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Dr. Darden - Question on Insulin/Insulin Resistance
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parker1

Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

https://www.drdavidludwig.com/...-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!
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Ellington Darden

parker1 wrote:
Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

https://www.drdavidludwig.com/...-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!


I've covered my views of low-carbohydrate dieting in The Body Fat Breakthrough, pages 251-254.

Ellington

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parker1

Thanks, Dr. Darden. Forgot about that section in your book.

How about Intermittent Fasting? I did some searches along with checking your more recent books and I couldn't find any comments.

Appreciate your feedback.
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Ellington Darden

parker1 wrote:
Thanks, Dr. Darden. Forgot about that section in your book.

How about Intermittent Fasting? I did some searches along with checking your more recent books and I couldn't find any comments.

Appreciate your feedback.


Intermittent fasting seems to be effective for some people.

Ellington

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Nwlifter

parker1 wrote:
Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

https://www.drdavidludwig.com/...-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!


this is an area I wish more people were interested in. Being a person with insulin resistance and having done years of research and so forth, I'd say Dr. Kraft's research is without equal.
He is the one who brought for the idea that even before a person's blood sugar rises, their insulin levels are higher due to insulin resistance. Some may maintain but many end up pre to full type 2 diabetic later.
According to the CDC, about 43% of th U.S. now has abnormal blood sugar.

Also, it's not just processed carbs.
Fast carbs have a higher but shorter peak insulin/blood sugar response. Slower complex carbs have a longer lasting but lower peak for insulin and blood sugar.
but the important part, is the AUC (area under the curve). ie 3 hours of slightly elevated is equal to 1 hour of higher elevated.

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Average Al

Nwlifter wrote:
parker1 wrote:
Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

www.drdavidludwig.com/case-low-carb-diet-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!

this is an area I wish more people were interested in. Being a person with insulin resistance and having done years of research and so forth, I'd say Dr. Kraft's research is without equal.
He is the one who brought for the idea that even before a person's blood sugar rises, their insulin levels are higher due to insulin resistance. Some may maintain but many end up pre to full type 2 diabetic later.
According to the CDC, about 43% of th U.S. now has abnormal blood sugar.

Also, it's not just processed carbs.
Fast carbs have a higher but shorter peak insulin/blood sugar response. Slower complex carbs have a longer lasting but lower peak for insulin and blood sugar.
but the important part, is the AUC (area under the curve). ie 3 hours of slightly elevated is equal to 1 hour of higher elevated.



Sounds familiar.

I've also read that impaired first stage insulin response is strongly predictive of risk for developing T2 diabetes, and this can be detected many years before elevated blood sugar levels actually occur. It may be related to having certain mutations or gene variants which leave you with a pancreas that produces a less robust insulin response when challenged with a large dump of glucose into the blood stream.

https://www.medicographia.com/...d-egg-question/
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Nwlifter

Average Al wrote:
Nwlifter wrote:
parker1 wrote:
Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

www.drdavidludwig.com/case-low-carb-diet-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!

this is an area I wish more people were interested in. Being a person with insulin resistance and having done years of research and so forth, I'd say Dr. Kraft's research is without equal.
He is the one who brought for the idea that even before a person's blood sugar rises, their insulin levels are higher due to insulin resistance. Some may maintain but many end up pre to full type 2 diabetic later.
According to the CDC, about 43% of th U.S. now has abnormal blood sugar.

Also, it's not just processed carbs.
Fast carbs have a higher but shorter peak insulin/blood sugar response. Slower complex carbs have a longer lasting but lower peak for insulin and blood sugar.
but the important part, is the AUC (area under the curve). ie 3 hours of slightly elevated is equal to 1 hour of higher elevated.



Sounds familiar.

