Protocol For Curing Type 2 Diabetes, Anyone?

[tankasnowgod]

I think this paper meshes very well with Peat's ideas. After reading this, I get to understand more what Peat was saying in Glucose and sucrose for diabetes. The one thing this paper diverges from Peat is its ascribing the variance of glucose uptake (as well as liver glucose production) among different people to genetics. Ray Peat ascribes this to PUFAs blocking glucose uptake.

Given insulin's role in inhibiting lipolysis and ketogenesis, as gleaned from the paper,it would be reasonable to infer that insulin promotes sugar metabolism. The consumption of fat enables fat oxidation, thus competing against glucose metabolism, and invariably lessens glucose uptake, contributing to higher blood sugar levels. And if the fat is PUFA, it also blocks glucose metabolism. Does this make a case for a low-fat dietary approach to counter diabetes?

And in the case of type II diabetes, where apart from PUFA inhibiting glucose uptake, an inability to produce sufficient insulin would make it hard to fully inhibit endogenous glucose production (by the liver), thus causing high blood sugar. Does this make a case for a high-carbohydrate approach, since both glucose and fructose would help restore the beta cells in the pancreas, thus increasing insulin production?

Kempner's approach looks to be validated. With the incorporation of Peat's ideas on PUFA elimination, even better.

It certainly seems to me like a long term low carb approach to diabetes is flawed. It seems that focusing on lowering iron would be much more beneficial. Although, I can see some merit in a lower carb approach with a focus on reducing iron stores, and cycling carbs up as iron gets near deficiency, maybe eventually ending up at what would be considered a high carb diet.

And it seems that, other than Peat, no one is really advocating getting the bulk of carbs from sugars rather than starches. I think that could also help solve a lot of problems.

By the way, Dr. Facchini had some good success with the approach of targeting iron. A Low-Iron-Available, Polyphenol-Enriched, Carbohydrate-Restricted Diet to Slow Progression of Diabetic Nephropathy

His experimental diet is labeled "carb restricted," but still had about 35% of calories from carbs, so more of a moderate than low carb approach.

 

[paymanz]

That insulin article is nice

 

[Elephanto]

Keep fat intake very low for a while, try to reduce stress (includes cutting down on caffeine if it applies), avoid darkness and blue lights, High Dose Niacinamide, B1, Magnesium (see Calcium Antagonists may treat diabetes thread), moderate cardio, keep CO2 high (controlled breathing, bag breathing, baking soda), take antioxidants to decrease pancreas and liver oxidation.

Niacinamide For Type II Diabetes

Calcium Antagonists May Completely Reverse Diabetes

Changes In Thiamine Levels May Be The First Sign Of Type I Diabetes

Thiamine: One Of The Main Limiting Factors For Proper Carbohydrate Metabolism

Emotional Stress Linked To Diabetes

Impact of moderate versus mild aerobic exercise training on inflammatory cytokines in obese type 2 diabetic patients: a randomized clinical trial

Rather, a stronger association has been observed between total fat and saturated fat intake and type 2 diabetes (75,76)

 

[Peater Piper]

Insulin resistance, but normal basal rates of glucose production in patients with newly diagnosed mild diabetes mellitus : Acta Endocrinologica

Basal glucose production and utilization between controls and diabetics is nearly the same in an unfed state. During insulin infusion, however, the diabetics have reduced suppression of endogenous glucose production. When glucose infusion is added to the insulin infusion, healthy subjects utilize the glucose at a very high rate, whereas the diabetics aren't able to increase utilization enough to prevent hyperglycemia.

 

[mostlylurking]

Ray Peat says all diabetics are by definition hypothyroid. So addressing this first makes really good sense to me. My husband (age 66) was diagnosed with "metabolic syndrome" and had high blood sugar. The doctor labeled him pre-diabetic and told him to go off of all sugar. Thankfully, she also put him on some natural desiccated thyroid medication. I talked him into cutting out all PUFA and adding a glass of orange juice with about 100 mg of niacinamide and 100 mg of thiamine three times a day. He lost 25 pounds in three months and feels a whole lot better. We usually have a large glass of milk with gelatin, sugar, and vanilla for dinner, along with some oranges .

