Man Makes Himself Insulin Resistant/type Two Diabetic By Drinking Olive Oil

[haidut]

Since when is TDEE the same as RMR ? You are comparing apples to oranges, so I am not even going to read that study .
Any other ?

They are not the same but TDEE includes RMR as a component. You should read the study, it touches upon that point as well.
"...Previously we reported that both 24-hour sedentary energy expenditure and sleeping metabolic rate measured in a respiratory chamber were reduced ∼6% beyond what was expected for the loss of metabolic mass (FFM and FM) [6]. This metabolic adaptation was also observed in RMR measured by a ventilated hood indirect calorimeter [7]. A portion of the reduction in sedentary energy expenditure was due to the reduced energy intake itself (thermic effect of food), and a reduction in the energy cost of spontaneous physical activity."

"...Behaviorally, a response to the semi starvation was also a tremendous decrease in physical activity. It was estimated that reduced physical activity accounted for 58% of the decreased total energy expenditure whereas RMR accounted for 32% and the thermic effect of food for only 10% [24]."

And if that is not enough, here are 3 other studies that measure only RMR adaptations and also found decrease.
Energy-metabolism adaptation in obese adults on a very-low-calorie diet. - PubMed - NCBI
"...The RMR-LBM ratio declined significantly during the VLCD period and decreased faster during the first week; the day 3, day 5, and day 21 ratio values were 94%, 91%, and 82%, respectively, of the original. The RMR-LBM ratio decrease after 21 d of a VLCD was near that found in chronic undernutrition. Results of previous studies that did not find any drop in the RMR-LBM ratio in obese adults on VLCDs might be explained by their LBM-assessment methods."

Short and long term effects of a very low calorie diet on resting metabolic rate and body composition. - PubMed - NCBI
"...Short and long term effects of a protein sparing modified fast (PSMF) diet on resting metabolic rate (RMR) and body composition were investigated. During a period of 6 months on diet, RMR decreased significantly, both in absolute value and after correction for fat-free mass (FFM). Short term evaluation with this type of diet showed no decrease in RMR. The results from this study indicate that the fall in RMR associated with a PSMF diet (weight loss) is not due to an acute adaptation to the lower energy intake. Changes in FFM are important in the change in RMR, but other factors have to be involved."

Physiological regulation of body weight and the issue of obesity. - PubMed - NCBI

 

[SAFarmer]

They are not the same but TDEE includes RMR as a component. You should read the study, it touches upon that point as well.

Again, ... you are now referencing other studies. Please stay on topic and 1 study at a time.
And, having RMR "included" in TDEE, without actually measuring it and comparing it directly on it's own, does again not provide the proof I am asking you for.

Also, the first study, the main 1 you claim is evidence of your belief, is a "free living" , "self reported" study that includes the words "estimated" etc. to all come to the conclusion what these people wanted to see , ie that extreme calorie restriction is good for longer living due to reduced metabolism and inflammation. They also make the mistake of estimating from the wrong base.
Interestingly in the CR group, the people kept losing weight, even in the weight maintenance period ... a further 2kg or more, even though the SMR stayed the same at M6 compared to M3. This is not explained.
Also looking at the data for the CR group (not a lot of data is given), the SMR (sedentary metabolic rate) did not fall significantly more than what could be expected for the weight loss.
It is a flawed study in many ways and offer no conclusive evidence for your belief.
I remain open to any other evidence you might find in your searches.

 

[SAFarmer]

And if that is not enough, here are 3 other studies that measure only RMR adaptations and also found decrease.

All 3 these studies that you claim as also evidence for your belief, are abstracts only with no open access to the full studies.
Did you read and study the full text ? Can you provide us with a copy if so ?
Also the 3rd study was done on rats, so would not count towards evidence in humans.
So based on the contents of the extracts only, I cannot see how you can offer this as evidence for your belief.

