Questions about Hyperinsulinemia/Diabetes

[MRC_Hans]

Whether modern lifestyle, pollution/environment is making us more anaaerobic? Excess Lactic acid( i don't know about pyruvate) can be immediate toxic/fatal. Can't it then encourage water retention to keep it diluted? Can't modern lifestyle, pollution etc. cause more Lactic acid production & prevalence?

No, no, and no.

Still there can be some different limit in different people. All can't become 100,200,300 Kgs.

And?

What for then Central obesity is meant for?

Who says it is meant for anything?

Triggering means most basic stage. If excess insulin will always result in hypoglycaemia, then how it is excess in IR & what is IR?

CONCLUSIONS: Insulin resistance is present even in young lean subjects at high risk to develop type 2 diabetes. Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease... From pubmed.

Is is not persistant high/excess level in blood in case of IR patients? I think insulin tests tells it.

It is high, but I make a distinction between high and excess.

High: Higher than in a healthy individual, but needed for glucose metabolism.

Excess: More than needed for glucose metabolism.

I have replied Rolfe's post accordingly. Can't excess insulin(naturally secreted or induced by medication) put some hold in proper excretion of sugar in urine? Can excess insulin effect renal threshhold of sugar absorption? There can be an impression of sugar need or it can be used due to excess insulin?

Read and UNDERSTAND Rolfe's post. You obviously haven't understood it. It answers your question.

Yes, you ARE going against the natural mechanisms--first creating it( bymodern lifestyle/environment/practices etc.) then treating it. Un-nature vs, un-nature..

Kumar, is your diet 90% vegetables? Is your BMI low? Do you exercise at least 1 hour a day? Would you be alive if you lived in the jungle? Are YOU "natural"?

Hans

 

[Badly Shaved Monkey]

Snippet from the source Kumar just quoted :


I think we might have a record here. Correct me if I'm wrong, but I cannot remember any other poster posting sources that directly and explicitly contradicted their ideas.



Hans

I just logged on again to say the same thing, so now I needn't bother.

I think the words have no meaning for him. He's like a magpie picking up shiny jargon terms wherever he can find them and stuffing them randomly into his nest.

 

[Kumar]

You were told: Animal insulin does not match the body perfectly and can give immune responses.

Do you ignore answers because:

a) Because you don't like them.

b) You are too lazy to read them.

c) You cannot really read English.

d) A combination of the above.

Hans

I don't have dispute on what you are saying, but I just want to clear, whether animal insulin can be more effective than synthetic human insulin in some cases or not? I simple yes or no can clear this point.

Most of the time my repeation is due to I am not satisfied with that reply except in some cases as of BSM, where language is a problem.

 

[Kumar]

It seems that there can be eventual damage to the beta cells in type 2 diabetes, but it is not a question of the beta cells being inactivated directly by high blood insulin levels, as you seem to be suggesting in another thread. If this were the case, an increase in blood insulin level would lead to reduced production of insulin by the pancreas, and hyperinsulinaemia would not develop.

Yes, this may be important point. Many thoughts can be there; There can be episodes of high & normal insulin levels in blood. It can be an inactivation & damage to beta cells due to persistant impression of excess insulin in blood due to IR. It can be a damage to beta cells due to persistant excess glucose. It can be a discouragement of insulin secretion due to less utilization of insulin in IR. It can be due to holding of excess insulin in blood due to presence of excess glucose in blood in IR condition. There may be some problem in excretion of its excess amount. Several factors can be thought at basic level, but which is true, is to be assessed.

 

[Kumar]

There is no difference between them. That's why synthetic human insulin is preferable to non-synthetic non-human insulin.

Is there any difference in different types/makes of different synthetic human insulin? Suppose hyperinsulinemia is a cause of getting IR condition, can excess injected synthetic haman insulin cause IR condition?

 

[MRC_Hans]

I don't have dispute on what you are saying, but I just want to clear, whether animal insulin can be more effective than synthetic human insulin in some cases or not? I simple yes or no can clear this point.

No.

Most of the time my repeation is due to I am not satisfied with that reply except in some cases as of BSM, where language is a problem.

Well, why do you keep asking questions, when you don't want to hear the answers?

Hans

 

[MRC_Hans]

Is there any difference in different types/makes of different synthetic human insulin? Suppose hyperinsulinemia is a cause of getting IR condition,

This is simply amazing. From the source YOU QUOTED YOURSELF:

CONCLUSIONS: Insulin resistance is present even in young lean subjects at high risk to develop type 2 diabetes. Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease... From pubmed.

Hyperinsulinemia IS NOT the cause if IR, it is the other way around.

can excess injected synthetic haman insulin cause IR condition?

No.