I think that over all, the changes he made were pretty simple and he has made them into long term habits. It has been 9 months and his weight seems to have stabilized at 25 pounds lighter.

 

[yerrag]

Ray Peat says all diabetics are by definition hypothyroid. So addressing this first makes really good sense to me. My husband (age 66) was diagnosed with "metabolic syndrome" and had high blood sugar. The doctor labeled him pre-diabetic and told him to go off of all sugar. Thankfully, she also put him on some natural desiccated thyroid medication. I talked him into cutting out all PUFA and adding a glass of orange juice with about 100 mg of niacinamide and 100 mg of thiamine three times a day. He lost 25 pounds in three months and feels a whole lot better. We usually have a large glass of milk with gelatin, sugar, and vanilla for dinner, along with some oranges .

I think that over all, the changes he made were pretty simple and he has made them into long term habits. It has been 9 months and his weight seems to have stabilized at 25 pounds lighter.

That looks pretty simple and easy to do. Good job!

 

[ecstatichamster]

this is pretty interesting:
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2362.2007.01838.x

Background  Although endothelial cells express insulin receptors, it is controversially discussed whether the endothelium represents an insulin‐responsive tissue. Since available data are primarily restricted to animal endothelial cells, this study tested (i) whether insulin affects glucose metabolism in human endothelium; (ii) whether insulin sensitivity is different in micro‐ versus macrovascular endothelial cells; and (iii) whether glucose concentration in the incubation medium affects the cells’ response to insulin.

Materials and methods  Human umbilical vein endothelial cells (HUVECs), human adult saphenous vein endothelial cells (HAVECs), human aortic endothelial cells (HAEC), and human retinal endothelial cells (HRECs) as well as human smooth muscle cells were incubated with/without insulin (0·3 nmol L−1 or 1 µmol L−1). Glucose transport, glycogen synthesis, glycogen content, lactate release, and expression of phospho‐Akt, Akt, and endothelial nitric oxide synthase (eNOS) were determined.

Results  In HUVECs and HRECs, insulin (1 µmol L−1) increased (P < 0·05) eNOS expression by ~70% and doubled Akt phosphorylation, but the latter was by far more pronounced in human smooth muscle cells (+1093 ± 500%, P < 0·05). In human smooth muscle cells, insulin (1 µmol L−1) stimulated glycogen synthesis by 67 ± 11% (P < 0·01). In human micro‐ (HRECs) and macrovascular endothelial cells (HUVECs, HAVECs and HAECs), insulin, however, failed to stimulate glucose transport, glycogen synthesis, glycogen content, or lactate release under various conditions, i.e. after glucose deprivation or in medium with normal (5·5 mmol L−1) or high glucose (30 mmol L−1).

Conclusions  Insulin stimulated glycogen synthesis and Akt phosphorylation in human smooth muscle cells. In human micro‐ and macrovascular endothelial cells, insulin, however, failed to affect glucose uptake and metabolism under all experimental conditions applied, whereas it increased Akt phosphorylation and eNOS expression.

 

[Rafe]

@Wilfrid Thank you for posting the respiratory quotient article. It's very straightforward. Saving.

Conclusions  Insulin stimulated glycogen synthesis and Akt phosphorylation in human smooth muscle cells. In human micro‐ and macrovascular endothelial cells, insulin, however, failed to affect glucose uptake and metabolism under all experimental conditions applied, whereas it increased Akt phosphorylation and eNOS expression.

This view of insulin must be really marginalized. It's so clearly coherent. Crazy. A person could get downright paranoid.
I think I get the Sonksen article now. The "metabolic mayhem" really is massive overavailability of substrates without any capacity to use them. So a mechanical view would go straight for an abstraction: "a diabetic eats too much and doesn't move enough." But that isn't it really. Pufa seems to jump out as the origin of toxicity that overwhelms the system in general and probably poisons the beta cells. And explains the rise in incidence. And contributes heavily to @mostlylurking the hypothyroidism that leads the derangement.

This view might also explain why bariatric surgery shows better diabetic control immediately, since less substrate of all kinds is available. And automatically less pufa, less tissue to produce and "futilely cycle," [thanks ham] nutrients. If it's immediate, then it can't be just about eating less, I'm thinking.

