Insulin Resistance

[Peata]

So far I seem to be losing, and at a slow but healthy rate. I use coconut oil, occasional evoo, occasional butter. Rare use of lard.

 

[Mittir]

Calcium and Heme Iron Absorption

There is another advantage of taking calcium with iron rich meal.
It blocks both heme and non-heme iron absorption within the range of
40 to 300 mg. In excess of 300 there is no extra inhibition.
Coffee does not inhibit heme iron. So it is a good idea to eat
iron rich meal ( liver, red meat etc) with coffee and milk or calcium.
Calcium carbonate and calcium acetate also block phosphorus absorption.
When i eat liver, i add both milk coffee and some calcium acetate lowering
absorption of both iron and phosphorus. RP has mentioned that heme iron
is more harmful than non-heme. Here is the article mentioning
calcium's ability to block heme iron.

The reported inhibition of iron
absorption by calcium is the same for nonheme and heme iron
(2, 11). Because heme and nonheme iron are absorbed by different
receptors on the mucosal surface, inhibition by calcium must
be located within the mucosal cell at some transfer step common
to the 2 kinds of iron. This difference between calcium and other
factors influencing iron absorption would by itself not cause
methodologic problems
The reported dose-effect relation between the amount of calcium
given and the degree of inhibition of iron absorption (2)
differs from other factors influencing iron absorption. No effect
of calcium on iron absorption is seen when < 40 mg Ca is present
in a meal and no further inhibition is seen when the calcium
content of the meal exceeds <300 mg. This flat, inverse
S-shaped relation between the amount of calcium in a meal and
the inhibition of iron absorption fits well with equations describing
one-site competitive binding. In practice, this means that
adding 200 mg Ca to a meal with, say, 100 mg Ca would reduce
iron absorption by 40%, whereas no effect would be seen if the
meal already contained <300 mg

Source:
Does calcium interfere with iron absorption?
http://ajcn.nutrition.org/content/68/1/3.full.pdf

 

[visionofstrength]

Eating carbs and fat together can cause insulin resistance, or at least it make it worse, try separating carbs from fats in your meals, also saturated fats(yes, even coconut oil) decrease insulin sensitivity, extra virgin olive oil improves it on the other hand, i looked a lot of studies to find this, i also did my own statistical analysis , the countries consuming more fat with carbohydrates are fatter and fatter, EXCEPT italy, although the fat intake is very high they are still one of the healthiest nations out there, also asian countries with the low fat intake have a very low obesity rate,...

As a courtesy to others, kindly provide links to at least some of these studies you refer to?

Peat thinks that estrogen and poly-unsaturated fats cause what is commonly termed "insulin resistance". Here is one explanation he provides:

One of estrogen's “excitatory” effects is to cause lipolysis, the release of fatty acids from storage fat; it directs the conversion of glucose into fat in the liver, so that the free fatty acids in the circulation remain chronically high under its influence. The free fatty acids inhibit the oxidation of glucose for energy, creating insulin resistance, the condition that normally increases with aging, and that can lead to hyperglycemia and “diabetes.”

He also cites a study that shows that only 8% of the changes in blood sugar result from insulin. He thinks that when the body is adequately energized, insulin is a hormone of stress that should not be needed at all.

You can search toxinless.com for the phrase "insulin resistance" to learn more about Peat's views on this topic.

 

[visionofstrength]

Re: Calcium and Heme Iron Absorption

Calcium carbonate and calcium acetate also block phosphorus absorption.

M, It seems calcium acetate does block phosphorus but the calcium is not as well absorbed as calcium carbonate and it also does not increase the calcium/phosphorus ratio?
http://www.ncbi.nlm.nih.gov/pubmed/2811066

I think Peat uses egg shell without the vinegar acetate?

 

[Mittir]

Calcium Carbonate as Phosphate binder

Calcium carbonate is a well known phosphate binder. In kidney patient goal is to
restrict both calcium and phosphorus absorption. Calcium acetate is more efficient
at binding phosphate with lesser amount of calcium. For peat followers, Calcium
carbonate will decrease phosphorus intake and increase calcium intake.
In this following study they are using almost twice the amount of calcium in
calcium carbonate to do the same job Calcium Acetate is doing.
Ratio of phosphate binding to calcium absorbed simply stating that we will
need more calcium in carbonate form to bind same amount of phosphate
bound by Acetate. This ratio is not talking about the ratio of calcium
and phosphorus absorbed.