I've also read that impaired first stage insulin response is strongly predictive of risk for developing T2 diabetes, and this can be detected many years before elevated blood sugar levels actually occur. It may be related to having certain mutations or gene variants which leave you with a pancreas that produces a less robust insulin response when challenged with a large dump of glucose into the blood stream.

https://www.medicographia.com/...d-egg-question/


that is 'possible', most likely though are dysfunctions related to cellular stress and ceramide accumulation over the years. They rarely see any dysfunction in children (save the very rare obese child with Metabolic Syndrome)to show an inherited dysfunction. Especially when early T2's can reverse these issues and restore first and second phase insulin secretion back to normal.
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Nwlifter

Average Al wrote:
Nwlifter wrote:
parker1 wrote:
Dr. Darden -

Background for my question: there are more and more concerns regarding processed carbs raising insulin levels potentially leading to fat storage Moreso, the current attention on "insulin resistance" and limiting carbs when one is trying to lean out. Dr. David Ludwig discusses processed carbs and the associated processes:

www.drdavidludwig.com/case-low-carb-diet-stronger-ever/

Finally, friend who is concerned about IR loaned me a book over the holidays written by Dr. Joseph Kraft who notes as we age the pancreas produces less insulin and insulin receptors diminish in capacity as well.

With this background,I wondered what your thoughts are on this growing body of information/research vs. your recommendations such as bagels, Kashi cereal, etc.?

Thank you!

this is an area I wish more people were interested in. Being a person with insulin resistance and having done years of research and so forth, I'd say Dr. Kraft's research is without equal.
He is the one who brought for the idea that even before a person's blood sugar rises, their insulin levels are higher due to insulin resistance. Some may maintain but many end up pre to full type 2 diabetic later.
According to the CDC, about 43% of th U.S. now has abnormal blood sugar.

Also, it's not just processed carbs.
Fast carbs have a higher but shorter peak insulin/blood sugar response. Slower complex carbs have a longer lasting but lower peak for insulin and blood sugar.
but the important part, is the AUC (area under the curve). ie 3 hours of slightly elevated is equal to 1 hour of higher elevated.



Sounds familiar.

I've also read that impaired first stage insulin response is strongly predictive of risk for developing T2 diabetes, and this can be detected many years before elevated blood sugar levels actually occur. It may be related to having certain mutations or gene variants which leave you with a pancreas that produces a less robust insulin response when challenged with a large dump of glucose into the blood stream.

https://www.medicographia.com/...d-egg-question/


You might find this interesting
https://www.ncbi.nlm.nih.gov/...les/PMC3168743/
Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol

Results
The first-phase insulin response increased during the study period (0.19 ? 0.02 to 0.46 ? 0.07 nmol min−1 m−2; p < 0.001) and approached control values (0.62 ? 0.15 nmol min−1 m−2; p = 0.42). Maximal insulin response became supranormal at 8 weeks (1.37 ? 0.27 vs controls 1.15 ? 0.18 nmol min−1 m−2). Pancreatic triacylglycerol decreased from 8.0 ? 1.6% to 6.2 ? 1.1% (p = 0.03).

---------------------------
https://care.diabetesjournals....
Pancreatic fat correlated negatively with β-cell function parameters, including the insulinogenic index adjusted for insulin resistance, early glucose-stimulated insulin secretion, β-cell glucose sensitivity, and rate sensitivity
----------------------------
Path of excess carbs to insulin resistance and beta cell dysfuntion
(tons of studies like these)

Excess carbohydrate converts to the FFA Palmitic Acid / Palmitate
https://journals.plos.org/...al.pone.0113605


Palmitate esterified in cells induces ceramides which induce insulin resistance and beta cell dysfunction (direct causal effects)
https://www.diva-portal.org/.../FULLTEXT01.pdf
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parker1

OTOH, you've got PhDs and researchers who have shown high carb diets reduce the need for insulin in Type 1 diabetics and completely reverse Type II diabetes in the vast marority of people. One example:

https://www.masteringdiabetes....

There is also quite a bit of information covering the association between cholesterol and insulin resistance. With Saturated Fatty acids having an inflammatory affect and animal "protein" affecting insulin (ref Reaven, Rosedale, et al), I wonder about the validity of keto/paleo diets for diseases like Type II diabetes/pre-diabetics (insulin resistance).
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Average Al

Thanks for the links. I will take a look when I have a bit more time.

My understanding of Cerasi's theory is this:

If you have gene variations which give you a robust insulin response, you can tolerate a high carb diet easily, and even get quite fat without having problems. There are many overweight people who do not develop diabetes.

