Potato = Good

[charlie]

I have had to give up on my potato included diet. Was doing good at first but slowly started sliding downhill.

After doing starch vs. no starch I have come to the conclusion I do not have the metabolic vigor to handle the extra endotoxin burden and whatever else happens when adding in starches.

 

[Mufasa]

I have had to give up on my potato included diet. Was doing good at first but slowly started sliding downhill.

After doing starch vs. no starch I have come to the conclusion I do not have the metabolic vigor to handle the extra endotoxin burden and whatever else happens when adding in starches.

So what do you use now for your carbs? Fruits?

 

[charlie]

So what do you use now for your carbs? Fruits?

Apple juice and milk right now.

 

[Mufasa]

Problem is 'we are all different' doesn't tell us anything. Sorry if that comes across as insulting, I just write quite bluntly. Accuracy is often quite blunt haha. We know why some people respond poorly to high fat, or dairy, or caffeine, or protein, or whatever else. I don't think this community, or Ray Peat himself, has put together a definitive mechanism for the different reactions (sugar v 'safe' starch), and that's what I'm hoping will come out of this thread. Or we realise there are puzzle pieces missing, and look to investigate further. The whole appeal of Peat is an accurate understanding of the interface of diet and human biology. And if one was selective they can find Peat saying certain starches are very good, nigh on essentials in the dietary toolkit.

I would find this interesting as well to get more understanding about this.

 

[Mufasa]

Apple juice and milk right now.

Nice, I love apple juice as well :) It is the only thing I drink when I go out, keeps me energized the whole night, while my friends can barely walk at the end of the night hehe. I wished it contains as much vitamins and minerals as orange juice though

 

[tyw]

Problem is 'we are all different' doesn't tell us anything. Sorry if that comes across as insulting, I just write quite bluntly. Accuracy is often quite blunt haha. We know why some people respond poorly to high fat, or dairy, or caffeine, or protein, or whatever else. I don't think this community, or Ray Peat himself, has put together a definitive mechanism for the different reactions (sugar v 'safe' starch), and that's what I'm hoping will come out of this thread. Or we realise there are puzzle pieces missing, and look to investigate further. The whole appeal of Peat is an accurate understanding of the interface of diet and human biology. And if one was selective they can find Peat saying certain starches are very good, nigh on essentials in the dietary toolkit.

Agree Progress is best made when mechanics are discussed as accurately and succinctly as possible. People can then look at those mechanics, decide if it applies to their context, and experiment accordingly.

----

Regarding the topic of starch, @Amazoniac posted some interesting info regarding different types of bacteria, and their preference to starch vs protein and/or fat -- Endotoxin And Fat Consumption

This opens up the door for further questions, like "Is it possible to determine from a gut biome analysis, the degree of starch a person can tolerate?"

----

Regarding Potatoes in particular, keep in mind that they are considered a "Nightshade", and contain compounds which may not be tolerated well (for whatever reason, we can discuss, but the observation is that there are those who mount an immune reaction to these compounds).

If you also don't tolerate things like tomatoes, eggplants / aubergines, strawberries, and similar nightshades, then the likelihood of you not tolerating potatoes is also high.

If this is the case, it is not necessarily the amylose or amylopectin that is causing issues, it is the other stuff in the potato.

A simple test would be to try "starch" sources that do not contain these compounds. Example: try sweet potatoes instead of potatoes, and see if you have the same issues.

If not, then the amylose or amylopectin is the issue.

If not, then further debugging can be done to see if there are functional differences between amylose and amylopectin.

----

Also, I've talked about the the differences between Amylose and Amylopectin quite a few times See that 'Endotoxin and Fat Consumption' thread for references to various other posts.

....

 

[Koveras]

Agree Progress is best made when mechanics are discussed as accurately and succinctly as possible. People can then look at those mechanics, decide if it applies to their context, and experiment accordingly.

----

Regarding the topic of starch, @Amazoniac posted some interesting info regarding different types of bacteria, and their preference to starch vs protein and/or fat -- Endotoxin And Fat Consumption

This opens up the door for further questions, like "Is it possible to determine from a gut biome analysis, the degree of starch a person can tolerate?"

----

Regarding Potatoes in particular, keep in mind that they are considered a "Nightshade", and contain compounds which may not be tolerated well (for whatever reason, we can discuss, but the observation is that there are those who mount an immune reaction to these compounds).

If you also don't tolerate things like tomatoes, eggplants / aubergines, strawberries, and similar nightshades, then the likelihood of you not tolerating potatoes is also high.

If this is the case, it is not necessarily the amylose or amylopectin that is causing issues, it is the other stuff in the potato.

A simple test would be to try "starch" sources that do not contain these compounds. Example: try sweet potatoes instead of potatoes, and see if you have the same issues.

If not, then the amylose or amylopectin is the issue.

