Do Carbohydrates Turn Into Fat?

[ecstatichamster]

I want to thank you all, especially @tyw, but everyone.

My weight hasn't budged. And I think I am consuming far too much sugar. My wife is going, "I've been telling you that all along, you never listen to me," LOL.

I wrote Ray and await his response. But today I started cutting WAY back on sugar. Still eating it, but not nearly as much, or as FAST. That's really the key too. I had half a glass of OJ. And I'm having milk without honey during the day.

Maybe this will help me lose weight. Maybe this is the missing piece. I feel like my liver must still be fatty. I just don't feel like I have that non-fatty lean metabolism.

I crash easily with coffee if I don't have enough food behind me, for instance.

And my appetite seems too high. I just feel like I'm hungry all the time. Not a great way to go. So now we hae a new tweak.

Less sugar, less often.

 

[Milena]

And my appetite seems too high. I just feel like I'm hungry all the time. Not a great way to go. So now we have a new tweak.

Less sugar, less often.

Do you eat protein, each meal, with your carbs? I find this makes me less hungry.

 

[ecstatichamster]

Do you eat protein, each meal, with your carbs? I find this makes me less hungry.

my diet is a few fried eggs, OJ, milk, cheese (not much), etc., so yes, I always do...

 

[Travis]

Just came across this. Thiamine is essential for three enzymes which catalyze three separate steps the glycolytic/Kreb's pathways

To assess the effect of high-dose oral thiamine supplements on glucose tolerance in patients with impaired glucose metabolism.

METHODS:
Twelve hyperglycemic subjects (10 cases of impaired glucose tolerance and 2 new cases of type 2 diabetes) completed this randomized, double-blind trial, where all participants received both placebo and thiamine capsules (3 × 100 mg/day) for 6 weeks in a cross-over manner. The main endpoint was changes in 2-h plasma glucose. Fasting plasma glucose and insulin, 2-h plasma insulin, the hemostatic model assessment of insulin resistance (HOMA-IR), renal function measurement and thiamin status were also evaluated at the commencement and completion of each treatment period.

RESULTS:
Thiamine supplementation resulted in significant decrease in 2-h plasma glucose relative to baseline (8.78 ± 2.20 vs. 9.89 ± 2.50 mmol/l, p = 0.004), with no significant change in the placebo arm. Fasting plasma glucose and insulin, and HOMA-IR increased significantly from baseline after 6 weeks in the placebo arm (p = 0.003, p = 0.04 and p = 0.02, respectively). These variables did not change with thiamine supplementation. There were no significant changes in 2-h plasma insulin or renal function marker, within or between arms.

CONCLUSION/INTERPRETATION:
Supplementation with high-dose thiamine may prevent deterioration in fasting glucose and insulin, and improve glucose tolerance in patients with hyperglycemia. High-dose thiamine supplementation may prevent or slow the progression of hyperglycemia toward diabetes mellitus in individuals with impaired glucose regulation.

High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial.

You might be able to use the sugar faster with thiamine.

 

[schultz]

I think most people get fatty liver either from excessive lipolysis or eating too much fat, usually combined with the soft drinks.

I think endotoxin is a huge part of it and possibly anything else that causes less than optimal liver function (like estrogen and PUFA). For the most part, I think fructose is the scapegoat because it happens to be at the scene of the crime, so-to-speak.

Take this paper for example....

"Several lines of evidence suggest that alterations of intestinal barrier function and an increased translocation of bacterial toxins like endotoxin are involved in the onset and probably the progression of NAFLD... In line with the results of human studies, results of animal studies have repeatedly shown that the development of NAFLD is associated with increased bacterial endotoxin levels in portal vein and an induction of TLRs in the liver. Furthermore, treatments with antibiotics targeting gram-negative bacteria in the gut have been shown to be associated with a marked attenuation of the development of NAFLD induced through feeding high fat- or high fructose diets"

So simply taking antibiotics can help clear up NAFLD.

In one of the East/West podcasts Ray tells this little anecdote...

Dr. Ray Peat: Just a few days ago I heard from someone in New Zealand who said he had been diagnosed a few months ago with non-alcoholic fatty liver disease and he said he started – I didn't get the details of the whole diet, but it included 300 grams of fructose everyday, and he now has a new diagnosis: his liver has no fat problem.

