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Dr. Darden - Question on Insulin/Insulin Resistance
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Average Al

Nwlifter wrote:

If so, I'd say that it's not an either/or but maybe an 'also'.


Agree! These diseases are multi-factorial. You can have bad genetics, or a bad diet, or a bad life style, or a combination of the above.

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Average Al

Some fascinating stuff in this paper too!

https://www.ncbi.nlm.nih.gov/...les/PMC4421107/

My initial thought after looking at this: DNL in adipose tissue is the preferred way to dispose of excess glucose (vs DNL in the liver); this may have evolved as a protective mechanism for feast and famine scenarios. As per the other paper, the fatty acids produced by this route of glucose disposal are not bad. But in the presence of chronic calorie excess and excess body fat, DNL via adipose tissue becomes impaired, and more DNL is done by the liver. That is when when bad things start to happen (ectopic deposition of fat).

So carbs may be just fine for lean and active people, who end up handling glucose spikes via direct utilization, and storage via DNL in adipose tissue. This supposes, of course, that your pancreas functions appropriately, and is not impaired by other things (poor genetics).

Thoughts?



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Nwlifter

Average Al wrote:
Nwlifter wrote:

If so, I'd say that it's not an either/or but maybe an 'also'.


Agree! These diseases are multi-factorial. You can have bad genetics, or a bad diet, or a bad life style, or a combination of the above.



true and also..
epigenetics

the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.
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Nwlifter

Average Al wrote:
Some fascinating stuff in this paper too!

https://www.ncbi.nlm.nih.gov/...les/PMC4421107/

My initial thought after looking at this: DNL in adipose tissue is the preferred way to dispose of excess glucose (vs DNL in the liver); this may have evolved as a protective mechanism for feast and famine scenarios. As per the other paper, the fatty acids produced by this route of glucose disposal are not bad. But in the presence of chronic calorie excess and excess body fat, DNL via adipose tissue becomes impaired, and more DNL is done by the liver. That is when when bad things start to happen (ectopic deposition of fat).

So carbs may be just fine for lean and active people, who end up handling glucose spikes via direct utilization, and storage via DNL in adipose tissue. This supposes, of course, that your pancreas functions appropriately, and is not impaired by other things (poor genetics).

Thoughts?





totally agree.
For 'most' people with metabolic issues and blood sugar issues, the root always seems to be, dysfunctional adipose cells.
They have IR so don't pull in enough glucose
they spew out too many fats (metabolic issues always show high fasting blood FFA levels)
This info. showing it forces the liver to make up for 'what they can't do', (very interesting!).

Now to note, the 'genetic pancreas' thing is pretty shaky... they are finding that the issue looks to be, pancreatic fats and ceramides, which have been actually seen to prevent beta cells from replicating like they should do in the presence of insulin resistance. One paper I read said lifestyle is so huge for this stuff that we can pretty much not even pay attention to genetics.

When they check most T2 diabetics with insulin resistance, their insulin levels are super high, not quite high enough to keep blood sugar normal, but still 5-10x what a normal lean person would have. So they can make a LOT of insulin. The big issue is ceramides also mess with beta cell signalling.
example
Normally, if blood sugar is 85, beta cells release insulin to keep it there. If it rises after a meal to 135, they 'see' 135 and bring it down to 85 again.

With signaling issues, when blood sugar is 110, they 'see' it as 85, so keep it at 110, it has to rise to 190 to 'seem like' 130. So the sensors are 'off' calibration. Ceramides block the input of the glucose molecules into the cells, so less get in than should for a given blood sugar concentration.
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Nwlifter

Average Al wrote:
Some fascinating stuff in this paper too!

https://www.ncbi.nlm.nih.gov/...les/PMC4421107/

My initial thought after looking at this: DNL in adipose tissue is the preferred way to dispose of excess glucose (vs DNL in the liver); this may have evolved as a protective mechanism for feast and famine scenarios. As per the other paper, the fatty acids produced by this route of glucose disposal are not bad. But in the presence of chronic calorie excess and excess body fat, DNL via adipose tissue becomes impaired, and more DNL is done by the liver. That is when when bad things start to happen (ectopic deposition of fat).