Am J Nephrol. 1994;14(3):192-6.
Calcium acetate versus calcium carbonate for the control of serum phosphorus in hemodialysis patients.
Almirall J1, Veciana L, Llibre J.
Author information
Abstract
Recent in vitro and in vivo studies have shown that calcium acetate (CaAC) is a more effective phosphorus binder than, among other calcium salts, calcium carbonate (CaCO3). More efficient binding allows serum phosphorus to be controlled with a lower dose; moreover, less calcium seems to be absorbed when CaAC is used. These properties could reduce the incidence of hypercalcemia; however, in clinical practice few reports have compared these two calcium salts, and results disagree. We evaluated in a 24-week prospective cross-over study the clinical efficiency of CaCO3 and CaAC in 10 selected chronic hemodialysis patients. Only 7 patients completed the study period. The patients were randomly assigned to start treatment with one of the two calcium salts; after 12 weeks they shifted to the other treatment. Serum analytical tests included weekly control of calcium, phosphorus, and alkaline phosphatase. PTH values (intact molecule) were obtained initially and at the end of every study period. The same good control of the phosphorus level (4.79 +/- 0.6 vs. 4.94 +/- 0.8 mg/dl) was obtained with CaAC (mean doses 4.1 +/- 0.3 g/day) as with CaCO3 (mean doses 4.01 +/- 0.8 g/day). The mean serum calcium levels were similar (10.36 +/- 0.5 vs. 10.20 +/- 0.5 mg/dl). The dose of elemental calcium administered was significantly less with CaAC (957 +/- 83 mg/day) than with CaCO3 (1,590 +/- 317 mg/day). However, the incidence of hypercalcemia (Ca > 11 mg/dl) was similar during the two treatment periods (13% with CaAC vs. 14% with CaCO3). Also the incidence of Ca x P products 765 was comparable (9.5 vs. 11.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
http://www.ncbi.nlm.nih.gov/pubmed/7977479

 

[Amazoniac]

From The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. - PubMed - NCBI:

"The major finding in this study was that the coingestion of fat with a carbohydrate meal reduced the postprandial glucose response to the carbohydrate load, but had no effect on the insulin response."

"However, despite the reduced blood glucose levels in the presence of fat, the insulin response was not affected. In other situations where blood glucose responses to carbohydrate meals have been reduced (eg, the addition of viscous fiber supplements to glucose [14] or reduced rate of starch digestion [15]) the insulin responses were also markedly reduced."

"One possible mechanism by which potentiation of the insulin response to glucose could occur is via GIP. Fat is a potent stimulus for GIP release and GIP has been shown to potentiate glucose-induced insulin secretion (16-18)."

"However, since the glucose concentration did not fall under these circumstances, it is possible that target tissue (hepatic and/or extra hepatic) sensitivity to the action of insulin in facilitating glucose transport was reduced after fat ingestion."

"This confirms previous reports that fat is the most potent dietary stimulant of GIP secretion (20, 21 ). GIP levels remained elevated for at least 4 h after fat ingestion, which probably reflects slow digestion and absorption ofthe fat."

"These changes found after the coingestion of fat may indicate an acute insulin insensitivity or at least a potentiation of insulin secretion which could form the basis of the insulin resistance associated with the chronic consumption of high fat diets. Thus, despite the apparent improvement in blood glucose levels which occurs when carbohydrate is ingested together with fat, the observation that the insulin levels were not reduced suggests that increasing the fat content of meals would not be beneficial for diabetics."

@Westside PUFAs

 

[Amazoniac]

Fats on starches

"The KANWU study suggested that SFA were more detrimental than MUFA when total fat intake was less than 37% of total calories, and the current study suggests that SFA are more detrimental than PUFA as well, at least when total fat intake is 30% of calories.