I don't intend that to be proof (not even close) but if it's true then it is at least interesting.

 

[schultz]

Just came across this. Thiamine is essential for three enzymes which catalyze three separate steps the glycolytic/Kreb's pathways



High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial.

You might be able to use the sugar faster with thiamine.

Good find. People often forget how important the b-vitamins are (I guess they're not in style anymore).

If someone eats a bunch of sugar everyday, in the form of pop or something, and develops health problems, it's easy to blame the sugar but it's really the absence of micro nutrients causing the health problems.

Does fructose directly cause NAFLD or is it also some deficiency, or at least partly.

I was taking CLA a while back and in the literature on it I noticed that it has been associated with fatty liver. I mentioned it to a friend of mine saying "I wonder if I am developing a fatty liver from the CLA?" and he mentioned that I would probably be fine since I eat liver regularly. He was referring to a Chris Masterjohn article on choline and NAFLD.

https://chrismasterjohnphd.com/2010/11/28/does-choline-deficiency-contribute-to/

The intro says this...

"I’m quite convinced that the development of fatty liver is pretty simple: anything that increases the amount of energy that the liver needs to process forms the first part; anything that impairs the ability of the liver to export that energy forms the second part. High intakes of total calories, sugar, fat, or alcohol can all contribute to fatty liver in animals. But the king of all nutrients needed to export that energy as fat, choline, protects against the disease in all of these animal models."

"Of course, a high intake of PUFA contributes to the inflammatory component, and when combined with other toxic factors may also contribute to the fatty component by preventing the liver from exporting its fat."

Aside from the choline, the important part of that is where he says "... anything that impairs the ability of the liver to export that energy forms the second part." I mentioned endotoxin in an earlier post. Endotoxin is one of these things that can impair the liver. According the Masterjohn, a deficiency of choline is another thing that can impair the export of energy from the liver.

Great thread btw.

 

[yoshiesque]

Im sorry but in my personal experiment carbohydrates can turn into fat. I tried a zero fat diet for a about a week. I just smashed out sugars like crazy. Fruit, fruit juices, plenty of white sugar and 2 cans of coke. I gained weight. I stopped the coke, cut down on white sugars and it was getting better.

 

[Wagner83]

Im sorry but in my personal experiment carbohydrates can turn into fat. I tried a zero fat diet for a about a week. I just smashed out sugars like crazy. Fruit, fruit juices, plenty of white sugar and 2 cans of coke. I gained weight. I stopped the coke, cut down on white sugars and it was getting better.

Did you try carbs in the form of potatoes/rice/starch with small amounts of fructose?

 

[ecstatichamster]

Im sorry but in my personal experiment carbohydrates can turn into fat. I tried a zero fat diet for a about a week. I just smashed out sugars like crazy. Fruit, fruit juices, plenty of white sugar and 2 cans of coke. I gained weight. I stopped the coke, cut down on white sugars and it was getting better.

this has been my experience too.

I am in the process of cutting back sugar and replacing it with boiled potatoes, rice, and just cutting back in general. So hopefully I won't be as hungry all the time.

So my plan is:

keep the nonfat milk with collagen
small amounts of OJ or guava juice
plenty of ripe fruit
rice or potatoes
a small amount of full fat cheese
dinner being a small portion of fish, chicken breast or lean grass fed beef and rice
1 Coke maximum per day

This will radically reduce my sugar intake and hopefully I can lose weight and feel good.

 

[haidut]

I think endotoxin is a huge part of it and possibly anything else that causes less than optimal liver function (like estrogen and PUFA). For the most part, I think fructose is the scapegoat because it happens to be at the scene of the crime, so-to-speak.

Take this paper for example....

"Several lines of evidence suggest that alterations of intestinal barrier function and an increased translocation of bacterial toxins like endotoxin are involved in the onset and probably the progression of NAFLD... In line with the results of human studies, results of animal studies have repeatedly shown that the development of NAFLD is associated with increased bacterial endotoxin levels in portal vein and an induction of TLRs in the liver. Furthermore, treatments with antibiotics targeting gram-negative bacteria in the gut have been shown to be associated with a marked attenuation of the development of NAFLD induced through feeding high fat- or high fructose diets"

So simply taking antibiotics can help clear up NAFLD.

