Do Carbohydrates Turn Into Fat?

Giraffe

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Except for hardcore Peaters and fruitians. With all the recommendations in this forum to drink lots of OJ & milk, eat lots of ice cream while avoiding starch (due to endotoxin), it's easy to hit over 100% of sugar within 10 minutes. Since starch is out of question, sucrose / fructore is the primary source of carbs.

I remember when I was 100% Peating and following the recommendations here 2 years ago, 100g of sugar per meal was minimum. Boy, my health hit rock bottom...
100 g sugar is:
  • orange juice or milk: 5-6 cups or
  • bananas: 4 large or
  • oranges 6 large or
  • honey: 6 tbsp or
  • table sugar: 25 tsp or
  • coke or icecream: 1 qt
Most people do not consume that amount of sugar in one meal, let alone in ten minutes. Please, don't say that the users here have not advised you to take it slow with dietary changes and supplements and to stop doing things that don't work for you.
 

Mito

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I believe Haidut drinks real sugar Pepsi so no fructose there.
There's no high fructose corn syrup in Pepsi Throwback (real sugar Pepsi) but there's still about 25g fructose per 20 oz bottle.
IMG_0681.jpg
 

tyw

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A flaw in many studies is that the observation time is limited to 120 minutes. This is also one of the flaws of the glycemic index. I looked for a study with longer observaton time. The participants here are type 2 diabetics.

Effect of Added Fat on Plasma Glucose and Insulin Response to Ingested Potato in Individuals With NIDDM


After ingestion of potato alone or potato plus different amounts of butter, insulin concentrations peaked at 60 min (120 min when 30 or 50 g fat was added). The insulin concentrations where near initial values after 300 min. After ingestion of 50 g glucose, the glucose concentration was below the initial value by 300 min. The insulin concentration was near initial value, but still elevated at 300 min.

This is a typical pattern. Insulin release to a bout of eating always has 2 phases, with an initial spike which lasts around 30-60mins, then a drop, and then a slight rise to a level that is maintained for until about 3 hours after the meal.

Measures of Glycaemic Index and Insulin Index typically last 120 mins / 2 hours, and are intended to measure the initial spike plus some of the second phase release. The typical pattern that we see with single meal in the single meal scenarios is that a lower first phase peak always leads to a lower second phase peak. This is what we saw in the 25g vs 50g vs 100g fructose vs sucrose vs glucose vs white bread study.

The potato study was talked about in detail here -- Tyw. Said Something That Makes Alot Of Sense!

It is still clear that adding fat to a meal reduced total insulin observed during that time. Whether or this is a good or bad thing is a different question, and is highly dependent on context. Almost every single study will be done in a single meal, overnight-fasted context (unless the study specifically set out to test the multi-meal scenario). How about different contexts?

- How will insulin release mechanics overlap with multiple closely-spaced meals?
- What happens if you ate a particularly large and fatty meal prior?
- What happens if you drink 100g of sugar over the course of 2 hours?
- What happens when you are under stress (cortisol antagonises insulin) .... etc ....

All the above will change insulin mechanics.

This is why I specifically did not focus my discussion of fructose on Insulin mechanics. Not only because it doesn't get affected much by insulin signalling, but because insulin signalling is secondary to total nutrient intake and the ability of tissues to use or store those nutrients. For fructose, the tissue that limits usage and storage is the liver, hence why my analysis was focused on that tissue.

I agree with the quote:

It's all about fuel tanks. Different individuals will use/fill different fuel tanks more/less efficiently based on lifestyle, history, age, activity, etc. Learning to keep the tanks close to full, without constant overfilling is the path to abundant energy at the healthiest level of body fat and musculature. searching for a perfect set calorie intake or macronutrient partition is probably futile. A dynamic organism will never have static energy needs.

And on that note, the best way to reduce systemic insulin levels is calorie restriction. Whether or not that is a good thing again, depends on context.