So carbs may be just fine for lean and active people, who end up handling glucose spikes via direct utilization, and storage via DNL in adipose tissue. This supposes, of course, that your pancreas functions appropriately, and is not impaired by other things (poor genetics).

Thoughts?





ha got off track with my recent post, forgot to finish! lol

But for sure, if fat cells are sucking in everything and working normal, blood sugar and blood fats will stay low.
Low blood FFA will keep ectopic fats low, that'll keep ceramides low too. All the stuff that causes issues will be 'sequestered' into the fat cells.
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Average Al

Nwlifter wrote:

Now to note, the 'genetic pancreas' thing is pretty shaky... they are finding that the issue looks to be, pancreatic fats and ceramides, which have been actually seen to prevent beta cells from replicating like they should do in the presence of insulin resistance. One paper I read said lifestyle is so huge for this stuff that we can pretty much not even pay attention to genetics.



Not my area of expertise of course. But it also isn't my theory. I got it from people who do research in this area; some of them think it is a possibility. Or at least they used to think that (circa 2000-2010):

https://diabetes.diabetesjourn...

Maybe the idea that there is a genetic component to the failure of beta cells to adapt to insulin resistance is a contrarian idea that just didn't pan out. Maybe it is correct but a minor secondary factor to the overwhelming impact of diet and lifestyle. I don't really know. I just thought it was an interesting idea that might explain individual variation in how people respond to a particular diet.

As a practical matter, I can't change my genetics, but I can change my diet and lifestyle. The trick is in knowing what to do.





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Nwlifter

Average Al wrote:
Nwlifter wrote:

Now to note, the 'genetic pancreas' thing is pretty shaky... they are finding that the issue looks to be, pancreatic fats and ceramides, which have been actually seen to prevent beta cells from replicating like they should do in the presence of insulin resistance. One paper I read said lifestyle is so huge for this stuff that we can pretty much not even pay attention to genetics.



Not my area of expertise of course. But it also isn't my theory. I got it from people who do research in this area; some of them think it is a possibility. Or at least they used to think that (circa 2000-2010):

https://diabetes.diabetesjourn...

Maybe the idea that there is a genetic component to the failure of beta cells to adapt to insulin resistance is a contrarian idea that just didn't pan out. Maybe it is correct but a minor secondary factor to the overwhelming impact of diet and lifestyle. I don't really know. I just thought it was an interesting idea that might explain individual variation in how people respond to a particular diet.

As a practical matter, I can't change my genetics, but I can change my diet and lifestyle. The trick is in knowing what to do.







I get the impression that overall, their might be genetic issues, but the genetic issues make a person more sensitive to the lifestyle factors. I've found some genetic traits, like fat cell number (the lower the worse), starting beta cell number as a child, even some genetic insulin sensitivity levels. It 'kinda' seems to me that it's not a gene that says 'yes your screwed' but more the total package, how 'sturdy' a person is set up. I wouldn't be surprised though too if beta cell increase ability isn't genetic too, just like how genetics affect muscle gains.
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Average Al

Nwlifter wrote:


I get the impression that overall, their might be genetic issues, but the genetic issues make a person more sensitive to the lifestyle factors. I've found some genetic traits, like fat cell number (the lower the worse), starting beta cell number as a child, even some genetic insulin sensitivity levels. It 'kinda' seems to me that it's not a gene that says 'yes your screwed' but more the total package, how 'sturdy' a person is set up. I wouldn't be surprised though too if beta cell increase ability isn't genetic too, just like how genetics affect muscle gains.


Yes, that is a pretty good view of how genetics (and other things) might come into play.


