Glucose loading cures everything?
-
@CrumblingCookie thanks for sharing your thoughts and findings!
I may have some more thoughts about this, but I am wondering what do you mean by "the glucose entering the brain"? I know that's something Dr. Stephens talk about, but what does that actually mean? Where in the brain? What in the brain is not having enough glucose, and is now getting enough glucose?
-
@gentlepotato said:
I may have some more thoughts about this, but I am wondering what do you mean by "the glucose entering the brain"? I know that's something Dr. Stephens talk about, but what does that actually mean?
That's the thing that we don't actually seem to know about yet. It was Dr. DS who raised the idea of an inhibited, down-regulated entry of glucose from the circulation into the brain. Which could be overridden by either a high enough glucose concentration gradient or the stability of its constant supply in the circulation. That could involve e.g. some very specific glucose transporters or other forced behaviours of the barrier/capillary lining cells responsible for the nutrient exchange. He speculates, that such uptake of glucose into the brain would normalize and rise to eventually provide the brain with all its original energy needs over time.
Dr. DS also hypothesizes that glucose from starches are taken up differently into the brain than glucose. Which always made me wonder how that could even physically work, since starches are made up of a network of glucose molecules, so the glucose molecules resulting from starch will be the same. It kind of sounded as if there would have to appear a magic portal or extra vein channeling all the dextrose glucose to the brain but not the starch glucose. Because once the glucose, regardless of its origin, is in the general circulation, it's the same!
- So perhaps it's about the spike of glucose absorption? But regular small amounts of glucose seems to work very well for many people, too, so that should not explain why a similar rate of glucose extracted over many hours from a big carbohydrate meal fails to provides similar benefits. On the other hand, we know that the whole process of digestion and maintenance of the gastrointestinal tract requires an enormous share of all incoming energy, especially so when things are out of whack. I therefore cannot even exclude the idea of a functional net caloric deficit being met with an all-net, not to be digested input of glucose.
- Perhaps we need to dissect the notion of a general circulation with regard to the locality of resorption? Which for dextrose starts as soon as it enters the mouth and then mostly in the stomach. Whereas glucose from starches will be taken up after enzymatic breakdown in or after the duodenum. And all throughout the ileum. And a remainder still in the colon.
Then, perhaps dextrose taken up from the stomach enters a more direct route to the brain, whereas everything further down the intestinal tract drains into the enterohepatic system, first benefitting the liver (and burdening the liver; see next point)? - Also, with digestion of carbohydrates spread out along most of the intestinal tract, there will be a range of bacterial metabolites and fatty acids produced. And of course the endotoxins. All going firstly to the liver, which if all goes well, just about balances the benefits with the burdens and fills up its glycogen stores first.
- Would any great excess amount of glucose supplied to the liver by the enterohepatic way perhaps preferably be fed into lipogenesis? Instead of passing it on/dumping it all into general circulation from which it would reach the brain? Similarities to the widely known significantly different metabolism of liposomalyl/transdermally/transgingivally applied steroid hormones as compared to them being taken orally with a first-pass through the liver?
- Or is the spillover of intestinal byproducts like fatty acids and endotoxins past the liver significantly great enough to suppress resorative results of glucose? If that were the case - and since taking dextrose with regular meals still brings about all the benefits - would it be the ratio of glucose to intestinal byproducts being crucial?
- Or is it the new thoughts above, with not the route or regulation of entry which takes glucose to the brain being decisive but a shutting-off of the entry of fatty acids by the brain when it's feasting on glucose? And subsequently, over time, ridding itself of such bad fatty acids and the aftermaths they had incurred?
Similar to the concept of the body/organs/bones/brain sucking up all other bivalent cations like lead and aluminium at an increased rate when there's deficiency in the actually required calcium?
@gentlepotato said:
What in the brain is not having enough glucose, and is now getting enough glucose?
Good thought. Maybe the whole matter is even particularly selective to certain brain regions. Like with the activities of dopamine and serotonine. On the other hand, the need for glucose is so basic and general that I doubt it matters. I don't know whether there are regional differences of capillary or perhaps even glympathic brain micro-anatomy which could point to local differences in the influx of nutrients or efflux of metabolites.
-
@CrumblingCookie less than we think is known about starch digestion. It could be that starch does not simply turn to maltose and then glucose.
It is always assumed that maltose turns into glucose somehow but I don’t think it does. It is very complex actually.
So actually, starch is NOTHING like eating glucose.
It is processed mostly in intestinal lumen and produces many sugars including sucrose and fructose and galactose and lactose.
image url) -
@CrumblingCookie said in Glucose loading cures everything?:
@S-Holmes said:
I've even cut back to under 100 grams of glucose a day and temp is still really good.
Under 100 grams of dextros per day? You are not going to starve out on us, I hope.
So about 4 months in you are needing less dextrose every day to maintain the benefits you've achieved so far? Have you cut back because of laziness or because of a decrease in the taste or craving for it?Here's a new thought of mine on the mysterious background mechanisms of glucose loading, and the origin of the causative shift to a lower metabolic brain set-point through repetitive experiences of great stress:
What if it's not only or at all about more glucose being transported into the brain but about the brain, once glucose-loaded and energy sufficient, keeping additional PUFAs out? Either by directly blocking the entry of free fatty acids into the brain or also by a much lower level of FFAs in overall circulation. Perhaps the glucose enters the brain just as much at the beginning of the dextrose protocol as it does many months later. And all this glucose saturating the brain in part overrides the anti-metabolic PUFAs, shifting the scales.
And over time, the already accumulated brain PUFAs naturally diminish mostly during inactive nighttime and sleep. And that brain PUFA diminishment, which removes the stress(FFAs!)-induced inhibitions on the metabolic rate, would be the actual effect of and reason for the benefit of the glucose protocol over the course of time?
It's fair to assume that there's more than one aspect and mechanism to the whole. Can anyone with a bit of brain expertise chime in and tell me about how naive or not this latest train of though is?
I'm needing to get my weight under control. Do not want to buy new clothes. The problem is that I don't know if the extra weight is from inflammation (water) from healing (I've had pcos for many years), or from actual fat. But I have gained one or the other on glucose. I also really struggled with gerd while on the high doses. My husband is still doing well on the high doses. In fact, on days when he doesn't get enough, his mood suffers, so I make sure to keep his glucose lemonade glass full.
I'm learning what glucose can and cannot do. I use glucose now instead of sucrose for sweetening beverages, etc. And when I get a new ice cream freezer will make fat free ice cream sweetened with dextrose.
I have permanently added glucose to my arsenal and when I start feeling blue or agitated, I take a little to restore equilibrium.
In other news, and something I'm very excited about...I have a doctor friend I've known for many years who maps and stimulates brain pathways for healing and symptom management. She has a few patients who are also friends of mine. I introduced them to Dr Stephens when he was here for the health conference and they are collaborating on a research project to learn more about how glucose heals. One friend has migraines and the other ADHD. It should be very interesting.
-
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.
-
@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.
-
@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.
-
@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 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.
-
@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.
-
@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
-
@S-Holmes far from clear. I would not say Peat was wrong.
-
@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.
-
@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. -
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
-
@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.
-
@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.
-
Dr. Stephens' new book:
Restored Hope: A Neuroscience Guide to Optimal Brain and Human Function -
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-2220Sjust 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.
-
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.