Breakthrough understanding in thyroid and glycogen link!

[EnergeticLeo]

Just wanted to share this recent development in my understanding of the energy system.
I had heard Peat say many times that glycogen storage wasn't great in hypothyroid individuals but I never understand the underlying mechanism - now I think I do.

First I came across this paper: The effect of the thyroid status on the activation of glycogen synthase in liver cells - PubMed

Isolated hepatocytes from hyperthyroid and euthyroid rats showed the same rate and extent of activation of glycogen synthase after addition of glucose (10 mM or 60 mM). In liver cells from hypothyroid rats this activation occurred at a 7-fold lower rate.

Then it struck me that glycogen formation is, like everything else in the body, a metabolic process, the rate of which is heavily influenced by how much thyroid hormone and fuel is in the system! It seems obvious and basic now but it really helped me understand my current situation - hopefully others will find it useful too.

Now it's clear to me why in a hypo-metabolic state, blood sugar control and hence energy stability can be poor.

 

[Peachy]

This is awesome. Thank you! Optimizing glycogen stores has been on the top of my mind lately and this is a lightbulb. What a vicious cycle this can get you in.

 

[EnergeticLeo]

This is awesome. Thank you! Optimizing glycogen stores has been on the top of my mind lately and this is a lightbulb. What a vicious cycle this can get you in.

Glad to hear it

Vicious it can be indeed - I'm trying hourly feeding intervals to try to compensate for poor glycogen storage, inspired by William Brown's diet in Glucose and sucrose for diabetes.

 

[Sitaruîm]

Could this mean that exercise performance and recovery could be used to test thyroid health? By measuring glycogen repletion, etc.

 

[EnergeticLeo]

Could this mean that exercise performance and recovery could be used to test thyroid health? By measuring glycogen repletion, etc.

That's a good point - I would think so.
In theory you could look at the rate of any metabolic process to get an idea of thyroid health. For example, as I've started to improve my own energy levels, I've noticed that my nails have been growing much faster.

 

[joaquin]

And why does eating popcorn at night seem to boost my glycogen stores better than anything else? I really want to stay away from corn, but it works.

 

[EnergeticLeo]

And why does eating popcorn at night seem to boost my glycogen stores better than anything else? I really want to stay away from corn, but it works.

Interesting observation. How are you gauging the improved glycogen stores?

 

[Sitaruîm]

And why does eating popcorn at night seem to boost my glycogen stores better than anything else? I really want to stay away from corn, but it works.

Probably because starch is best to replenish glycogen, due to it being insulinogenic, I'm thinking.

 

[joaquin]

Interesting observation. How are you gauging the improved glycogen stores?

I sleep much deeper and stay asleep for 7.5 hours usually. That is my main gauge.

 

[SamYo123]

Probably because starch is best to replenish glycogen, due to it being insulinogenic, I'm thinking.

These a reason why most edurance athletes use rice/pasta before a long race...

 

[mostlylurking]

Now it's clear to me why in a hypo-metabolic state, blood sugar control and hence energy stability can be poor.

Optimizing glycogen stores has been on the top of my mind lately and this is a lightbulb.

Another related thing to keep in mind: The liver (along with the rest of the body) needs good oxidative metabolic function to do its jobs and be healthy. Good oxidative metabolism needs thyroid hormone (T3) to work. It also requires a supply of thiamine which acts as a co-enzyme in multiple stages of the metabolic process. In addition, the thyroid needs thiamine to do its job of making thyroid hormone and the liver needs thiamine to have the energy to convert T4 into T3.

High-dose vitamin B1 therapy prevents the development of experimental fatty liver driven by overnutrition - PubMed

Fatty liver is an abnormal metabolic condition of excess intrahepatic fat. This condition, referred to as hepatic steatosis, is tightly associated with chronic liver disease and systemic metabolic morbidity. The most prevalent form in humans, i.e. non-alcoholic fatty liver, generally develops...

