Questions about Hyperinsulinemia/Diabetes

[Kumar]

...Concentrations above the renal glucose threshold lead to glycosuria and osmotic diuresis as an inevitable result of the way the kidney works. I don't think that either the glycosuria or the polyuria/polydipsia are really beneficial to the patient, and I don't think they're a deliberate mechanism evolved by the body to cope with hyperglycaemia. (Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold, apparently an adaptive response to avoid losing so much glucose in the urine, which would suggest that it isn't beneficial.) I think it just happens, because that's the way the kidney works.

Rolfe.

I want to understand;

Why glycosuria or the polyuria/polydipsia are not really beneficial to the patient & why they're not deliberate mechanism evolved by the body to cope with hyperglycaemia? Is it not good to excrete excess sugar into urine by encouraging
polyuria/polydipsia? Much adverse effects are not indicated of glycosuria.

"Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold,"

Can't it happen due to medications/hyperinsulinemia?

The renal thresholds for various substances can be altered by many drugs and also change in characteristic ways during illnesses, as for example infections of various types.
http://en.wikipedia.org/wiki/Renal_threshold

 

[Rolfe]

I want to understand;

Why glycosuria or the polyuria/polydipsia are not really beneficial to the patient & why they're not deliberate mechanism evolved by the body to cope with hyperglycaemia? Is it not good to excrete excess sugar into urine by encouraging
polyuria/polydipsia? Much adverse effects are not indicated of glycosuria.

No. The amount of glucose lost (not "excreted") in the urine is pretty insignificant as far as controlling hyperglycaemia is concerned. Also, any event which increases the blood glucose above the renal glucose threshold will lead to glycosuria - such as intravenous glucose treatment or, as you noted, a high consumption of carbohydrate short-term - it's not a specific mechanism related to diabetes. It's just the way the kidney works, it's not a desirable or beneficial effect.

Man has evolved in an environment of food scarcity. All adaptive mechanisms are geared to conserving calories where possible. No adaptive response wants to waste glucose. It's just that the kidney didn't evolve to cope with blood glucose over about 10mmol/l because that is never seen for more than very short (and insignificant) periods in healthy people. So when blood glucose is high in diabetes, you get an overspill effect.

Glycosuria is an adverse event. It leads to osmotic diuresis, polyuria, and dehydration (if not corrected by polydipsia). It also predisposes to serious urinary tract infections. It is not a good thing to have.

Also, encouraging polydipsia does not lead to glycosuria. If you deliberately drink more, you will not get glucose in your urine unless your blood glucose is over the renal threshold - and if it is, you will not be able to help drinking more, because the excess glucose in the urine will force you to do it.

The glycosuria is the primary event, causing the polyuria, which then causes polydipsia. But of course Kumar's been at the bass-ackwards machine again.[/B][/QUOTE]"Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold,"

Can't it happen due to medications/hyperinsulinemia? [/B][/QUOTE] Long-term diabetic patients do not have hyperinsulinaemia. Unless they've been injecting too much insulin. In which case they become hypoglycaemic and suffer faints and collapse. Low blood glucose will not lead to an increased renal threshold. Once again Kumar has been at the bass-ackwards machine.

Kumar, diabetic patients do not have "too much" insulin! Quite the opposite! Early type II patients might have abnormally high levels, but that's a different matter. If they are hyperglycaemic, they do not have "too much". They still don't have enough. It is too much glucose that causes insulin resistance, not insulin.

And if a diabtic patient takes too much insulin, he will not become insulin resistant, he will become hypoglycaemic.

And the presence of glucose in the urine is a meaningless side-effect of the functioning of the kidney when blood glucose is above a certain level, there is no deep significance to be found in that.

Oh, why do I bother.

BSM, shoot me now.

Rolfe.

 

[Badly Shaved Monkey]

BSM, shoot me now.

Rolfe.

No. I'll ask a question instead. I've never been sure and have been unable to confirm, what does glycosuria do to urine SG? If a diabetic with glycosuria has a high SG does that confirm renal concentration capacity is intact, or is it just the sugariness that raises the SG?

 

[Rolfe]

No. I'll ask a question instead. I've never been sure and have been unable to confirm, what does glycosuria do to urine SG? If a diabetic with glycosuria has a high SG does that confirm renal concentration capacity is intact, or is it just the sugariness that raises the SG?

It's the sugariness. That's the pukka, out-of-the-book answer. However, I note that some pretty high-glucose samples are still low-SG. Which makes me conclude that the amount of diuresis must be pretty spectacular. But even though it's a significant calorie loss to the body, it never makes any difference to the blood glucose.