So, "starvation improves the metabolic state" [paraphrase] for 3 weeks, and Peat's dad took only brewer's yeast "for a few weeks." Besides the fact that super-low nutrition for more than 3 weeks would just be straight starvation instead of therapy, got any ideas about what is significant about the 3 weeks? Beta cell recovery time? I'm thinking that.

 

[rei]

dr. jason fung has cured hundreds of type2 diabetics by using fasting as a therapeutic intervention, both intermittent fasting and prolonged fasting. He cannot say that he cures the patients but puts them in remission because officially t2d cannot be cured. Medical regulation is quite strict so he really has the data to back up all his claims. I suggest you look up some of his videos on youtube, he does not do anything extreme, and in fact i believe he could further improve his protocol by integrating some peaty ideas, mainly very small amounts of saturated fat during the fasting to combat the stress from released PUFA.

 

[Wilfrid]

@yerrag , have you heard about a guy named Rajinder Bhalla?
Take a look of his advices for health through his website: One Cure for All Diseases - One Cure for All Diseases
I think that the guy is really onto something with his protocol. His method to deal with diabetes reminds me of Pierre Alphonse Piorry's one. Ray has already spoke about Piorry , as well as one of his english fellow William Budd, in his articles about diabete.
Rajinder's website deserves a scrupulous reading.

 

[yerrag]

@yerrag , have you heard about a guy named Rajinder Bhalla?
Take a look of his advices for health through his website: One Cure for All Diseases - One Cure for All Diseases
I think that the guy is really onto something with his protocol. His method to deal with diabetes reminds me of Pierre Alphonse Piorry's one. Ray has already spoke about Piorry , as well as one of his english fellow William Budd, in his articles about diabete.
Rajinder's website deserves a scrupulous reading.

Thanks a lot for the link Wilfrid. If it were just any other poster, I would likely ignore this. The title is very clickbaity, and the solution he proposes seems to good to be true. But as I followed along, I began to think whether I would be free enough to follow his advice for the next 3 to 4 months. His story about how his elderly father and mother recovered for what I would see as irreversible disease with elderly people says he is either a liar or he has found a solution. He talks also about diabetes and how it can be cured. While I don't have diabetes, I think I can benefit from drinking water his way, being able to time it at the right time and drinking the quantity he recommends. The simple walking and rest cycle is something easy enough to try as well. I urinate a lot, and now I think I could be drinking too much water.

 

[Texon]

I think what matters is fasted insulin readings. I don’t really think it matters to spike glucose high, as long as minimal insulin is required in response. Stuff consistently hits the fan when fasted insulin is high (double digits already too high imo), sensitivity declines etc.

A year ago my father and I got the same fasted blood glucose upwards of 90, but my insulin was a third of his. Means a lot

@ecstatichamster benaoao I find this to be a fascinating discussion as I am 67, lean at 6'5"/195 lbs and as of recent labs had fasting glucose of 90 and a1c of 5.8. Nevertheless I may have stumbled on to something related to monk fruit benefits from of all things the diabetes council..

Why Monk Fruit is A Power Food for Diabetes

I had also recently become concerned about potential kidney issues (intermittently foamy urine etc.). Recent gfr was 60 and I would like it to be higher. Being that it is thanksgiving, my diet has been distinctly unfavorable to all this. However recent liberal use of the monk fruit/erythritol based sweetener Lankato has stopped the foamy urine in its tracks. Plus I have started very low doses of arimidex since I am on a modest trt protocol. I hope this might help clear fairly prominent age spots on the backs of both hands as well. I am looking at adding low hcg once a week too per your suggestion benaoao. Anyway I wanted to see what you guys think about the monk fruit idea.

 

[Katty]

dr. jason fung has cured hundreds of type2 diabetics by using fasting as a therapeutic intervention, both intermittent fasting and prolonged fasting. He cannot say that he cures the patients but puts them in remission because officially t2d cannot be cured. Medical regulation is quite strict so he really has the data to back up all his claims. I suggest you look up some of his videos on youtube, he does not do anything extreme, and in fact i believe he could further improve his protocol by integrating some peaty ideas, mainly very small amounts of saturated fat during the fasting to combat the stress from released PUFA.