pubmed.ncbi.nlm.nih.gov

Abstract ​

Fatty liver is an abnormal metabolic condition of excess intrahepatic fat. This condition, referred to as hepatic steatosis, is tightly associated with chronic liver disease and systemic metabolic morbidity. The most prevalent form in humans, i.e. non-alcoholic fatty liver, generally develops due to overnutrition and sedentary lifestyle, and has as yet no approved drug therapy. Previously, we have developed a relevant large-animal model in which overnourished sheep raised on a high-calorie carbohydrate-rich diet develop hyperglycemia, hyperinsulinemia, insulin resistance, and hepatic steatosis. Here, we tested the hypothesis that treatment with thiamine (vitamin B1) can counter the development of hepatic steatosis driven by overnutrition. Remarkably, the thiamine-treated animals presented with completely normal levels of intrahepatic fat, despite consuming the same amount of liver-fattening diet. Thiamine treatment also decreased hyperglycemia and increased the glycogen content of the liver, but it did not improve insulin sensitivity, suggesting that steatosis can be addressed independently of targeting insulin resistance. Thiamine increased the catalytic capacity for hepatic oxidation of carbohydrates and fatty acids. However, at gene-expression levels, more-pronounced effects were observed on lipid-droplet formation and lipidation of very-low-density lipoprotein, suggesting that thiamine affects lipid metabolism not only through its known classic coenzyme roles. This discovery of the potent anti-steatotic effect of thiamine may prove clinically useful in managing fatty liver-related disorders.This article has an associated First Person interview with the joint first authors of the paper.
-end-

In addition, the thyroid needs thiamine to do its job of making thyroid hormone and the liver needs thiamine to have the energy to convert T4 into T3.

These a reason why most edurance athletes use rice/pasta before a long race...

An additional detail to keep in mind: a person's thiamine stores are used up processing carbohydrates so it is important to try to keep the supply of thiamine in sync with the amount of carbs consumed. Refined carbs like white rice and white flour have lost their thiamine stores when milled and refined.

 

[PeskyPeater]

Probably because starch is best to replenish glycogen, due to it being insulinogenic, I'm thinking.

nah, glucose is faster to fill the glycogen stores, but fructose makes for 30% more energy per glycogen molecule

 

[PeskyPeater]

Am J Clin Nutr 1993 Nov;58(5 Suppl):766S-770S. Fructose and dietary thermogenesis. Tappy L, Jequier E. “Fructose ingestion induces a greater thermogenesis than does glucose. This can be explained by the hydrolysis of 3.5-4.5 mol ATP/mol fructose stored as glycogen, vs 2.5 mol ATP/mol glucose stored. Therefore the large thermogenesis of fructose corresponds essentially to an increase in obligatory thermogenesis. Obese individuals and obese patients with non-insulin-dependent diabetes mellitus commonly have a decrease in glucose-induced thermogenesis. These individuals in contrast display a normal thermogenesis after ingestion of fructose. This may be explained by the fact that the initial hepatic fructose metabolism is independent of insulin.” Glycemia, starch, and sugar in context

Several potential mechanisms for the decreased
glycaemic response caused by a catalytic small
amount of fructose have been considered: fruc-
tose-induced malabsorption of carbohydrates, en-
hanced insulin secretion, and stimulation of hepatic
glucose uptake secondary to hepatic glucokinase
translocation (34). However, malabsorption should
not be a problem with the small dose of fructose
(7.5-10 g) used in the three studies (30,32), since in
one recent study of 21 healthy subjects in whom
malabsorption was demonstrated after ingestion of
50 g fructose, only four individuals experienced
malabsorption when consuming 25 g fructose (35).
Enhanced insulin secretion caused by fructose also
seems not to be the case. Two of the three studies
measured also the insulin AUC. In the study with
healthy subjects no difference was seen between the
OGTT with and without fructose, and in the study
with type 2 diabetic patients, the insulin AUC
decreased by 21% with fructose administration.
Therefore, the most probable mechanism for the
decreased glycaemic response may be fructose-
induced stimulation of hepatic glucose uptake. It
has been established that in hepatocytes, fructose is
rapidly phosphorylated to fructose-1-phosphate,
which competes with fructose-6-phosphate for bind-
ing on a glucokinase regulatory protein (GKRP).
As a result of this competition, glucokinase is
released from GKRP and the liberated glucokinase
diffuses to the cytosol. The glucokinase transloca-
tion stimulates the hepatic glucose uptake by
converting glucose to glycogen, and phosphoryla-
tion of glucose by glucokinase, which is a rate-
determining step for hepatic glucose metabolism.
Thus, the primary difference between hepatic fruc-
tose and glucose metabolism is that fructose mole-
cules by-pass the main rate-controlling step in
glycolysis, 6-phosphofructokinase. This hypothesis
has been demonstrated in studies with dogs (36, 37).
Although the fructose-induced stimulation of hepa-
tic glucose uptake seems to be the most obvious
mechanism of catalytic effect of fructose, more
studies are needed to confirm the mechanism in
humans. https://www.researchgate.net/public...m_body_weight_and_glucose_tolerance_in_humans