 

[haidut]

All 3 these studies that you claim as also evidence for your belief, are abstracts only with no open access to the full studies.
Did you read and study the full text ? Can you provide us with a copy if so ?
Also the 3rd study was done on rats, so would not count towards evidence in humans.
So based on the contents of the extracts only, I cannot see how you can offer this as evidence for your belief.

I read one of the subsequent studies so far. When I get a chance will read the other one, as the third one is on rats (as you said) and probably not directly relevant. If they allow PDF to be downloaded I will post here. Look, you seem hellbent on disagreeing with me but these are the conclusions of the studies. If you have a problem with their design or conclusions that's another story altogether. But the very goal of study 1 and its references is to make exactly that claim - i.e. chronic dieting lowers RMR beyond what the RMR is in control subjects with the same weight. You asked for a control group and there was one in that study. Now, it is a problem with the study design. As far as RMR and its relation to TDEE - that's what the quote from the first study was for - if 1/3 of the decrease in TDEE is due to RMR, then the 6%-10% decline of TDEE would be (all other things being equal) due to decrease in RMR, adjusted for FFM and compared to controls.

 

[WestCoaster]

I love how threads take turns. When I was first here it was about buddy making himself insulin resistant through drinking olive oil (even though he eats pizza before his test), now it seems were talking about weight loss, RMR, BMR, TDEE, cold thermogeneis, and what looks like CICO (Calories in Calories out).

So here is the coles notes on weight loss, and by weight loss I mean FAT loss. The more insulin circulating in your system, the less body fat you're able to burn, simple as that. Remember, glucose is used up for energy first in the body, not fat (ketones); if glucose is present, the body wont burn fat. If your insulin is elevated, your blood sugar is elevated. CICO and calories have jack squat to do with this. Where people seem to get screwed up is they seem to forget that what type of foods react in one person, don't react the same in another. Lets take 2 people for example here:, Lets call them Bob and Bill. Bob has good insulin sensitivity, Bill does not. Lets assume their twins, same height, same weight. Bill's fasting blood sugar is slightly higher than Bob's due to insulin problems. Both Bob and Bill decide to eat 1500 calories a day of whole foods. Let's assume Bob's fasting blood sugar is 85 and Bill's is 100. Right off the bat, Bill is going to have a little more difficult burning fat due to elevated levels of blood sugar. His insulin is having more difficult than Bob's to lower his blood sugar.

Breakfast consists of a couple eggs, a couple sausages, an apple, an orange, and some water. Bob and his great insulin sensitivity peak at 100 30 min after he eats then quickly lowers back to 85 within the hour. Bill on the other hand, his blood sugar rockets up to 160 because again, his insulin is having difficulty clearing the glucose. Not only does it go up to 160, but stays there for 3 hours before coming back down to 100. Poor Bill spends longer trying to clear his glucose than Bob, so Bill has a longer period of time of glucose burning, and less time burning fat.

For arguments sake, lets assume their other 2 meals are the same thing and equal 1500 calories (I know they don't but bare with me). Lets also assume, they eat the same thing every day for 1 month. At the end of the month, Bob has spent more time burning fat than Bill. Bob loses 5lbs, Bill loses nothing. Bob says "Great CICO works!" Bill says "screw you, it doesn't work, I lost nothing", and thus the argument of BMR, RMR, TDEE, and CICO ensue. Some people have good insulin sensitivity, others do not. More accurately I should say, most people don't have good insulin sensitivity. In Bill's case, the only way he will match Bob's 5lb fat loss in a month is he will have to get his blood sugar and insulin sensitivity in check to match Bob's. That mean his has to drop to 85, and his glucose and insulin can stay no longer in his system than Bob's. Now what food choices would Bill have to make to reach that goal? Impossible to say, the only way he could do that is if he constantly monitors his blood glucose which simply isn't going to happen. Not only that, other things as you guys know affect blood sugar, like cortisol from either environmental stress or poor sleep. Cortisol drags blood sugar up halting fat loss.

