Insulin resistance - Dr Jason Fung's video (again)

[Just-a-little-prick]

Today (07/08/2023) Dr Fung's video on insulin resistance has been aired yet again. I have two negative responses. 1] He incorrectly states, more than once, "Too much insulin causes insulin resistance". 2] He refers, more than once, only to Type II diabetes.
But Type I diabetics also can suffer from insulin resistance - I'm one of them. The only reason that I inject more insulin is because my body is increasingly resistant to it - the opposite of this doctor's concept. To be specific, I currently have to inject around 140 units total per day (basal + fast acting Humalog). Most of it is wasted. My current HBA1c is 6.5, so I have good control. I am 84 years old, late onset for 30 years.
I believe, from my knowledge and research, that Dr Fung's video is misleading. Research is clear - the recognition of pre-diabetic insulin resistance by GPs is the key to prevention of diabetes, especially Type II. The immediate physical evidence is the presence of a 'beer belly' - which, of course is an old wive's tale, it is actually now known to be caused by the deposit of fats that results from the inabilty of food to be transferred into the cells, because of insulin resistance. This fat deposit cannot be dieted away - Dr Fung's view is wrong.
Obviously there is always a relationship between food quality & quantity - but there is also a limit below which you cannot go, especially if your body is not able to fully use what you eat, because of ineffective insulin usage.
Any chance of Dr Fung clarifying his views on this forum, and with particular and specific reference to Type I?

 

[catinahat]

Too much insulin causes insulin resistance". 2] He refers, more than once, only to Type II diabetes.

The reason he probably refers to T2 is because if you have T2 you are definitely insulin resistant.
T2 is insulin resistance, our bodies resist the action of our insulin, our blood sugar remains higher than it should be so our pancreas is forced to produce more insulin just to get the blood sugar into normal range.
There are many theories on what causes insulin resistance, a popular one often repeated by the media is that it's caused by fat, so by eating the same diet as everyone else we have caused our own problems. What about the 10% of T2's who are not overweight, well they must be thin on the outside but fat on the inside, or perhaps Dr Jason Fung's idea could make sense.
Insulin resistance causes our pancreas to produce more and more of the fat storage hormone insulin. Our insulin struggles to make the glucose available for our bodies to use for energy so it has no option but to store it as fat, the high levels of insulin and the storage of fat makes us even more resistant to insulin.
High carb diet = high blood sugar= high insulin levels = fat storage and insulin resistance
Dr Jason Fung's solution is to combine intermittent fasting with a low carb diet. When we fast the stores of glucose get used up first, when that's reduced our pancreas can take a break from churning out insulin so as our sugar levels fall so does our insulin levels, without the presence of the fat storage hormone we can now use our fat stores for fuel.
Fasting + low carb = low blood sugar= low insulin= fat burning+ improving insulin resistance
Now T1's who don't have any functioning beta cells obviously have their own set of problems and I don't think Dr Jason Fung's books or videos are particularly aimed at T1's being mainly about obesity and insulin resistance. Although having T1 will not mean you are immune from insulin resistance. Whatever has caused me to become resistant to insulin can affect anyone else and I would have thought that the same principles apply.
High carb diet = high blood sugar= a higher insulin requirement
Lower carb. = Lower blood sugar= less insulin required

 

[jonathan183]

My understanding ...
Working beta cells in pancreas produce insulin, acts on alpha cells to reduce glucagon production, remaining insulin down portal vein to liver and reduces glucose production, what's left goes to general circulation and rest of the body.

Type 1 no/low insulin from beta cells in pancreas due to destruction. Insulin injected into fat, gets into general circulation, from there some gets to the liver and some gets to the pancreas. The insulin starts in the wrong place so will be at a higher level in the general circulation. You will have more insulin in the general circulation to get the same effect on the liver and alpha cells in the pancreas

 

[Just-a-little-prick]

The reason he probably refers to T2 is because if you have T2 you are definitely insulin resistant.
T2 is insulin resistance, our bodies resist the action of our insulin, our blood sugar remains higher than it should be so our pancreas is forced to produce more insulin just to get the blood sugar into normal range.
There are many theories on what causes insulin resistance, a popular one often repeated by the media is that it's caused by fat, so by eating the same diet as everyone else we have caused our own problems. What about the 10% of T2's who are not overweight, well they must be thin on the outside but fat on the inside, or perhaps Dr Jason Fung's idea could make sense.
Insulin resistance causes our pancreas to produce more and more of the fat storage hormone insulin. Our insulin struggles to make the glucose available for our bodies to use for energy so it has no option but to store it as fat, the high levels of insulin and the storage of fat makes us even more resistant to insulin.
High carb diet = high blood sugar= high insulin levels = fat storage and insulin resistance
Dr Jason Fung's solution is to combine intermittent fasting with a low carb diet. When we fast the stores of glucose get used up first, when that's reduced our pancreas can take a break from churning out insulin so as our sugar levels fall so does our insulin levels, without the presence of the fat storage hormone we can now use our fat stores for fuel.
Fasting + low carb = low blood sugar= low insulin= fat burning+ improving insulin resistance
Now T1's who don't have any functioning beta cells obviously have their own set of problems and I don't think Dr Jason Fung's books or videos are particularly aimed at T1's being mainly about obesity and insulin resistance. Although having T1 will not mean you are immune from insulin resistance. Whatever has caused me to become resistant to insulin can affect anyone else and I would have thought that the same principles apply.
High carb diet = high blood sugar= a higher insulin requirement
Lower carb. = Lower blood sugar= less insulin required