If not, then further debugging can be done to see if there are functional differences between amylose and amylopectin.

----

Also, I've talked about the the differences between Amylose and Amylopectin quite a few times See that 'Endotoxin and Fat Consumption' thread for references to various other posts.

....

I would add that individuals who produce more amylase in their saliva (such as through variations in AMY1 gene copy numbers) break down starch in sugars more quickly, and higher up in the digestive system, and tend to have better blood sugar responses to starch, and less obesity (possibly through reduced endotoxin with less starch reaching the large intestine).

High endogenous salivary amylase activity is associated with improved glycemic homeostasis following starch ingestion in adults. - PubMed - NCBI

Diet and the evolution of human amylase gene copy number variation. - PubMed - NCBI

Low copy number of the salivary amylase gene predisposes to obesity. - PubMed - NCBI

Copy number polymorphism of the salivary amylase gene: implications in human nutrition research. - PubMed - NCBI

 

[wiggles92]

Agree Progress is best made when mechanics are discussed as accurately and succinctly as possible. People can then look at those mechanics, decide if it applies to their context, and experiment accordingly.

----

Regarding the topic of starch, @Amazoniac posted some interesting info regarding different types of bacteria, and their preference to starch vs protein and/or fat -- Endotoxin And Fat Consumption

This opens up the door for further questions, like "Is it possible to determine from a gut biome analysis, the degree of starch a person can tolerate?"

----

Regarding Potatoes in particular, keep in mind that they are considered a "Nightshade", and contain compounds which may not be tolerated well (for whatever reason, we can discuss, but the observation is that there are those who mount an immune reaction to these compounds).

If you also don't tolerate things like tomatoes, eggplants / aubergines, strawberries, and similar nightshades, then the likelihood of you not tolerating potatoes is also high.

If this is the case, it is not necessarily the amylose or amylopectin that is causing issues, it is the other stuff in the potato.

A simple test would be to try "starch" sources that do not contain these compounds. Example: try sweet potatoes instead of potatoes, and see if you have the same issues.

If not, then the amylose or amylopectin is the issue.

If not, then further debugging can be done to see if there are functional differences between amylose and amylopectin.

----

Also, I've talked about the the differences between Amylose and Amylopectin quite a few times See that 'Endotoxin and Fat Consumption' thread for references to various other posts.

....

The hypothesis:

The starch molecules themselves are not problematic. So then like you say the allergens bundled with the starches are problematic. I also expect different preparation methods could yield very different levels of these allergens.

Potato: nightshade compounds
Oats: ???
Wheat: phytates? gluten?
Rice: ???
Corn: ???

It may well be the case that some cope better without any starch. But many will still want what I lovingly call a "proper meal". Even just once every few days. Given that, understanding why certain starches are tolerable is important.

There may be others, like me, who do better with more starch, but perhaps also get problems from the allergens contained within their favourite starches. In that scenario they will shift to no starch, which in such conditions would lead to poorer health than they could otherwise achieve.

So that's another good reason to understand what's going on.

 

[wiggles92]

I would add that individuals who produce more amylase in their saliva (such as through variations in AMY1 gene copy numbers) break down starch in sugars more quickly, and higher up in the digestive system, and tend to have better blood sugar responses to starch, and less obesity (possibly through reduced endotoxin with less starch reaching the large intestine).

High endogenous salivary amylase activity is associated with improved glycemic homeostasis following starch ingestion in adults. - PubMed - NCBI

Diet and the evolution of human amylase gene copy number variation. - PubMed - NCBI

Low copy number of the salivary amylase gene predisposes to obesity. - PubMed - NCBI

Copy number polymorphism of the salivary amylase gene: implications in human nutrition research. - PubMed - NCBI

Is there any way to increase salivary amylase? Are there any studies of differences in salivary amylase between men, women, age, general health markers, race, those with certain other health issues? Basically are there any correlations, or is it just random?

 

[Peater Piper]

I would add that individuals who produce more amylase in their saliva (such as through variations in AMY1 gene copy numbers) break down starch in sugars more quickly, and higher up in the digestive system, and tend to have better blood sugar responses to starch, and less obesity (possibly through reduced endotoxin with less starch reaching the large intestine).

Regarding the last point, many Asian cultures that rely on starch heavy diets also frequently consume teas with their meals. Green tea is especially potent at inhibiting a-amylase (along with a number of other digestive enzymes), and a number of spices also inhibit amylase, so in fact, they may be less prone to obesity because they're malabsorbing quite a bit of the starch they're consuming. Of course, some of those calories will be made up for when they're broken down into short chain fatty acids in the colon (which are protective against endotoxin), and they may derive some vitamins from the bacterial fermentation as well. I think endotoxin is really only an issue when there's dysbiosis involved, or the fermentation is occurring in the small intestine.

