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What do you think about this specific sentence I read on a blog post, I want your guys opinions on this.
- Thread starter Ali Akin
- Start Date
Resurgam
Master
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- Type of diabetes
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- Diet only
As type 2s don't generally get any testing of their insulin resistance and don't have a DNA analysis done at diagnosis, such statements are as trustworthy as saturated fat is a killer and smoking helps to clear the lungs.
Well said man you are totally right, he is giving dangerous advice to people telling them if they don’t have the genes for diabetes they can go crazy and gain as much weight as you want and you will never get diabetes. Unfortunately that’s not how it works, genes may make a person more likely to get type 2 diabetes but they don’t actually cause the disease, the actual disease. This guy also says other very ridiculous things about cholesterol and also one more thing he says this: “People without the genes for insulin resistance have a1c of 25 to 30, and if you are above 30 you have pretty bad insulin resistance”. Then he says “oh I have 500 pound Paitents with a1c 25, so they don’t even have a lick of insulin resistance”. He even admitted in an interview he doesn’t check fasting insulin levels for such Paitents as he thinks there is no way they have insulin resistance having an a1c of 25. Unfortunately that’s not how it works you can have a low a1c like this kept by Sky High levels of insulin. He’s a cardiologist not an endocrinologist and is not qualified to be saying such things, he is making things up. And oh one last thing: he says that a1c of 25 to 30 is in people without the genes for insulin resistance and he said this is proved in studies, I have yet to see a study on this.
You stated that the extract is from a blog. I believe that saying something on a blog is an opinion not advice, and should not be considered as such.
Well the question is what do you think about this opinion then? I mean it’s an opinion not a fact, an opinion isn’t a fact.
Chris24Main
Well-Known Member
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- I reversed my Type 2
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So, here then is a fact.
Everyone goes through a period of insulin resistance at least once in their lives. You, @Ali Akin have just come through it, it's called puberty. You have to overcome insulin's control of energy in order to grow at the rate needed. Pregnancy is another such period, which is why gestational diabetes is a thing. (for some people, according to their genetic disposition and gene expression via epigenetics, and environmental impact on that)
If it was as simple as "having the genes for it" - then you would expect out of a population, some would go through puberty and some would be stuck in childhood. Maybe that's correct, but my opinion is that it's unlikely.
The problem with insulin resistance, is that it's complicated. Every cell in your body has an interaction with insulin, and insulin has over 100 jobs to do throughout your body. Dealing with blood glucose is only the best-known effect, and even that has wildly different effects on different tissue types. Then - there are large numbers of processes that drive insulin resistance at the cellular level that have nothing to do with glucose. Fructose (and it's cousin, alcohol) will directly drive insulin resistance in visceral adipose tissue by causing the mass production of ROS and cytokines due to hypertrophy - and the effect of that is the meta increase in insulin resistance around the body (simply requiring more of a thing to do the same job) - you have to understand the effects at cellular, organic and whole-body level. I've been studying hard on this all year, and only know that I know very little.
However - my solid opinion is that anyone who suggests that there is a "gene" for dealing with insulin resistance, firstly doesn't understand anything about genetic expression and how translation factors work, or anything about epigenetics at all, because it's such a reductive over-simplification that it's practically meaningless. And that's before you consider how unlikely it is that we evolved a genetic switch to flip something as fiendishly complicated (and necessary) as all the things that insulin does.
But - as humans - we like a simple story, especially a simple story that sound convincing - and that's really what the sentence you stared with is - it's just very out of date, and lacking in understanding of genetics and insulin resistance.
Everyone goes through a period of insulin resistance at least once in their lives. You, @Ali Akin have just come through it, it's called puberty. You have to overcome insulin's control of energy in order to grow at the rate needed. Pregnancy is another such period, which is why gestational diabetes is a thing. (for some people, according to their genetic disposition and gene expression via epigenetics, and environmental impact on that)
If it was as simple as "having the genes for it" - then you would expect out of a population, some would go through puberty and some would be stuck in childhood. Maybe that's correct, but my opinion is that it's unlikely.
The problem with insulin resistance, is that it's complicated. Every cell in your body has an interaction with insulin, and insulin has over 100 jobs to do throughout your body. Dealing with blood glucose is only the best-known effect, and even that has wildly different effects on different tissue types. Then - there are large numbers of processes that drive insulin resistance at the cellular level that have nothing to do with glucose. Fructose (and it's cousin, alcohol) will directly drive insulin resistance in visceral adipose tissue by causing the mass production of ROS and cytokines due to hypertrophy - and the effect of that is the meta increase in insulin resistance around the body (simply requiring more of a thing to do the same job) - you have to understand the effects at cellular, organic and whole-body level. I've been studying hard on this all year, and only know that I know very little.