During my recent reading, I found one paper with the title "The natural history of Beta cell adaptation and failure in type 2 diabetes". It went into great detail about all the things that can affect the development and performance of beta cells from conception to old age. An extraordinary number of things can go wrong along the way....
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hit4me

Florida, USA

I am no expert on this insulin subject, as a matter of fact I know very little of this matter....however, some of the questions I have is based on knowing individuals or have known individuals who are diabetic and those who are now diabetic

I know of a few people who are diabetic or pre-diabetic and are not overweight..as a matter of fact they are quite thin
and then I know of a few that are obese and are not diabetic...and when I say obese, my mother is 89, 4'8" and 200 lbs and is not diabetic....a fellow at work is 6'5", never exercises and is 400 lbs and is not diabetic

so, for the individual like me who knows nothing about this subject....it really is confusing to decipher what the causes of diabetes is....which leads me to think it is mostly genetic...but like I said I know nothing
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Frank Scott

Well Mr Entwhistle, you wanted something other than sets and reps. Have a crack at this!
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Nwlifter

hit4me wrote:
I am no expert on this insulin subject, as a matter of fact I know very little of this matter....however, some of the questions I have is based on knowing individuals or have known individuals who are diabetic and those who are now diabetic

I know of a few people who are diabetic or pre-diabetic and are not overweight..as a matter of fact they are quite thin
and then I know of a few that are obese and are not diabetic...and when I say obese, my mother is 89, 4'8" and 200 lbs and is not diabetic....a fellow at work is 6'5", never exercises and is 400 lbs and is not diabetic

so, for the individual like me who knows nothing about this subject....it really is confusing to decipher what the causes of diabetes is....which leads me to think it is mostly genetic...but like I said I know nothing


I've researched all that a LOT, and had huge long discussions with other on that diabetes forum.

Here some some ideas from research..
1) It's not being over weight in general that causes issues. It's being overweight for 'you' that may. People have a huge variation in fat cell numbers, some thin people are thin because they lack enough fat cells, so then the ones they have are as large as they can get, the issues start, yet the person still isn't 'overweight' in the general sense.
2) There are also what they call TOFI's (thin on the outside, fat inside), the critical area for fat, the internal visceral fat, can be higher while outer bodyfat isn't. This may be a genetic 'trait' (not a diabetes gene per se', but a genetic train that makes someone more at risk for it ).
3) Almost all actually obese people do have metabolic issues, there are studies actually on the 'super rare metabolically healthy obese'. It's such a rare thing that a person can be really over weight and not have any insulin resistance, blood pressure issues, etc.
4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.
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Nwlifter

Average Al wrote:
Nwlifter wrote:


I get the impression that overall, their might be genetic issues, but the genetic issues make a person more sensitive to the lifestyle factors. I've found some genetic traits, like fat cell number (the lower the worse), starting beta cell number as a child, even some genetic insulin sensitivity levels. It 'kinda' seems to me that it's not a gene that says 'yes your screwed' but more the total package, how 'sturdy' a person is set up. I wouldn't be surprised though too if beta cell increase ability isn't genetic too, just like how genetics affect muscle gains.

Yes, that is a pretty good view of how genetics (and other things) might come into play.


During my recent reading, I found one paper with the title "The natural history of Beta cell adaptation and failure in type 2 diabetes". It went into great detail about all the things that can affect the development and performance of beta cells from conception to old age. An extraordinary number of things can go wrong along the way....


Yes true!
And this may also be of interest on this to you....
https://www.bioworld.com/...betes?v=preview

http://www.understandinganimal...

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Average Al

Nwlifter wrote:

And this may also be of interest on this to you....
https://www.bioworld.com/...betes?v=preview

http://www.understandinganimal...



Wow! That seems encouraging, because that kind of effect might be easier to reverse, even if they don't presently know how to do it.

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Nwlifter

Average Al wrote:
Nwlifter wrote:

And this may also be of interest on this to you....
https://www.bioworld.com/...betes?v=preview

http://www.understandinganimal...



Wow! That seems encouraging, because that kind of effect might be easier to reverse, even if they don't presently know how to do it.