I know this is an old thread, but I have a question about the reference to Dr. Jason Fung's discussion of diabetes. I'm aware of Peat's views on fasting and diabetes, but I'm curious about something Fung said in this video:


View: https://www.youtube.com/watch?v=6KS7M0s2fJM


Dr. Fung asserts that diabetes is a problem of too much insulin, which causes too much glucose to enter the cell (not just in the blood). And that the blood sugar increases because there's already too much glucose in the cell and no room for more glucose molecules to enter. He then says that the excess glucose in the cell ends up creating TOO MUCH ATP. He doesn't really come back to this point. He goes on to say the cells in the liver don't like to store so much glucose, so they turn the glucose into fat, which makes a person gain body fat.

My first question... is Dr. Fung correct in his assertion that diabetics create TOO MUCH ATP? If that were true, why do diabetics have a subjective feeling of being tired/sleepy, especially in those hours after a meal. Wouldn't too much ATP mean a person feels energetic?

My second question... Dr. Fung says that a person who loses weight will start to heal/reverse the diabetes, which I know can be true sometimes (though there are some lean Type 2 diabetics). But it doesn't seem to fit in with his theory... because why would loss of adipose tissue help someone become more insulin sensitive if it's the glucose, and not the fat, that is clogging up the cell?

 

[Serge]

Dr. Fung asserts that diabetes is a problem of too much insulin, which causes too much glucose to enter the cell (not just in the blood). And that the blood sugar increases because there's already too much glucose in the cell and no room for more glucose molecules to enter.

Glucose is quite easy to deplete by not eating it and excercising. Strangely, - well, not really, - after you do this, the body will still have problems handling even small amounts of sugar - eat a couple of potatoes again, and BG numbers will run as high as before if not higher. I don't think his theory holds water.

 

[Katty]

Glucose is quite easy to deplete by not eating it and excercising. Strangely, - well, not really, - after you do this, the body will still have problems handling even small amounts of sugar - eat a couple of potatoes again, and BG numbers will run as high as before if not higher. I don't think his theory holds water.

Yes, I agree with that observation. But are you saying that, with diabetes, there is not extra glucose in the cell, and thus there is not an overproduction if ATP?

 

[Serge]

Yes, I agree with that observation. But are you saying that, with diabetes, there is not extra glucose in the cell, and thus there is not an overproduction if ATP?

Strictly speaking, there's only one way to know: by some intricate lab experiment. Other than that I can only say that feeling like a withered plant most of the time, I don't feel like swimming in ATP :) but who knows, excess could potentially cause tiredness as well. But pure logic can't decide anything related to biochemistry, only biochemical experiment can tell...

 

[CLASH]

I know this is an old thread, but I have a question about the reference to Dr. Jason Fung's discussion of diabetes. I'm aware of Peat's views on fasting and diabetes, but I'm curious about something Fung said in this video:


View: https://www.youtube.com/watch?v=6KS7M0s2fJM


Dr. Fung asserts that diabetes is a problem of too much insulin, which causes too much glucose to enter the cell (not just in the blood). And that the blood sugar increases because there's already too much glucose in the cell and no room for more glucose molecules to enter. He then says that the excess glucose in the cell ends up creating TOO MUCH ATP. He doesn't really come back to this point. He goes on to say the cells in the liver don't like to store so much glucose, so they turn the glucose into fat, which makes a person gain body fat.

My first question... is Dr. Fung correct in his assertion that diabetics create TOO MUCH ATP? If that were true, why do diabetics have a subjective feeling of being tired/sleepy, especially in those hours after a meal. Wouldn't too much ATP mean a person feels energetic?

My second question... Dr. Fung says that a person who loses weight will start to heal/reverse the diabetes, which I know can be true sometimes (though there are some lean Type 2 diabetics). But it doesn't seem to fit in with his theory... because why would loss of adipose tissue help someone become more insulin sensitive if it's the glucose, and not the fat, that is clogging up the cell?

I haven't watched the video, so I am responding purely to your statements.