Why is it that SFA appear more detrimental both in the short-term meal and when consumed habitually? It may be because SFA induce a larger post-meal increase in NEFA than MUFA or PUFA, which are the culprit behind insulin resistance in the short-term. Regarding habitual intake, there is a direct association between the amount of saturated fat stored within the muscle and the proportion of SFA in muscle cell membranes and insulin resistance, and both of these reflect the fat composition of the diet."

"..adding fat to a starchy carbohydrate may indeed lower the glycemic response – but only if the habitual diet is not high in fat, as research in humans suggests that anything above 40% may lead to gastrointestinal adaptations that ultimately speed the gastric transit time of fatty meals which would consequently remove the beneficial reduction of post-prandial glycemia."

"These data indicate that when a second meal contained butter with potato but the first meal consisted of only potato, a smaller glucose rise occurred with the second meal. That is, the presence of butter resulted in an attenuated glucose area response just as when it was present in the first meal. However, if both meals contained fat, the glucose area was not decreased with the second meal."

Key points from the link:

"The evidence thus far suggests that consuming fat alongside starchy carbohydrates such as potatoes and rice acts to reduce and delay the initial blood glucose spike that would occur if no fat was consumed. However, ultimately the amount of glucose entering the blood will be the same because the fat only acts to slow the absorption of glucose into the bloodstream. Therefore, fat may lower the postprandial glucose spike, but it will cause the body to be in a state of hyperglycemia for a longer time period.

Fat also appears to cause a temporary and acute state of insulin resistance whereby more insulin is required to dispose of the same or in some cases less glucose than if no fat was consumed alongside a starchy carbohydrate. Moreover, the insulin response is prolonged, meaning that blood insulin levels remain elevated for a longer period of time."

"The insulin resistance effects are most pronounced with SFAs, as evidenced primarily by research using butter. Oils containing predominantly MUFA and PUFA appear to act similar to one-another, both of which are less insulinemic than SFAs. Additionally, animal fats appear to act similar to oils, perhaps because at least half of their fat content is unsaturated. Regardless of the fat, a reasonably “safe” upper limit of consumption appears to be about 15 grams of total fat in a meal."

"Additionally, when you eat starchy carbohydrates such as potatoes, legumes, or grains, there is no need to load them up on added fats such as cooking oils and butter. If you want added flavor, use some spices or vinegar."

--
The study from the previous post is the one by Collier and others, from 1983. They used a lot of butter to induce those effects: "In the present study we examined the effect of coingestion of 50 g fat (butter) on the postprandial glucose, insulin, and gastric inhibitory polypeptide responses to 50 g carbohydrate (potato) or 50 g protein (low fat veal) in eight normal subjects"

 

[ecstatichamster]

Incidentally, from what I've read of Peat, he just says a little butter or coconut oil with potatoes, not a ton of it. Of course a lot of fat with a lot of carbs will cause insulin resistance for hours. As that article says.

 

[schultz]

So butter with starch creates a higher and longer lasting insulin level? This could be a good anabolic tool to promote muscle growth. It seems like it would be an especially good idea before going to sleep as it would let the glucose stay elevated longer and therefore prevent a nocturnal rise in cortisol. Insulin suppresses muscle protein breakdown as well, so the result could be very anti-catabolic.

 

[James IV]

So butter with starch creates a higher and longer lasting insulin level? This could be a good anabolic tool to promote muscle growth. It seems like it would be an especially good idea before going to sleep as it would let the glucose stay elevated longer and therefore prevent a nocturnal rise in cortisol. Insulin suppresses muscle protein breakdown as well, so the result could be very anti-catabolic.

Excatly. Hyperglycemia is what provides you energy from a meal. The primary reason we eat is to raise blood sugar. Transient insulin resistance allows blood sugar to stay up longer, providing you with sustained energy. Which is why higher fat meals allow you to eat less often.
Hearing hyperglycemia and insulin resistance automatically makes people think "bad." This is not the case in practice.
Ray peat acknowledges that high blood sugar (hyperglycemia) is perfectly safe, and beneficial. It's major changes in blood sugar that can be harmful. Id argue that a low fat diet makes you more suceptable to the latter unless you are stringent with your meal macros and timing.
Which do you think will cause more drastic changes in blood sugar. 2 large mixed meals that digest for 6-10hours each, or 6-8 small meals that digest rapidly.
Both CAN work, but the latter, I've observed, can create a lifestyle of constant preoccupation with food, and stress induced "panic" hunger. Or tiredness/poor mood/ hunger from over stimulating insulin and incurring hypoglycemia.
I see this daily with low fat bodybuilders. They HAVE to eat by the clock, or they dont function well.