On a related matter, when I was at the RVC I used to fight with the surgeons who perpetually put their patients on dextrose saline for maintenance. They had all these grossly hyperglycaemic patients, except they didn't know because "we don't need no steenkin blood tests". Kathy Clarke used to say, well, you shouldn't use isotonic saline, because the sodium will be excreted and that will draw water with it and dehydrate the patient. I don't think I quite found the courage at the time to explain that the dextrose/glucose was doing the same thing but with bells on! And I was getting all these hypokalaemic patients who weren't recovering fast enough because of the muscle weakness.... I had an uphill struggle to advance the case for Hartmann's, but I think that argument has been won by now.

Rolfe.

 

[Kumar]

Man has evolved in an environment of food scarcity. All adaptive mechanisms are geared to conserving calories where possible. No adaptive response wants to waste glucose. It's just that the kidney didn't evolve to cope with blood glucose over about 10mmol/l because that is never seen for more than very short (and insignificant) periods in healthy people. So when blood glucose is high in diabetes, you get an overspill effect.

Thanks Rolfe.

You said; "No adaptive response wants to waste glucose". As you say that higher insulin level will always be hypoglycaemic, excess glucose level in blood will only be due to less availabilty of insulin. Does it not tell that, glycosuria will always be insulin dependent? Higher insulin low glycosuria, low insulin more glycosuria. Under this consideration we can say that, insulin is a cause to getting or not getting glycosuria, polyuria & polydipsia. Its lower level will encourage glycosuria, polyuria & polydipsia & its higher level will discourage these. Right?

Long-term diabetic patients do not have hyperinsulinaemia. Unless they've been injecting too much insulin. In which case they become hypoglycaemic and suffer faints and collapse. Low blood glucose will not lead to an increased renal threshold. Once again Kumar has been at the bass-ackwards machine.Kumar, diabetic patients do not have "too much" insulin! Quite the opposite! Early type II patients might have abnormally high levels, but that's a different matter. If they are hyperglycaemic, they do not have "too much". They still don't have enough. It is too much glucose that causes insulin resistance, not insulin.



Is it not medications oriented?

And if a diabtic patient takes too much insulin, he will not become insulin resistant, he will become hypoglycaemic.

But can it encourage glucose conversion into fats & fats store--making a person obese so IR? Can a person still convert glucose into fats & store it, when he is insulin resistant?

Btw, whether insulin test measures both exo/endo-genous amount of insulin present in blood?

 

[Kumar]

In other words, Kumar fails to grasp even the basics of diabetes and the difference between the two types.No, Kumar type 1 is not a later stage of type 2. Type 2 patients often progress to insulin dependent type 2, but that is NOT the same as type 1.Excess insulin of any kind does not acuse IR in a type 1 diabetic.

Excess insulin does not cause IR in anybody, it causes hypo.

Hans

Sorry, there is a backlog in replying but I am trying. Don't consider my reply to you previous post but consider, what is quoted.

Do you mean to say type1 and other autoimmune diseases are not a progressive diseases(in one or in sevaral generations)? If progressive, can you tell stages of DM type1?

But can't it encourage glucose conversion into fats & fats store--making a person obese so IR?

 

[Kumar]

No. See here: Insulin resistance is a problem with sugar metabolism, not fat metabolism. An insulin resistant patient is not totally unable to utilise blood sugar.

Thanks for good link. Can we now forget obesity as a cause of IR? Can we now think that IR may be due to hyperinsulinemia? T

This is characteristic of type 1 diabetics, not type 2 (I wish you would make up your mind which you are trying to discuss).

Hyperinsulinemia may also be not a characteristic of type 1 diabetics but excess BG levels can be? If glucose metabolism is is a reson, why type1 do not become insulin/glucose-resistant(should be right world if you are right)?

Weight loss can be observed in insulin resistant patients, particularly in the later stages when the condition is more severe,

How it happens in later stage when patient is taking sufficient medications?

but if they're not expending more calories than they are able to take in, they won't lose weight, just the same as anyone else.

What about in IR condition?


No.No. Insulin resistance is caused by persistently elevated blood sugar levels. If there were a problem with absorbtion of sugar by the gut, it wouldn't lead to increased blood sugar levels, would it? Try to use a little common sense.

The problem can also be related to absorbing excess sugar in intestines--may be due to excess mucus/sodium.

No. This has already been explained to you. How could excessive excretion of sugar in the urine increase the blood sugar level? Try to use a little common sense.As 2 and 3 do not occur, they can't be aggravated. Try to use a little common sense.

Sorry, you see only one side. Any problem/imbalance can be related to both higher or lower side. Excessive excretion of sugar in the urine will decrease the blood sugar level, but what about lesser excretion/loss of sugar in urine(low renal threshold)? Can't this not be possible due to any disorder of kidney or other parts?

 

[MRC_Hans]

.. Incomprehensible gibberish .... backwards assumptions .... misrepresentations ..... idiocy ....

NO.

