Anti-Peat Low Carb Eating Does Not Cause Hypothyroid

B___Danny

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Hyperlipid: Are you free, T3?

"You can get an idea of whether the brain thinks there is enough T3 sitting on its receptors by whether it is asking for more. It asks for more using (eventually, after several steps) TSH, thyroid stimulating hormone. This is released from the pituitary as a signal to the thyroid to increase production.

So the rule of thumb with a suspected hypothyroid patient is to ask whether the TSH level is elevated, ie is the brain unhappy with the current thyroid level. When you don't have the time or finances available for that courier to swim the Atlantic, this is what we use. It's a surrogate, but useful."

"However, even with the greater fall in total T3 under LC eating, the brain is happy with whatever level of free T3 it is "seeing", as judged by TSH level. Should the brain be happy?

There are hints. In particular the TEE was reduced least in the LC phase of the study. There was a reduction in TEE of course. But less than for either of the other two phases imposing weight stability at reduced BMI. Despite the largest drop in total T3. It seems like a reasonable idea that both free T3 and receptor bound T3 might actually be higher under LC eating. As so many times, we will never know.

Another way of looking at the change would be to consider whether as much free T3 is needed on a LC diet. Sam Knox provided this rather nice link in the comments to The lost 300 post. It's certainly worth thinking about. Of course, I quite like the idea. But then I would!

So will low carbohydrate eating lead to thyroid deficiency? Who knows, in the long term. This was a very short study. But in this paper the brain seems quite happy with 108ng/dl of total T3 as judged by a TSH of 1.11microIU/ml."


It doesn't make logical sense that low-carb eating can ever cause hypothyroid LONG TERM (although it may appear to do so in the short-term). The problem is that low-carb eating is almost always synonymous with intermittent fasting/(starving) and caloric restriction with people trying to lose weight. The only logical thing that would cause the thyroid to not be able to produce enough T4/T3 is because it has been catabolized due to low calorie eating. Otherwise, the organ will stay strong and be able to play its roll in the body.
 
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Hyperlipid: Are you free, T3?

"You can get an idea of whether the brain thinks there is enough T3 sitting on its receptors by whether it is asking for more. It asks for more using (eventually, after several steps) TSH, thyroid stimulating hormone. This is released from the pituitary as a signal to the thyroid to increase production.

So the rule of thumb with a suspected hypothyroid patient is to ask whether the TSH level is elevated, ie is the brain unhappy with the current thyroid level. When you don't have the time or finances available for that courier to swim the Atlantic, this is what we use. It's a surrogate, but useful."

"However, even with the greater fall in total T3 under LC eating, the brain is happy with whatever level of free T3 it is "seeing", as judged by TSH level. Should the brain be happy?

There are hints. In particular the TEE was reduced least in the LC phase of the study. There was a reduction in TEE of course. But less than for either of the other two phases imposing weight stability at reduced BMI. Despite the largest drop in total T3. It seems like a reasonable idea that both free T3 and receptor bound T3 might actually be higher under LC eating. As so many times, we will never know.

Another way of looking at the change would be to consider whether as much free T3 is needed on a LC diet. Sam Knox provided this rather nice link in the comments to The lost 300 post. It's certainly worth thinking about. Of course, I quite like the idea. But then I would!

So will low carbohydrate eating lead to thyroid deficiency? Who knows, in the long term. This was a very short study. But in this paper the brain seems quite happy with 108ng/dl of total T3 as judged by a TSH of 1.11microIU/ml."


It doesn't make logical sense that low-carb eating can ever cause hypothyroid LONG TERM (although it may appear to do so in the short-term). The problem is that low-carb eating is almost always synonymous with intermittent fasting/(starving) and caloric restriction with people trying to lose weight. The only logical thing that would cause the thyroid to not be able to produce enough T4/T3 is because it has been catabolized due to low calorie eating. Otherwise, the organ will stay strong and be able to play its roll in the body.

yeah. Im trying Keto since 2-3 months and im warm&toasty, did not measure temperature objectively though. Seems plausible, biologically plausible that the User-Facing readings and labworks are off via the many ways of endogenous thyroidal activity measurements or skewed in the literature by confounding low calorie Dieting artefacts. A lot of Animals are Keto, and if you look at Arctic dogs like huskys and their extreme condition resilience, you better believe that their thyroid is going places.
 