1) Insulin Resistance and Upregulated Glucagon:
-In diabetes the insulin dependent cells are not effectively responding to insulin, this is the concept of insulin resistance i.e. even in the presence of insulin the glucose is impaired in its ability to be pushed into the cell. Furthermore, an element not described here by this perspective is that diabetes is characterized by an increased level of glucagon, which is not turned down despite an increased insulin/ blood glucose level (these two things generally decrease glucagon secretion by pancreatic alpha cells). Glucagon's function is to increase the generation of glucose at the liver, in the absence of exogenous glucose intake with a decreasing blood sugar level. So you have a double whammy here, 1) an increased blood glucose level from an elevated glucose production by the liver stimulated by glucagon, and 2) an impairment of glucose uptake in response to insulin. So the assumption that too much glucose is entering the cell in the diabetic state is quite contradictory from this perspective. If anything the insulin levels are increased in a compensatory manner due to the increased glucose concentrations from both of these aforementioned mechanisms (increased gluconeogensis and insulin resistance). See below:

*Insulin Resistance Quote:
"Insulin resistance is identified as an impaired biologic response to insulin stimulation of target tissues, primarily the liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in a compensatory increase in beta-cell insulin production and hyperinsulinemia."

*Excess Glucagon in Diabetes Quote:
"Excessive production of glucose by the liver contributes to fasting and postprandial hyperglycaemia, hallmarks of type 2 diabetes. A central feature of this pathologic response is insufficient hepatic insulin action, due to a combination of insulin resistance and impaired β-cell function. However, a case can be made that glucagon also plays a role in dysregulated hepatic glucose production and abnormal glucose homeostasis. Plasma glucagon concentrations are inappropriately elevated in diabetic individuals, and α-cell suppression by hyperglycaemia is blunted. Experimental evidence suggests that this contributes to greater rates of hepatic glucose production in the fasting state and attenuated reduction after meals. Recent studies in animal models indicate that reduction of glucagon action can have profound effects to mitigate hyperglycaemia even in the face of severe hypoinsulinaemia."

The role of dysregulated glucagon secretion in type 2 diabetes - PubMed

Excessive production of glucose by the liver contributes to fasting and postprandial hyperglycaemia, hallmarks of type 2 diabetes. A central feature of this pathologic response is insufficient hepatic insulin action, due to a combination of insulin resistance and impaired β-cell function...

pubmed.ncbi.nlm.nih.gov

---------------------------


2) Excess Fatty Acid Oxidation/ Decreased ATP generation in Diabetics:
-Furthermore, diabetes, obesity, insulin resistance are characterized by an increase in fatty acid oxidation. This elevated fatty acid oxidation actually drives insulin resistance directly. This further contradicts the idea that too much glucose oxidation is going on in the diabetic state, if anything there is too much fatty acid oxidation. Also, the idea the there is an excess of ATP is questionable, most of the papers I have read have characterized diabetes, obesity, insulin resistance as a state of cellular energy deficiency. Please see below for both points:

*Excess Fatty Acid Oxidation in Diabetics Quote:
"An imbalance between fatty acid uptake and oxidation is believed to be responsible for this lipid accumulation, and is thought to be a major cause of insulin resistance in obesity and diabetes, due to lipid accumulation and inhibition of one or more steps in the insulin-signaling cascade. As a result, decreasing muscle fatty acid uptake can improve insulin sensitivity. However, the potential role of increasing fatty acid beta-oxidation in the heart or skeletal muscle in order to prevent cytoplasmic lipid accumulation and decrease insulin resistance is controversial. While increased fatty acid beta-oxidation may lower cytoplasmic lipid accumulation, increasing fatty acid beta-oxidation can decrease muscle glucose metabolism, and incomplete fatty acid oxidation has the potential to also contribute to insulin resistance."