However - my solid opinion is that anyone who suggests that there is a "gene" for dealing with insulin resistance, firstly doesn't understand anything about genetic expression and how translation factors work, or anything about epigenetics at all, because it's such a reductive over-simplification that it's practically meaningless. And that's before you consider how unlikely it is that we evolved a genetic switch to flip something as fiendishly complicated (and necessary) as all the things that insulin does.
But - as humans - we like a simple story, especially a simple story that sound convincing - and that's really what the sentence you stared with is - it's just very out of date, and lacking in understanding of genetics and insulin resistance.
Wow this is an amazing reply, really enjoyed reading it. Thanks for taking the time to write such an amazing masterpiece! It was very informative.
Is this to do with your course work? If it is, you certainly are receiving plenty of useful information.
Nah I just am just involved with this stuff for fun, for my own health. It’s just an interest or mine really.
Chris24Main
Well-Known Member
- Messages
- 1,024
- Type of diabetes
- I reversed my Type 2
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Just try to remember that it's much more than that for many members of this forum. Getting accurate information, and sometimes just basic human encouragement, can make all the difference between just hanging on, and turning this thing around. You will appreciate that it's very much not fun for many on here.
Yea I totally understand man! Just I am very interested in human metabolism and health. I personally had a big health scare with my Liver, it had lots of fat in it, which we know is related in the development of insulin resistance, prediabetes, type 2 diabetes etc. And this problem of Fatty Liver happened at a young age, due to me being obese. Luckily I managed to reverse the fatty liver by just a weight loss of 28kgs. So now like for the rest of my life I want to be careful of my weight and general health, the mantra is if I keep this weight for the rest of my life I will be fine. For me the issue was quite mild so I didn’t cut out carbs I just did a calorie deficit really. But yea I get what you mean totally it wasn’t easy managing my own health issues too, loosing the weight wasn’t easy.
Last edited:
Lamont D
Oracle
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- I do not have diabetes
I do get that. But as @Chris24Main describes it is so complicated and to trawl through the medical jargon to understand it all. For some, it is too much. Opinion of their medical doctors are important in treatment.
I like it simple, then I have the options, to either ignore or follow. Or a version of what is required to improve my future health issues.
When you hear that, you have to do something that you don't believe, that for all your life, is healthy for everyone.
that the best advice from professionals, is to carry on doing so.
Opinions of the uninformed in our treatment is too widespread within our health services.
I had to find my way through it all. The tests that got me my diagnosis, I learned from them, done the science thing, followed the theories and made decisions based on my own personal experience and information gaining the knowledge from good sources and the basis of the people involved.
Plus, someone, on here, who had had issues from young.
The ensuing months of experimentation and recording. Because there was none. Finding about intolerance to food, finding how my body reacts to food. Trusting my judgement, asking questions to my endocrinologist, doing more research, more testing, more experimenting, more recording. Concluding, with the evidence in front of me. Conclusion and my GP confirmed. I'm weird.
We are all different, we are unique, are needs are singular, to stay as healthy for as long as possible. To know your body, it's limitations and the logical way to keep it that way.
I'm seventy soon. My health is very good.
It wouldn't be if I didn't do all that research.
I do believe, that I would have been a sheep with T2.
But I didn't have any other resource but my endocrinologist. And he didn't know everything about my condition.
His opinion was valuable and did change my life dramatically.
I didn't accept the general consensus of how to treat it.
I have said it many times.
When young, it was found I had lactose intolerance.
I was told to stay away from dairy products.
In my diagnosis of Reactive Hypoglycaemia, which I found to be into!enfant to carbs, I was repeatedly told to eat healthy carbs. Why?
Not logical!
Even, with hindsight, my endocrinologist eventually agreed with me. I shouldn't have carbs but my ever revolving door of GP's, still question my decision making. Only one GP, who who was fascinated with my evidence and knowledge, an hour I will never get back.
There is too much not known, opinions sometimes, is what those who don't understand is what we have to go by.
Don't stop learning.
Have an open mind.