If you have the gene variation that doesn't give you a very robust insulin response, but you grow up in conditions were food isn't too readily available, and you have to perform a lot of physical labor to acquire food, then you tend to stay fairly lean, and you can most likely escape the problem. He points out that, in Europe, during and immediately after the war, when many people faced significant food insecurity, the frequency of T2 diabetes dropped significantly. The genetic component only became apparent when people began doing gene profiles on populations where food was abundant and readily available, such that greater numbers of people were being diagnosed. (That there are genetic risk factors for the disease seems undisputed at this point.)

The disease is most prevalent when vulnerable individuals are placed in a challenging environment: sedentary life, abundant food, with a lot of sugar and refined carbs. In other words, weak pancreas plus excessive carb and calorie load equals high risk. Even then, the problem doesn't develop immediately. If you have impaired first stage response, but adequate overall insulin capacity, then eventually you produce enough insulin to bring blood sugar back down. But you are exposed to elevated levels of insulin and glucose for longer periods of time than someone with a more robust response. This starts to wear down the beta cells, perhaps by some of the mechanisms you mention. Eventually you reach a level of insufficiency where control of glucose level is lost.

In all of this, insulin resistance serves as an amplifying factor, by further increasing the amount of insulin needed from a pancreas which is already subpar. Accumulation of fat in the liver and pancreas is likely a contributing factor as well, both for insulin resistance and insulin response.

Because the robustness of insulin response varies with genetics, you have some people who can get fat and not have problems, and others who put on just a little bit of weight (skinny fat) and have an issue. (I gather that South East Asian populations - India and China - show much higher prevalence of T2 diabetes with only modest degrees of excess weight. That might be partially genetic.)

So what is the answer? Cerasi says: "For the majority of type 2 diabetics, to prevent hyperglycemia and its consequences either food intake has to be reduced drastically, or the cell enforced to cope with the increased workload. Neither seems easy. "

So, as the most interesting man in the world might say: Stay hungry my friends, and hope for medications that pump up your beta cells.

And a post script: 5 distinct types of diabetes that have now been identified, each with unique characteristics. Apparently, it is more complicated than commonly believed.

https://www.medicalnewstoday.c...
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hit4me

Florida, USA

is it "processed carbs" that are the problem.....or is it the amount of "processed carbs", i.e. everything is supersized, therefore we are over consuming processed carbs along with proteins and fat.....could it also be consuming processed carbs along with high fat, therefore one of these will be stored and the other used for energy
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Average Al

parker1 wrote:
OTOH, you've got PhDs and researchers who have shown high carb diets reduce the need for insulin in Type 1 diabetics and completely reverse Type II diabetes in the vast marority of people. One example:

www.masteringdiabetes.org/reverse-insulin-resistance-presentation/



I've seen that claim before, that low fat diets can reverse T2 diabetes. When I have looked at the data from the intervention studies that are cited as proof, I've often been disappointed: often, the diet is shown to improve blood sugar control, and even get some subjects off medications, but does not necessarily get them to normal blood sugar levels.

Note that the levels of A1C and fasting blood sugar that are considered "acceptable" by medical experts for management of T1 and T2 diabetes are often still higher than what is considered normal or optimal. So look closely at the details before accepting claims of a cure.

I also see that on the Mastering Diabetes web site, the claim is that they can "reverse insulin resistance", which is not quite the same as claiming a cure for diabetes.



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Nwlifter

Average Al wrote:
parker1 wrote:
OTOH, you've got PhDs and researchers who have shown high carb diets reduce the need for insulin in Type 1 diabetics and completely reverse Type II diabetes in the vast marority of people. One example:

www.masteringdiabetes.org/reverse-insulin-resistance-presentation/



I've seen that claim before, that low fat diets can reverse T2 diabetes. When I have looked at the data from the intervention studies that are cited as proof, I've often been disappointed: often, the diet is shown to improve blood sugar control, and even get some subjects off medications, but does not necessarily get them to normal blood sugar levels.

