New Paradigm For Insulin Resistance

[Brunneria]

This is an interesting one too!

 

[Indy51]

This is an interesting one too!

The part of the video relevant to this discussion starts at around 1hr 4mins into the lecture and the paper he references is well worth reading: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082845/

My takeaway from the paper was that overnutrition is the root cause of typical Type 2 and all the metabolic consequences including insulin resistance flow on from that.

My eyes still glaze over when I try to work out those metabolic pathways though

 

[ickihun]

Th

I feel diabetes type 2 is the creation of the wrong 'fat' cells and how those cells reject insulin.
Insulin resistance is due to those fat cells not being processed, everytime as only the right 'fat' cell can be accessed.
The more wrong cells, the more insulin resistant. Has dr fung or anyone explored the wrong fat cell theory?
I'm sorry if I'm dum but this theory feels right to me.
Carb intolerance causes the wrong fat cell but in reducing carbs it reduces the amount of wrong fat cells being made.
Total conversion only possible when more good fat cells more than bad fat cells which need killing off in the body asap.
Low bad fat cells will cure type 2 diabetes.
Empty bad fat cells still confuse insulin.

That is why only some type 2s put it in good remission @KevinPotts or reverse their diabetes. I feel you are a prime example of a person with empty 'bad/wrong' fat cells. If I am right they could eradicate your empty bad fat cells leaving you cured. I sincerely believe that.
I hope one day I'm proven right and you are one of the first to be cured. Your efforts lately are commendable.
Do you also agree?
Do you think this theory explains your body and system?

 

[KevinPotts]

Th

That is why only some type 2s put it in good remission @KevinPotts or reverse their diabetes. I feel you are a prime example of a person with empty 'bad/wrong' fat cells. If I am right they could eradicate your empty bad fat cells leaving you cured. I sincerely believe that.
I hope one day I'm proven right and you are one of the first to be cured. Your efforts lately are commendable.
Do you also agree?
Do you think this theory explains your body and system?

From my fairly extensive reading and studying over the last 5 months it seems that the prevailing consensus is that many of us with T2 can improve their insulin sensitivity (some very significantly, some less so) primarily via a regime of lowering carbs, exercise and for some IF

 

[ickihun]

We can definitely grow more fat cells. But it only happens when our original fat cells are full. So it takes a level of obesity before the body says 'yikes, my existing fat stores are full, I had better make more cells to cope.'

This is one of the reasons why it is so much more difficult for obese people to slim down and stay slim than for slightly overweight people to slim down and stay slim.

Once your body has created these extra fat cells, they are likely to be there for a very long time. They don't pop out of existence if we lose weight. And the body keeps them functioning, so expects to have fat stores in them... What effectively happens, is that once you have created extra fat cells, then your body re-sets its 'normal' fat storage levels higher, and will fight to maintain that level.

So losing weight below that level becomes more challenging, because our own body is trying to bounce us back up to the 'normal' it likes. This is one of the reasons why rebound weight gain is so common.

Just had a thought. Overweight people (people with more fat cells) need to produce more Insulin. Deemed insulin resistant because they are producing more insulin but its not enough for the fat cells. Empty fat cells might be why diabetes cannot process the insulin. Maybe only fat cells with something in them can be converted to energy. Or carb making fat in cells cannot be processed?
Which backs up my theory of good fat eaten in lchf diet can replace bad fat in cells.
But what empties or kills carb fat not good fat?
Ultimately I believe its the cell which needs killing off not its contents per say.
Fat cells around the pancreas was named as the culprit some months ago. I'll take that further and say its the fat cells which need killing off and not recreated thereafter to cure diabetes.
Good fat cells keep diabetes at bay. That is why some people obese are diabetc and others arent. Maybe?

 

[ickihun]

Briefly (and it a while since I checked) I think it went something like:

1. Before bariatric surgery, need to shrink the liver. [So you can find the stomach.]
2. Crash diet - very low calorie - seems to do this
3. Hang on - some people reversing T2 before the surgery

Followed by a study into why this unexpected thing happened.

So it appears that a crash VLC diet targets the liver above general body fat. So in turn this means that this may be more effective than a slow reduction (if your viscera doggedly hang onto their layer of fat). Then again RT now says that the total loss is more important than the speed of loss. Go figure.

I absolutely totally agree. I thought as much myself.

 

[ickihun]

From my fairly extensive reading and studying over the last 5 months it seems that the prevailing consensus is that many of us with T2 can improve their insulin sensitivity (some very significantly, some less so) primarily via a regime of lowering carbs, exercise and for some IF

Yes increase sensitivity but not cure diabetes.
I feel you are closer than most to a cure and fat cells filled with good fat might be the key but bad fat cells need to be destroyed too.