Role of fatty acid uptake and fatty acid beta-oxidation in mediating insulin resistance in heart and skeletal muscle - PubMed

Fatty acids are a major fuel source used to sustain contractile function in heart and oxidative skeletal muscle. To meet the energy demands of these muscles, the uptake and beta-oxidation of fatty acids must be coordinately regulated in order to ensure an adequate, but not excessive, supply for...

pubmed.ncbi.nlm.nih.gov

*Decreased ATP generation in Diabetics Quote:
"Patients with diabetes had 27% lower fasting ATP synthetic flux compared to younger controls (p = 0.031). Insulin stimulation increased ATP synthetic flux only in controls (younger: 26%, 95% CI 13%–42%; older: 11%, 95% CI 2%–25%), but failed to increase even during hyperglycemic hyperinsulinemia in patients with T2DM. Fasting free fatty acids and waist-to-hip ratios explained 44% of basal ATP synthetic flux. Insulin sensitivity explained 30% of insulin-stimulated ATP synthetic flux."

"Patients with diabetes and the older controls had lower fasting ATP synthesis rates than the young controls and, whereas insulin stimulation increased ATP synthesis in all the controls, it had no effect in the patients with diabetes. In addition, fasting blood fatty acid levels were inversely related to basal ATP synthesis, whereas insulin sensitivity was directly related to insulin-stimulated ATP synthesis."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1858707/pdf/pmed.0040154.pdf

---------------------------


Overall, I'm not sure where Dr. Fung got his idea of increased glucose oxidation, and increased ATP production in diabetics (if he did indeed propose these things; I didn't watch the video, just going off of the initial posters questions/ statements). If anything its entirely the opposite here; decreased ATP, and impaired glucose oxidation.

 

[Katty]

Strictly speaking, there's only one way to know: by some intricate lab experiment. Other than that I can only say that feeling like a withered plant most of the time, I don't feel like swimming in ATP :) but who knows, excess could potentially cause tiredness as well. But pure logic can't decide anything related to biochemistry, only biochemical experiment can tell...

Agreed. Unless we're all misunderstanding ATP's role.

 

[Katty]

I haven't watched the video, so I am responding purely to your statements.

1) Insulin Resistance and Upregulated Glucagon:
-In diabetes the insulin dependent cells are not effectively responding to insulin, this is the concept of insulin resistance i.e. even in the presence of insulin the glucose is impaired in its ability to be pushed into the cell. Furthermore, an element not described here by this perspective is that diabetes is characterized by an increased level of glucagon, which is not turned down despite an increased insulin/ blood glucose level (these two things generally decrease glucagon secretion by pancreatic alpha cells). Glucagon's function is to increase the generation of glucose at the liver, in the absence of exogenous glucose intake with a decreasing blood sugar level. So you have a double whammy here, 1) an increased blood glucose level from an elevated glucose production by the liver stimulated by glucagon, and 2) an impairment of glucose uptake in response to insulin. So the assumption that too much glucose is entering the cell in the diabetic state is quite contradictory from this perspective. If anything the insulin levels are increased in a compensatory manner due to the increased glucose concentrations from both of these aforementioned mechanisms (increased gluconeogensis and insulin resistance). See below:

*Insulin Resistance Quote:
"Insulin resistance is identified as an impaired biologic response to insulin stimulation of target tissues, primarily the liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in a compensatory increase in beta-cell insulin production and hyperinsulinemia."

*Excess Glucagon in Diabetes Quote:
"Excessive production of glucose by the liver contributes to fasting and postprandial hyperglycaemia, hallmarks of type 2 diabetes. A central feature of this pathologic response is insufficient hepatic insulin action, due to a combination of insulin resistance and impaired β-cell function. However, a case can be made that glucagon also plays a role in dysregulated hepatic glucose production and abnormal glucose homeostasis. Plasma glucagon concentrations are inappropriately elevated in diabetic individuals, and α-cell suppression by hyperglycaemia is blunted. Experimental evidence suggests that this contributes to greater rates of hepatic glucose production in the fasting state and attenuated reduction after meals. Recent studies in animal models indicate that reduction of glucagon action can have profound effects to mitigate hyperglycaemia even in the face of severe hypoinsulinaemia."

