Squire Fulwood
Expert
I've been doing a lot of reading about insulin resistance. I'm not a scientist so it's hard going but I'm getting the gist. I think that IR underlies a lot of the weight issues in our society.
So do I.
I've been doing a lot of reading about insulin resistance. I'm not a scientist so it's hard going but I'm getting the gist. I think that IR underlies a lot of the weight issues in our society.
That's very true. I don't normally have IR, and my insulin production is relatively mildly impaired, but in my last two pregnancies I developed IR. Both times once the pregnancy was over the IR apparently vanished, but I do wonder about scarring and whether I'm now more vulnerable to IR.But (as I'm sure you have already read) there are other things that increase insulin resistance as well as a fatty liver. These include subcutaneous fat, hormone conditions (eg PCOS) and some drugs. There are probably more.
Plus there is also the question of scarring.
Me too.
And I'm intimately acquainted with IR.
But (as I'm sure you have already read) there are other things that increase insulin resistance as well as a fatty liver. These include subcutaneous fat, hormone conditions (eg PCOS) and some drugs. There are probably more.
Plus there is also the question of scarring.
I was surprised to read this when I came across it, but now it seems perfectly obvious... A liver isn't designed to get fat and then defat. And rather like alcoholic cirrhosis of the liver, scars can develop in the liver. These scars can inhibit normal function.
So there is no guarantee that defattifying will restore normal liver function, or that it is even possible to get beneath the personal fat threshold, because the personal fat threshold changes over time, depending on many things, including age, liver scarring, fitness level, and all those other IR generating factors.
It's a hugely complex issue, and sadly it all boils down to the individual's body and lifestyle and environment, much of which is unquantifiable. Even if a person defats and 'reverses' their T2 at 40, and keeps the weight off, there is no guarantee they won't get the symptoms of D back, years later, as their PFT shifts downwards with age.
So it's unpredictable, variable and very frustrating!
That's very true. I don't normally have IR, and my insulin production is relatively mildly impaired, but in my last two pregnancies I developed IR. Both times once the pregnancy was over the IR apparently vanished, but I do wonder about scarring and whether I'm now more vulnerable to IR.
Unpredictable, variable and frustrating is about right!
Kate
What is the body defending against?Just a thought.
I posted this on another thread, but it definitely relates to this one too as it investigates why different people respond differently to fasting/calorie reduction: http://www.sciencedaily.com/releases/2015/05/150511162918.htm
I really think a lifetime of yo-yo dieting can screw up our metabolism big time![]()
I think one of the mysteries is what really happens to insulin levels when BG rises. We take a rise in BG as a proxy/clue for insulin levels but who knows what's really going on? The models are based on "normal" people. (and mice.) They make it sound as if the body works brilliantly - you eat something and the body produces just the right amount of insulin and it all works perfectly. So you "should" be able to lose weight if you cut calories. Well, why do the experts think that people with metabolic issues follow their models?
Suppose as a result of eating sugary type carbs my body produces MORE insulin than it needs to clear the BG. Then I'm hungry again very quickly. Or, maybe my IR is preventing the glucose from getting into the cells...still hungry.
So many unknowns.
http://care.diabetesjournals.org/content/16/1/369.abstractWe estimated that the traditional Pima diet, although seasonably variable, was ∼ 70–80% carbohydrate, 8–12% fat, and 12–18% protein
"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 signaling from the cells as if they were foreign bodies They may die so called apoptosis and they made they initiate local inflammation and the 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 tthe cells insulin resistant, which in this context may be seen as a defense mechanism since insulin blocks the release of fat from the cells"
The process may also effect the beta cells in the pancreatic islets, and thereby impede their ability to respond to increase 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.
That 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 high BMI get diabetes. Those who don't get diabetes are not filled their fat depots up to the limits and hence have not reached the step that elicit the processes that induce insulin resistance..................... On the other hand, the theory explains why some people with normal or even low BMI may run an increased risk of diabetes. They have a small capacity to store fat, they may essentially fill up the stores and initiate the processes leading to insulin resistance. In the most extreme cases, this is seen in patients with lipodystrophy, where the adipose tissue does not work properly for various reasons, such as genetic disorders or side effects to some drugs
re the Kendrick article
The reasons why the Pima in the US have high rates of diabetes and obesity have been the subject of study for decades.