I really appreciate your well-considered reply to my post, Cat. Thank you. You have some interesting concepts - though I don't agree with all of them.
I can see that my complaint about Dr Fung's video starts with the headline that it is about 'Insulin Resistance'. More correctly it should be 'Insulin resistance in Type 2 diabetes', perhaps. Because - as you say in your final para - "Type 1's have their own set of problems". You have summed up my complaint very well!
Maybe it would be interesting to address a couple of your points though, even if they do apply specifically to Type 2.
For example, you say "if you have T2 you are definitely insulin resistant". I don't think that follows. The treatment of Type 2, such as dietary control and Metformin, are based merely on your pancreas not producing sufficient insulin for your body's needs. You may be resistant too, of course, and that's why I made the observation about the current need for GPs to spot the signs of pre-diabetes. But it is not universal, surely?
You refer to insulin as "the fat storage hormone". That's an interesting concept - but a bit of a stretch! At best it is a description of the consequences of poor blood sugar control. It is not the normal function of the hormone.
Your concept of "fasting + low carb" (ie.'dieting') as a strategy is also not borne out by research studies. Fat deposited on the inner stomach wall as a consequence of insulin resistance is not responsive to dieting. This is one of the unexplained and unknown factors of insulin resistance.
Which leaves us with the - in my opinion and experience - incorrect explanation, which you also quote, that the resistance is "caused by fat". Dr. Fang certainly appears to support this theory. But it makes no sense. The fat does not come first, take it from me - it is a consequence of the resistance in your body's functioning. What causes that has not been identified, to my knowledge.
My fundamental complaint/problem remains - I can find no research, much less explanatory videos from any doc, which provide any answers for Type 1 diabetics, who produce no insulin, are well balanced and controlled by calculated insulin injections, and yet can still (like me) have serious problems arising from the onset of insulin resistance. I wish that Dr Fang would address this.

 

[Just-a-little-prick]

My understanding ...
Working beta cells in pancreas produce insulin, acts on alpha cells to reduce glucagon production, remaining insulin down portal vein to liver and reduces glucose production, what's left goes to general circulation and rest of the body.

Type 1 no/low insulin from beta cells in pancreas due to destruction. Insulin injected into fat, gets into general circulation, from there some gets to the liver and some gets to the pancreas. The insulin starts in the wrong place so will be at a higher level in the general circulation. You will have more insulin in the general circulation to get the same effect on the liver and alpha cells in the pancreas

Thanks, Jonathan - I can understand your explanation that the insulin 'starts in the wrong place' because it is injected into the outer skin (not, to be fair, necessarily into 'fat'). I don't think that "some gets to the pancreas" is part of the physiology, though. My pancreas, like most Type 1's, is non-functioning after all these years.
Certainly, therefore, there may be 'a higher level of insulin in the general circulation' if it is injected externally, and not produced naturally. But that is not an explanation for insulin resistance - sorry. In my own case, as an example, I still maintain an excellent HBA1c reading every time - but I am injecting more than double the amount of insulin that I used to.

 

[jonathan183]

My pancreas, like most Type 1's, is non-functioning after all these years.

alpha cells producing glucagon still function ... beta cells which would produce insulin killed by immune system

 

[catinahat]

For example, you say "if you have T2 you are definitely insulin resistant". I don't think that follows. The treatment of Type 2, such as dietary control and Metformin, are based merely on your pancreas not producing sufficient insulin for your body's needs

Most if not all newly diagnosed T2's have high insulin levels and high blood sugar levels, if they did not have insulin resistance that extra insulin would cause low blood sugar.
It's a pity Dr's don't do a c peptide test as a general health screening. The potential for pre and T2 would be picked up long before high blood sugar became a problem

Copied from herehttps://my.clevelandclinic.org/health/diseases/24178-hyperinsulinemia

In most cases, hyperinsulinemia results from insulin resistance, which happens when cells in your muscles, fat and liver don’t respond as they should to insulin. The development of insulin resistance typically increases insulin production (hyperinsulinemia) so that your body can maintain healthy blood sugar levels

Chronic insulin resistance and hyperinsulinemia can result in chronic high blood sugar (hyperglycemia), which leads to prediabetes and Type 2 diabetes.

You refer to insulin as "the fat storage hormone". That's an interesting concept - but a bit of a stretch! At best it is a description of the consequences of poor blood sugar control. It is not the normal function of the hormone.

Copied from here https://www.nuvidarx.com/blog/why-insulin-is-called-the-fat-storage-hormone

How does insulin store fat?​

If your body works correctly, insulin is a significant hormone that controls your blood sugar and gives you the energy you need to survive and function.

However, when your diet is high in carbohydrates or simple sugars, it increases your blood glucose levels. Because your cells can only absorb so much glucose, the excess has to go somewhere so your blood sugar returns to normal levels.

When too much glucose is circulating in your blood, insulin pushes the excess into your fat cells, muscles, and liver and stores it as fat. But why fat