Shman Frontal

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Well, when Thyroid increases (ft3 and ft4) than you need higher amounts of nutrients and calories, otherwise you will collapse. They are many people who take thyroid and get sugar issues/black in front of the eyes when getting up etc. So its not just your body isnt happy, your body adapt to the circumstances. Eating enough carbs is essential.
 

John Estrada

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I've seen someone go Keto and they wore a Fitbit which tracked their resting heart rate. Over the course of a few months their resting heart rate dropped over 20 BPM. As far as I know it hasn't recovered since.
 

B___Danny

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I've seen someone go Keto and they wore a Fitbit which tracked their resting heart rate. Over the course of a few months their resting heart rate dropped over 20 BPM. As far as I know it hasn't recovered since.
Was it a low calorie diet (i.e. less than 3000-4000 caloeies)?
 

Maljam

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I've seen someone go Keto and they wore a Fitbit which tracked their resting heart rate. Over the course of a few months their resting heart rate dropped over 20 BPM. As far as I know it hasn't recovered since.

What was the start and end bpm? Your anecdote isn't useful without them, as the implications behind say 105>85 are different to 75>55 for example.
 

Zigzag

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The problem is that low-carb eating is almost always synonymous with intermittent fasting/(starving) and caloric restriction with people trying to lose weight
Yes, that's definitely an issue. Imagine you had to eat less than 100g of carbs a day and still maintain, for example, a 3500kcal diet. That's barely possible because all that protein+fat you'd have to eat, would make you throw up. That's why keto is so easy to stick to. You just physically can't eat that much, because of satiety.
 

B___Danny

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Yes, that's definitely an issue. Imagine you had to eat less than 100g of carbs a day and still maintain, for example, a 3500kcal diet. That's barely possible because all that protein+fat you'd have to eat, would make you throw up. That's why keto is so easy to stick to. You just physically can't eat that much, because of satiety.
Exactly. But people with eating disorders (most keto dieters) consider this a plus because they think that eating is bad so the less you eat the better. That not having an appetite/being hungry is a good thing.

I think keto could work if you are deliberate about eating every 2-4 hours and high calorie. Keto really becomes a problem when you are making ketones and glucose from your own tissues which is an adaptation with many negative long term consequences. A high fat diet is only “ketogenic” per se if calories are restricted/you go more than 4 hours without eating.
 

Jessie

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I don't think the bioenergetic view claims low-carb causes long-term hypothyroidism. This has never really been claimed as far as my understanding on the topic. The issue with low-carb diets is 1) there's less CO2 production, because fats (including saturated fats) produce less CO2 than carbohydrate, and 2) less liver glycogen means less T4 gets converted into T3.

If your only issue is low liver glycogen, then simply reintroducing sugar into the diet will start up the oxidative metabolism again. But that's a big if. 99% of the people have far more issues then low liver glycogen. They have bacterial overgrowth, impaired glycolosis, electron transport problems, soft tissue calcification, high estrogen, high prolactin, low vitamin D, and a vast array of multiple other issues.

Most of these things because of our degraded food supply. It's always worse on the proceeding generation as well. The 1st generation exposed to these inflammatory substances, like PUFA oils for example, were able to handle them better than us today. Their metabolisms were healthy starting off. Now days we're born in a uphill battle.
 

B___Danny

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I don't think the bioenergetic view claims low-carb causes long-term hypothyroidism. This has never really been claimed as far as my understanding on the topic. The issue with low-carb diets is 1) there's less CO2 production, because fats (including saturated fats) produce less CO2 than carbohydrate, and 2) less liver glycogen means less T4 gets converted into T3.

If your only issue is low liver glycogen, then simply reintroducing sugar into the diet will start up the oxidative metabolism again. But that's a big if. 99% of the people have far more issues then low liver glycogen. They have bacterial overgrowth, impaired glycolosis, electron transport problems, soft tissue calcification, high estrogen, high prolactin, low vitamin D, and a vast array of multiple other issues.