Importantly, the Pima as a "race" do not have high rates of diabetes, only those that are in the reservations of the US.
Their genetically identical cousins in the Sierra Mardre mountains in Mexico are not overweight and don't have a diabetes problem. They continue to eat nearer to their traditional diet (which was very high carb/fibre and much lower in fat) The diet eaten in the US reservations was very different, energy dense and nutrient poor.
There are other factors involved Far too much to go into here but this website gives a lot of information http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm
traditional diet of the Pima ie in the 19th century pre diabetes
http://care.diabetesjournals.org/content/16/1/369.abstract
re fat cells and people who don't have any.ie generalised lipodystrophy’
. The current hypothesis accepted by many researchers is similar to Dr Kendrick's explanation. The difference as he says is in the order but there is a lot more to it than he suggests.
Fat is meant to stay in adipose cells ie fat cells. That's what they are for. That's the case with the very fat Sumo or even the many people who are overweight but not diabetic.
It's when they overspill that problems arrive
Rather than explain I will quote because it's hard to summarise any more than this.
The body doesn't want that fat to overflow and be deposited elsewhere in the liver or around the pancreas because that leads to further problems .
Thorkild I A Sorensen, Professor of Metabolic and Clinical Epidemiology Faculty of Health and Medical Sciences, University of Copenhagen.( part of lecture from Coursera Global diabetes course)
This is very much the theory behind Dr Taylors research. He has been able to produce images of fat deposited around the liver and pancreas. When this is reduced and fat is back to where it should be in the fat cells then people become less insulin resistant.Just as above he suggests that people have their own individual fat thresholds.
Primer on fat storage http://science.howstuffworks.com/life/cellular-microscopic/fat-cell2.htm
re the Kendrick article
The reasons why the Pima in the US have high rates of diabetes and obesity have been the subject of study for decades.
Importantly, the Pima as a "race" do not have high rates of diabetes, only those that are in the reservations of the US.
Their genetically identical cousins in the Sierra Mardre mountains in Mexico are not overweight and don't have a diabetes problem. They continue to eat nearer to their traditional diet (which was very high carb/fibre and much lower in fat) The diet eaten in the US reservations was very different, energy dense and nutrient poor.
There are other factors involved Far too much to go into here but this website gives a lot of information http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm
traditional diet of the Pima ie in the 19th century pre diabetes
http://care.diabetesjournals.org/content/16/1/369.abstract
re fat cells and people who don't have any.ie generalised lipodystrophy’
. The current hypothesis accepted by many researchers is similar to Dr Kendrick's explanation. The difference as he says is in the order but there is a lot more to it than he suggests.
Fat is meant to stay in adipose cells ie fat cells. That's what they are for. That's the case with the very fat Sumo or even the many people who are overweight but not diabetic.
It's when they overspill that problems arrive
Rather than explain I will quote because it's hard to summarise any more than this.
The body doesn't want that fat to overflow and be deposited elsewhere in the liver or around the pancreas because that leads to further problems .
Thorkild I A Sorensen, Professor of Metabolic and Clinical Epidemiology Faculty of Health and Medical Sciences, University of Copenhagen.( part of lecture from Coursera Global diabetes course)
This is very much the theory behind Dr Taylors research. He has been able to produce images of fat deposited around the liver and pancreas. When this is reduced and fat is back to where it should be in the fat cells then people become less insulin resistant.Just as above he suggests that people have their own individual fat thresholds.
Primer on fat storage http://science.howstuffworks.com/life/cellular-microscopic/fat-cell2.htm
Bmi is not really a good indicator of diabetes risk, it is what kind of fat that you have, how much of it, and where it is stored that is important.This is a realy interesting thread... Are there any accounts regarding India's high number of Diabetics.??
The fat overspill theory is a simple answer that accounts for this ; groups with certain genetics have fewer fat cells but you probably have to go beyond genetics. There are many factors that may play a part.Heres one researches ideas http://www.hindawi.com/journals/ije/2014/593982/This is a realy interesting thread... Are there any accounts regarding India's high number of Diabetics.??