Note that the levels of A1C and fasting blood sugar that are considered "acceptable" by medical experts for management of T1 and T2 diabetes are often still higher than what is considered normal or optimal. So look closely at the details before accepting claims of a cure.

I also see that on the Mastering Diabetes web site, the claim is that they can "reverse insulin resistance", which is not quite the same as claiming a cure for diabetes.





Right agree.

the issue with the path they have found (to parker1 also), is this....

Excess nutrients increase fat cell size
As fat cell size increases, the larger a fat cell , the more insulin resistance it has.
The more insulin resistance it has, the more it releases FFA into the blood stream
Blood FFA (free fatty acids) are higher 24 hours a day
The higher FFA in the blood, increases ectopic fats (ectopic tissues take in FFA based on blood levels)
If blood consists of high palmitic acid, when the cells esterify it for storage, that process creates a ceramide molecule
Ceramides reduce cellular signaling levels (insulin resistance or glucose sensing in beta cells).

So yes a low calories diet of any kind, that reduces fat storage size, reducing insulin resistance of the adipose tissues, this will lower blood FFA and that will allow ectopic fats to lower also. But the one little key point is, the issues are mostly caused from ceramides in the cells and those come from palmitate which is mostly from excess carbohydrate. The palmitate in 'meat' is short lived in the blood after a meal and usually has enough oleate included (the right ratio) to negate the palmitate.
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parker1

hit4me wrote:
is it "processed carbs" that are the problem.....or is it the amount of "processed carbs", i.e. everything is supersized, therefore we are over consuming processed carbs along with proteins and fat.....could it also be consuming processed carbs along with high fat, therefore one of these will be stored and the other used for energy


Great point.

I travel to Europe and Asia and the portion sizes, compared to the US, are significantly smaller. While in Milano, Italy, at lunch, an engineer I was working with laughed at my lunch (a miserable piece of dry chicken**, salad, a tiny bit of pasta) and said Americans don't understand food. We eat pasta and enjoy meals -- do you see fat Italians? He was right...they eat very, very slowly forks down between meals and enjoy their food. No gulping down Super Sized meals or huge plates of food. (**Meat, poultry is expensive in Europe hence it isn't common to see it served as a main course everywhere. Also, you don't see the silly protein powder BS everywhere in gyms, etc., in Europe like the US.)

Japan, Taiwan, the same...the basis of their meals include noodles or rice with small amounts of pork or fish. (NOTE: fast food is on the rise in Asia and the younger groups, not older generations, are the customers. The WSJ and other business sites have said China, Japan are the #1 growth markets for KFC, for example. I have pictures of KFC delivery scooters from the streets of Taipei.)

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parker1

Average Al wrote:
parker1 wrote:
OTOH, you've got PhDs and researchers who have shown high carb diets reduce the need for insulin in Type 1 diabetics and completely reverse Type II diabetes in the vast marority of people. One example:

www.masteringdiabetes.org/reverse-insulin-resistance-presentation/



I've seen that claim before, that low fat diets can reverse T2 diabetes. When I have looked at the data from the intervention studies that are cited as proof, I've often been disappointed: often, the diet is shown to improve blood sugar control, and even get some subjects off medications, but does not necessarily get them to normal blood sugar levels.

Note that the levels of A1C and fasting blood sugar that are considered "acceptable" by medical experts for management of T1 and T2 diabetes are often still higher than what is considered normal or optimal. So look closely at the details before accepting claims of a cure.

I also see that on the Mastering Diabetes web site, the claim is that they can "reverse insulin resistance", which is not quite the same as claiming a cure for diabetes.


If you eliminate the cause for insulin resistance/T2 diabetes, you've provided the cure. A long time friend had T2 diabetes, went on a hard core diet after he started have issues with his eyes and has been off of his meds for over 15 years. Not my words, but, his doctor said his diet 'cured' him. He does watch his blood sugar like crazy and knows which foods to avoid and tries to avoid foods/fats higher in SFAs, focusing on fats higher in MUFAs/lower in SFAs.