Is there any way to increase salivary amylase? Are there any studies of differences in salivary amylase between men, women, age, general health markers, race, those with certain other health issues? Basically are there any correlations, or is it just random?

The number of copies of the AMY1 gene is genetic. The fact that people with more copies of the gene handle starch better (although there's some conflicting information on this) is probably indicative of other genetic advantages resulting from their ancestors consuming starch. That said, pancreatic production of a-amylase can be modulated, at least in rats. In the following study, rats were fed either raw or cooked ginger extract and amylase activity was measured after four weeks. In non-diabetic rats, raw ginger increased pancreatic amylase by 28% over the control, cooked by 7%. In diabetic rats, raw ginger increased pancreatic amylase by 50%(!) and cooked ginger by 30%. The ginger basically cured the diabetic rats, so possibly amylase secretion was increased due to improved insulin signaling and sensitivity.

http://www.interesjournals.org/full...zotocin-induced-diabetic-rats.pdf?view=inline

 

[tyw]

@wiggles92 and @Koveras

I agree that salivary amylase count is a big factor in carbohydrate digestion and use

Like @Peater Piper I do not think that salivary amylase is a sole mechanism, but part of a suite of adaptations that made humans uniquely adapted to using carbohydrate. It just happens to be one of the significant markers that represents this suite of adaptations.

​

Yes, there is going to be increased salivary activity, but I don't think this makes much of a difference .... Here's a study showing barely any difference in amylose digestion after 5 mins salivary amylose exposure. Note that salivary amylase basically becomes inactivated in the pH of the stomach, so all its activity must be in the mouth (and do people really sit and chew for 5 mins ). Chewing seems to be the more important factor here -- The Effect of a Brief Salivary α-Amylase Exposure During Chewing on Subsequent in Vitro Starch Digestion Curve Profiles

​

Therefore, I tend not to be eager to attribute mechanical analyses to genetic markers like this. A metric like salivary amylase gene count is better seen as a correlative factor to other adaptations that enable better amylose digestion. eg: it seems like the AMY1 gene counts also come with greater AMY2 and AMY3 activity (pancreatic). Now we have real plausible mechanism.

----

The above doesn't change the observation that there will be some people who just do not do as well on starch sources

----

As for the time-directionality of adaptation. It is my opinion that Humans evolved this starch-eating capacity, and then as they migrated out of Africa, some populations slowly lost this adaptation.

The fact that all humans still have much more salivary amylase gene counts than any other primate, is indicative that there was some selection pressure put all the common ancestor of all present living humans, to be able to process starch.

"Not being able to digest starch" should be seen as a prior adaptation that has been lost to some degree, for whatever reason.

That still doesn't change the observed fact that some people do not do well on starch sources ...

----

Sidenote: as much as some Asian cultures do drink tea. Lots of cultures which consume a lot of starch have no clue what it is

Tea is a more modern discovery. Starch was eaten by early humans. The adaptation to starch is independent of any modern behaviours.

----

I am specific to say "starch sources" and not "amylose / amylopectin". I do think that the source for obtaining amylose and amylopectin does matter, and each source can contain compounds that are not well tolerated by a particular individual.

There are no answers here, and no way to determine beforehand if you're going to be able to tolerate potatoes and their solanoids right here, right now. (Don't forget that immune system activity changes on a minute to minute basis ....)

I've said before that personally, potatoes are a hit or miss for me. Sometimes I get a little bloated, and if I'm really stressed out, potatoes give even worse bloat. It's definitely not the "starch" in my case, because rice has the opposite effect of reducing bloat almost every time

.....

 

[Westside PUFAs]

I agree that salivary amylase count is a big factor in carbohydrate digestion and use

There's also pancreatic amylase.

The fact that all humans still have much more salivary amylase gene counts than any other primate, is indicative that there was some selection pressure put all the common ancestor of all present living humans, to be able to process starch.

And that amylase starts to show after weaning years indicating when you are done with mommy's milk its time to dig.

 

[Peater Piper]

Sidenote: as much as some Asian cultures do drink tea. Lots of cultures which consume a lot of starch have no clue what it is

Tea is a more modern discovery. Starch was eaten by early humans. The adaptation to starch is independent of any modern behaviours.

Agreed that tea didn't play a role in evolution, but tea, coffee, high polyphenol spices, and acetic acid (vinegar) do slow digestion of carbohydrates, especially starches, effectively lowering the glycemic index of the meal. Some cooked or fermented low starch vegetables also slows the digestion a bit. It's just interesting that so many cultures gravitated to food products that blunt the post-prandial glucose response (and unlike fat, they won't inhibit insulin sensitivity, and may even improve it). It could be a coincidence, but potentially a beneficial one.