There is many factors at play here, so using all encompassing things like BMR, RMR, TDEE, CICO, is a losing battle. You simply do not know how what someone is eating, how they are feeling, how they slept is affecting their blood sugar. Nor do you know if there are any hidden diseases going on causing it to stay elevated either from stress, or flat out insulin problems.

You simply cannot tell somebody to "eat less and exercise more" if eating less causes metabolism to slow down, and cortisol to elevate, while exercising more causes cortisol to elevate and remain elevated. Your best bet is to tell them to grab a glucometer that tests ketones as well. The goal being get ketones up while blood sugar is down, that is when FAT loss will occur. Then how they get that to occur is something they have to figure out on their own

 

[Westside PUFAs]

(even though he eats pizza before his test)

Pizza has fat. And the starch in pizza is flour which has different absorbtion and effects than a boiled/steamed potato/rice/squash/cassava/taro which are non-flour and have potassium which acts like insulin and other nutrients.

So here is the coles notes on weight loss, and by weight loss I mean FAT loss.

The question is how did that fat there in the first place. What did the person eat to get fat in the first place.

The more insulin circulating in your system, the less body fat you're able to burn, simple as that.

This is the Gary Taubes theory which has been debunked many times. See here:

Is Obesity Selected For By Evolution?

Glucose Fatty Acid Cycle and Insulin Resistance

Lets call them Bob and Bill. Bob has good insulin sensitivity, Bill does not.

The question is why is Bill insulin resistant.

Lets also assume, they eat the same thing every day for 1 month.

It depends on what they are eating.

You simply do not know how what someone is eating, how they are feeling, how they slept is affecting their blood sugar. Nor do you know if there are any hidden diseases going on causing it to stay elevated either from stress, or flat out insulin problems.

Yes.

You simply cannot tell somebody to "eat less and exercise more"

I never said that. I said the fat you eat is the fat your wear, as evidence by testing the fat tissue of cadavers and donors:

National Human Adipose Tissue Survey (Nhats) | Risk Assessment Portal | US EPA

Peat has said that the body will store PUFA first because it wants to burn the good stuff first (sugar). He's also said that MUFA from olive olive is fattening, and I've posted his numerous quotes on how dairy which is saturated can be fattening. So again, the fat you eat is the fat you wear, only to be turned into ketones if needed. But even though ketones by themselves are a safe fuel, they are the back up fuel for the brain and not 100% at that, we still always need some sugar even when in deep ketosis. The process of ketosis is too stressful to be in everyday, which isn't what ketosis was meant for evolutionarily.

that is when FAT loss will occur.

And then how does one eat daily, every day, for the rest of their life after they lose fat? - "So, since we can make all of the saturated fats, palmitate, stearate and we can desaturate stearic acid to make oleic acid and our own series of polyunsaturates, I think it's best to get as much sugar and starch in your diet, preferably sugars from fruit and milk, and minimize the exposure to the unstable and n-6 and n-3 fatty acids." So Peat is saying it's best to be a sugar burner, not a fat burner.

Here is true ketosis at work. This guy didn't eat for 21 days. And here is he breaking his fast by drinking juice. Notice how much fat and water he lost. That is ketosis, not meant for every day outside of a water fasting context. Notice when he is laying down on the bed how little energy he has when in ketosis. Because that is real ketosis' purpose, to survive a famine, or to do what he did and turn much of his adipose tissue into ketones which resulted in less body fat, and reset his taste buds, not a state to be in every day for life long term.

 

[James IV]

So would you say overfeeding on sugar causes adrenaline? There is a study that compared sucrose to starch and in the sucrose group their adrenaline was much higher throughout the day. I could never reconcile this. I have had issues with adrenaline for over 2 yrs. I don't overeat calories but I do eat lots of sugary food.

Absolutely. Some may disagree, but I think thats why sugar increases your metabolic rate so much, adrenaline.

I want to be clear I don't believe in CICO. I do however believe that fat loss/gain is an energy balance issue.

 

[NathanK]

Wanted to add to this conversation and back up one of @haidut core points that fat mass does not equate to diabetes/IR as commonly believed.