 

[Amazoniac]

It's probably not a good anabolic tool. And chronic elevation of insulin can't be a good thing; same for hyperglycemia. Otherwise diabetes would be a great condition.
At least for me, this issue doesn't appear to be so simple. I would not be surprised if a bit of olive oil or some slices of avocadoes become the darlings for starchy meals back again.
Although butter and coconut oil are safer fats when stored/metabolized, with olive oil and avocado in modest amounts it seems that you get the benefits of both sides: a more controlled deliver of glucose and less insulin insensitivity than the other fats on starchy meals.
At first I thought that there was a threshold of fat intake that would be significant, that if you stayed below that, it wouldn't make much difference the fatty acid profile and how it affects the meal. But apparently there isn't. And a fat free starchy meal is also completely different than one with a bit of added fat.

I'm not on any side, by the way. In fact, I don't like olive oil and avocadoes at all, but I'm open to that idea..

 

[James IV]

It's probably not a good anabolic tool. And chronic elevation of insulin can't be a good thing; same for hyperglycemia. Otherwise diabetes would be a great condition.
At least for me, this issue doesn't appear to be so simple. I would not be surprised if a bit of olive oil or some slices of avocadoes become the darlings for starchy meals back again.
Although butter and coconut oil are safer fats when stored/metabolized, with olive oil and avocado in modest amounts it seems that you get the benefits of both sides: a more controlled deliver of glucose and less insulin insensitivity than the other fats on starchy meals.
At first I thought that there was a threshold of fat intake that would be significant, that if you stayed below that, it wouldn't make much difference the fatty acid profile and how it affects the meal. But apparently there isn't. And a fat free starchy meal is also completely different than one with a bit of added fat.

I'm not on any side, by the way. In fact, I don't like olive oil and avocadoes at all, but I'm open to that idea..

I am on no side either, but again, youre still accerting all IR is bad. There is a big difference between phisiological IR and transient IR. In this case we are discussin the latter, so the comparison to diabetes is unfounded. And if elevated blood FFA caused diabetes (t2), then fasting or extreme caloric restriction would make it worse, not cure it.
Eating mixed meals will not give you diabetes, or almost everyone would have diabetes. Fattening your pancreas by chronically eating beyond your metabolic capacity/needs, likely will.

both food, and bodyfat (subcutaneous, visceral) are sources of energy. When more of one is available, the other will be utilized less. There is no magic macro ratio that will circumvent this. If you need to lose bodyfat, eat/live in a way that provides you with the most energy output (nutrition) with the least energy intake. It is that simple, and that complicated.

 

[Amazoniac]

I am on no side either, but again, youre still accerting all IR is bad. There is a big difference between phisiological IR and transient IR. In this case we are discussin the latter, so the comparison to diabetes is unfounded. And if elevated blood FFA caused diabetes (t2), then fasting or extreme caloric restriction would make it worse, not cure it.
Eating mixed meals will not give you diabetes, or almost everyone would have diabetes. Fattening your pancreas by chronically eating beyond your metabolic capacity/needs, likely will.

both food, and bodyfat (subcutaneous, visceral) are sources of energy. When more of one is available, the other will be utilized less. There is no magic macro ratio that will circumvent this. If you need to lose bodyfat, eat/live in a way that provides you with the most energy output with the least energy intake. It is that simple, and that complicated.

Prince, as far as I know, hyperglycemia by itself is already something beyond your metabolic capacity; even if it's a state that was induced temporarily. The question here is not if it's beneficial or not to add fat, but if by adding fats that are predominantly MUFA, you get those benefits without impairing the use of glucose as much as it happens with SaFA..