 

[tyw]

Agreed that tea didn't play a role in evolution, but tea, coffee, high polyphenol spices, and acetic acid (vinegar) do slow digestion of carbohydrates, especially starches, effectively lowering the glycemic index of the meal. Some cooked or fermented low starch vegetables also slows the digestion a bit. It's just interesting that so many cultures gravitated to food products that blunt the post-prandial glucose response (and unlike fat, they won't inhibit insulin sensitivity, and may even improve it). It could be a coincidence, but potentially a beneficial one.

(NOTE: what I write below should be treated as miscellaneous rantings, inspired by the quoted text, but not directly responding to it personally)

I tend to:

(a) err on the side of uncertainty, and try not to attribute positive mechanics to anything, and
(b) tend not to favour terminology that is subject to heavy contextual variance

Regarding (b), terms like "Glycemic Index" are really only broadly useful, and become pretty useless once we get to real life scenarios .....

First off, what are we trying to achieve? We cannot just chase a metric for the sake of chasing a metric. What does a "low glycemic index" represent?

Once we have asked that question, we can start to formulate more useful goals. For example, an actually useful metric is -- We want to get ingested glucose stored away as safely as possible, and then mobilised as needed. We DO NOT want it lingering in the blood. Tight endogenous control over glucose supply is the assumed goal.

----
Conflicting Research

Now we return to the definition of Glycemic Index -- Area under the curve for post prandial blood glucose levels, following an ingestion of a fixed amount of carbohydrate from a food source (usually 50-75g carbohydrate), with respect to the Area under the curve for white bread.

We can immediately see that this is a relative measure, which is going to be dependent on both assimilation rate, as well as storage rate.

This also means that statements like "Green Tea lowers your blood glucose response" is not going to be true in all contexts (and may not even be true in most contexts).

We need to mechanically explain completely contradictory results like these:

- Overweight patients + green tea => no effect when no exercise, lower blood glucose with exercise + green tea -- An Error Occurred Setting Your User Cookie

- High dose (3.3g) green tea vs low dose (0.6g) green tea. Higher dose, lower post prandial blood glucose -- Additional benefit of higher dose green tea in lowering postprandial blood glucose | Lahirin | Medical Journal of Indonesia

- Higher glucose levels at 120min with green tea compared to without -- Does green tea affect postprandial glucose, insulin and satiety in healthy subjects: a randomized controlled trial. - PubMed - NCBI

- Green Tea + Cinnamon + Ginger resulting in much lower GI with white bread consumption -- http://docsdrive.com/pdfs/ansinet/pjbs/2013/74-79.pdf

- And one study on coffee, which increased Glycemic Index very substantially (140+%) -- Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men

I will talk about this in the next few sections.

----
Contexts

To start our base of thinking, we can construct extreme scenarios:

(1) Healthy and lean athlete, heavy exercise for 1 hour from 3pm to 4pm (timing is important, in that exercise at this time will increase skeletal muscle glucose uptake capacity, whereas adipose tissue insulin sensitivity declines).

GLUT4 receptors maximally up-regulated, muscle glycogen stores slightly depleted, good baseline insulin sensitivity to begin with.

Why would such a person want to slow down rate of digestion of carbohydrate? Any carbohydrate they consume will be shuttled directly into storage, until those are full, and even then, will likely be continued to be oxidised anyway. That is to say, any digestable carbohydrate is a "low glycemic carbohydrate" at this stage, because by definition, blood glucose levels will be blunted by skeletal muscle uptake.

(2) Diabetic who sees 300+ mg/dL glucose values after eating 20g of carbohydrate. Near zero carbohydrate storage capacity.

Why would such a person even be eating blood glucose raising carbohydrates at all? (Sidenote: moderate quantities of sucrose will probably be a better bet here. "Moderate" means like 50-100g a day).

Any glucose-containing carbohydrate whatsoever is a "High GI carbohydrate" in this case.

----

Realistically, most people will fall in the middle of these 2 extremes, depending on their state of health, the type of carbohydrate they are eating, the time of the day, and many many many other factors.

Taking something like green tea, which yes, has been shown to inhibit certain amylases, and therefore slow down carbohydrate digestion, should be seen as a plain mechanic, without any value judgement.

We can construct a context where it is good -- eg: mixed meal containing fat and carbs, slow-down of carbohydrate absorption may attenuate excessive glucose rises in this context.

We can construct a context where it is bad -- eg: primarily carbohydrate meal, slow-down of carbohydrate absorption may lead to more opportunities for bacterial grown and endotoxin production.

But how do we know whether a compound like green tea is useful in our context, at this very moment? No clue ..... I eat using my body, not my mind, and just trust certain instincts at that point in time.

----
Muscle Glucose Uptake

The other mechanic that something like green tea and/or cinnamon affects may be the ability for skeletal muscle to uptake glucose. This is completely separate from digestion, since it is strictly a Post-digestion effect.

I view this shuttling of glucose out of the bloodstream and into storage, as a good thing in all contexts.