Obesity is nothing more than a symptom of IR in as much as it is for any malady. The att paper shows NEFA is tightly regulated in the body independent of fat mass. It may be that excessive estrogen (once again!) is the dysregulating force of FFA and thereby saturating the blood, increasing lipolysis, and causing IR.

People who improve their IR by losing weight may be doing so via lowering estrogen -> increasing protective hormones-> lowering lipolysis -> returning to FFA homeostasis. It wasnt intended, but I can attest to vitamin E lowering my A1C within 3 weeks (5.4 to 5.2). Thats a pretty good drop for what is considered a long range measure of blood sugar.

Diabetes | Mobile

(I posted this in a thread over a year ago so here is just a quick glance excerpt):
FASTING NEFA RELEASE IN RELATION TO FAT MASS OR
FASTING INSULIN
As noted above, the literature suggests that NEFA con-
centrations do not increase in proportion to fat mass, with
a clear corollary that lipolysis per kilogram fat mass must
be reduced in obesity. This has been repeatedly seen in
studies of adipocytes from obese individuals in vitro (66,67)
and is associated with downregulation of the expression of
the key enzymes of fat mobilization, hormone-sensitive li-
pase and adipose triglyceride lipase (12,66,68,69).
This aspect of adipose tissue function in obesity has been
studied with isotopic turnover techniques. Mittendorfer
et al. (70) studied NEFA turnover in individuals with
a range of BMIs (18–44 kg/m2
). The systemic rate of ap-
pearance of NEFA, when expressed per kilogram fat mass,
clearly decreased across a wide range of fat mass (corre-
lation coefficient 20.81, P , 0.001). Although not high-
lighted by the authors, a similarly negative association was
present (r = 20.64, P = 0.06, n = 8 [men]) when recalcu-
lating raw data presented in the very first article describing
NEFA turnover in obesity (71). We have shown this also
when comparing a group of abdominally obese men with
lean control subjects over a 24-h period (12).
This downregulation of lipolysis per kilogram of fat
mass will tend to normalize plasma NEFA concentrations
in obese individuals. Some extreme examples are seen in
the literature. Reeds et al. (72) studied extremely obese
insulin-resistant young women compared with lean control
subjects. Despite a sixfold difference in fat mass, basal
NEFA concentrations were identical in the two groups. In
our own studies, abdominally obese men with 2.5 times the
adipose tissue mass of a lean control group had almost
identical NEFA concentrations over a 24-h period (12

Btw, there are plenty of studies showing fasting increases NEFA. This all comes back to Ray's recommendation to keep FFA low by keeping stress hormones low with our usual toolbox of food and vitamins.

 

[InChristAlone]

Absolutely. Some may disagree, but I think thats why sugar increases your metabolic rate so much, adrenaline.

I want to be clear I don't believe in CICO. I do however believe that fat loss/gain is an energy balance issue.

Problem is I can tell the difference between adrenaline and a good metabolism. Adrenaline is for sure cold hands and feet, fight or flight stress hormone. And that doesn't always happen with a high sugar intake. I think it can happen if you are trying to increase metabolism and the resources aren't there.

 

[schultz]

I want to be clear I don't believe in CICO. I do however believe that fat loss/gain is an energy balance issue.

Are these not the same thing?

If your body uses 3,000 calories a day and you intake 2,900 calories a day, you will lose weight. If you reverse those numbers you will gain weight.

Obviously the body doesn't burn a preset, and static, amount of calories. I'm sure it varies depending on lots of external factors. Simply eating more calories likely results in the body burning more calories. What I mean is, just say you eat 2,000 calories and burn 2,000 calories. If you increase your intake to 4,000 calories, maybe the body burns 2,500 (or whatever).

Lots of things contribute to the amount of calories your body uses each day, but it's still a matter of fuel intake/ fuel burned, right? Is this not what calories in/calories out means?