 

[James IV]

Prince, as far as I know, hyperglycemia by itself is already something beyond your metabolic capacity; even if it's a state that was induced temporarily. The question here is not if it's beneficial or not to add fat, but if by adding fats that are predominantly MUFA, you get those benefits without impairing the use of glucose as much as it happens with SaFA..

Prince?
Hyperglycemia is necessary if you wish to do pretty much any type of physical or even strenuous mental exercise. Even Dr Peat says you want higher blood sugar during the daylight hours. Beyond a certain degree it does appear that hyperglycemia can be detrimental, but this is directly related to energy intake, not macro intake.
In a healthy, fasted, individual, a 500kcal meal of pure starch will cause fast and large hyperglycemia and equally fast fall back to baseline with the cells using the glucose they immediately need, and converting what isn't immediately needed to glycogen, fat, or heat. A 500kcal mixed meal will cause slower and smaller hyperglycemia and an equally slow return to baseline. In the end the cellular energy exposure is the same. The difference is the mixed meal person will likely not be hungry as quickly after the meal, since low blood sugar is a well known stimulus for hunger.
This is all in a metabolically perfect individual, which is likely a small percentage of people. Metabolically damaged individuals will likely put themselves in more danger eating the starch meal, rather than the mixed, because thier capacity for energy utilization/conversion is going to be damaged, which can lead to excessive cellular energy exposure.

 

[Amazoniac]

Prince?
Hyperglycemia is necessary if you wish to do pretty much any type of physical or even strenuous mental exercise. Even Dr Peat says you want higher blood sugar during the daylight hours. Beyond a certain degree it does appear that hyperglycemia can be detrimental, but this is directly related to energy intake, not macro intake.
In a healthy, fasted, individual, a 500kcal meal of pure starch will cause fast and large hyperglycemia and equally fast fall back to baseline with the cells using the glucose they immediately need, and converting what isn't immediately needed to glycogen, fat, or heat. A 500kcal mixed meal will cause slower and smaller hyperglycemia and an equally slow return to baseline. In the end the cellular energy exposure is the same. The difference is the mixed meal person will likely not be hungry as quickly after the meal, since low blood sugar is a well known stimulus for hunger.
This is all in a metabolically perfect individual, which is likely a small percentage of people. Metabolically damaged individuals will likely put themselves in more danger eating the starch meal, rather than the mixed, because thier capacity for energy utilization/conversion is going to be damaged, which can lead to excessive cellular energy exposure.

Ok, prince was too warming, what about Barber of Seville?
The problem with all that is that when the person is dealing with sugar issues, even what people in general would consider a small amount, is enough to cause problems. Fasting heals those problems but so do consistent meals with plain starches and no added fats. What I mean by hyperglycemia, is toxicity, not just slightly elevated.
Back to the main point: fat clearly interferes with the use of glucose, and the fats affect differently.
From what you imply, the fact that saturated fats interfere the most, is not a problem; might even be beneficial (on healthy lords). Now, how much?
And also, following that same logic: pizzas, hamburguers, etc, are all fine as long as the ingredients are good?

Now tell me honestly, this isn't going to get anywhere, right?

 

[James IV]

Ok, prince was too warming, what about Barber of Seville?
The problem with all that is that when the person is dealing with sugar issues, even what people in general would consider a small amount, is enough to cause problems. Fasting heals those problems but so do consistent meals with plain starches and no added fats. What I mean by hyperglycemia, is toxicity, not just slightly elevated.
Back to the main point: fat clearly interferes with the use of glucose, and the fats affect differently.
From what you imply, the fact that saturated fats interfere the most, is not a problem; might even be beneficial (on healthy lords). Now, how much?
And also, following that same logic: pizzas, hamburguers, etc, are all fine as long as the ingredients are good?

Now tell me honestly, this isn't going to get anywhere, right?

