212S-2220S

just rings all the bells of what Dr. DS is on about as the authors are making it very clear that it's not even the malnutrition per se doing most of the long-lasting harm but the emotional responses concomitant with such stressful events:

"However, recent neuropharmacological research has revealed long-lasting, if not permanent, 
changes in brain neural receptor function resulting from an early episode of malnutrition. 
These more recent findings indicate that the kinds of behaviors and cognitive functions 
impaired by malnutrition may be more related to emotional responses to stressful events 
than to cognitive deficits per se, the age range of vulnerability to 
these long-term effects of malnutrition may be much greater than we had suspected 
and the minimal amount of malnutrition (hunger) necessary 
to produce these long-term alterations is unknown."

Again, this also reminds me of the extensive findings off the Massachusetts Starvation Experiment (MSE) and the very long-lasting aftereffects on its participants from "a meager" 3-4 months of not even full starvation but a caloric cut to about c. 1800 kcal IIRC (The MSE was a trial run for what came to be applied, intensely and extensively for several years, on the population of the defeated German Reich). Remember that lots of folks actually subsist on such caloric intakes nowadays and that metabolism and body overall body temperatures were much higher a hundred years ago.

Do you know the range of dose required to heal the body from these stresses? I had many traumas as a child: emotional abuse, sexual abuse (incident), malnutrition/starvation from birth to age 20, and others. (My father punished my mother for minor offenses by withholding the meager sum he gave her to buy groceries. She had to feed a family of 6 on a pittance.)

I just restocked my pyridoxine today. Do you think P5P is safer than pyridoxine in high or adequate doses?

[Ecstatic_Hamster]

@S-Holmes I have always thought so. P5P is all I recommend.

[CrumblingCookie]

@Ecstatic_Hamster said:

P5P is all I recommend.

I'm also scrapping all supplement products with pyridoxine, which I had used or bookmarked, from future use to replace them with products which contain only P5P=PLP.

@S-Holmes said:

Do you know the range of dose required to heal the body from these stresses?

I'm sorry you had to live through such experiences. It really hurts just from reading about it.
In that pyrithioxine in Developmental dysphasia study above they used an enormous 12-15mg/kg or 200-250mg in 3-5 year old kids. A scaringly high dose.

I've looked into treatments of inborn vitamin B6-dependent epilepsies because they go most in-depth with the clinical practicalities of vitamer B6 dosing.
Clinicians for those recommend equally high doses of between 10-50(at the very most!)mg/kg of either PLP or pyridoxine (PN).
Which is wild, as that would come to >840mg PLP daily for an 70kg adult. On the other hand they use to set an upper threshold of 200-300mg/daily for all - be they adults or lightweight infants.
That essentially breaks down the dosage question to empiric observation of the individual. It's being stressed to use as low a dose as needed for clearance of symptoms.
Given the absence of clearly distinguishable acute fits as a marker in non-epileptics, I suppose dosing PLP comes down to subjective intuition and feeling over the short and long term, as well as meeting recognition of possible adverse effects with an ensuing dose-reduction.

I reckon that, ultimately, it's most important to go with steady, regular PLP supplementation. Similarly as with dextrose. Similarly as with oral thiamin.
Those epilepsy clinicians recommend 4-6x daily dosing. I.e. every 4-6 hours.
I think this seems very sensible. That matches up with what I saw in graphs of serum-concentration over time for PN, PL, PLP. It matches up with my own experiences of needing B6 several times daily irrespective of how high the single dose.

To summarize my own experiences with pyridoxine are btw the following:
PN quickly shows initial benefits during the first 1-2 days. Then everything turns sour and even though some things like twitchings gradually improved over the course of months, in general PN feels like an uncomfortable trade-off and overall burden for me. Empirically, I agree with saying anything above c. 10mg PN per single dose becomes intolerable and reverses most benefits.

What those clinicians for inborn B6 conditions also clearly stress is that PLP should preferably always be used, from the start and in general, because PLP is about equally inexpensive as PN and - irrespective of the different pharmacokinetics which apply to everyone "normal" - because of those genetic epilepsy conditions with inhibited conversion of PN->PLP.
They further acknowledge that there's no "pharmaceutical grade"/"pharmacopeia"/"USP" PLP, so "non-drug" chemical supplies or nutraceuticals must be used even for those patients with clearly diagnosed genetic causes. Which I'm finding strange and wrong, but unsurprising.

I'm planning to take 25mg PLP 3-5x per day along with the dextrose. Which translates to 1-2mg PLP/kg. I'll need to find out which single dose feels good and then take that as regularly as possible.

[gentlepotato]

Has anyone read the new book? Wondering what it's about.