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Average Al

hit4me wrote:
is it "processed carbs" that are the problem.....or is it the amount of "processed carbs", i.e. everything is supersized, therefore we are over consuming processed carbs along with proteins and fat.....could it also be consuming processed carbs along with high fat, therefore one of these will be stored and the other used for energy


Good questions.

I think the standard american diet is a a problem in many regards:

- Plenty of fat, particularly saturated fat, which does decrease insulin sensitivity and therefore raise insulin requirements for a given level of carbohydrate intake.

- Plenty of refined carbs with little fiber, so glucose is dumped quickly into the blood stream presenting a challenge to the pancreas, especially if insulin resistance is present.

- Excessive calories, which makes people fat, and adds to insulin resistance, as well as increasing the load on the pancreas.

- Too frequent meals and snacking just add to the challenges facing the pancreas. It just never gets a break from trying to drive down blood sugar.

- As above problems persist, you get chronically elevate blood sugar and insulin levels, which is damaging to the body. Fat can also start to build up in the liver and pancreas, making everything that much worse.


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Nwlifter

parker1 wrote:
OTOH, you've got PhDs and researchers who have shown high carb diets reduce the need for insulin in Type 1 diabetics and completely reverse Type II diabetes in the vast marority of people. One example:

https://www.masteringdiabetes....

There is also quite a bit of information covering the association between cholesterol and insulin resistance. With Saturated Fatty acids having an inflammatory affect and animal "protein" affecting insulin (ref Reaven, Rosedale, et al), I wonder about the validity of keto/paleo diets for diseases like Type II diabetes/pre-diabetics (insulin resistance).


For T1 diabetics, more carbs always means higher insulin usage (they have to use more bolus to cover the postprandial glucose rise).

I have been part of a diabetes forum for over 4 years, I've watched many many members on there with various diets. I can say for sure that newly diagnosed who are overweight but still have good pancreas function, can improve and a few have reversed their issues purely by a good amount of weight loss to lower insulin resistance. The rest who have a great A1C and great blood sugar have been following low carb and many are ketogenic. A couple members have been keto for many many years. One lady on there almost 10 years and maintaining an A1C under 5. Keto lowered her trigs down to amazing levels (trigs are totally related to carb intake) her cholesterol and all blood work is perfect.
I wish I had the stomach to eat a pure keto diet.....
So for sure, most T2 diabetics do way way better with low carb diets. Absolutely no doubt
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Average Al

parker1 wrote:

If you eliminate the cause for insulin resistance/T2 diabetes, you've provided the cure. A long time friend had T2 diabetes, went on a hard core diet after he started have issues with his eyes and has been off of his meds for over 15 years. Not my words, but, his doctor said his diet 'cured' him. He does watch his blood sugar like crazy and knows which foods to avoid and tries to avoid foods/fats higher in SFAs, focusing on fats higher in MUFAs/lower in SFAs.



No doubt, dietary interventions can have a profound beneficial impact for diabetics.

But there is a difference between keeping your blood sugar at an acceptable level by following a highly restrictive diet, versus just being able to let your body take care of things, without having to severely limit a particular macronutrient (carbohydrates, in the case of a ketogenic diet, or fat, in the case of a very low fat vegan diet).


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Nwlifter

Average Al wrote:
hit4me wrote:
is it "processed carbs" that are the problem.....or is it the amount of "processed carbs", i.e. everything is supersized, therefore we are over consuming processed carbs along with proteins and fat.....could it also be consuming processed carbs along with high fat, therefore one of these will be stored and the other used for energy

Good questions.

I think the standard american diet is a a problem in many regards:

- Plenty of fat, particularly saturated fat, which does decrease insulin sensitivity and therefore raise insulin requirements for a given level of carbohydrate intake.

- Plenty of refined carbs with little fiber, so glucose is dumped quickly into the blood stream presenting a challenge to the pancreas, especially if insulin resistance is present.

- Excessive calories, which makes people fat, and adds to insulin resistance, as well as increasing the load on the pancreas.

- Too frequent meals and snacking just add to the challenges facing the pancreas. It just never gets a break from trying to drive down blood sugar.

- As above problems persist, you get chronically elevate blood sugar and insulin levels, which is damaging to the body. Fat can also start to build up in the liver and pancreas, making everything that much worse.




