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.
" were reported to contain no live Oxf [10.1016/j.urology.2014.11.013], "Ocheck" and "Oxbact" don't seem great either).