Protocol For Curing Type 2 Diabetes, Anyone?

[Apple]

@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.

Did you have any luck with this water cure regimen ?

 

[CLASH]

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



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 :)

Here are quotes from the same article you extracted your quote from, directly preceding and following your quote:

"Since there is a dynamic steady state during short‐term fasting, glucose production exactly matches glucose clearance from the plasma. In the face of hyperglycaemia, glucose clearance represents both tissue glucose metabolism and urinary glucose loss. By collecting urine and measuring the losses directly, tissue glucose metabolism can be calculated readily. Such calculations show that, in the face of hyperglycaemia, tissue glucose uptake is usually increased above normal even when insulin deficiency is severe."

This method of determining glucose uptake doesn't tell us much about glucose oxidation. Even if the cell is able to uptake glucose, is it able to oxidize it. Also, as we will see in the next quote, which you alluded to, glucose doesn't necessarily require insulin to be taken up. This is widely known, which is why in the quote I quoted above they specifically mention the liver, adipose tissues and muscles as uniquely insulin dependent. These are the tissues that largely rely on GLUT-4, which is an insulin dependent glucose transporter. Other tissues such as the organs/ systems, RBC's, CNS, etc. use other glucose transporters that aren't insulin dependent. With these elements in mind, the idea that glucose uptake being increased in hyperglycemia with insulin deficiency doesn't invalidate the idea of insulin resistance in target insulin dependent tissues. Also, insulin resistance isn't generally understood as a complete inability of the cells to uptake glucose, it implies a decrease metabolism of glucose at these insulin sensitive tissues with adjustments in uptake. See the quote below for talk about the different glucose transporters from the same article:

"We now know the detailed mechanisms involved and can explain this. Glucose uptake by all cells is by means of a specific transport protein (glucose transporter) of which at least six isomers (Glut 1 to Glut 6) are known. Glucose is a highly polar substance, being freely soluble in water but insoluble in fat. It cannot enter cells except through the specific transport system utilizing Glut 1–6. Glut 4 is the transport protein present in muscle and adipose tissue, which is known to be ‘insulin sensitive’. This means that, in addition to the transporters resident in the cell membrane at any given moment, there is a pool of glucose transporter molecules in the cytoplasm of the cell which can be recruited in response to a rise in plasma insulin, to join those already in the cell membrane in the fasting state. We now know, from experiments like those illustrated in Fig. 3, that even in the fasting state or in a state of absolute insulin deficiency, there are sufficient glucose transporters already in place in the cell membrane to allow glucose uptake to exceed that of a normal individual when the gradient of glucose concentration across the cell membrane is sufficiently high."

***I can't access figure 3 to see what specifically they are referring to.***

Furthermore the authors discuss ketones as molecules that can block glucose oxidation and then seemingly allude to the randle cycle without directly mentioning it. The thing is both ketones and fatty acids can block glucose oxidation by similar mechanisms implied by the authors. Also, something they discuss here as well is even if glucose can enter the cell, if it cannot be effectively oxidized, there is the possibility that it can be excreted. It may also be metabolized to other components, rather than being converted to energy. If I recall correctly diabetics actually tend to have higher glycogen levels in the cell. It has been hypothesized that this occurs due to a shifting of the carbohydrate towards glycogen storage due to an inability to properly oxidize the carbohydrate.

"When ketone concentrations in the plasma are high (above about 15 mmol litre–1), their metabolism can account for most of the energy needs of the Krebs’ cycle. This results in a physiological ‘damming back’ of glycolysis from glucose. As a result, the concentration of the intermediate compounds in the glycolytic pathway increases until the tissue concentration of glucose 6‐phosphate is so high that further phosphorylation of glucose that has been transported into the cell becomes inhibited. Even when this stage is reached, glucose transport into the cell continues but, rather than being phosphorylated and passing down the glycolytic pathway and oxidized in the Krebs’ cycle, glucose is transported back out of the cell (‘futile cycling’). The glucose transporter is specific for glucose and cannot transport glucose 6‐phosphate."

Overall this quote still isn't supporting Dr. Fung's arguments. All we are seeing with these series of quotes is that glucose can be taken up without insulin via separate GLUT transporters. Whether this is occurring in the insulin dependent tissues is hard to parse out from this study as I can't access figure 3 right now. This still doesn't support increased glucose oxidation or excess ATP generation (to be fair I know you directly mentioned that increased ATP isn't discussed by this quote). If anything this article supports the idea that excess fatty acid oxidation/ ketone oxidation in the diabetic state is impairing glucose oxidation and subsequently backing up glycolysis (randle cylce), and that excess glucagon (I didn't quote this section) is involved in driving the diabetic state.