Yes for sure! there is another paper where they explained some of this.
Since they can't image a human pancreas in vivo, the only method they have had was autopsy of diabetics. What the did was use a dye to stain all the beta cells so the ones with insulin would show up. So they 'assumed' that since way less were insulin positive, that the rest must have died off. But when they used better newer imaging techniques , they saw that no, the other cells were alive and well, just didn't have very much insulin in them so wouldn't show up with the dye/stain. now they are finding that eventually they even kinda revert back to an earlier 'generic' pancreas cell, just like they are in like a fetus before they actual end up as an insulin positive beta cell. I bet there is some trick, some 'thing' that they can do, or have the person do that will pop them back into beta cells with insulin again.
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hit4me

Florida, USA

Nwlifter wrote:
hit4me wrote:
I am no expert on this insulin subject, as a matter of fact I know very little of this matter....however, some of the questions I have is based on knowing individuals or have known individuals who are diabetic and those who are now diabetic

I know of a few people who are diabetic or pre-diabetic and are not overweight..as a matter of fact they are quite thin
and then I know of a few that are obese and are not diabetic...and when I say obese, my mother is 89, 4'8" and 200 lbs and is not diabetic....a fellow at work is 6'5", never exercises and is 400 lbs and is not diabetic

so, for the individual like me who knows nothing about this subject....it really is confusing to decipher what the causes of diabetes is....which leads me to think it is mostly genetic...but like I said I know nothing

I've researched all that a LOT, and had huge long discussions with other on that diabetes forum.

Here some some ideas from research..
1) It's not being over weight in general that causes issues. It's being overweight for 'you' that may. People have a huge variation in fat cell numbers, some thin people are thin because they lack enough fat cells, so then the ones they have are as large as they can get, the issues start, yet the person still isn't 'overweight' in the general sense.
2) There are also what they call TOFI's (thin on the outside, fat inside), the critical area for fat, the internal visceral fat, can be higher while outer bodyfat isn't. This may be a genetic 'trait' (not a diabetes gene per se', but a genetic train that makes someone more at risk for it ).
3) Almost all actually obese people do have metabolic issues, there are studies actually on the 'super rare metabolically healthy obese'. It's such a rare thing that a person can be really over weight and not have any insulin resistance, blood pressure issues, etc.
4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.


thx Sir
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Nwlifter

hit4me wrote:
Nwlifter wrote:
hit4me wrote:
I am no expert on this insulin subject, as a matter of fact I know very little of this matter....however, some of the questions I have is based on knowing individuals or have known individuals who are diabetic and those who are now diabetic

I know of a few people who are diabetic or pre-diabetic and are not overweight..as a matter of fact they are quite thin
and then I know of a few that are obese and are not diabetic...and when I say obese, my mother is 89, 4'8" and 200 lbs and is not diabetic....a fellow at work is 6'5", never exercises and is 400 lbs and is not diabetic

so, for the individual like me who knows nothing about this subject....it really is confusing to decipher what the causes of diabetes is....which leads me to think it is mostly genetic...but like I said I know nothing

I've researched all that a LOT, and had huge long discussions with other on that diabetes forum.

Here some some ideas from research..
1) It's not being over weight in general that causes issues. It's being overweight for 'you' that may. People have a huge variation in fat cell numbers, some thin people are thin because they lack enough fat cells, so then the ones they have are as large as they can get, the issues start, yet the person still isn't 'overweight' in the general sense.
2) There are also what they call TOFI's (thin on the outside, fat inside), the critical area for fat, the internal visceral fat, can be higher while outer bodyfat isn't. This may be a genetic 'trait' (not a diabetes gene per se', but a genetic train that makes someone more at risk for it ).
3) Almost all actually obese people do have metabolic issues, there are studies actually on the 'super rare metabolically healthy obese'. It's such a rare thing that a person can be really over weight and not have any insulin resistance, blood pressure issues, etc.
4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.

thx Sir


Sure anytime :)
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Average Al

Nwlifter wrote:

4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.