Chris24Main
Well-Known Member
- Messages
- 1,024
- Type of diabetes
- I reversed my Type 2
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@Ali Akin - with the proviso that almost everything going on with the body of a 50 odd year old is totally different to someone approaching 20, my starting point was definitely about trying to understand the boundary between fatty liver and insulin resistance and diabetes (clearly T2DM, but I wasn't so clear about even that at the time, I was totally clueless) - but - for what it's worth, let me lay out a year of learning in a paragraph or two - I'm always trying to be conscious that I could be wrong about things, but there is quite a lot that seems to me to be uncontroversial.
The first thing to consider is that non-alcoholic fatty liver is relatively new - up till about a generation ago - all fatty liver was considered to be a consequence of alcohol, and one step towards cirrhosis. Given that the liver uniquely has to metabolise both alcohol and fructose, that's a reasonably big clue right there.
I previously laid out all the ways you need to consider the ways that insulin affects the body - but it's just as useful to totally over-simplify and think of it as being the master arbiter of energy management, and that it's triggered in response to foods that easily break down into glucose - so one of the big ways it manages energy is by clearing out glucose into wherever will have it by any means necessary throughout the body - but since there is a kind of cascade of possibilities, that first means around the liver itself, in large muscles, and fat storage cells (first turning it into thing that can be stored in these places).
Sugars and Starch - too much blood glucose - insulin response - less blood glucose - more glucose around the body, starting around the liver.
As we use energy - glucose being consumed in the cells (not exclusively - the heart runs mainly on fat whatever else is going on, for example, but it's always a special case) it gets replenished, starting from the most easily converted storage, the glycogen in the liver (think animal starch) - of which we typically have about a 24 hour capacity, in the liver and muscles.
So - you end up with a kind of "big bucket - little bucket" concept of the body - we fill up the little bucket fairly quickly if we eat sugars and starches, (the liver, short term storage) and then we have to fill up the big bucket - the rest of the body. When we use energy, we use it from the little bucket.
Almost everything then can be thought of as the answer to this question - what happens when we eat another meal before the little bucket is empty?
Your genetics clearly play a part in the answer, because the answer depends on what the food is, and what your body does with it, but for most of us, the answer is that the little bucket is already full, and we keep topping up the big bucket - and then the big bucket starts to over-fill. For some that means putting on weight, for others T2DM, for others all sorts of inflammatory conditions and brain disorders .. but to explain any of that you have to get much more complicated than "big bucket - little bucket".
However - the body can handle this for a long time, you could be talking about 20 years before you even notice an increase in blood glucose, which is where fructose plays a special part.
In what I understand a flexible metabolism to be, your digestive system is in fairly complex coordination with your fat storage and brain, and you absorb nutrients (mainly from protein and fat together) and store them, and use them, and the liver does the fine tuning, also having a direct line to the brain. In diets dominated by surgars and starches, everything (more or less) goes through the liver and it does all the heavy lifting (as described) - but when you have fructose - that; only the liver can deal with, and it can only turn it into fat and store it locally.
That - cramming of fat into storage around the liver - causes the cells to swell up like balloons (fat storage cells, they are meant to do this and can become really huge, comparatively). This is what visceral fat is, and why apparently thin people can have fatty livers. Although fat cells can cope, the danger comes from their coping mechanisms to this swelling. Firstly, they literally push back - like a balloon. How this happens is quite complicated, but the analogy works - this is direct resistance to insulin, like a balloon gets harder to blow as it gets bigger. Secondly - as it gets bigger, it gets further from blood supply, and starts shouting for more blood vessels closer to it - this is the cytokine response, and is literally chronic inflammation (again, directly - nothing else but that fructose). The third thing is also more complicated, but essentially you have more fuel in the cell than the "fire" needs, so the way that energy is produced is altered - if you think of putting too much wood on the fire, that's close enough, and you get too much smoke (ROS or what used to be called free radicals).
So - all of that is not good - directly causes inflammation and oxidative stress, AND - insulin resistance.
The net effect of this is that fructose acts as a catalyst to the otherwise slow process of insulin resistance building up over time, more insulin causing the "normal" to raise, and that requiring more insulin, becoming less sensitive to the action of insulin, requiring more... and so on. Sugar -table sugar- is of course both glucose and fructose which means that it has both effects at the same time, but having lots of fructose because you believe it to be natural - as I did - is a very bad idea.
The most obvious example of this in food industry is the production of Foi Gras. Literally meaning "fat goose" - it is the ground liver of geese specially fed to have fat livers - and how do they do this - well, it's no secret, you feed them high fructose corn syrup for the last couple of months of their life.
So - that's essentially why - as a teen (therefore never having had the 20 or so years or gradually increasing insulin resistance that typically leads to T2DM) you can still develop a fatty liver.