How much of a practical significance does this actually have? No clue, but it will definitely depend on factors like ratio of lean-tissue to adipose tissue, how quickly the person can actually digest the carbohydrate, etc ....

----
Traditional Diets

Whether or not traditional diets incorporated such practices is a secondary point. There are just as many harmful traditional practices as there are helpful ones, and some of the "helpful practices" may only be helpful in the context of the already harmful practices. eg: Take a look at some of the traditional Indian diets, and you will see PUFA galore. Northern Chinese diets contain scary levels of wheat and PUFA of all forms. And if you look at any of the traditional South-East Asian diets, wow do you see PUFAs

Also, there are many high starch eating cultures that never really gravitated towards tea or any other of the aforementioned compounds. Kitava, papua new guinea, etc ....

So yes, I am actually in support of any consumption of these compounds being a coincidence, and whether or not these are beneficial is a dubious proposition.

----
Insulin

Sweet potatoes have one of the highest insulin indexes (have to download research paper and look at Appendix 3, with the Food Insulin Index (FII) database -- The Sydney eScholarship Repository: Clinical Application of the Food Insulin Index to Diabetes Mellitus)

Does this make sweet potatoes "good" or "bad"? One can say that this high insulin index encourages the storage of glucose as rapidly as possible, and prevents blood glucose rise. One can also say that if the body cannot respond to said insulin response (due to insulin resistance or whatever), then this leads to uncontrolled blood glucose and possible complications.

The effects are not clear, and definitely not uniform across people.

----
Conclusion

This is complicated as all hell. I avoid making any conclusions whatsoever .

The only philosophical stance I will take is "Avoid harm, and don't be obsessed with chasing benefits".

.....

 

[Braveheart]

(NOTE: what I write below should be treated as miscellaneous rantings, inspired by the quoted text, but not directly responding to it personally)

I tend to:

(a) err on the side of uncertainty, and try not to attribute positive mechanics to anything, and
(b) tend not to favour terminology that is subject to heavy contextual variance

Regarding (b), terms like "Glycemic Index" are really only broadly useful, and become pretty useless once we get to real life scenarios .....

First off, what are we trying to achieve? We cannot just chase a metric for the sake of chasing a metric. What does a "low glycemic index" represent?

Once we have asked that question, we can start to formulate more useful goals. For example, an actually useful metric is -- We want to get ingested glucose stored away as safely as possible, and then mobilised as needed. We DO NOT want it lingering in the blood. Tight endogenous control over glucose supply is the assumed goal.

----
Conflicting Research

Now we return to the definition of Glycemic Index -- Area under the curve for post prandial blood glucose levels, following an ingestion of a fixed amount of carbohydrate from a food source (usually 50-75g carbohydrate), with respect to the Area under the curve for white bread.

We can immediately see that this is a relative measure, which is going to be dependent on both assimilation rate, as well as storage rate.

This also means that statements like "Green Tea lowers your blood glucose response" is not going to be true in all contexts (and may not even be true in most contexts).

We need to mechanically explain completely contradictory results like these:

- Overweight patients + green tea => no effect when no exercise, lower blood glucose with exercise + green tea -- An Error Occurred Setting Your User Cookie

- High dose (3.3g) green tea vs low dose (0.6g) green tea. Higher dose, lower post prandial blood glucose -- Additional benefit of higher dose green tea in lowering postprandial blood glucose | Lahirin | Medical Journal of Indonesia

- Higher glucose levels at 120min with green tea compared to without -- Does green tea affect postprandial glucose, insulin and satiety in healthy subjects: a randomized controlled trial. - PubMed - NCBI

- Green Tea + Cinnamon + Ginger resulting in much lower GI with white bread consumption -- http://docsdrive.com/pdfs/ansinet/pjbs/2013/74-79.pdf

- And one study on coffee, which increased Glycemic Index very substantially (140+%) -- Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men

I will talk about this in the next few sections.

----
Contexts

To start our base of thinking, we can construct extreme scenarios:

(1) Healthy and lean athlete, heavy exercise for 1 hour from 3pm to 4pm (timing is important, in that exercise at this time will increase skeletal muscle glucose uptake capacity, whereas adipose tissue insulin sensitivity declines).

GLUT4 receptors maximally up-regulated, muscle glycogen stores slightly depleted, good baseline insulin sensitivity to begin with.

Why would such a person want to slow down rate of digestion of carbohydrate? Any carbohydrate they consume will be shuttled directly into storage, until those are full, and even then, will likely be continued to be oxidised anyway. That is to say, any digestable carbohydrate is a "low glycemic carbohydrate" at this stage, because by definition, blood glucose levels will be blunted by skeletal muscle uptake.

(2) Diabetic who sees 300+ mg/dL glucose values after eating 20g of carbohydrate. Near zero carbohydrate storage capacity.