You simply don't get it. You don't understand anything, not even the simplest things.



Hans

 

[Kumar]

Let me refresh my doubts:-


1. Excess glucose can be converted into fats & stored in fat cells in the presence of insulin. Can this conversion of glucose into fats is also possible in insulin resistance condition when both insulin & glucose levels are higher in blood?

2. Can high or excess insulin levels in blood cause IR condition OR impairing of insulin secretion from beta cells?

3. Whether any disorder related to decrease in renal threshold for sugar can be possible in diabetes/IR patients resulting into elevated level of blood glucose? Can hyperinsulinemia trigger it?

4. Can there be some disorder in intestinal absorption of sugar which may result into more glucose in blood in DM type2/IR patients(think abourt Na/sugar co-transported & more Na in thick intestinal mucus via Na/KATP pump may cause it)? Can hyperinsulinemia encourage/trigger to it?

5. Whether obesity/cenral obesity is a prime cause of getting IR condition or it is due to IR condition?

6. Can there be some role of acid, base, water(mucus) imbalances in metabolic pathway in getting diabetes/IR conditions?

7. Can central obesity be due to gas/blotting, fluid(LA) or fats accumulations in muscles/cavaties?

I am asking these questions considering Insulin secretion is not impaired in patient with insulin resistance, so it may not be a beta cell defect.

 

[Mojo]

Do you mean to say type1 and other autoimmune diseases are not a progressive diseases(in one or in sevaral generations)? If progressive, can you tell stages of DM type1?

But can't it encourage glucose conversion into fats & fats store--making a person obese so IR?

No, type 1 diabetes does not encourage glucose conversion to fat. This is because the high blood glucose level in diabetics is caused by their cells being unable to take up and metabolise glucose. You have been told this over and over again.

If diabetics are overweight, it's because they are eating too much and/or not getting enough exercise, possibly as a result of spending all their spare time on the internet.

 

[Mojo]

As you say that higher insulin level will always be hypoglycaemic, excess glucose level in blood will only be due to less availabilty of insulin. Does it not tell that, glycosuria will always be insulin dependent? Higher insulin low glycosuria, low insulin more glycosuria.

I don't think Rolfe has said this. In fact, she's indicated that glycosuria is caused by hyperglycaemia, not hypoinsulinaemia:

Also, any event which increases the blood glucose above the renal glucose threshold will lead to glycosuria - such as intravenous glucose treatment or, as you noted, a high consumption of carbohydrate short-term - it's not a specific mechanism related to diabetes.

This was in the very post you were replying to (although, of course, you neglected to quote this particular sentence).

 

[Kumar]

Kumar, common sense? Incompatible .

Hans

Yes, different, dynamic, uncommon...senses can add/research whereas routine, static, common...senses can just tell, repeat or teach. What should be practiced here & there except in class-room?

I may present on one day dynamic/different thoughts as;

Can excess intake of Na/salt & modern lifestyle/environment related effects(stress/pH related) be a prime resong of getting modern diseases--diabetes, hypertention etc.?

Effects of use of"Talcum powder", some other cosmatics, tree cover etc. on BG/BP levels and IR?

 

[Mojo]

Can we now forget obesity as a cause of IR? Can we now think that IR may be due to hyperinsulinemia?

No. As you have been repeatedly told, insulin resistance is caused by long-term hyperglycaemia, and obesity is a contributing factor.

Hyperinsulinemia may also be not a characteristic of type 1 diabetics but excess BG levels can be?

Yes, in type 1 diabetes hypoinsulinaemia, caused by the beta cells not producing enough insulin, leads to hyperglycaemia.

Weight loss can be observed in insulin resistant patients, particularly in the later stages when the condition is more severe,

How it happens in later stage when patient is taking sufficient medications?

If a patient is taking "sufficient medications" their glucose metabolism should be more or less normal, and their weight will be dependent on diet and exercise, the same as anyone else's. Weight loss in the later stages of type 2 diabetes is caused by their not being able to take up and utilise glucose from the blood as a result of not having sufficient levels of insulin to overcome resistance.

but if they're not expending more calories than they are able to take in, they won't lose weight, just the same as anyone else.

What about in IR condition?

Just the same as for anyone else.

The problem can also be related to absorbing excess sugar in intestines--may be due to excess mucus/sodium.

The intestines have evolved to absorb as much sugar as possible. "Excess sugar," as you put it, will be absorbed if there is too much sugar in the diet. This is certainly not a defect in the gut itself.

Any problem/imbalance can be related to both higher or lower side. Excessive excretion of sugar in the urine will decrease the blood sugar level, but what about lesser excretion/loss of sugar in urine(low renal threshold)? Can't this not be possible due to any disorder of kidney or other parts?

No. The kidneys, as you have already been told, are not part of the body's system for regulating blood sugar levels.