Even if two people eat the same thing (like "Bob and Bill") and one person loses more than the other, what about the other factors? Who gets more activity, who gets more sunlight, who has more initial muscle mass, who has more stored fat soluble vitamins, who has more stored PUFA (the release of which could slow one persons metabolism). There are many factors.

Remember, glucose is used up for energy first in the body, not fat (ketones); if glucose is present, the body wont burn fat.

The muscles burn fat at rest, even if glucose is present in the body. Just like you can still burn fat while taking aspirin and niacin (which inhibit lipolysis). If you drank a liter of juice and then went for an hour walk, would your muscles not burn fat?

Note: I understand there is some internet definition of what CICO is, and it possibly includes the idea that all types of calories have the same effect on the body or something. But the phrase "calories in/calories out" by itself, with no additional definition, is true. It has to be according to our current understanding of physics.

Just because someone says calories in/calories out is true, doesn't necessarily mean they are saying 1g of PUFA and 1g of sugar will have the same effect on the body metabolically.

To lose weight you need to create a deficit of calories, in one way or another! The idea is simple, it's the how that is the complicated part.

 

[Peater Piper]

Obesity is nothing more than a symptom of IR in as much as it is for any malady. The att paper shows NEFA is tightly regulated in the body independent of fat mass. It may be that excessive estrogen (once again!) is the dysregulating force of FFA and thereby saturating the blood, increasing lipolysis, and causing IR.

Wow, doesn't that call into major question the role FFA plays in insulin resistance? The paper you linked is stating that FFA probably becomes dysregulated after metabolic syndrome has already taken hold. Thus, insulin resistance begins (due to bad diet, stress, whatever), the body increases insulin and lipolysis is downregulated to compensate, and only when these measures fail do you get the elevated NEFA, which probably exacerbates things further.

They also mention this:

"Insulin resistance associated with longer-term lipid overload is now considered to involve accumulation of lipids in insulin-responsive tissues other than adipose tissue, so-called ectopic fat deposition (55). Fatty acid uptake by insulin-sensitive tissues is also likely to be modulated by altered function/expression of transporter proteins (56). The detrimental effects on insulin sensitivity and other cellular processes are known as lipotoxicity (57). In skeletal muscle, an increase in intramyocellular lipid (cellular TG), associated with insulin resistance, is seen during Intralipid/heparin infusion and clearly represents increased supply (58). Although it is as yet unresolved as to whether regulatory defects in mitochondrial fatty acid oxidation, with the apparently concomitant intramyocellular TG accumulation, are primary or secondary to insulin resistance, the phenomena appear to be strongly linked (59)."

I've posted the following study before, but it shows some people probably carry genetic defects that prevent them from upregulating beta oxidation when necessary, which would lead to increases in TG. Their energy expenditure in response to a high fat meal was also lower than the controls, which could lead to weight gain over time. I'm wondering if it's these people that respond so poorly to higher fat diets, whereas some people seem to be able to thrive with more fat.

Diabetes

 

[zztr]

if glucose is present, the body wont burn fat

You're always burning fat. It's just a question of proportion. This is why it ultimately boils down to calories and these macro dogma discussions are so dumb. In the real world it boils down to calories and any reasonable intake of saturated fat relative to carbs doesn't matter very much.

You simply cannot tell somebody to "eat less and exercise more" if eating less causes metabolism to slow down, and cortisol to elevate, while exercising more causes cortisol to elevate and remain elevated.

Exercise and eating less don't do that. Crash diets are a problem, so don't crash diet. But knocking it off with the deserts every night and the soda all day will not lower metabolism. Going on walk every day will not lower metabolism.

Sheesh, it's like some people refuse to observe the real world around them. You've never known someone who lost weight and kept it off? I've seen loads. It's always a simple story of eating less and exercising more.

 

[Westside PUFAs]

"if glucose is present, the body wont burn fat"

If that's true then how did this guy burn so much fat, 50 kilos/100 pounds, with high glucose/insulin? A pure starch/glucose diet for a whole year.