 

[Katty]

Here are quotes from the same article you extracted your quote from, directly preceding and following your quote:

"Since there is a dynamic steady state during short‐term fasting, glucose production exactly matches glucose clearance from the plasma. In the face of hyperglycaemia, glucose clearance represents both tissue glucose metabolism and urinary glucose loss. By collecting urine and measuring the losses directly, tissue glucose metabolism can be calculated readily. Such calculations show that, in the face of hyperglycaemia, tissue glucose uptake is usually increased above normal even when insulin deficiency is severe."

This method of determining glucose uptake doesn't tell us much about glucose oxidation. Even if the cell is able to uptake glucose, is it able to oxidize it. Also, as we will see in the next quote, which you alluded to, glucose doesn't necessarily require insulin to be taken up. This is widely known, which is why in the quote I quoted above they specifically mention the liver, adipose tissues and muscles as uniquely insulin dependent. These are the tissues that largely rely on GLUT-4, which is an insulin dependent glucose transporter. Other tissues such as the organs/ systems, RBC's, CNS, etc. use other glucose transporters that aren't insulin dependent. With these elements in mind, the idea that glucose uptake being increased in hyperglycemia with insulin deficiency doesn't invalidate the idea of insulin resistance in target insulin dependent tissues. Also, insulin resistance isn't generally understood as a complete inability of the cells to uptake glucose, it implies a decrease metabolism of glucose at these insulin sensitive tissues with adjustments in uptake. See the quote below for talk about the different glucose transporters from the same article:

"We now know the detailed mechanisms involved and can explain this. Glucose uptake by all cells is by means of a specific transport protein (glucose transporter) of which at least six isomers (Glut 1 to Glut 6) are known. Glucose is a highly polar substance, being freely soluble in water but insoluble in fat. It cannot enter cells except through the specific transport system utilizing Glut 1–6. Glut 4 is the transport protein present in muscle and adipose tissue, which is known to be ‘insulin sensitive’. This means that, in addition to the transporters resident in the cell membrane at any given moment, there is a pool of glucose transporter molecules in the cytoplasm of the cell which can be recruited in response to a rise in plasma insulin, to join those already in the cell membrane in the fasting state. We now know, from experiments like those illustrated in Fig. 3, that even in the fasting state or in a state of absolute insulin deficiency, there are sufficient glucose transporters already in place in the cell membrane to allow glucose uptake to exceed that of a normal individual when the gradient of glucose concentration across the cell membrane is sufficiently high."

***I can't access figure 3 to see what specifically they are referring to.***

Furthermore the authors discuss ketones as molecules that can block glucose oxidation and then seemingly allude to the randle cycle without directly mentioning it. The thing is both ketones and fatty acids can block glucose oxidation by similar mechanisms implied by the authors. Also, something they discuss here as well is even if glucose can enter the cell, if it cannot be effectively oxidized, there is the possibility that it can be excreted. It may also be metabolized to other components, rather than being converted to energy. If I recall correctly diabetics actually tend to have higher glycogen levels in the cell. It has been hypothesized that this occurs due to a shifting of the carbohydrate towards glycogen storage due to an inability to properly oxidize the carbohydrate.

"When ketone concentrations in the plasma are high (above about 15 mmol litre–1), their metabolism can account for most of the energy needs of the Krebs’ cycle. This results in a physiological ‘damming back’ of glycolysis from glucose. As a result, the concentration of the intermediate compounds in the glycolytic pathway increases until the tissue concentration of glucose 6‐phosphate is so high that further phosphorylation of glucose that has been transported into the cell becomes inhibited. Even when this stage is reached, glucose transport into the cell continues but, rather than being phosphorylated and passing down the glycolytic pathway and oxidized in the Krebs’ cycle, glucose is transported back out of the cell (‘futile cycling’). The glucose transporter is specific for glucose and cannot transport glucose 6‐phosphate."

Overall this quote still isn't supporting Dr. Fung's arguments. All we are seeing with these series of quotes is that glucose can be taken up without insulin via separate GLUT transporters. Whether this is occurring in the insulin dependent tissues is hard to parse out from this study as I can't access figure 3 right now. This still doesn't support increased glucose oxidation or excess ATP generation (to be fair I know you directly mentioned that increased ATP isn't discussed by this quote). If anything this article supports the idea that excess fatty acid oxidation/ ketone oxidation in the diabetic state is impairing glucose oxidation and subsequently backing up glycolysis (randle cylce), and that excess glucagon (I didn't quote this section) is involved in driving the diabetic state.

Thanks, @CLASH. So the question is still how do we oxidize the glucose? Low fat, B3/niacinamide, aspirin. Now I'm wondering why Kempner's low fat rice diet didn't work for about 40% of participants. What was blocking glucose oxidation for those that were eating super low fat?