In one of the East/West podcasts Ray tells this little anecdote...

Dr. Ray Peat: Just a few days ago I heard from someone in New Zealand who said he had been diagnosed a few months ago with non-alcoholic fatty liver disease and he said he started – I didn't get the details of the whole diet, but it included 300 grams of fructose everyday, and he now has a new diagnosis: his liver has no fat problem.

I don't intend that to be proof (not even close) but if it's true then it is at least interesting.

Absolutely, there are even quite a few companies trying to get drugs approved for NAFLD and even cirrhosis. Google for "TLR4 antagonist NAFLD". So, the carrot salad, less soluble fiber to feed the bacteria, antibiotics, cascara/emodin, methylene blue, and even vitamin K should all help. Coincidentally, there are studied for all of these substances and NAFLD.

 

[Travis]

You should enter your food into the cronometer.

 

[schultz]

I just smashed out sugars like crazy.

I gained weight.

Yah that'll do it!

Do you happen to know how many calories you were getting?

A week isn't a long time. Maybe the weight you gained was water + glycogen? Sort of like a carb load.

 

[schultz]

Absolutely, there are even quite a few companies trying to get drugs approved for NAFLD and even cirrhosis. Google for "TLR4 antagonist NAFLD". So, the carrot salad, less soluble fiber to feed the bacteria, antibiotics, cascara/emodin, methylene blue, and even vitamin K should all help. Coincidentally, there are studied for all of these substances and NAFLD.

https://www.researchgate.net/publication/279302142_Hepatic_TLR4_signaling_in_obese_NAFLD

"The bacterial endotoxin lipopolysaccharide (LPS) and total free fatty acid levels were significantly increased in plasma of NASH patients."

I suppose the question is, does endotoxin impair liver function and cause the liver not to be able to deal with the excess energy, or does fructose impair liver function causing the liver not to be able to deal with endotoxin like it normally does (hence the elevated endotoxin in the blood). The latter seems unlikely to me, but I probably harbour a pre-existing bias on the subject.

I have seen some studies say that fructose actually allows endotoxin in from the gut, through the portal vein I suppose. The way they worded it made it seem like it was the fault of fructose.

Then you have studies like this

"This concept is best studied for the quintessential TLR agonist, LPS, which activates TLR4. In mice, high-fat diets result in increased gut permeability and modest but significantly increased levels of circulating LPS, termed metabolic endotoxemia, that drives metabolic disease. The concept that reduced intestinal barrier function can result in gut microbiota products breaching the intestine, sometimes referred to as "leaky gut syndrome", is increasingly thought to play a central role in liver disease."

Sort of off topic, but I am reminded of a study I read about drinking alcohol. A few hours after a large amount of alcohol has been consumed there is a drop in endotoxin, but after 24 hours (or some number) there is a large influx. I suppose it may be possible that alcohol is not the cause, or at least only partially the cause, of alcoholic liver disease, and that it is endotoxin doing the damage, albeit facilitated by alcohol in some way (possibly increasing gut permeability).

I think this is the study I was thinking off: Acute binge drinking increases serum endotoxin and bacterial DNA levels in healthy individuals. - PubMed - NCBI

"Our findings indicate that even a single alcohol binge results in increased serum endotoxin levels likely due to translocation of gut bacterial products and disturbs innate immune responses that can contribute to the deleterious effects of binge drinking."

 

[haidut]

https://www.researchgate.net/publication/279302142_Hepatic_TLR4_signaling_in_obese_NAFLD

"The bacterial endotoxin lipopolysaccharide (LPS) and total free fatty acid levels were significantly increased in plasma of NASH patients."

I suppose the question is, does endotoxin impair liver function and cause the liver not to be able to deal with the excess energy, or does fructose impair liver function causing the liver not to be able to deal with endotoxin like it normally does (hence the elevated endotoxin in the blood). The latter seems unlikely to me, but I probably harbour a pre-existing bias on the subject.

I have seen some studies say that fructose actually allows endotoxin in from the gut, through the portal vein I suppose. The way they worded it made it seem like it was the fault of fructose.