My current impression is this:

1) Classic type 1 is complete insulin deficiency, from an autoimmune attack on beta cells. Classic T1 is also called Juvenile Diabetes because it typically develops in children, and the onset is rapid. There is also something called Latent Autoimmune Diabetes of Adults (LADA). It occurs later in life, and the onset is slower, meaning insulin production is slowly lost over time, and it can produce complete loss of insulin production. I think it has an autoimmune cause (given the name), which is why I listed it as a T1 variant.


2) In the past, anything not fitting the classic Type 1 profile was called T2. But actually, there are several different forms of disease found within the traditional T2 category:

a) Insulin deficiency that is not complete, but sometimes severe, resulting from well known genetic factors (see link below). These are now often called Mature Onset Diabetes of the Young (or Mody Type N, with perhaps 4 or 5 types). These kinds of conditions can be made worse by poor lifestyle and insulin resistance.

2) Classic T2 associated with age and lifestyle factors. Genetics may play a role, but how is less obvious and more complex. Basically you end up with a collection of genes that make you more susceptible to lifestyle factors. Genetics could influence both your tendency to become insulin resistant, and the ability of your pancreas to adjust to insulin resistance. In the past, it is likely than many people carried these genes but didn't get into trouble because of more favorable lifestyles (less food abundance, less refined foods, more activity).

Type 2b (classic T2) is a milder form of the disease, and is the kind that is most "reversible" through diet and exercise. It is the kind that has become more common as people have gotten fatter and more sedentary. If the condition is allowed to persist significant insulin deficiency can develop, to the point that exogenous insulin is needed. At that point, reversing the condition may not be possible. This used to be attributed to beta cell death. As noted in an earlier post, that might not be strictly true, so perhaps a way to reverse even this condition will be forthcoming.

http://www.independentnurse.co...


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Nwlifter

Average Al wrote:
Nwlifter wrote:

4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.

My current impression is this:

1) Classic type 1 is complete insulin deficiency, from an autoimmune attack on beta cells. Classic T1 is also called Juvenile Diabetes because it typically develops in children, and the onset is rapid. There is also something called Latent Autoimmune Diabetes of Adults (LADA). It occurs later in life, and the onset is slower, meaning insulin production is slowly lost over time, and it can produce complete loss of insulin production. I think it has an autoimmune cause (given the name), which is why I listed it as a T1 variant.


2) In the past, anything not fitting the classic Type 1 profile was called T2. But actually, there are several different forms of disease found within the traditional T2 category:

a) Insulin deficiency that is not complete, but sometimes severe, resulting from well known genetic factors (see link below). These are now often called Mature Onset Diabetes of the Young (or Mody Type N, with perhaps 4 or 5 types). These kinds of conditions can be made worse by poor lifestyle and insulin resistance.

2) Classic T2 associated with age and lifestyle factors. Genetics may play a role, but how is less obvious and more complex. Basically you end up with a collection of genes that make you more susceptible to lifestyle factors. Genetics could influence both your tendency to become insulin resistant, and the ability of your pancreas to adjust to insulin resistance. In the past, it is likely than many people carried these genes but didn't get into trouble because of more favorable lifestyles (less food abundance, less refined foods, more activity).

Type 2b (classic T2) is a milder form of the disease, and is the kind that is most "reversible" through diet and exercise. It is the kind that has become more common as people have gotten fatter and more sedentary. If the condition is allowed to persist significant insulin deficiency can develop, to the point that exogenous insulin is needed. At that point, reversing the condition may not be possible. This used to be attributed to beta cell death. As noted in an earlier post, that might not be strictly true, so perhaps a way to reverse even this condition will be forthcoming.

http://www.independentnurse.co...




OK that's really close to how they classify.
MODY is pure genetic, not in the T2 category. it's monogenic, single bad inherited gene. 11 variants found so far.

Yes spot on with T1 and LADA , both are insulin deficiency.