 

[James IV]

Are these not the same thing?

If your body uses 3,000 calories a day and you intake 2,900 calories a day, you will lose weight. If you reverse those numbers you will gain weight.

Obviously the body doesn't burn a preset, and static, amount of calories. I'm sure it varies depending on lots of external factors. Simply eating more calories likely results in the body burning more calories. What I mean is, just say you eat 2,000 calories and burn 2,000 calories. If you increase your intake to 4,000 calories, maybe the body burns 2,500 (or whatever).

Lots of things contribute to the amount of calories your body uses each day, but it's still a matter of fuel intake/ fuel burned, right? Is this not what calories in/calories out means?

Even if two people eat the same thing (like "Bob and Bill") and one person loses more than the other, what about the other factors? Who gets more activity, who gets more sunlight, who has more initial muscle mass, who has more stored fat soluble vitamins, who has more stored PUFA (the release of which could slow one persons metabolism). There are many factors.



The muscles burn fat at rest, even if glucose is present in the body. Just like you can still burn fat while taking aspirin and niacin (which inhibit lipolysis). If you drank a liter of juice and then went for an hour walk, would your muscles not burn fat?

Note: I understand there is some internet definition of what CICO is, and it possibly includes the idea that all types of calories have the same effect on the body or something. But the phrase "calories in/calories out" by itself, with no additional definition, is true. It has to be according to our current understanding of physics.

Just because someone says calories in/calories out is true, doesn't necessarily mean they are saying 1g of PUFA and 1g of sugar will have the same effect on the body metabolically.

To lose weight you need to create a deficit of calories, in one way or another! The idea is simple, it's the how that is the complicated part.

I meant I don't believe that you be successful getting lean and healthy and maintain it, simply by reducing calories. In other words, the CICO "diet."

 

[James IV]

Agree with WSP on this one. You can definitely burn fat with glucose present. Glucose is always present.

 

[James IV]

Problem is I can tell the difference between adrenaline and a good metabolism. Adrenaline is for sure cold hands and feet, fight or flight stress hormone. And that doesn't always happen with a high sugar intake. I think it can happen if you are trying to increase metabolism and the resources aren't there.

Agree. But those symptoms aren't always reliable. Adrenaline can be high without them. Exercise increases adrenaline, but rarely do people get those symptoms.

 

[NathanK]

Wow, doesn't that call into major question the role FFA plays in insulin resistance? The paper you linked is stating that FFA probably becomes dysregulated after metabolic syndrome has already taken hold. Thus, insulin resistance begins (due to bad diet, stress, whatever), the body increases insulin and lipolysis is downregulated to compensate, and only when these measures fail do you get the elevated NEFA, which probably exacerbates things further.

They also mention this:

"Insulin resistance associated with longer-term lipid overload is now considered to involve accumulation of lipids in insulin-responsive tissues other than adipose tissue, so-called ectopic fat deposition (55). Fatty acid uptake by insulin-sensitive tissues is also likely to be modulated by altered function/expression of transporter proteins (56). The detrimental effects on insulin sensitivity and other cellular processes are known as lipotoxicity (57). In skeletal muscle, an increase in intramyocellular lipid (cellular TG), associated with insulin resistance, is seen during Intralipid/heparin infusion and clearly represents increased supply (58). Although it is as yet unresolved as to whether regulatory defects in mitochondrial fatty acid oxidation, with the apparently concomitant intramyocellular TG accumulation, are primary or secondary to insulin resistance, the phenomena appear to be strongly linked (59)."

I'm having a hard time wrapping my head the broader implications of this, tbh. Like, "...However, it is clear that insulin resistance, even severe insulin resistance, can exist in obesity without elevation of NEFA concentrations..." or, "...Women have very significantly raised NEFA concentrations compared with men ((19–22), and this difference becomes more marked with short fasting (23,24)), yet tend to be more insulin-sensitive and to have better lipid profiles.... . Wouldn't this imply that women should have markedly more cases of T2D?