 

[Lamont D]

Just had a thought. Overweight people (people with more fat cells) need to produce more Insulin. Deemed insulin resistant because they are producing more insulin but its not enough for the fat cells. Empty fat cells might be why diabetes cannot process the insulin. Maybe only fat cells with something in them can be converted to energy. Or carb making fat in cells cannot be processed?
Which backs up my theory of good fat eaten in lchf diet can replace bad fat in cells.
But what empties or kills carb fat not good fat?
Ultimately I believe its the cell which needs killing off not its contents per say.
Fat cells around the pancreas was named as the culprit some months ago. I'll take that further and say its the fat cells which need killing off and not recreated thereafter to cure diabetes.
Good fat cells keep diabetes at bay. That is why some people obese are diabetc and others arent. Maybe?

Maybe, yes!
But more likely a combination of different factors.
As someone who has been very obese and lost a lot because of very low carb and not producing excess insulin. (That is my cause of obesity!, insulin!)
The gut flora bacteria, how much, as well as insulin, hormone imbalance, insulin resistance and our own individual cells that can or cannot help our food processing. There are many different factors including fat threshold, how much food, how many calories we actually need, how much fat, minerals and not forgetting water, to get through one day, and what exercise you use, daily!
Our lifestyle, environment, not forgetting what has been handed down from our parents.

I think you could pick a lot more, if you wanted to!

Maybe?

Maybe, it's a lottery, and if you get T2, T1, etc! Then that's it!

But, why did I pick RH?

And why didn't my medical people recognise it?

 

[phoenix]

Just had a thought. Overweight people (people with more fat cells) need to produce more Insulin. Deemed insulin resistant because they are producing more insulin but its not enough for the fat cells. Empty fat cells might be why diabetes cannot process the insulin. Maybe only fat cells with something in them can be converted to energy. Or carb making fat in cells cannot be processed?
Which backs up my theory of good fat eaten in lchf diet can replace bad fat in cells.
But what empties or kills carb fat not good fat?
Ultimately I believe its the cell which needs killing off not its contents per say.
Fat cells around the pancreas was named as the culprit some months ago. I'll take that further and say its the fat cells which need killing off and not recreated thereafter to cure diabetes.
Good fat cells keep diabetes at bay. That is why some people obese are diabetc and others arent. Maybe?

If you had lots of fat cells or large fat cells then according to the 'fat overflow' theory you wouldn't become insulin resistant; fat cells are where fat is meant to be. Some people have far fewer fat cells than others and become diabetic at relatively low BM1s (indeed there are some rare conditions where people can't store fat but are diabetic because all fat ends up where it shouldn't be and the body reacts accordingly ) this applies to one of the para olympic cyclists http://www.bbc.com/news/health-22903537 )
I'm not going to try to explain I'll leave it to a specialist ( I've chopped it a bit but think I've included the main part)

"A commonly investigated and plausible theory implies, that the fatness itself manifests in triglycerides, put into the small intracellular droplets is biologically inert, irrespective of where it's deposited, whether in the adipocytes of the adipose tissue in the hip or thigh region or in the liver cells. Fatty acids stored as triglyceride in cells is basically a way of storing energy for the future use and is a mechanism used for this purpose by most living organisms. And, and for many of them, essential for survival. For example, for those living in the Arctic or Antarctic areas, and for hibernating animals and migrating birds. [COUGH]

What matters in relation to diabetes risk is according to that theory, the capacity to store the triglycerides determined by size of the cellular droplets and the number of fat cells. And hence, the expandability of the fat stores. The peripheral subcutaneous adipose tissue, especially around the hips and the thighs, is considered the primary fat storage site. At any point in time, there is, for each individual an upper limit to how much fat that can be stored in the depot. Then the filling of the interabdominal depots and subsequently the position outside of adipose tissue is a consequence of continuous loading of the body with fat, in spite of the four primary stores in the periphery. (snip)