T2 is insulin resistance. What happens is really long term insulin resistance can 'lead to' pancreas insulin secretion issues. Dr. Kraft found some cool information.
A person develops IR, insulin rises, blood sugar normal. As the years progress, usually IR keeps going up, insulin goes up more but eventually (and now they know usually it's from fatty pancreas), the insulin can't keep up with the high IR so even though insulin output is high, it's not quite high enough for the IR level. If people reverse IR while the pancreas is still capable of good enough insulin secretion, they can have normal blood sugar again.
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Nwlifter

Average Al wrote:
Nwlifter wrote:

4) A lot of this research now too is finding that a person can gain weight in a more healthy way as apposed to a more unhealthy way. (the types of fats ect. that are taken in and stored). If the pancreas gets fatty and has ceramide issues, that can halt the very thing that compensates for insulin resistance. Beta cell / insulin increases are limited by that.
It more seems that it's a 'genetic setup' rather than a 'diabetes gene', how resilient the body is to a poor lifestyle.
5) They also are finding that a lot of the thin people who are 'deemed' regular type 2 diabetic, might actually have a true genetic form of diabetes (like one of the MODY versions, or even LADA). True type 2 is almost unseen in lean competitive athletes.

My current impression is this:

1) Classic type 1 is complete insulin deficiency, from an autoimmune attack on beta cells. Classic T1 is also called Juvenile Diabetes because it typically develops in children, and the onset is rapid. There is also something called Latent Autoimmune Diabetes of Adults (LADA). It occurs later in life, and the onset is slower, meaning insulin production is slowly lost over time, and it can produce complete loss of insulin production. I think it has an autoimmune cause (given the name), which is why I listed it as a T1 variant.


2) In the past, anything not fitting the classic Type 1 profile was called T2. But actually, there are several different forms of disease found within the traditional T2 category:

a) Insulin deficiency that is not complete, but sometimes severe, resulting from well known genetic factors (see link below). These are now often called Mature Onset Diabetes of the Young (or Mody Type N, with perhaps 4 or 5 types). These kinds of conditions can be made worse by poor lifestyle and insulin resistance.

2) Classic T2 associated with age and lifestyle factors. Genetics may play a role, but how is less obvious and more complex. Basically you end up with a collection of genes that make you more susceptible to lifestyle factors. Genetics could influence both your tendency to become insulin resistant, and the ability of your pancreas to adjust to insulin resistance. In the past, it is likely than many people carried these genes but didn't get into trouble because of more favorable lifestyles (less food abundance, less refined foods, more activity).

Type 2b (classic T2) is a milder form of the disease, and is the kind that is most "reversible" through diet and exercise. It is the kind that has become more common as people have gotten fatter and more sedentary. If the condition is allowed to persist significant insulin deficiency can develop, to the point that exogenous insulin is needed. At that point, reversing the condition may not be possible. This used to be attributed to beta cell death. As noted in an earlier post, that might not be strictly true, so perhaps a way to reverse even this condition will be forthcoming.

http://www.independentnurse.co...




Here are a couple real life data points that might be of interest.....

On that diabetes forum I have been on for years...

1) Quite a few people, some had A1C's as high as 10 or more, moved to a keto diet and now have normal A1C's and normal blood sugar. Of course they can't eat carbs or their levels go up, but they are on no meds, no insulin, etc. Just super low carb diet. They have great BP, and all other blood work.

2) One guy on there that I even emailed with and got to know, was the obese T2, at diagnosis, his A1C was over 10, glucose was over 200. He went on insulin and was super perfect with it, he kept his blood sugar totally in the normal range with it. This would protect the pancreas from being 'over worked'. As he lost weight, his insulin needs dropped to the point of not needing it at all. Then he could eat anything he wanted and have normal blood sugar and a normal A1C.
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Average Al

Nwlifter wrote:

OK that's really close to how they classify.

MODY is pure genetic, not in the T2 category. it's monogenic, single bad inherited gene. 11 variants found so far.



It would make sense to classify those with genetically driven deficiency as different from those with lifestyle driven insulin resistance. But before the various forms of MODY were clearly identified, T2 seemed to be the default if you were not clearly T1. So that might account for some of the anecdotal reports of T2 diabetics who are thin and not insulin resistant.