Agree with all that.
I will say though, there is something to the carbohydrate - insulin connection.

If we take the root of 80% of the T2 diabetic diagnosis levels, which is being overweight, and knowing that insulin inhibits HSL, thus keeping fatty acids locked up in fat cells, and insulin causes fat cells to absorb glucose, where it then becomes stored trigs, I can't see any way around the facts that a person eating 4 high carb meals a day with a massively higher 24 AUC of insulin compared to a low carb diet, wouldn't have a higher chance of 'getting fat' in the first place and starting the whole cascade.
I've seen far too many 'real people' over the years just shed fat (myself included) like crazy on low carb with plenty of food to satiate the appetite.
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Nwlifter

Here is how 'fat mass' affects glucose and insulin levels, even in people who are still 'under the cutoff' for being diagnosed with glucose issues.

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Average Al

Nwlifter wrote:

But the one little key point is, the issues are mostly caused from ceramides in the cells and those come from palmitate which is mostly from excess carbohydrate.


The role of ceramides is something I am not familiar with, so I am curious about this.

I understand that excess carbohydrates can be converted to fat, but I thought that the overall conversion rate was quite low, unless your carbohydrate intake exceeds your total calorie requirement by a good margin. In other words, you need to eat a boat load of carbs to really ramp up de novo lipogenesis.

So lets say you are eating 3000 calories a day, 1500 from carbs, and your total calorie requirements are only 2500. Since your carb intake does not exceed 2500 calories, there shouldn't be a large amount of DNL occurring. Instead the body will just store fat in excess of what is needed. Are ceramides still an issue in this circumstance?
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Nwlifter

Average Al wrote:
Nwlifter wrote:

But the one little key point is, the issues are mostly caused from ceramides in the cells and those come from palmitate which is mostly from excess carbohydrate.

The role of ceramides is something I am not familiar with, so I am curious about this.

I understand that excess carbohydrates can be converted to fat, but I thought that the overall conversion rate was quite low, unless your carbohydrate intake exceeds your total calorie requirement by a good margin. In other words, you need to eat a boat load of carbs to really ramp up de novo lipogenesis.

So lets say you are eating 3000 calories a day, 1500 from carbs, and your total calorie requirements are only 2500. Since your carb intake does not exceed 2500 calories, there shouldn't be a large amount of DNL occurring. Instead the body will just store fat in excess of what is needed. Are ceramides still an issue in this circumstance?


It seems that if calories exceed, carbs are always the 'extra' unless the muscles and liver are super depleted (like maybe after a marathon), the amount it takes to normal restore glycogen is really small.
If fat cells are small and able to take in all excess FFA, the palmitate created from the excess glucose will be rapidly stored in the fat cells instead of ending up in ectopic and muscle cells.

But, if the person becomes overweight (which is relative to their actual total fat cell number and fat cell max sizes), now their adipose tissue is a very high proportion of palmitate, as their cells leak and release trigs and FFA, their blood palmitate levels are high 24/7, this feeds muscle and ectopic tissues.
If blood glucose is low, the ectopic cells 'run on the fats', but when glucose rises after a carbohydrate meal, the cells switch to glucose as a fuel and esterify and store the incoming palmitate, that process creates ceramide molecules and those directly affect cell signaling.

https://www.sciencedirect.com/...212877818308056

Ectopic causes ceramides


https://www.hindawi.com/...dr/2014/765784/
High insulin increase ceramides

http://diabetes.diabetesjourna...

