I think it's more likely that obesity causes diabetes, buying into the fat threshold idea. Yes, insulin goes up with insulin resistants and type II (until it can't). But it goes up in part because the body is resistant to storing more nutrients, but also largely because of dysfunction in the liver and pancreas due to an increase in certain aspects of lipid metabolism. Subcutaneous tissue is overwhelmed in its ability to sequester fat, internal organs are exposed to increased levels of fatty acids and sugar, this is damaging to the tissues.

The increased insulin might help to make the subcutaneous fat grow beyond where it would otherwise have--but first there's a failure at the level of the subcutaneous tissue that has consequences to internal organs that increases that insulin that might further increase subcutaneous tissue.

Which came first, the chicken or the egg? My answer is fish, I think there were eggs long before there were chickens. :lol:

From what Ive veen learning......

Obesity , storage of extra energy, develops when other areas of storage is full, like the liver. Cells fill up with triglycerides or similar, cant remember exact name. The insulin is the key to all cells , facilitating removal of excess glucose from the blood, because too much bg is harmful, so storage form is prefered.

When the fat storage becomes maximized, the cell no lo nger responds to the insulin, leaving more glucose in the blood than is ideal.

At this point, Insulin Resistance is the problem.

The level of disfunction becomes more extreme, and gets named type 2 diabetes.

Im no expert. This is what lots of reading and sluthing has revealed.

Accirding to this model, obesity is a normal storage method. Not a disease state.

Furthet reading suggested that to restore insulin senditivity, reduce the need for insulin. Not supplying MORE, but the opposite. Go keto, or fast, yo allow healing and fixing. To restore sensitivity.

Im sorry I cant remember which sources to quote. My focus at the time was to understand

1. throwing insulin at T2D is stupid and causes more damage

2. altering diet to keto or fasting will fix insulin resistance and T2D

hypertriglyceridemia?

Anything ending in -emia is specific to the blood. Usually for muscle you'll see elevated or excess intramyocellular lipids, for the liver, fatty liver or steatotis, I've also seen fatty kidney or fatty pancreas used. Or ectopic fat is used, ectopic just means out of it's usual place. When dealing with damage caused by out of place fat usually lipotoxicity is used--that's more about free fatty acids and excess production of products of their metabolism, usually ceramides come up. Triglycerides themselves aren't necessarily a problem--there are studies showing that some things that actually increase triglycerides in liver or pancreatic cells can actually be protective. Triglycerides are basically metabolically inert, so driving free fatty acids towards triglyceride synthesis can sometimes decrease ceramide formation and also decrease competition with glucose for oxidation, facilitating glucose disposal in that way as well. There are studies in mice where choline deficiency prevents diabetes on a diet that would normally cause it--this causes a large increase in fatty liver.

Also lipotoxicity is a bit misnamed, sometimes gluco-lipo-toxicity is used. Elevated glucose or fatty acids seem to be relatively harmless to individual cells, it's when both are elevated that pathways that lead to ceramide excess etc. are elevated.

https://www.youtube.com/watch?v=VjQkqFSdDOc

Really good talk on diabetes, role of glucagon, etc.

I was looking at an article the other day that was looking at muscle triglycerides in athletes versus type II diabetics. Endurance athletes get fattier muscles, but have high muscle insulin sensitivity/low resistance. They were looking at the saturation of the fat in the muscle, the diabetic's muscle fat was more saturated compared to the athletes. In lipotoxicity studies, the saturated fat especially palmitic seems to be the problem--sort of. When exposed to palmitic acid and sugar, those ceramides are produced and damage occurs. Adding a little bit of oleic acid, monounsaturated fat, or some polyunsaturated fats increases triglyceride synthesis--fat stores increase in the cells, giving a way to dispose of excess free fatty acids (only really excess given the excess elevation of glucose also present), this protects the cells from damage.