 

[Kumar]

Tell me Kumar, which of the words in the sentence "IR is not caused by hyperinsulinemia" is it you don't understand?

Hans

"Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease"

Can't pathogenesis of this disease be- excess/high secretion of insuln/gastic acid which may encourage & result into all other conditions?

 

[MRC_Hans]

Yes, different, dynamic, uncommon...senses can add/research whereas routine, static, common...senses can just tell, repeat or teach. What should be practiced here & there except in class-room?

I may present on one day dynamic/different thoughts as;

Can excess intake of Na/salt & modern lifestyle/environment related effects(stress/pH related) be a prime resong of getting modern diseases--diabetes, hypertention etc.?

Effects of use of"Talcum powder", some other cosmatics, tree cover etc. on BG/BP levels and IR?

Nope, Kumar, that is not what you are doing. Just shooting ideas into space to see if they orbit can be productive in certain situations (think of a brainstorming session), although to do it in general science is virtually certain to be a waste of time.

However, that is not what you are doing, Kumar. Because if you just were airing ideas, you would accept it with grace when they were shot down, and go on to the next idea. But in fact you do the opposite: You cling desperately to even the most silly notions forever, never really abandoning them even after people have been lecturing you endlessly on why you are wrong. You show a profound and arrogant disrespect to the prople you are communicating with when you keep ignoring their answers. Just look at this post of yours, right above:

Let me refresh my doubts:-


1. Excess glucose can be converted into fats & stored in fat cells in the presence of insulin. Can this conversion of glucose into fats is also possible in insulin resistance condition when both insulin & glucose levels are higher in blood?

2. Can high or excess insulin levels in blood cause IR condition OR impairing of insulin secretion from beta cells?

3. Whether any disorder related to decrease in renal threshold for sugar can be possible in diabetes/IR patients resulting into elevated level of blood glucose? Can hyperinsulinemia trigger it?

4. Can there be some disorder in intestinal absorption of sugar which may result into more glucose in blood in DM type2/IR patients(think abourt Na/sugar co-transported & more Na in thick intestinal mucus via Na/KATP pump may cause it)? Can hyperinsulinemia encourage/trigger to it?

5. Whether obesity/cenral obesity is a prime cause of getting IR condition or it is due to IR condition?

6. Can there be some role of acid, base, water(mucus) imbalances in metabolic pathway in getting diabetes/IR conditions?

7. Can central obesity be due to gas/blotting, fluid(LA) or fats accumulations in muscles/cavaties?

I am asking these questions considering Insulin secretion is not impaired in patient with insulin resistance, so it may not be a beta cell defect.

EVERY single question in that post has been painstakingly and carefully answered IN THIS VERY THREAD, some of them several times. It is incredibly inulting to the people who have taken time to answer you, when you just restate those questions.

I will not express my opinion of you as it would most certainly violate rule 8, but I for one am done with you. Do not expect any more tolerance from me.

Hans

 

[Mojo]

I am asking these questions considering Insulin secretion is not impaired in patient with insulin resistance, so it may not be a beta cell defect.

You have already been told that insulin resistance is not a defect of the beta cells. It is a defect of the body's cells which prevents them from reacting properly to the insulin that the beta cells produce.

 

[Kumar]

"not"

 

[Mojo]

"Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease"

Do you really think this quotation supports your contention that insulin resistance is caused by hyperinsulaemia?

Can't pathogenesis of this disease be- excess/high secretion of insuln/gastic acid which may encourage & result into all other conditions?

No. Quite apart from anything else, the low pH in the stomach is to enable the digestion of protein, not carbohydrates.

 

[MRC_Hans]

You have already been told that insulin resistance is not a defect of the beta cells. It is a defect of the body's cells which prevents them from reacting properly to the insulin that the beta cells produce.

I am trying hard to be so charitable as to assume that Kumar simply does master enough English to understand neither his own questions nor the many replies to them. Unfortunately, he does occasionally show that he can both read, write, and apply logic, so I'm really left with a much less flattering conclusion than sheer idiocy.

Hans

 

[Kumar]

In Kumar's second post on the JREF forum, a thread he started himself, and touching on what appeared to be his main motivation for coming here to debate, he postulated that excess injected insulin could exacerbate diabetes, and reducing insulin dosage (or discontinuing it) would cure the patient. This was close to two years ago. He was told then that insulin does not cause insulin resistance, and people have been telling him the same thing on almost a daily basis ever since.

I've seens a number of cases of wilful refusal to learn, but this really caps the lot.

Rolfe.

Sorry to say/ask this: Should anyone accept everything absolutely, said by you/science? One should be satisfied or not esp. when backed by some practical observations & experiances, logics, differenciating informations, fishy smells here & there etc.?? Should we think dynamically & differently or not to add/research OR just follow routines?