There are things missing and a lot of chicken or egg first questions. The answer may be somewhere in the muscles (and liver's) ability to dispose and uptake fatty acids. My guess was estrogen is the disrupting factor, which is found in ectopic muscle and liver fat. It's possible that NEFA is as indicative of Type II in as much as a ketogenisis is of cancer (okay, i'm exaggerating...). I may send to Ray to see what he thinks

NEFA under stress:
...[NEFA] They are suppressed during high-carbohydrate diets (25) and increased in stress states, e.g., concentrations of 1,720 mmol/L were found in racing drivers before a race (26). During exercise, when fat is mobilized from adipose tissue to supply the working muscles, concentrations may rise somewhat (2), but often plasma NEFA concentrations remain relatively stable as removal by muscle increases to match adipose tissue lipolysis (27,28)..."

High carb v. high fat
In a recent study by Hernandez et al. (78) comparing the metabolic effects of weight loss in groups on either a high-carbohydrate or a high-fat diet, the fasting NEFA concentration was not different between the groups whereas the postprandial and diurnal suppression of NEFA was almost completely abolished in the high-fat diet group, leading to drastically higher 24-h NEFA concentrations.

I've posted the following study before, but it shows some people probably carry genetic defects that prevent them from upregulating beta oxidation when necessary, which would lead to increases in TG. Their energy expenditure in response to a high fat meal was also lower than the controls, which could lead to weight gain over time. I'm wondering if it's these people that respond so poorly to higher fat diets, whereas some people seem to be able to thrive with more fat.

Diabetes

Anytime I hear hereditary, or all the family members suffer similar consequences, I start thinking grandma or great grandpa was on a ketogenic diet

 

[Peater Piper]

I'm having a hard time wrapping my head the broader implications of this, tbh. Like, "...However, it is clear that insulin resistance, even severe insulin resistance, can exist in obesity without elevation of NEFA concentrations..." or, "...Women have very significantly raised NEFA concentrations compared with men ((19–22), and this difference becomes more marked with short fasting (23,24)), yet tend to be more insulin-sensitive and to have better lipid profiles.... . Wouldn't this imply that women should have markedly more cases of T2D?

There are things missing and a lot of chicken or egg first questions. The answer may be somewhere in the muscles (and liver's) ability to dispose and uptake fatty acids. My guess was estrogen is the disrupting factor, which is found in ectopic muscle and liver fat. It's possible that NEFA is as indicative of Type II in as much as a ketogenisis is of cancer (okay, i'm exaggerating...). I may send to Ray to see what he thinks

NEFA under stress:
...[NEFA] They are suppressed during high-carbohydrate diets (25) and increased in stress states, e.g., concentrations of 1,720 mmol/L were found in racing drivers before a race (26). During exercise, when fat is mobilized from adipose tissue to supply the working muscles, concentrations may rise somewhat (2), but often plasma NEFA concentrations remain relatively stable as removal by muscle increases to match adipose tissue lipolysis (27,28)..."

High carb v. high fat
In a recent study by Hernandez et al. (78) comparing the metabolic effects of weight loss in groups on either a high-carbohydrate or a high-fat diet, the fasting NEFA concentration was not different between the groups whereas the postprandial and diurnal suppression of NEFA was almost completely abolished in the high-fat diet group, leading to drastically higher 24-h NEFA concentrations.

The forum was being wonky and I couldn't log-in for a while, but that paper's really awesome. I didn't see it when you originally posted it, but it's forced me to change my viewpoint on some things.

 

[NathanK]

The forum was being wonky and I couldn't log-in for a while, but that paper's really awesome. I didn't see it when you originally posted it, but it's forced me to change my viewpoint on some things.

I had weird issues replying this week, but seems fixed. May have been the mobile platform.

Ultimately, this just confirms to me that there is a lot of things still unexplained--no matter how much we try to wrap a bow around certain concepts and feel they are largely solved.

 

[paymanz]

Surely high FFA levels are involved in process to make him T2D.