----

Thanks @tyw, a last question, I have seen you talk about the proteins found in starchy foods or legumes not being relevant and usable proteins (or something along those lines) compared to animal foods , do you think the same is true for steamed potatoes? Of course Peat has talked repeatedly about the quality of those proteins and the ones in mushrooms but I'm curious how valuable this information is in the context of regular cooking ( =/= potatoe juice).

Did you see the study I posted on high sucrose diet not leading to weight loss while high starch/ glucose diet did?

Hmm, I do not recall saying that proteins from plant sources are not relevant to overall consumption. They are certainly not as bioavailable as some animal protein sources, and specific plants may have a relative lack of a particular amino acid, but eating enough variety and quantity of plant protein sources can certainly meet people's protein needs. At worst, this means that slightly more net protein needs to be consumed, if they are all going to be plant sourced.

Any amino acids found in Potatoes will be usable. As an aside, I personally rely mostly on plant proteins, and there are many people in the online fitness world who get more than enough protein on a vegan and build muscle just fine.

This should not be confused with keto acids, which are not sources of nitrogen at all -- Protein Vs Keto Acids

If you want details, I am again, biased towards Lyle McDonald's multi part overview about most aspects of protein.

- What Are Good Sources of Protein? - Introduction : Bodyrecomposition
- What Are Good Sources of Protein? - Digestibility : Bodyrecomposition
- What Are Good Sources of Protein? - Speed of Digestion Pt. 1 : Bodyrecomposition
- Good Sources of Protein? - Speed of Digestion Part 2 : Bodyrecomposition
- What Are Good Sources of Protein? - Speed of Digestion Part 3 : Bodyrecomposition
- What Are Good Sources of Protein? - Protein Quality : Bodyrecomposition
- What Are Good Sources of Protein? - Amino Acid Profile Part 1 : Bodyrecomposition
- Good Sources of Protein? - Amino Acid Profile Part 2 : Bodyrecomposition
- Good Sources of Protein? - Amino Acid Profile Part 3 : Bodyrecomposition
- What Are Good Sources of Protein? - Micronutrient Content : Bodyrecomposition
- What Are Good Sources of Protein? - Dietary Fat Content : Bodyrecomposition
- What Are Good Sources of Protein? - Wrapping it Up : Bodyrecomposition

----

I did not see the study of sucrose vs glucose on weight loss. Can you link to the post?

.....
 

Dan W

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As an aside, I personally rely mostly on plant proteins
I might've missed some details of your diet, but am I correct that it's a much lower calcium : phosphate ratio than many of us Peat-peeps try to maintain?

I did not see the study of sucrose vs glucose on weight loss. Can you link to the post?
I think he's referring to the first one here:
Studies On Sucrose And Starch
 

Giraffe

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This is a typical pattern. Insulin release to a bout of eating always has 2 phases, with an initial spike which lasts around 30-60mins, then a drop, and then a slight rise to a level that is maintained for until about 3 hours after the meal.

Measures of Glycaemic Index and Insulin Index typically last 120 mins / 2 hours, and are intended to measure the initial spike plus some of the second phase release. The typical pattern that we see with single meal in the single meal scenarios is that a lower first phase peak always leads to a lower second phase peak. This is what we saw in the 25g vs 50g vs 100g fructose vs sucrose vs glucose vs white bread study.

I think, this is complete nonsense.

Under physiological conditions (as in eating a meal) there is no such thing as a first phase response. The so-called first phase response has only been observed after bolus intravenous glucose administration.

The first phase takes place almost instantaneously after the beginning of the stimulation, and, at any glucose level, the rapid rise and decay of the first phase occur within 3–4 min. The second phase can last several hours if the β-cell is continuously exposed to glucose.

In fact, the first-phase insulin response to intravenous glucose can be interpreted as the magnification of one of the insulin bursts detected in the portal circulation in response to a physiological stimulus.

First-phase insulin secretion: does it exist in real life? Considerations on shape and function
 

tyw

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Cairns, Australia
I think, this is complete nonsense.