Most of these things because of our degraded food supply. It's always worse on the proceeding generation as well. The 1st generation exposed to these inflammatory substances, like PUFA oils for example, were able to handle them better than us today. Their metabolisms were healthy starting off. Now days we're born in a uphill battle.
Most of the problems you named are symptoms of long term starvation i.e. eating less than 4000 calories per day. “Inflammation” is also just a buzz word that people know nothing about.
 
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Kvothe

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Hyperlipid: Are you free, T3?

"You can get an idea of whether the brain thinks there is enough T3 sitting on its receptors by whether it is asking for more. It asks for more using (eventually, after several steps) TSH, thyroid stimulating hormone. This is released from the pituitary as a signal to the thyroid to increase production.

So the rule of thumb with a suspected hypothyroid patient is to ask whether the TSH level is elevated, ie is the brain unhappy with the current thyroid level. When you don't have the time or finances available for that courier to swim the Atlantic, this is what we use. It's a surrogate, but useful."

"However, even with the greater fall in total T3 under LC eating, the brain is happy with whatever level of free T3 it is "seeing", as judged by TSH level. Should the brain be happy?

There are hints. In particular the TEE was reduced least in the LC phase of the study. There was a reduction in TEE of course. But less than for either of the other two phases imposing weight stability at reduced BMI. Despite the largest drop in total T3. It seems like a reasonable idea that both free T3 and receptor bound T3 might actually be higher under LC eating. As so many times, we will never know.

Another way of looking at the change would be to consider whether as much free T3 is needed on a LC diet. Sam Knox provided this rather nice link in the comments to The lost 300 post. It's certainly worth thinking about. Of course, I quite like the idea. But then I would!

So will low carbohydrate eating lead to thyroid deficiency? Who knows, in the long term. This was a very short study. But in this paper the brain seems quite happy with 108ng/dl of total T3 as judged by a TSH of 1.11microIU/ml."


It doesn't make logical sense that low-carb eating can ever cause hypothyroid LONG TERM (although it may appear to do so in the short-term). The problem is that low-carb eating is almost always synonymous with intermittent fasting/(starving) and caloric restriction with people trying to lose weight. The only logical thing that would cause the thyroid to not be able to produce enough T4/T3 is because it has been catabolized due to low calorie eating. Otherwise, the organ will stay strong and be able to play its roll in the body.

- Significantly reduced resting respiratory quotient
- 20% higher cortisol
- Significantly lower serum T3
- Significantly reduced hepatic and peripheral insulin sensitivity

... sounds wonderful. Peter will twist anything he gets long enough until it somehow says low carb diets are splendid. His logic that a lower TSH is somehow a sign of the brain/body being happy with a lower metabolic rate is absurd, in my humble opinion. Low T3 and low TSH, at the same time, are possibly the worst combination possible. It's basically saying that you are on your way to becoming a frozen vegetable. High fat, especially high PUFA, diets are very good at getting your there.

Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults
I H Ullrich, P J Peters, M J Albrink

A low-carbohydrate diet, frequently used for treatment of reactive hypoglycemia, hypertriglyceridemia, and obesity may affect thyroid function. We studied the effects of replacing the deleted carbohydrate with either fat or protein in seven healthy young adults. Subjects were randomly assigned to receive seven days of each of two isocaloric liquid-formula, low-carbohydrate diets consecutively. One diet was high in polyunsaturated fat (HF), with 10%, 55%, and 35% of total calories derived from protein, fat, and carbohydrate, respectively. The other was high in protein (HP) with 35%, 30%, and 35% of total calories derived from protein, fat, and carbohydrate. Fasting blood samples were obtained at baseline and on day 8 of each diet. A meal tolerance test representative of each diet was given on day 7. The triiodothyronine (T3) declined more (P less than .05) following the HF diet than the HP diet (baseline 198 micrograms/dl, HP 138, HF 113). Thyroxine (T4) and reverse T3 (rT3) did not change significantly. Thyroid-stimulating hormone (TSH) declined equally after both diets. The insulin level was significantly higher 30 minutes after the HP meal (148 microU/ml) than after the HF meal (90 microU/ml). The two-hour glucose level for the HP meal was less, 85 mg/dl, than after the HF meal (103 mg/dl). Serum triglycerides decreased more after the HF diet (HF 52 mg/dl, HP 67 mg/dl). Apparent benefits of replacing carbohydrate with polyunsaturated fat rather than protein are less insulin response and less postpeak decrease in blood glucose and lower triglycerides. The significance of the lower T3 level is unknown.

Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults - PubMed


It doesn't make logical sense that low-carb eating can ever cause hypothyroid LONG TERM (although it may appear to do so in the short-term). The problem is that low-carb eating is almost always synonymous with intermittent fasting/(starving) and caloric restriction with people trying to lose weight. The only logical thing that would cause the thyroid to not be able to produce enough T4/T3 is because it has been catabolized due to low calorie eating. Otherwise, the organ will stay strong and be able to play its roll in the body.

This is simply not true. Dozens of studies have shown that carbohydrate is essential for normal T3 production, and the carbohydrate content is much more important than total calorie intake.


Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism

R Pasquali, M Parenti, L Mattioli, M Capelli, G Cavazzini, G Baraldi, G Sorrenti, G De Benedettis, P Biso, N Melchionda


The effect of different hypocaloric carbohydrate (CHO) intakes was evaluated in 8 groups of obese patients in order to assess the role of the CHO and the other dietary sources in modulating the peripheral thyroid hormone metabolism. These changes were independent of those of bw. Serum T3 concentrations appear to be more easily affected than those of reverse T3 by dietary manipulation and CHO content of the diet. A fall in T3 levels during the entire period of study with respect to the basal levels occurred only when the CHO of the diet was 120 g/day or less, independent of caloric intake (360, 645 or 1200 calories). Moreover, reverse T3 concentrations were found increased during the entire period of study when total CHO were very low (40 to 50 g/day) while they demonstrated only a transient increase when CHO were at least 105 g/day (with 645 or more total calories). Indeed, our data indicate that a threshold may exist in dietary CHO, independent of caloric intake, below which modifications occur in thyroid hormone concentrations. From these results it appears that the CHO content of the diet is more important than non-CHO sources in modulating peripheral thyroid hormone metabolism and that the influence of total calories is perhaps as pronounced as that of CHO when a "permissive" amount of CHO is ingested.

Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism - PubMed
 
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B___Danny

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- Significantly reduced resting respiratory quotient
- 20% higher cortisol
- Significantly lower serum T3
- Significantly reduced hepatic and peripheral insulin sensitivity

... sounds wonderful. Peter will twist anything he gets long enough until it somehow says low carb diets are splendid. His logic that a lower TSH is somehow a sign of the brain/body being happy with a lower metabolic rate is absurd, in my humble opinion. Low T3 and low TSH, at the same time, are possibly the worst combination possible. It's basically saying that you are on your way to becoming a frozen vegetable. High fat, especially high PUFA, diets are very good at getting your there.

Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults
I H Ullrich, P J Peters, M J Albrink

A low-carbohydrate diet, frequently used for treatment of reactive hypoglycemia, hypertriglyceridemia, and obesity may affect thyroid function. We studied the effects of replacing the deleted carbohydrate with either fat or protein in seven healthy young adults. Subjects were randomly assigned to receive seven days of each of two isocaloric liquid-formula, low-carbohydrate diets consecutively. One diet was high in polyunsaturated fat (HF), with 10%, 55%, and 35% of total calories derived from protein, fat, and carbohydrate, respectively. The other was high in protein (HP) with 35%, 30%, and 35% of total calories derived from protein, fat, and carbohydrate. Fasting blood samples were obtained at baseline and on day 8 of each diet. A meal tolerance test representative of each diet was given on day 7. The triiodothyronine (T3) declined more (P less than .05) following the HF diet than the HP diet (baseline 198 micrograms/dl, HP 138, HF 113). Thyroxine (T4) and reverse T3 (rT3) did not change significantly. Thyroid-stimulating hormone (TSH) declined equally after both diets. The insulin level was significantly higher 30 minutes after the HP meal (148 microU/ml) than after the HF meal (90 microU/ml). The two-hour glucose level for the HP meal was less, 85 mg/dl, than after the HF meal (103 mg/dl). Serum triglycerides decreased more after the HF diet (HF 52 mg/dl, HP 67 mg/dl). Apparent benefits of replacing carbohydrate with polyunsaturated fat rather than protein are less insulin response and less postpeak decrease in blood glucose and lower triglycerides. The significance of the lower T3 level is unknown.

Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults - PubMed




This is simply not true. Dozens of studies have shown that carbohydrate is essential for normal T3 production, and the carbohydrate content is much more important than total calorie intake.


Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism

R Pasquali, M Parenti, L Mattioli, M Capelli, G Cavazzini, G Baraldi, G Sorrenti, G De Benedettis, P Biso, N Melchionda


The effect of different hypocaloric carbohydrate (CHO) intakes was evaluated in 8 groups of obese patients in order to assess the role of the CHO and the other dietary sources in modulating the peripheral thyroid hormone metabolism. These changes were independent of those of bw. Serum T3 concentrations appear to be more easily affected than those of reverse T3 by dietary manipulation and CHO content of the diet. A fall in T3 levels during the entire period of study with respect to the basal levels occurred only when the CHO of the diet was 120 g/day or less, independent of caloric intake (360, 645 or 1200 calories). Moreover, reverse T3 concentrations were found increased during the entire period of study when total CHO were very low (40 to 50 g/day) while they demonstrated only a transient increase when CHO were at least 105 g/day (with 645 or more total calories). Indeed, our data indicate that a threshold may exist in dietary CHO, independent of caloric intake, below which modifications occur in thyroid hormone concentrations. From these results it appears that the CHO content of the diet is more important than non-CHO sources in modulating peripheral thyroid hormone metabolism and that the influence of total calories is perhaps as pronounced as that of CHO when a "permissive" amount of CHO is ingested.

Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism - PubMed
Thank you for the rebuttal. Will look into it. But it also doesnt make sense to me that we would have made it this far as humans while not always having access to carbohydrates. I am not saying that carbohydrates are damaging, i actually think they are helpful. But I think that saying that the lack of them leads to disease is as fallacious as saying that a heavy supply of them leads to disease.the real problem at hand is multi generational caloric restriction habits.
 

baccheion

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The only way to do keto is with truly pastured organic raw egg yolks. And maybe some electrolyted water..

Egg yolks are a pure model of food meant to be eaten in isolation for an extended period of time. Everything is present and cohesive, even serving up keto/5-20-75% macros.
 

John Estrada

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What was the start and end bpm? Your anecdote isn't useful without them, as the implications behind say 105>85 are different to 75>55 for example.
Probably closer to the to 75>55 range. It was a steady decline in average BPM over a month or two of Keto.
 

Jessie

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Most of the problems you named are symptoms of long term starvation i.e. eating less than 4000 calories per day. “Inflammation” is also just a buzz word that people know nothing about.
Actually one of the benefits to calorie restricted diets is a reduction in bacterial endotoxin. Also for most people, 4,000 calories per day is hypercaloric. A healthy adult needs roughly 50-60% of that. Someone with an impaired metabolism probably even less, unless getting fat isn't a concern for them.

I agree many people loosely throw around words like inflammation and don't properly understand the connotations to it
 

baccheion

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Actually one of the benefits to calorie restricted diets is a reduction in bacterial endotoxin. Also for most people, 4,000 calories per day is hypercaloric. A healthy adult needs roughly 50-60% of that. Someone with an impaired metabolism probably even less, unless getting fat isn't a concern for them.

I agree many people loosely throw around words like inflammation and don't properly understand the connotations to it
Adding less than 300 calories/week, hypermetabolic is the point at which there's fat gain out of proportion with lean mass gain (ie, more fat gain than lean mass).
 

Jessie

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Adding less than 300 calories/week

I don't understand what you're saying here. Someone eating 300 calories a week is starvation.

hypermetabolic is the point at which there's fat gain out of proportion with lean mass gain (ie, more fat gain than lean mass).

Ray's opinion is hyperthyroidism is rare, and most of them are just hypo with really high stress hormones compensate their symptoms.
 
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