Could it possibly be a circular argument and that what causes obesity also contributes to developing T2D? I emphasize the word "contributes." This condition is often referred to as a syndrome meaning many variables contributing to cause and many symptoms representing the condition. No easy button here, as it's likely a different set of variables contributing to the condition in each individual depending on phenotypes.

Sort of? Personal fat threshold doesn't even require a person to become obese or even overweight. People with the sort of dyslipidemia where they can barely even accumulate normal fat tissue can get insulin resistance/type II diabetes. It isn't so much the fat as it is the fat showing up at the wrong time, in the wrong place. I don't think there's any question that obesity can contribute to diabetes. A might cause both B and C--that doesn't mean B doesn't increase C and vice versa.

Robert Lustig has compared fructose to a high fat/high carbohydrate diet. It does seem to worsen the effect. The liver is exposed to increased carbohydrate metabolism--but without the insulin response, fat metabolism is not adequately decreased, so maybe you get this mix of the two. I do think this is a case where fructose can both increase obesity and increase insulin resistance and risk of diabetes--so both having a single cause. But that doesn't mean that the weight gain itself can't make things worse and still contribute to the development of diabetes. The most fattening diet for rodents isn't necessarily high fructose, fructose is mostly used in the diet for models of insulin resistance/diabetes.

I haven't seen anything showing that once a person is insulin resistant, with higher peripheral insulin, they're more easily fattened. Or I don't think I have, maybe I missed it. I've seen claims, theories that that's the case. I think it's more likely it's harder to get fatter at that point, although of course you can blow through stalls with exogenous insulin and various diabetes drugs (they call the weight gain a side effect, but it's probably pretty much the very mechanism by which they have the desired effect).

That's why I proposed the circular argument, as I've heard too often that obesity causes diabetes. Yet, people who don't appear obese are diabetes candidates as well. It's never as simple as people would like, no single smoking gun. Personal fat threshold is the "unnoticeable" variable here, and is merely one contributing variable.

What I have learned, obesity is a storage method; the insulin resistance and the T2D is when it all goes awry; Hence obesity is not required in all cases. And in fact, most people are in biochemical trouble long before obesity is pointed at.

For those just becoming aware of IF and Jason Fung, this is an excellent video from earlier this year. For those already aware, this is a recent summary and detailed discussion with Bret Scher of DD:

https://www.youtube.com/watch?v=rQs...24ed1-102468937

I should add that this video covers fasting and more with cited research related to diet, cancer, hormonal influence, and many other metabolic dynamics. Very good education overall.

So Dr. Fung's Big News has dropped. The IDM page is now:

https://thefastingmethod.com

The program has fees, though at least for now, the long history of blog posts are still available.

I'm happy that Dr. Fung can be a positive resource to many. A lot has changed over the past few years when his site provided much information and advice for no fee. Also, a lot has changed over the past few years in opinions of fasting for health along with TRF/E and the knowledge that many do best when they aren't spiking insulin by eating continually during their waking hours. If I were in dire straights with T2D, I would do well by enrolling in the fasting method. The fees would be well spent. I hope they will continue to maintain a no fee area of information, as I've found it very helpful.

Blog is still accessible.

Since so many follow Dr. Fung directly with his emails, FB and many, many podcast interviews and talks on DietDoctor and elsewhere, I haven't updated this in months. Today's email had a link to a long-format one hour interview with an NPR host who has been fasting himself (and worried he's lost too much!):

"In Conversation with Dr. Fung
Catch this podcast from WAMC!

This week, Dr. Fung was featured on WAMC’s Alan Chartock In Conversation With, tackling Intermittent Fasting and type 2 Diabetes. Don’t miss the podcast, hosted by Northeast Public Radio in NY.

He's also been back on the LowCarbMD podcasts with an update on his new services."

In reading Dr Fung's diet plan, he allows fruits - for example.

So my question is - does IF depend upon a low carb program to be effective - or can you eat anything at all as Dr Fung seems to suggest.

Just confusedabout Dr Fung's message