Under physiological conditions (as in eating a meal) there is no such thing as a first phase response. The so-called first phase response has only been observed after bolus intravenous glucose administration.

First-phase insulin secretion: does it exist in real life? Considerations on shape and function

There is an obvious peak-then-drop-then-rise behaviour in insulin secretion seen in most studies done in an overnight fasted context. The graphs from the previous sucrose vs fructose vs glucose vs white bread study are clearly indicative of this sort of behaviour -- https://raypeatforum.com/community/attachments/screen-shot-2017-04-23-at-6-37-24-am-png.5174/

The potato + different kind of fat study also showed this sort of behaviour, and still, different fats caused different Area under the curve for insulin measurement. ie: different total insulin secretion over measured period with different type of nutrients despite same caloric and carbohydrate load.

There is clearly this sort of behaviour in isolated feeding during a fasted state as well, and not just through IV administration. Real world data supports this observation, specifically after an overnight fast, with the specified nutrients being given. In real world scenarios, this is irrelevant to all but the first meal of the day, and even then, composition of the meal can drastically alter nutrient absorption kinetics.

Once again, I do not focus on insulin mechanics before talking about total and type of nutrient intake. This thread was about fructose, and I discussed the potential for it to overload the liver. Insulin is not a relevant to fructose-induced liver overload, and I did not bring it up in the first place because of its irrelevance.

----

I might've missed some details of your diet, but am I correct that it's a much lower calcium : phosphate ratio than many of us Peat-peeps try to maintain?

TBH, I never bothered tracking any of this at all. I did post about how my calcium intake has been habitually low. Calcium requirements are most likely dictated by ancestral habitual calcium concentration, and my ancestors probably ate a low calcium diet, such that I do not need much calcium (even 300mg a day is more than enough).

Then recently, I've reduced animal food intake a fair bit, and even the legumes that I eat at the quantities that I eat them, won't provide too much phosphorus to cause any issues.

Once again, context specific to my case, and so far I've managed to make this sort of diet work for about 1.5 years now.

I think he's referring to the first one here:
Studies On Sucrose And Starch

I will comment separately in that thread.

.....
 

Giraffe

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There is an obvious peak-then-drop-then-rise behaviour in insulin secretion seen in most studies done in an overnight fasted context. The graphs from the previous sucrose vs fructose vs glucose vs white bread study are clearly indicative of this sort of behaviour -- https://raypeatforum.com/community/attachments/screen-shot-2017-04-23-at-6-37-24-am-png.5174/

The potato + different kind of fat study also showed this sort of behaviour, and still, different fats caused different Area under the curve for insulin measurement. ie: different total insulin secretion over measured period with different type of nutrients despite same caloric and carbohydrate load.

There is clearly this sort of behaviour in isolated feeding during a fasted state as well, and not just through IV administration. Real world data supports this observation, specifically after an overnight fast, with the specified nutrients being given. In real world scenarios, this is irrelevant to all but the first meal of the day, and even then, composition of the meal can drastically alter nutrient absorption kinetics.
Neither the potato study you linked, nor the potato study I linked show this "peak-then-drop-then-rise" behavior. Why do you pretend the potato study you linked does? The bread etc study shows this only at 100 g carbohydrates, but not at lower intakes.

Once again, I do not focus on insulin mechanics before talking about total and type of nutrient intake. This thread was about fructose, and I discussed the potential for it to overload the liver. Insulin is not a relevant to fructose-induced liver overload, and I did not bring it up in the first place because of its irrelevance.
No. This thread was about ne novo lipogenesis. It's stimulated by insulin, isn't it?
 

tyw

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Neither the potato study you linked, nor the potato study I linked show this "peak-then-drop-then-rise" behavior. Why do you pretend the potato study you linked does? The bread etc study shows this only at 100 g carbohydrates, but not at lower intakes.

No. This thread was about ne novo lipogenesis. It's stimulated by insulin, isn't it?

Went back and looked at the potato study again, you are right, it was a linear increase until 1hr, and then a slow decline. Sorry, was rushing around and posting in between work.