I would guess that specialists are now well aware of the difference. I wonder how many primary care doctors are up to date on this? Likewise, how many diet guru's and public health experts understand the distinction?

What I don't really know is the relative prevalence of T2 (correctly diagnosed) vs MODY (correctly diagnosed).

Here is an example of why it can be important. There is a women who runs a web site that you probably have encountered - Jenny Ruhl at Diabetes 101. When she was first diagnosed as T2, she embraced the idea that it was lifestyle driven. So she hunted for the right diet, and ended up a low carb advocate. She also dieted like crazy, and really beat herself up with tons of cardio because T2 was from her bad choices. Despite this, she struggle with controlling her blood sugar. Later on, she had some genetic testing which suggested she had MODY like genetic variants (though not the specific ones that are currently known). In any case, she switched to a medication known to work well for certain MODY patients, and ended up doing much better. So understanding that she (probably) had a genetic condition lead to better medical treatment, and also meant she could stop punishing herself for failing to find a full cure with lifestyle interventions.
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Average Al

Nwlifter wrote:

Here are a couple real life data points that might be of interest.....

On that diabetes forum I have been on for years...

1) Quite a few people, some had A1C's as high as 10 or more, moved to a keto diet and now have normal A1C's and normal blood sugar. Of course they can't eat carbs or their levels go up, but they are on no meds, no insulin, etc. Just super low carb diet. They have great BP, and all other blood work.



I can believe it. But anecdotes can be all over the place.

I remember reading one story on the McDougal web site about a guy who lost 150-200 lbs with an extreme low fat diet. His A1C dropped from over 10 to a very low number, like around 4.2 (In hindsight, that almost seems too low - not healthy either?)

In contrast, after losing 45 lbs and following a low carb diet, my A1C still ran toward the high end of normal, more like 5.8 plus/minus a tenth of a point. I was disappointed that I didn't get a bigger drop (though I never got above 6.5, even when fat).



2) One guy on there that I even emailed with and got to know, was the obese T2, at diagnosis, his A1C was over 10, glucose was over 200. He went on insulin and was super perfect with it, he kept his blood sugar totally in the normal range with it. This would protect the pancreas from being 'over worked'. As he lost weight, his insulin needs dropped to the point of not needing it at all. Then he could eat anything he wanted and have normal blood sugar and a normal A1C.


Interesting. I do recall some internet personality suggesting that maybe insulin should be started sooner with T2 diabetics, in the hopes of preserving whatever native beta cell capacity still exists, and also to give the pancreas a break. He/she suggested it might even promote healing or recovery of the beta cells. That anecdote seems to validate the suggestion.

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Nwlifter

Average Al wrote:
Nwlifter wrote:

OK that's really close to how they classify.

MODY is pure genetic, not in the T2 category. it's monogenic, single bad inherited gene. 11 variants found so far.



It would make sense to classify those with genetically driven deficiency as different from those with lifestyle driven insulin resistance. But before the various forms of MODY were clearly identified, T2 seemed to be the default if you were not clearly T1. So that might account for some of the anecdotal reports of T2 diabetics who are thin and not insulin resistant.

I would guess that specialists are now well aware of the difference. I wonder how many primary care doctors are up to date on this? Likewise, how many diet guru's and public health experts understand the distinction?


Unfortunately they don't pursue that. Their view is 'high blood sugar, here's your meds'. MODY testing is very expensive and extensive. So for the average person, they just call em T2 and give em meds.

What I don't really know is the relative prevalence of T2 (correctly diagnosed) vs MODY (correctly diagnosed).

Yes they have no idea with the difficulty of testing for MODY :(

Here is an example of why it can be important. There is a women who runs a web site that you probably have encountered - Jenny Ruhl at Diabetes 101. When she was first diagnosed as T2, she embraced the idea that it was lifestyle driven. So she hunted for the right diet, and ended up a low carb advocate. She also dieted like crazy, and really beat herself up with tons of cardio because T2 was from her bad choices. Despite this, she struggle with controlling her blood sugar. Later on, she had some genetic testing which suggested she had MODY like genetic variants (though not the specific ones that are currently known). In any case, she switched to a medication known to work well for certain MODY patients, and ended up doing much better. So understanding that she (probably) had a genetic condition lead to better medical treatment, and also meant she could stop punishing herself for failing to find a full cure with lifestyle interventions.