Why would such a person even be eating blood glucose raising carbohydrates at all? (Sidenote: moderate quantities of sucrose will probably be a better bet here. "Moderate" means like 50-100g a day).

Any glucose-containing carbohydrate whatsoever is a "High GI carbohydrate" in this case.

----

Realistically, most people will fall in the middle of these 2 extremes, depending on their state of health, the type of carbohydrate they are eating, the time of the day, and many many many other factors.

Taking something like green tea, which yes, has been shown to inhibit certain amylases, and therefore slow down carbohydrate digestion, should be seen as a plain mechanic, without any value judgement.

We can construct a context where it is good -- eg: mixed meal containing fat and carbs, slow-down of carbohydrate absorption may attenuate excessive glucose rises in this context.

We can construct a context where it is bad -- eg: primarily carbohydrate meal, slow-down of carbohydrate absorption may lead to more opportunities for bacterial grown and endotoxin production.

But how do we know whether a compound like green tea is useful in our context, at this very moment? No clue ..... I eat using my body, not my mind, and just trust certain instincts at that point in time.

----
Muscle Glucose Uptake

The other mechanic that something like green tea and/or cinnamon affects may be the ability for skeletal muscle to uptake glucose. This is completely separate from digestion, since it is strictly a Post-digestion effect.

I view this shuttling of glucose out of the bloodstream and into storage, as a good thing in all contexts.

How much of a practical significance does this actually have? No clue, but it will definitely depend on factors like ratio of lean-tissue to adipose tissue, how quickly the person can actually digest the carbohydrate, etc ....

----
Traditional Diets

Whether or not traditional diets incorporated such practices is a secondary point. There are just as many harmful traditional practices as there are helpful ones, and some of the "helpful practices" may only be helpful in the context of the already harmful practices. eg: Take a look at some of the traditional Indian diets, and you will see PUFA galore. Northern Chinese diets contain scary levels of wheat and PUFA of all forms. And if you look at any of the traditional South-East Asian diets, wow do you see PUFAs

Also, there are many high starch eating cultures that never really gravitated towards tea or any other of the aforementioned compounds. Kitava, papua new guinea, etc ....

So yes, I am actually in support of any consumption of these compounds being a coincidence, and whether or not these are beneficial is a dubious proposition.

----
Insulin

Sweet potatoes have one of the highest insulin indexes (have to download research paper and look at Appendix 3, with the Food Insulin Index (FII) database -- The Sydney eScholarship Repository: Clinical Application of the Food Insulin Index to Diabetes Mellitus)

Does this make sweet potatoes "good" or "bad"? One can say that this high insulin index encourages the storage of glucose as rapidly as possible, and prevents blood glucose rise. One can also say that if the body cannot respond to said insulin response (due to insulin resistance or whatever), then this leads to uncontrolled blood glucose and possible complications.

The effects are not clear, and definitely not uniform across people.

----
Conclusion

This is complicated as all hell. I avoid making any conclusions whatsoever .

The only philosophical stance I will take is "Avoid harm, and don't be obsessed with chasing benefits".

.....

"Avoid harm, and don't be obsessed with chasing benefits".

Well said!!

 

[Parsifal]

Apple juice and milk right now.

No fibers?

 

[Parsifal]

Agree Progress is best made when mechanics are discussed as accurately and succinctly as possible. People can then look at those mechanics, decide if it applies to their context, and experiment accordingly.

----

Regarding the topic of starch, @Amazoniac posted some interesting info regarding different types of bacteria, and their preference to starch vs protein and/or fat -- Endotoxin And Fat Consumption

This opens up the door for further questions, like "Is it possible to determine from a gut biome analysis, the degree of starch a person can tolerate?"

----

Regarding Potatoes in particular, keep in mind that they are considered a "Nightshade", and contain compounds which may not be tolerated well (for whatever reason, we can discuss, but the observation is that there are those who mount an immune reaction to these compounds).

If you also don't tolerate things like tomatoes, eggplants / aubergines, strawberries, and similar nightshades, then the likelihood of you not tolerating potatoes is also high.

If this is the case, it is not necessarily the amylose or amylopectin that is causing issues, it is the other stuff in the potato.

A simple test would be to try "starch" sources that do not contain these compounds. Example: try sweet potatoes instead of potatoes, and see if you have the same issues.

If not, then the amylose or amylopectin is the issue.

If not, then further debugging can be done to see if there are functional differences between amylose and amylopectin.

----

Also, I've talked about the the differences between Amylose and Amylopectin quite a few times See that 'Endotoxin and Fat Consumption' thread for references to various other posts.

....

Hasn't Peat said that sweet potatoes are high in estrogens?

 

[Peater Piper]

Regarding (b), terms like "Glycemic Index" are really only broadly useful, and become pretty useless once we get to real life scenarios .....