Still, total insulin over the 4 hour period either was increased or decreased depending on the type of fat eaten, indicating different mechanics even in isolated food studies in a fasted state.

The reason the bread study showed this oscillatory behaviour was likely due to absorption kinetics.

But once I again, I do not see the relevance of this discussion to DNL. First, I explained beforehand why DNL needs to be separated between Adipose tissue DNL, and Hepatic DNL.

Then, the only reason for DNL in either of the cases, is if:
(a) the body perceives that it needs to make more fat due to lack of fat
(b) there is an overload of carbohydrate to the tissue, so much so that DNL becomes a disposal pathway

Insulin is relevant to Adipose DNL, whereby insulin can drive nutrient overload of adipose tissue. This is a minor pathway in cases outside of extreme overfeeding, and is not very relevant.

Hepatic DNL is driven by localised hepatic overload, particularly by fructose, but gross nutrient excess of any form can do this too. All the information has already been presented. The fructose-driven overload pathway has little to do with insulin.

....
 

JRB22

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Except for hardcore Peaters and fruitians. With all the recommendations in this forum to drink lots of OJ & milk, eat lots of ice cream while avoiding starch (due to endotoxin), it's easy to hit over 100% of sugar within 10 minutes. Since starch is out of question, sucrose / fructore is the primary source of carbs.

I remember when I was 100% Peating and following the recommendations here 2 years ago, 100g of sugar per meal was minimum. Boy, my health hit rock bottom...



I followed tyw's advice and replaced sugar with white rice. Now my weight hovers around 160-170lbs-ish. And I feel way better, like a normal, healthy dude. It's been awhile.

Make that n=2... very similarly I have found much more success with increases in starch intake in lieu of sugar. Weight gained through strict Peating has come off, more stable blood sugars between meals and no sweaty, heart pounding middle of the night awakenings since making the switch.
 

Milena

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100 g sugar is:
  • honey: 6 tbsp or
Most people do not consume that amount of sugar in one meal, let alone in ten minutes. Please, don't say that the users here have not advised you to take it slow with dietary changes and supplements and to stop doing things that don't work for you.

Honey is a sneaky. I can easily eat that amount in 10 mins :) I have to limit my honey and only buy the solid sort in jars. Squeezy honey is sooo tempting.
 

Wagner83

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Hmm, I do not recall saying that proteins from plant sources are not relevant to overall consumption. They are certainly not as bioavailable as some animal protein sources, and specific plants may have a relative lack of a particular amino acid, but eating enough variety and quantity of plant protein sources can certainly meet people's protein needs. At worst, this means that slightly more net protein needs to be consumed, if they are all going to be plant sourced.

Any amino acids found in Potatoes will be usable. As an aside, I personally rely mostly on plant proteins, and there are many people in the online fitness world who get more than enough protein on a vegan and build muscle just fine.

This should not be confused with keto acids, which are not sources of nitrogen at all -- Protein Vs Keto Acids

If you want details, I am again, biased towards Lyle McDonald's multi part overview about most aspects of protein.

- What Are Good Sources of Protein? - Introduction : Bodyrecomposition
- What Are Good Sources of Protein? - Digestibility : Bodyrecomposition
- What Are Good Sources of Protein? - Speed of Digestion Pt. 1 : Bodyrecomposition
- Good Sources of Protein? - Speed of Digestion Part 2 : Bodyrecomposition
- What Are Good Sources of Protein? - Speed of Digestion Part 3 : Bodyrecomposition
- What Are Good Sources of Protein? - Protein Quality : Bodyrecomposition
- What Are Good Sources of Protein? - Amino Acid Profile Part 1 : Bodyrecomposition
- Good Sources of Protein? - Amino Acid Profile Part 2 : Bodyrecomposition
- Good Sources of Protein? - Amino Acid Profile Part 3 : Bodyrecomposition
- What Are Good Sources of Protein? - Micronutrient Content : Bodyrecomposition
- What Are Good Sources of Protein? - Dietary Fat Content : Bodyrecomposition
- What Are Good Sources of Protein? - Wrapping it Up : Bodyrecomposition

----

I did not see the study of sucrose vs glucose on weight loss. Can you link to the post?