Then you have studies like this

"This concept is best studied for the quintessential TLR agonist, LPS, which activates TLR4. In mice, high-fat diets result in increased gut permeability and modest but significantly increased levels of circulating LPS, termed metabolic endotoxemia, that drives metabolic disease. The concept that reduced intestinal barrier function can result in gut microbiota products breaching the intestine, sometimes referred to as "leaky gut syndrome", is increasingly thought to play a central role in liver disease."

Sort of off topic, but I am reminded of a study I read about drinking alcohol. A few hours after a large amount of alcohol has been consumed there is a drop in endotoxin, but after 24 hours (or some number) there is a large influx. I suppose it may be possible that alcohol is not the cause, or at least only partially the cause, of alcoholic liver disease, and that it is endotoxin doing the damage, albeit facilitated by alcohol in some way (possibly increasing gut permeability).

I think this is the study I was thinking off: Acute binge drinking increases serum endotoxin and bacterial DNA levels in healthy individuals. - PubMed - NCBI

"Our findings indicate that even a single alcohol binge results in increased serum endotoxin levels likely due to translocation of gut bacterial products and disturbs innate immune responses that can contribute to the deleterious effects of binge drinking."

Alcohol is TLR4 agonist, along with opioids like morphine. Alcohol also increases gut permeability, which allows for even more endotoxin to enter the blood. Liver disease is not due to carbs of any kind, including fructose. Peat wrote once that cirrhosis cannot form without presence of PUFA and the studies on reversing liver fibrosis with saturated fat confirm this. TLR4 antagonists like ketotifen can also reverse fibrotic states like cirrhosis and systemic sclerosis, but ketotifen is also a histamine, serotonin, and leukotriene antagonist so I doubt its benefits are due just to endotoxin antagonism. I think fructose is pretty clearly a scapegoat, just like cholestrol (which it incidentally raises) is for CVD.

 

[Mito]

I think fructose is pretty clearly a scapegoat, just like cholestrol (which it incidentally raises) is for CVD.

Interesting analogy. In CVD, the oxidizing PUFA's in the phospholipid membrane of the LDL particles contribute to formation of atherosclerotic plaques. Without PUFA's in the LDL particle membrane, they would loose their bad reputation. How does PUFA contribute to fructose potentially increasing liver fat? Would it be by slowing down the liver's ability to quickly metabolize the fructose?

 

[schultz]

Alcohol is TLR4 agonist, along with opioids like morphine. Alcohol also increases gut permeability, which allows for even more endotoxin to enter the blood. Liver disease is not due to carbs of any kind, including fructose. Peat wrote once that cirrhosis cannot form without presence of PUFA and the studies on reversing liver fibrosis with saturated fat confirm this. TLR4 antagonists like ketotifen can also reverse fibrotic states like cirrhosis and systemic sclerosis, but ketotifen is also a histamine, serotonin, and leukotriene antagonist so I doubt its benefits are due just to endotoxin antagonism. I think fructose is pretty clearly a scapegoat, just like cholestrol (which it incidentally raises) is for CVD.

That effect of alcohol, in regards to gut permeability, does it happen with any dose or just an excessive dose (whatever that is)?

Ray does tend to be right.

 

[m_arch]

A bigger waist is probably considered more attractive.

.... said no one, ever D:

 

[schultz]

.... said no one, ever D:

lol

 

[haidut]

That effect of alcohol, in regards to gut permeability, does it happen with any dose or just an excessive dose (whatever that is)?

Ray does tend to be right.

I think this is one area where the official recommendations may be accurate - i.e. up to 2-3 drinks per day is probably OK and would not seriously raise permeability, assuming careful diet and keeping estrogen/endotoxin/PUFA under control. I think for people with sensitive guts that are easily disturbed by things like starch, alcohol should not be consumed every day to allow the barrier to recover. Magnesium and vitamin A are known to restore barrier function.
Btw, despite the estrogenicity of beer I find it gives me the least amount of problems after drinking it. It has a lot of B vitamins so that may be one reason why.

 

[yoshiesque]

Did you try carbs in the form of potatoes/rice/starch with small amounts of fructose?

I did no starch at all. I have not tried it with small amounts of fructose but I certainly do believe starch makes you fatter. My personal experiments have shown that clearly. So while losing weight, I tend to avoid all starches. Once I am at a relatively healthy weight, Ill add them back in.