First off, what are we trying to achieve? We cannot just chase a metric for the sake of chasing a metric. What does a "low glycemic index" represent?

Once we have asked that question, we can start to formulate more useful goals. For example, an actually useful metric is -- We want to get ingested glucose stored away as safely as possible, and then mobilised as needed. We DO NOT want it lingering in the blood. Tight endogenous control over glucose supply is the assumed goal.

Lowered post prandial spikes to reduce peak blood glucose levels, as there's some evidence that higher levels can cause damage, and AGEs rise in a non-linear fashion. From a more Peat perspective, by slowing absorption, you gain a steadier supply of glucose over a longer period of time, rather than having blood glucose drop like a rock, potentially raising cortisol and reverting back to primarily fat oxidation. One of the reasons (out of many) that Peat likes fructose is he believes it slows the absorption of glucose from the intestines.

"RP: Yeah, and the only place fructose slows down glucose is in the absorption from the intestine. The fructose itself is slow to be absorbed compared to glucose, and so if you eat starch, like white rice or white bread, you get a very sharp increase in the amount of glucose in the blood. That will stimulate insulin to handle that rising glucose, and that stimulates cortisol to prevent the reverse reaction from too much insulin and not enough sustained glucose. But when you eat sugar, the glucose half is broken off, and the fructose lags a little bit in being absorbed."

We need to mechanically explain completely contradictory results like these:

- Overweight patients + green tea => no effect when no exercise, lower blood glucose with exercise + green tea -- An Error Occurred Setting Your User Cookie

- High dose (3.3g) green tea vs low dose (0.6g) green tea. Higher dose, lower post prandial blood glucose -- Additional benefit of higher dose green tea in lowering postprandial blood glucose | Lahirin | Medical Journal of Indonesia

- Higher glucose levels at 120min with green tea compared to without -- Does green tea affect postprandial glucose, insulin and satiety in healthy subjects: a randomized controlled trial. - PubMed - NCBI

- Green Tea + Cinnamon + Ginger resulting in much lower GI with white bread consumption -- http://docsdrive.com/pdfs/ansinet/pjbs/2013/74-79.pdf

- And one study on coffee, which increased Glycemic Index very substantially (140+%) -- Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men

The first study used a glucose drink. I'm assuming that means it was glucose monosacharides. If we're talking about enzyme inhibitors here, the methods need to be tested with polysaccharides. This is one of the reasons there's conflicting results with cinnamon, because it really only seems to be effective when consumed with starch, not so much with sugar or monosaccharides. The second study mentions a "test meal", and specifically tested for enzyme inhibition, so I'm assuming polysaccharaides were used and the results were as expected. The third study does indeed seem to be contradictory, though small and not in line with most I've read that used proper testing methods. Regarding the coffee study, so many times I see caffeine or coffee ingestion, followed by a delay, then the test meal. Not only will you get no enzyme inhibition in this way, but of course adrenaline and free fatty acids will rise, resulting in reduced glucose tolerance when tested.

You mention delayed glucose absorption possibly feeding endotoxin. The same can be said for having a very large meal of glucose compared to smaller more frequent meals. A large amount of starch is almost certainly going to travel further down the intestine. Green tea, coffee, cinnamon, and ginger all have antimicrobial properties. I can only speak for myself that my digestion improves when I consistently have one of the above mentioned items with my meals. In terms of glucose control, my fasting is around 80. 100 grams of carbs from starch can spike me to 140-150 or so at an hour, by two hours I'm back at 80 and usually not feeling so well. Both green tea and coffee (normal and decaf) consumed with or immediately after a meal consistently lower my 1-hour spike to 120-130, and 2-hours it's usually between 100 and 110, and I'm back at baseline at 3-hours. My energy is better sustained eating in this fashion. I'm not saying it will work for everyone, but it sure seems to line up with the proposed mechanisms involved.

Whether or not traditional diets incorporated such practices is a secondary point. There are just as many harmful traditional practices as there are helpful ones, and some of the "helpful practices" may only be helpful in the context of the already harmful practices. eg: Take a look at some of the traditional Indian diets, and you will see PUFA galore. Northern Chinese diets contain scary levels of wheat and PUFA of all forms. And if you look at any of the traditional South-East Asian diets, wow do you see PUFAs

Excessive PUFA consumption would be a relatively new thing when seed oils became viable.

 

[charlie]

No fibers?

Mushrooms twice a day.

 

[tyw]

@Peater Piper

Firstly, I do not give specific prescriptions If what works for you works, that's great.

My discussion is of mechanics, which are often very uncertain.

Example: Chris Masterjohn had a very good article about Glycation -- Where Do Most AGEs Come From? O Glycation, How Thy Name Hast Deceived Me!

The most recent podcast episodes on Glycation were pretty good as well.