.....

Thanks to Dan Wich for posting the link, the study I mentioned was in reference to ecstatichamster's post but somehow when you quoted my message his quote within my own post disappeared. Your comments in the threads are welcome, I'm also interested in the idea of fructose/sucrose leading to glucose intolerance which is mentioned in the two studies (one on rats, one on humans).

Thanks your for the links I have had a look and will read more, the writer does not seem to be a big fan of non animal sources of proteins besides soy. I won't derail the thread further.

---
Not sure if by 100 g of sugar you guys mean sucrose/fructose but recently I ate 1 kg of potatoes at once on a few occasions without issues other than feeling pretty nice. It depends on the potatoes and probably other things I have not pinned down.
 
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Braveheart

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I did not see the study of sucrose vs glucose on weight loss. Can you link to the post?
 

haidut

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@haidut From some of your recent posts it appears that you personally make no attempt to limit fructose consumption. For example 2-3 bottles (assuming 20 oz bottles) of Pepsi alone is around 80-100g of fructose (http://www.sciencedirect.com/science/article/pii/S0899900714001920). It was suggested in this thread (quote below) that a limit of 50g/day of fructose is a conservative target to decrease the likelihood of liver fat accumulation. Since your daily diet includes at least 2x (and maybe even more) that recommendation, I am curious as to your thoughts on the risk of liver fat accumulation considering the amount of fructose in your diet.

I have no reason to limit fructose, my liver tests are normal and my trigs and other blood lipid profiles are also in range. So, I eat to taste, as I mentioned before, with the restrictions on PUFA, legumes, and starch in place (in that order).
Btw, I am not sure there is an RDA for fructose especially when combined with at least 1:1 ratio of glucose. I think most people get fatty liver either from excessive lipolysis or eating too much fat, usually combined with the soft drinks. There have been plenty of human studies with normal-weight people being placed on high soda-drink diet and they did not get fatty liver or obesity.
 

Waynish

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"The very rapid rise of blood sugar stimulates massive release of insulin, and rapidly converts much of the carbohydrate into fat." -- Ray Peat, Glycemia, starch, and sugar in context.
 

haidut

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Do you have any of those links?


The first one here: Studies On Sucrose And Starch

I have to dig a bit for them. But as far as the study you referred to in the other post on sucrose/starch - these were formerly obese people, which due to dieting are usually all profoundly hypothyroid as we discussed in the threads on lowering RMR with dieting/fasting. So, I would not take them as solid evidence. What is needed are studies on non-obese humans consuming the different diets and those have been done but are older. Here are some of the ones I have seen with focus on fructose.
http://www.tandfonline.com/doi/abs/10.1080/10408390903461426?journalCode=bfsn20
"...The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in healthy, normal weight humans, using an evidence-based approach. The results of the analysis indicate that fructose does not cause biologically relevant changes in TG or body weight when consumed at levels approaching 95th percentile estimates of intake."

http://www.tandfonline.com/doi/full/10.3109/10408363.2015.1084990?src=recsys
"...However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate."

Even in obese people, fructose does not seem to worsen the condition.
http://www.tandfonline.com/doi/full/10.1080/10408398.2010.512990?src=recsys
"...The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in overweight or obese humans, using an evidence-based approach. The results of the analysis indicate that there is no evidence which shows that the consumption of fructose at normal levels of intake causes biologically relevant changes in triglycerides (TG) or body weight in overweight or obese individuals."

But I will find the intervention studies and post here as those contained information on specific dietary measures that may have influenced the findings. Speaking of which, did anybody verify that the "sucrose" diet in that study comparing with starch was not in fact a high-fat+high-sucrose diet as is commonly done in metabolic studies?
 
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