Yes exactly, she is a great example. If they would/could test all people, it would save a lot of wrong treatment paths. One lady on the D forum suspects she is MODY, but cannot afford the test. Insurance won't cover it, it's like 5,000 and only tests for a few common versions, not all 11 versions.

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Nwlifter

Average Al wrote:



I can believe it. But anecdotes can be all over the place.

I remember reading one story on the McDougal web site about a guy who lost 150-200 lbs with an extreme low fat diet. His A1C dropped from over 10 to a very low number, like around 4.2 (In hindsight, that almost seems too low - not healthy either?)


wow that is LOW low. I've heard of some being low like that. Some people when they lose weight, have a LOT of 'insulin power' so to speak left over from the higher IR so for a while, they have extra low blood sugar. People who have gastric bypass have that too, they end up goign hypo all the time, some have to have some of the pancreas removed to lower their insulin levels.

In contrast, after losing 45 lbs and following a low carb diet, my A1C still ran toward the high end of normal, more like 5.8 plus/minus a tenth of a point. I was disappointed that I didn't get a bigger drop (though I never got above 6.5, even when fat).

Oh wow you came down good though. I didn't know you had the pre D battle too. My highest was 6.1, haven't tested it in a couple years, should to that again. But I used a meter every day and keep an eye on fasting and many post meal levels.




Interesting. I do recall some internet personality suggesting that maybe insulin should be started sooner with T2 diabetics, in the hopes of preserving whatever native beta cell capacity still exists, and also to give the pancreas a break. He/she suggested it might even promote healing or recovery of the beta cells. That anecdote seems to validate the suggestion.



Yes lots of studies on this too, early insulin shows a LOT of help.

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Average Al

Nwlifter wrote:
Average Al wrote:

I remember reading one story on the McDougal web site about a guy who lost 150-200 lbs with an extreme low fat diet. His A1C dropped from over 10 to a very low number, like around 4.2 (In hindsight, that almost seems too low - not healthy either?)

wow that is LOW low.


Now I'm doubting my memory on that number. I am pretty sure he got below 5.0, but maybe it was more like 4.9




Oh wow you came down good though. I didn't know you had the pre D battle too. My highest was 6.1, haven't tested it in a couple years, should to that again. But I used a meter every day and keep an eye on fasting and many post meal levels.



Having a doctor tell me that I was very close to diabetes diagnosis was a real shock, and a wake up call.

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Nwlifter

Average Al wrote:
Nwlifter wrote:
Average Al wrote:

I remember reading one story on the McDougal web site about a guy who lost 150-200 lbs with an extreme low fat diet. His A1C dropped from over 10 to a very low number, like around 4.2 (In hindsight, that almost seems too low - not healthy either?)

wow that is LOW low.


Now I'm doubting my memory on that number. I am pretty sure he got below 5.0, but maybe it was more like 4.9




Oh wow you came down good though. I didn't know you had the pre D battle too. My highest was 6.1, haven't tested it in a couple years, should to that again. But I used a meter every day and keep an eye on fasting and many post meal levels.



Having a doctor tell me that I was very close to diabetes diagnosis was a real shock, and a wake up call.



oh ok, 4.9 is like perfection for A1C, that's really great to hit that level. A lady on that diabetes forum lost like 80 pounds and now has that exact A1C (4.9).

Man I hear ya, I found out myself, my wife is full T2, uses insulin and such, 4 years ago , one morning I was just curious and checked my blood sugar with her meter, I saw 118 and almost crapped my pants lol. I right away got a meter myself, started reading up on it and went on a mass diet (low cal and low carb), I lost 35 lbs of fat in a few months and tracked my blood sugar. I didn't get all the way back to totally normal numbers but pretty darned close.
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