- The Daily Lipid Podcast Episode 13: Wait a Second, Is Glycation Actually GOOD For You?
- The Daily Lipid Podcast Episode 012: What Is Measuring Our Hba1c REALLY Telling Us About Our Blood Glucose and Diabetes Risk?

We will see that even the blood sugar => glycation link is fuzzy. The blood sugar => Hb1Ac connection is more robust, but even that is going to be subject to so much variation based upon what the body decides to do with HbA1c.​

I find it very hard to come to conclusions regarding glycemic indexes, slower absorption of carbohydrates, actual blood sugar values, and regulation of carbohydrate storage mechanisms.

I've quoted this study before, but it's worth quoting again -- Four grams of glucose

If a human has 5L of blood, then a blood glucose concentration of 80mg/dL is 0.08 * 5000 / 100 = 4.0 grams of glucose circulating. That is not a lot of glucose .... the difference between 80mg/dL glucose and 200mg/dL glucose, is 6 grams of glucose. Basically a teaspoon worth of glucose.

Digestion rates for carbohydrates can vary, with peak values of around 1.75 grams per minute, to rates which are possibly much lower. What your specific rate of digestion of carbohydrate will be unknown.

So just how much does "slowing absorption from the gut" actually affect this sort of tight regulation? What does "slowing absorption mean"? How does slowing absorption via enzymatic inhibition work vs mixing carbs and fat?

For example, enzymatic inhibition may work to reduce average rate of glucose absorption from the small intestine. If so, then this is effective if the person's lack of glucose control is due to an inability to deal with peak rates of assimilation.

But if for example, that another mechanism of "slowing down digestion" is to prevent enzymes from reaching the carbohydrate in the first place, and then dumping the carbs in a huge lump after a certain delay, then this will do nothing for the person who is limited by peak carbohydrate assimilation rate.

Possible Example: eat pasta with lots of fat --> enzymes do not get to work on the carbohydrates until 3 hours after the meal --> carbs are "freed from the fat" --> sudden burst of carbohydrate. (This is actually a pattern which some people have seen while eating pasta .... nothing for awhile, then sudden blood sugar spike)

----

Personally, I knew things weren't adding up, when I was eating literally 400g of carbs in a sitting, and never seeing blood glucose go above 130mg . Blood Glucose monitoring over the last few months has led to the same results -- fasting glucose around 90mg/dL, post meal jumps to 120-130mg which stays there for about 4 hours after meals of around 300g carbohydrate (mostly glucose), and then a reduction back to baseline.

This is again, as much a question of glucose storage regulation, as it is about upstream factors like digestion speed.

In any one person, I cannot say which factor is more important

In this light, the studies I quoted were used to show contradictory effects of the compounds listed, and to show that depending on the context, we will have regulation of carbohydrate intake bottlenecked by a particular process in the chain.

ie: It will never be always the case of slower digestion implying better glucose control. Sometimes it will be muscle glycogen uptake. Sometimes it will be intestinal absorption rates (which are distinct from enzymatic breakdown rates). etc ....

The compounds listed, such as Green Tea and Cinnamon, affect all these processes in mechanistic ways. Whether or not those effects lead to better blood glucose assimilation will likely depend on how the individual responds to those mechanics, and it is exactly this sort of major variance that we see in real life.

----

I dunno about that Peat quote regarding fructose .... when we put fructose and glucose together in a sports context, we almost always get much faster absorption and oxidation rates -- A Step Towards Personalized Sports Nutrition: Carbohydrate Intake During Exercise

In fact, one of the primary benefits that Peat touts regarding fructose is that it increases the oxidation rates of glucose at even an intake of 10% total carbohydrate as fructose.

As an aside I did give more opinions on fructose in the following post -- Fructose Alters Brain Genes Negatively. How To Counter This From Peat Perspective?​

----

PUFA consumption of Asian populations is actually something that I am uncertain of

I do know that sesame oil and other similar seed oils were present long before tea was cultivated (you'll definitely find sesame oil 2,000 years ago, and some records point to 5,000 year-old production methods), but I do not know how widespread its consumption would have been.

The same goes for truly higher phytoestrogenic foods like Tofu, whereby production also extends back at least 2,000 years.

In any case, I refuse to draw any conclusions about what foods were good or bad in ancient history. All I see are people taking advantage of whatever was available to them at the time, and then making discoveries later, and for no apparent reason at all. (the Ancient Chinese discovery stories are always the most hilarious ... "how did u discover Chinese medicine?" --> "some god told me")


Sidenote: @Parsifal I do not know of any mechanism by which sweet potatoes would be excessively estrogenic. Yams may contains some amount of the compound diosgenin, which is thought to be a phytoestrogen. Sweet potatoes are not yams, and contain barely any of this compound. But then again, the data for diosgenin actually being estrogenic is not conclusive as well.

....