The role of dysregulated glucagon secretion in type 2 diabetes - PubMed

Excessive production of glucose by the liver contributes to fasting and postprandial hyperglycaemia, hallmarks of type 2 diabetes. A central feature of this pathologic response is insufficient hepatic insulin action, due to a combination of insulin resistance and impaired β-cell function...

pubmed.ncbi.nlm.nih.gov

---------------------------


2) Excess Fatty Acid Oxidation/ Decreased ATP generation in Diabetics:
-Furthermore, diabetes, obesity, insulin resistance are characterized by an increase in fatty acid oxidation. This elevated fatty acid oxidation actually drives insulin resistance directly. This further contradicts the idea that too much glucose oxidation is going on in the diabetic state, if anything there is too much fatty acid oxidation. Also, the idea the there is an excess of ATP is questionable, most of the papers I have read have characterized diabetes, obesity, insulin resistance as a state of cellular energy deficiency. Please see below for both points:

*Excess Fatty Acid Oxidation in Diabetics Quote:
"An imbalance between fatty acid uptake and oxidation is believed to be responsible for this lipid accumulation, and is thought to be a major cause of insulin resistance in obesity and diabetes, due to lipid accumulation and inhibition of one or more steps in the insulin-signaling cascade. As a result, decreasing muscle fatty acid uptake can improve insulin sensitivity. However, the potential role of increasing fatty acid beta-oxidation in the heart or skeletal muscle in order to prevent cytoplasmic lipid accumulation and decrease insulin resistance is controversial. While increased fatty acid beta-oxidation may lower cytoplasmic lipid accumulation, increasing fatty acid beta-oxidation can decrease muscle glucose metabolism, and incomplete fatty acid oxidation has the potential to also contribute to insulin resistance."

Role of fatty acid uptake and fatty acid beta-oxidation in mediating insulin resistance in heart and skeletal muscle - PubMed

Fatty acids are a major fuel source used to sustain contractile function in heart and oxidative skeletal muscle. To meet the energy demands of these muscles, the uptake and beta-oxidation of fatty acids must be coordinately regulated in order to ensure an adequate, but not excessive, supply for...

pubmed.ncbi.nlm.nih.gov

*Decreased ATP generation in Diabetics Quote:
"Patients with diabetes had 27% lower fasting ATP synthetic flux compared to younger controls (p = 0.031). Insulin stimulation increased ATP synthetic flux only in controls (younger: 26%, 95% CI 13%–42%; older: 11%, 95% CI 2%–25%), but failed to increase even during hyperglycemic hyperinsulinemia in patients with T2DM. Fasting free fatty acids and waist-to-hip ratios explained 44% of basal ATP synthetic flux. Insulin sensitivity explained 30% of insulin-stimulated ATP synthetic flux."

"Patients with diabetes and the older controls had lower fasting ATP synthesis rates than the young controls and, whereas insulin stimulation increased ATP synthesis in all the controls, it had no effect in the patients with diabetes. In addition, fasting blood fatty acid levels were inversely related to basal ATP synthesis, whereas insulin sensitivity was directly related to insulin-stimulated ATP synthesis."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1858707/pdf/pmed.0040154.pdf

---------------------------


Overall, I'm not sure where Dr. Fung got his idea of increased glucose oxidation, and increased ATP production in diabetics (if he did indeed propose these things; I didn't watch the video, just going off of the initial posters questions/ statements). If anything its entirely the opposite here; decreased ATP, and impaired glucose oxidation.

Thanks for this thorough response. I had the same understanding of diabetes, which is why Dr. Fung's explanation about ATP was confusing.

 

[Serge]

Dr. Fung asserts that diabetes is a problem of too much insulin, which causes too much glucose to enter the cell (not just in the blood). And that the blood sugar increases because there's already too much glucose in the cell and no room for more glucose molecules to enter.

Hm interesting :) Previously in this very thread there is a link to an article that says:

Glucose uptake into cells is usually normal and often high in untreated diabetes​

...the observations which show unequivocally that tissue glucose uptake can exceed normal even in the face of severe insulin deficiency such as occurs in uncontrolled diabetes mellitus.

though it does not happen with all people. Besides, the article says that the role of insulin in glucose coming into the cell is exaggerated, glucose can come inside the cell using other agents. It doesn't talk about ATP. Anyways, I just find it interesting that it seems that glucose is abundant in the cells, according to this.

Sorry if it creates more confusion :)