Oh I see, you were making a stab at my character, ok.
So regarding the discussion; Fat will interfere with the use of carbohydrate in the sense that only limited amounts of each can enter the Randal Cycle at a time. But in the big picture both substrates will get used eventually if energy intake is appropriate. You are implying that dietary fat is the issue, and overconsumption of energy is the issue. If fat in the bloodstream is harmful, why does the human body store so much excess energy as fat? Why wouldn't we have a practically unlimited capacity for glucose storage if we are designed to run purely on glucose. Getting fat is a protective response to limit excess cellular energy. Getting fat makes you insulin resistant. So removing fat will not fix the problem if the person does not create an energy deficit and lose bodyfat.
That's the goal.

My observation is in most real life situations, it's much easier and more applicable for people to drastically limit carbohydrate than to drastically limit fat when eating ad libitum. There is a reason the Atkins diet is the most popular diet of all time, it works. And it works for thousands of people that had no results with traditional low fat and calorie restriction. Restricting starch has been a well known cure for obesity for hundreds, if not thousands of years. I think there is a also mitochondrial and gut biome effect to high fat/low carb that is possibly advantageous to individuals with a history of overeating.
I'm not implying severe carbohydrate restriction is the optimal way to eat long term, although I'm not saying it isn't. However for bodyfat loss with muscle retention, and ease of application, it's a great option for many people.

Looking at the transient chemistry of post prandial blood work is not seeing the forest through the trees.

 

[Amazoniac]

Oh I see, you were making a stab at my character, ok.
So regarding the discussion; Fat will interfere with the use of carbohydrate in the sense that only limited amounts of each can enter the Randal Cycle at a time. But in the big picture both substrates will get used eventually if energy intake is appropriate. You are implying that dietary fat is the issue, and overconsumption of energy is the issue. If fat in the bloodstream is harmful, why does the human body store so much excess energy as fat? Why wouldn't we have a practically unlimited capacity for glucose storage if we are designed to run purely on glucose. Getting fat is a protective response to limit excess cellular energy. Getting fat makes you insulin resistant. So removing fat will not fix the problem if the person does not create an energy deficit and lose bodyfat.
That's the goal.

My observation is in most real life situations, it's much easier and more applicable for people to drastically limit carbohydrate than to drastically limit fat when eating ad libitum. There is a reason the Atkins diet is the most popular diet of all time, it works. And it works for thousands of people that had no results with traditional low fat and calorie restriction. Restricting starch has been a well known cure for obesity for hundreds, if not thousands of years. I think there is a also mitochondrial and gut biome effect to high fat/low carb that is possibly advantageous to individuals with a history of overeating.
I'm not implying severe carbohydrate restriction is the optimal way to eat long term, although I'm not saying it isn't. However for bodyfat loss with muscle retention, and ease of application, it's a great option for many people.

Looking at the transient chemistry of post prandial blood work is not seeing the forest through the trees.

Member that releases elevator tension by opening and closing the message app 30x despite not receiving one in a while,

I didn't write that dietary fat is an issue; if I'm trying to understand how much and what type of fat is better, it's quite the opposite of that interpretation.
But what I do insist is that it's not good to create unnecessary oxidative stress by keeping blood sugar and insulin excessively and chronically elevated, something that is not difficult to achieve with a starchy meal with a decent amount of added fat, especially considering that most people are not at their best condition; and something that definitely will happen when there's energy excess.

Now, James my little lord, don't quote me, otherwise my multiple edits become @Pointless

 

[James IV]

Member that releases elevator tension by opening and closing the message app 30x despite not receiving one in a while,

I didn't write that dietary fat is an issue; if I'm trying to understand how much and what type of fat is better, it's quite the opposite of that interpretation.
But what I do insist is that it's not good to create unnecessary oxidative stress by keeping blood sugar and insulin excessively and chronically elevated, something that is not difficult to achieve with a starchy meal with a decent amount of added fat, especially considering that most people are not at their best condition; and something that definitely will happen when there's energy excess.

Now, James my little lord, don't quote me, otherwise my multiple edits become @Pointless

I unsure what your first paragraph is referring to. And im not sure why you've adopted a patronizing tone, but it isn't going to change my thoughts on this matter.