The good news, is (as you have shown) that your metabolism is so active at that age, that fairly small changes can have big, long-term effects. Those of us figuring this out in our later years have a tougher time of it.
The first thing to consider is that non-alcoholic fatty liver is relatively new - up till about a generation ago - all fatty liver was considered to be a consequence of alcohol, and one step towards cirrhosis. Given that the liver uniquely has to metabolise both alcohol and fructose, that's a reasonably big clue right there.
I previously laid out all the ways you need to consider the ways that insulin affects the body - but it's just as useful to totally over-simplify and think of it as being the master arbiter of energy management, and that it's triggered in response to foods that easily break down into glucose - so one of the big ways it manages energy is by clearing out glucose into wherever will have it by any means necessary throughout the body - but since there is a kind of cascade of possibilities, that first means around the liver itself, in large muscles, and fat storage cells (first turning it into thing that can be stored in these places).
Sugars and Starch - too much blood glucose - insulin response - less blood glucose - more glucose around the body, starting around the liver.
As we use energy - glucose being consumed in the cells (not exclusively - the heart runs mainly on fat whatever else is going on, for example, but it's always a special case) it gets replenished, starting from the most easily converted storage, the glycogen in the liver (think animal starch) - of which we typically have about a 24 hour capacity, in the liver and muscles.
So - you end up with a kind of "big bucket - little bucket" concept of the body - we fill up the little bucket fairly quickly if we eat sugars and starches, (the liver, short term storage) and then we have to fill up the big bucket - the rest of the body. When we use energy, we use it from the little bucket.
Almost everything then can be thought of as the answer to this question - what happens when we eat another meal before the little bucket is empty?
Your genetics clearly play a part in the answer, because the answer depends on what the food is, and what your body does with it, but for most of us, the answer is that the little bucket is already full, and we keep topping up the big bucket - and then the big bucket starts to over-fill. For some that means putting on weight, for others T2DM, for others all sorts of inflammatory conditions and brain disorders .. but to explain any of that you have to get much more complicated than "big bucket - little bucket".
However - the body can handle this for a long time, you could be talking about 20 years before you even notice an increase in blood glucose, which is where fructose plays a special part.
In what I understand a flexible metabolism to be, your digestive system is in fairly complex coordination with your fat storage and brain, and you absorb nutrients (mainly from protein and fat together) and store them, and use them, and the liver does the fine tuning, also having a direct line to the brain. In diets dominated by surgars and starches, everything (more or less) goes through the liver and it does all the heavy lifting (as described) - but when you have fructose - that; only the liver can deal with, and it can only turn it into fat and store it locally.
That - cramming of fat into storage around the liver - causes the cells to swell up like balloons (fat storage cells, they are meant to do this and can become really huge, comparatively). This is what visceral fat is, and why apparently thin people can have fatty livers. Although fat cells can cope, the danger comes from their coping mechanisms to this swelling. Firstly, they literally push back - like a balloon. How this happens is quite complicated, but the analogy works - this is direct resistance to insulin, like a balloon gets harder to blow as it gets bigger. Secondly - as it gets bigger, it gets further from blood supply, and starts shouting for more blood vessels closer to it - this is the cytokine response, and is literally chronic inflammation (again, directly - nothing else but that fructose). The third thing is also more complicated, but essentially you have more fuel in the cell than the "fire" needs, so the way that energy is produced is altered - if you think of putting too much wood on the fire, that's close enough, and you get too much smoke (ROS or what used to be called free radicals).
So - all of that is not good - directly causes inflammation and oxidative stress, AND - insulin resistance.
The net effect of this is that fructose acts as a catalyst to the otherwise slow process of insulin resistance building up over time, more insulin causing the "normal" to raise, and that requiring more insulin, becoming less sensitive to the action of insulin, requiring more... and so on. Sugar -table sugar- is of course both glucose and fructose which means that it has both effects at the same time, but having lots of fructose because you believe it to be natural - as I did - is a very bad idea.
The most obvious example of this in food industry is the production of Foi Gras. Literally meaning "fat goose" - it is the ground liver of geese specially fed to have fat livers - and how do they do this - well, it's no secret, you feed them high fructose corn syrup for the last couple of months of their life.
So - that's essentially why - as a teen (therefore never having had the 20 or so years or gradually increasing insulin resistance that typically leads to T2DM) you can still develop a fatty liver.
The good news, is (as you have shown) that your metabolism is so active at that age, that fairly small changes can have big, long-term effects. Those of us figuring this out in our later years have a tougher time of it.