Ceramide is a potent lipid-signaling molecule that can cause insulin resistance by inhibiting the ability of insulin to activate Akt (6) and/or via the activation of c-jun amino terminal kinase (JNK) (7,8). Importantly, preventing ceramide accumulation by inhibiting de novo ceramide synthesis protects against the development of insulin resistance (9,10).


http://www.jbc.org/...2/17/12583.full

Elevated non-esterified fatty acids, triglyceride, diacylglycerol, and ceramide have all been associated with insulin resistance in muscle. We set out to investigate the role of intramyocellular lipid metabolites in the induction of insulin resistance in human primary myoblast cultures. Muscle cells were subjected to adenovirus-mediated expression of perilipin or incubated with fatty acids for 18 h, prior to insulin stimulation and measurement of lipid metabolites and rates of glycogen synthesis. Adenovirus-driven perilipin expression lead to significant accumulation of triacylglycerol in myoblasts, without any detectable effect on insulin sensitivity, as judged by the ability of insulin to stimulate glycogen synthesis. Similarly, incubation of cells with the monounsaturated fatty acid oleate resulted in triacylglycerol accumulation without inhibiting insulin action. By contrast, the saturated fatty acid palmitate induced insulin resistance. Palmitate treatment caused less accumulation of triacylglycerol than did oleate but also induced significant accumulation of both diacylglycerol and ceramide. Insulin resistance was also caused by cell-permeable analogues of ceramide, and palmitate-induced resistance was blocked in the presence of inhibitors of de novo ceramide synthesis. Oleate co-incubation completely prevented the insulin resistance induced by palmitate. Our data are consistent with ceramide being the agent responsible for insulin resistance caused by palmitate exposure. Furthermore, the triacylglycerol derived from oleate was able to exert a protective role in sequestering palmitate, thus preventing its conversion to ceramide.


Carbs increase palmitate
https://journals.plos.org/...al.pone.0113605

Even obese youth had high palmitate
http://www.ncbi.nlm.nih.gov/...pubmed/27064244
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Average Al

Nwlifter wrote:
Average Al wrote:


If we take the root of 80% of the T2 diabetic diagnosis levels, which is being overweight, and knowing that insulin inhibits HSL, thus keeping fatty acids locked up in fat cells, and insulin causes fat cells to absorb glucose, where it then becomes stored trigs, I can't see any way around the facts that a person eating 4 high carb meals a day with a massively higher 24 AUC of insulin compared to a low carb diet, wouldn't have a higher chance of 'getting fat' in the first place and starting the whole cascade.
I've seen far too many 'real people' over the years just shed fat (myself included) like crazy on low carb with plenty of food to satiate the appetite.


I'm afraid you lost me here...

Calories being equal, and not in excess of need, I'd guess that someone eating a high carb diet would need more insulin than someone on a low carb diet. But as long as calories are not excessive, there shouldn't be risk of weight gain.

If calories were controlled, but in excess of need, then I guess I don't really know which diet would be more fattening.

As for the ad libitum situation, it probably depends a lot on the individual.
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Average Al

Nwlifter wrote:
Here is how 'fat mass' affects glucose and insulin levels, even in people who are still 'under the cutoff' for being diagnosed with glucose issues.



Higher % IBW means more fat mass? It shows some correlation, but also a few outliers...
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Nwlifter

Average Al wrote:
Nwlifter wrote:
Average Al wrote:


If we take the root of 80% of the T2 diabetic diagnosis levels, which is being overweight, and knowing that insulin inhibits HSL, thus keeping fatty acids locked up in fat cells, and insulin causes fat cells to absorb glucose, where it then becomes stored trigs, I can't see any way around the facts that a person eating 4 high carb meals a day with a massively higher 24 AUC of insulin compared to a low carb diet, wouldn't have a higher chance of 'getting fat' in the first place and starting the whole cascade.
I've seen far too many 'real people' over the years just shed fat (myself included) like crazy on low carb with plenty of food to satiate the appetite.

I'm afraid you lost me here...

Calories being equal, and not in excess of need, I'd guess that someone eating a high carb diet would need more insulin than someone on a low carb diet. But as long as calories are not excessive, there shouldn't be risk of weight gain.

If calories were controlled, but in excess of need, then I guess I don't really know which diet would be more fattening.

As for the ad libitum situation, it probably depends a lot on the individual.


remember though, maintenance calories, which determine what level 'is' excess, depends on BMR, high carb high insulin, lowers metabolic rate.
Studies show that in people with more insulin resistance, a high carb diet's maintenance level might be as high as 500 calories less than a low carb diet due to metabolic rate changes.
So the high insulin, locking fats in, keeps metabolic rate lower so we 'burn' less calories at rest.
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