Anyway, your statements are now becoming a bit muddied. Your original assertion indicated that you beleived dietary fat was the driver of phisiological insulin resistance, and that removing fat from your diet will cure or heal an insulin resistant person. Now you seem to be saying that it's an energy balance issue, which was my point. Although you also seem to imply that fat is still more detrimental than carbohydrate, in the environment of energy excess? Which I don't agree with, and I would say that's actually backwards. In an overfed environment, fat will likely cause the least amount of damage to the cells.

I will succeed this debate, because I agree that it's not going anywhere.

 

[Amazoniac]

I unsure what your first paragraph is referring to. And im not sure why you've adopted a patronizing tone, but it isn't going to change my thoughts on this matter.

Anyway, your statements are now becoming a bit muddied. Your original assertion indicated that you beleived dietary fat was the driver of phisiological insulin resistance, and that removing fat from your diet will cure or heal an insulin resistant person. Now you seem to be saying that it's an energy balance issue, which was my point. Although you also seem to imply that fat is still an issue in the environment of energy excess? Which I don't agree with, and would say that's actually backwards. In an overfed environment, fat will likely cause the least amount of damage to the cells.

I will succeed this debate, because I agree that it's not going anywhere.

One more time, please don't skim: I don't have any problem with added fats. I'm just trying to find what type of fat is best and how much of it.
The best outcome is a controlled glucose response and the least insulin insensitivity; because if insulin can't do its job, the utilization of glucose would be impaired, and that can't be a good thing in the long term. That effect is dose-dependent and remains for hours after a given meal rich in starches and fats.
You gave a extreme example of healing diabetes by fasting, I gave one by removing all added fats.
If the utilization of a nutrient is impaired (as in the case of mixing a great amount of both, starches and fats), that leaves you in a state of excess, which is something beyond your capacity at that time; and that in turn creates unnecessary stress. In this case a sustained hyperglycemia and hyperinsulinemia.
There's nothing getting muddy, except for our romance, that seems to be succumbing. But don't take those jokes personally, because they're not, they're quite random in fact; and I wouldn't joke with people that I don't like..

 

[Amazoniac]

The Randle cycle revisited: a new head for an old hat

"Glucose toxicity.
High values of ΔΨ lead to proton leak, reversed electron flow, and ROS production (Fig. 7). As described above, active fatty acid oxidation induces such a state. Flooding the system with glucose on top of fatty acids is expected to induce considerable damage to the mitochondria if energy demand is not concomitantly increased. An overabundant diet rich in carbohydrates and fat (184) should force-feed electrons from glucose into the respiratory chain, in which the already prevailing high ΔΨ prevents electron flow. This excessive energy supply, not matched by energy demand, will further worsen the jamming of electrons in the respiratory chain and eventually result in massive ROS production and mitochondrial damage (Fig. 7). In addition, a saturated flux through the glycolytic pathway could result in an overflow into the hexosamine biosynthetic pathway leading to protein glycosylation by O-linked β-N-acetylglucosamine (67, 106, 192). The persistent combination of these two effects probably explains glucose toxicity. By contrast, the beneficial effects of physical activity and muscle exercise could prevent mitochondrial damage by decreasing ΔΨ and favoring the overall oxidation of substrates to fulfill the increased energy demand. Last, one might even wonder whether glucose intolerance and insulin resistance are not a protective mechanism that prevents glucose toxicity."

"The slowly progressing pathological process could be the consequence of a continuous overabundant diet enriched in both carbohydrate and lipid, unmatched by physical activity. In the mitochondria, the redox pressure from both substrates would provoke a continuous production of ROS, resulting first in minimal damage but deteriorating with time into more extensive and irreversible lesions. This interpretation is in agreement with recent data showing that mitochondrial alterations do not precede the onset of insulin resistance and result from increased ROS production in muscle in diet-induced diabetic mice (15). In addition, the importance of physical activity and energy utilization is fully taken into account in our interpretation, because they are expected to protect the mitochondria by decreasing ROS production. One may also wonder whether the beneficial effect of metformin, the most widely used drug for the treatment of type 2 diabetes, may be due to its capacity to decrease mitochondrial ROS production by inhibiting the reversed electron flow at the level of the complex 1 of the respiratory chain (11, 103)."

James, this is not an indirect quote towards you. I'm learning along, if you don't believe me check the horror show from my first posts here on the forum.