When the cells become full of as much fat they can hold, and there is obviously an upper limit for the cells, they become dysfunctional. When fatty acids cannot be easily used as fuel in the body and in the metabolism, or be deposited as reserve energy and triglyceride in the fat cells , the accumulation of free fatty acids and also, mono and diglyceride takes place. These compounds are toxic and the so called state of lipotoxicity develops, this initiates inflammatory signalling from the cells as if they were foreign bodies and they may die; so called apoptosis and they may initiate local inflammation and formation of collagen networks around the cells, like the fibrosis occurring in other inflamed tissues. The state of lipotoxicity and inflammatory process and signals make the cells insulin resistant, which in this context may be seen as a defence mechanism since insulin blocks the release of fat from the cells so-called lipolysis and stimulates formation of fat from glucose in the cells so-called lipogenesis. If the process continues, the insulin resistance leads to impaired glucose tolerance and eventually diabetes. The process may also effect the beta cells in the pancreatic islets, and thereby impede their ability to respond to increased needs of insulin to overcome the insulin resistance and to maintain glucose homeostasis.
Assuming this theory to be true, it nicely explains how diabetes is related to overweight and obesity. To apply this theory however, we need to assume that there are considerable individual differences in the fat storage capacity. The greater BMI is associated with increased risk of diabetes is explained by the increasing likelihood that the greater the fat mass, the more people have used those capacity for storage of fat. Thus paving the way to insulin resistance by continuous fat overloading. It also explains why only some of the people with a high BMI get diabetes. Those who don't get diabetes have not filled their fat depots up to the limits and hence have not reached the step that elicits the processes that induces insulin resistance.

Thorkild I A Sorensen, Professor of Metabolic and Clinical Epidemiology Faculty of Health and Medical Sciences, University of Copenhagen Global Diabetes, Coursera

 

[Indy51]

I thought I remembered a topic with this title - Dr Fung has just published a blogpost with the exact same title

https://intensivedietarymanagement.com/the-central-paradox-t2d-23/

 

[ickihun]

I thought I remembered a topic with this title - Dr Fung has just published a blogpost with the exact same title

https://intensivedietarymanagement.com/the-central-paradox-t2d-23/

What I take from that is lchf and IF are just treating the symptoms not the cause. Like insulin injections for some type 2s who are still producing their own.
I have regulated high bgs when I forget to take my insulin. I have no first response and then my body caps my high bgs to 14 -15mmol/l max. Why is my high bgs being capped?
Is that what circulating insulin is waiting for. Emergency resource incase of needing a cap to protect the brain and other organs from ketosis. Type 1s produce no insulin but type 2s do. Is that insulin being stored for an emergency/shock/stress mechanism? Does the fight or flight theory hold the answer?

 

[lindisfel]

I don't think ickyhun there is a cure for some of us, particularly those of us with a delayed or missing initial insulin response. Like many medical interventions and dietary ones, we are just compensating for the complex and individual ways this marvellous chemical factory of the human body works.For some of us carbs are poison. D.

 

[kokhongw]

I thought I remembered a topic with this title - Dr Fung has just published a blogpost with the exact same title

https://intensivedietarymanagement.com/the-central-paradox-t2d-23/

His proposed model even if it doesn't explain everyting seems to work better by lowering circulating insulin than the conventional model of lock and key which continue to force more insulin into the system.

But I am looking forward to the new research on FGF1 protein which holds the promise of improving/restoring insulin signaling.

 

[Lamont D]

What I take from that is lchf and IF are just treating the symptoms not the cause. Like insulin injections for some type 2s who are still producing their own.
I have regulated high bgs when I forget to take my insulin. I have no first response and then my body caps my high bgs to 14 -15mmol/l max. Why is my high bgs being capped?
Is that what circulating insulin is waiting for. Emergency resource incase of needing a cap to protect the brain and other organs from ketosis. Type 1s produce no insulin but type 2s do. Is that insulin being stored for an emergency/shock/stress mechanism? Does the fight or flight theory hold the answer?

Hi,
Do we fast or very low carb to treat the symptoms or the cause of either high insulin or insulin resistance?
The problem is to stop the symptoms, you reduce your low carb enough to reduce your initial and secondary insulin response., which reduces both insulin production and converts your energy from carbs to muscle fat, hence ketosis.
As usual it's a lot more complicated than that but reduction of insulin resistance is paramount to being healthy.
By stopping insulin production and insulin resistance your body reduces the high glucose in your blood as well. Your body works better.
By doing both fasting and low carbing, your body can cope better with its metabolic condition. You are treating the cause and the effect.
If like me, the cause is unknown as well as the cure, if something like fasting and low carb works and you feel as good as I do, then the whys and how's, negate the need to find the answers. Sometimes you just need to move on and live your life.
I have accepted that a lot of food is poisonous to me because my tolerance to them is really bad. So I avoid them.
As in exercise, if I avoid strenuous exercise and do moderate exercise, the same cause and effect as eating carbs happens. Once the trigger, is switched on, my pancreas goes into overdrive and insulin floods my blood.
Insulinoma and hyperinsulinaemia can be the precursor to prediabetes and T2.
If this is found to be the cause, why is it not tested for more often?
Hormone imbalance, is still not really understood, that's why the whys and how's are still in debate and not understood.
You, like me have to find our own way with how we deal with our conditions.
Best wishes.