 

[xeliex]

High-dose vitamin B1 therapy prevents the development of experimental fatty liver driven by overnutrition - PubMed

Fatty liver is an abnormal metabolic condition of excess intrahepatic fat. This condition, referred to as hepatic steatosis, is tightly associated with chronic liver disease and systemic metabolic morbidity. The most prevalent form in humans, i.e. non-alcoholic fatty liver, generally develops...

pubmed.ncbi.nlm.nih.gov

Good stuff Mostlythiamine!

 

[mostlylurking]

Am J Clin Nutr 1993 Nov;58(5 Suppl):766S-770S. Fructose and dietary thermogenesis. Tappy L, Jequier E. “Fructose ingestion induces a greater thermogenesis than does glucose. This can be explained by the hydrolysis of 3.5-4.5 mol ATP/mol fructose stored as glycogen, vs 2.5 mol ATP/mol glucose stored. Therefore the large thermogenesis of fructose corresponds essentially to an increase in obligatory thermogenesis. Obese individuals and obese patients with non-insulin-dependent diabetes mellitus commonly have a decrease in glucose-induced thermogenesis. These individuals in contrast display a normal thermogenesis after ingestion of fructose. This may be explained by the fact that the initial hepatic fructose metabolism is independent of insulin.” Glycemia, starch, and sugar in context

A biotin deficiency can derail the successful utilization of fructose. Biotin supplementation can help

Protective effect of supplementation with biotin against high-fructose-induced metabolic syndrome in rats

Several reports have demonstrated that pharmacological concentrations of biotin reduce hyperglycemia, hypertriglyceridemia, and hypertension. We hypot…

www.sciencedirect.com

Abstract​

Several reports have demonstrated that pharmacological concentrations of biotin reduce hyperglycemia, hypertriglyceridemia, and hypertension. We hypothesized that biotin could exert a protective effect on some illness-associated metabolic syndrome. To test this hypothesis, male Wistar rats were fed a diet containing 30% fructose in drinking water and classified into four groups: C, the control group; B, the group receiving biotin (intraperitoneal injection, 2 mg/kg); F, the group receiving fructose (30% w/v); and FB, the group receiving fructose-biotin. The administration of biotin began after the rats had been on a high-fructose diet for 12 weeks and continued for 4 weeks. Our results showed that food and fluid intake were diminished in the F and FB groups. However, the final body weights were similar between the groups. A significant increase in hepatic triglyceride and cholesterol content, plasma cholesterol, triglycerides, transaminases, low-density lipoprotein cholesterol (LDL-c), systolic blood pressure, and vasocontraction, as well as a decrease in high-density lipoprotein cholesterol (HDL-c) were observed in the F group. Glucose tolerance and insulin tolerance were also impaired in the F group. The administration of biotin ameliorated all these changes. Hepatic oxidative stress as well as macrovesicular fatty changes in hepatocytes caused by a high-fructose diet were also improved by biotin. Our findings demonstrate that biotin has a protective role against metabolic syndrome by improving insulin resistance associated with normal hepatic and serum levels of triglyceride and cholesterol, blood pressure, and the prevention of steatosis and hepatic oxidative damage. Therefore, biotin could be used as a therapeutic strategy in the pharmacological treatment of metabolic syndrome.

Good stuff Mostlythiamine!

thanks.

 

[PeskyPeater]

A biotin deficiency can derail the successful utilization of fructose. Biotin supplementation can help

Yeah biotin may help utilize sugar, but not on its own. Also preventing triggering the randle effect is a must. Like with niacinamide aspirin and vitamin E.

and alcohol is a danger for it reduces the absorption of biotin from food, like raw eggs do