Well, at least we get your raw idiocy clearly exposed here. It is now the 8th time you are told this IN THIS THREAD ALONE, and it has been said repeatedly before.

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



Hans

 

[Kumar]

Let's have a little fun. Kumar, please explain the snippet you just quoted. Show us how much of it you understand .

Hans

It tells me two conditions. The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency. Probably, insulin secretion deficient T2DM may not be obese(esp. centrally) because insulin deficient so not insulin resistant untill medicated if this can result hyperinsulinemia. Insulin resistant can be obese--naturally & medicated.

 

[Darat]

...snip...

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



Hans

"not"

 

[Rolfe]

Suppose hyperinsulinemia is a cause of getting IR condition....

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.

 

[MRC_Hans]

It tells me two conditions. The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency. Probably, insulin secretion deficient T2DM may not be obese(esp. centrally) because insulin deficient so not insulin resistant untill medicated if this can result hyperinsulinemia. Insulin resistant can be obese--naturally & medicated.

The snippet in question read:

The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency....
...In conclusion, in IRS-2G1057D variation DD genotype apparently showed two phenotypes. The insulin sensitivity of non-obese subjects with DD genotype was increased; which indicated that DD genotype might be the protective factor of T2DM. The insulin sensitivity of obese (especially central obesity) subjects with DD genotype was decreased; which indicated that DD genotype might be the risk factor of T2DM occurrence. All of these results demonstrated that the IRS-2G1057D variation and obesity were connected to T2DM.

So:

It tells me two conditions. The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency.

Well, cut and paste does not show understanding. We already know you can cut and paste .

Probably, insulin secretion deficient T2DM may not be obese

This is not incorrect, since not all type 2 patients are obese, but that is not what the text says.

(esp. centrally) because insulin deficient so not insulin resistant untill medicated if this can result hyperinsulinemia.

Kumar tries to reassemble the words in the text to support his pet theory. Kumar, I have news for you: In English, the sequence of the words have an impact on the meaning, so you can't just shuffle them about at will.

Insulin resistant can be obese--naturally & medicated.

How can you be medicated obese?

Well, thank you for your sincere effort, Kumar. Unfortunately, it confirms what we already know: You are largely unable to gain information from written sources. You either cut and paste indiscriminately, or you misunderstand and misrepresent the text.

Kumar, you say you are on a mission to show science where it has failed. I'm afraid you are not even marginally equipped for such a mission. And to wit, in all the time I have watched your strivings, you have not acieved anything but providing involuntary entertainment and much frustration among well-educated people who have made an honest attempt to educate you.

Except as a clown, you are a total failure, and even as a clown you are rather boring.

And now Kumar will reply by saying that he is thinking dynamically, while I am unable to do so because of my vested interests etc. He will tell me it is my duty as scientist to find the reason for mass. .etc.



Hans

 

[Kumar]

No, no, and no.

Peobaby it may change un furthur understandings.
Can lactic acidoses be an "acute candition" as arising from eg, metformin toxicity AND "chronic" condition arising from some other conditions-- MELAS (Mitochondrial myopathy, encephalopathy, lactacidosis, stroke)? We may be able to tollerate chronic condition for some time but acute condition can be immediat fatal.

And?

What for then Central obesity is meant for?

Who says it is meant for anything?

Above that individual limit of fat store, ine may start getting IR condition. Central obesity is thought to be more related to IR. HOW?


CONCLUSIONS: Insulin resistance is present even in young lean subjects at high risk to develop type 2 diabetes. Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease... From pubmed.

Lean person may be having lean fat store limit. Above it he may get IR, still looks lean. Furthur, it may be just a start if IR where he might have not yet stored much fats so looked lean.

It is high, but I make a distinction between high and excess.

High: Higher than in a healthy individual, but needed for glucose metabolism.

Excess: More than needed for glucose metabolism.

Good, dynamic & different definitions. How you can say excess, if elevated BG level is there & it is still pending to be used but can't due to IR? Can we take it as excess, if total amount of insulin available in blood is higher that normal requirement to metabolize total sugar as present in blood?

Read and UNDERSTAND Rolfe's post. You obviously haven't understood it. It answers your question.

No I understood it but it is not complete.

Kumar, is your diet 90% vegetables? Is your BMI low? Do you exercise at least 1 hour a day? Would you be alive if you lived in the jungle? Are YOU "natural"?

No, therefore "Un-nature vs. un-nature", so justified. Many time I mentioned "modern systems are most valid & entitled in current age" due to "Un-nature vs. un-nature", or "modern vs. modern". One can't fight with sticks & swords against guns & bombs.

 

[Donks]

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.

Can you imagine what it must have been like for Kumar's teachers? They probably wished for the sweet release of death on a daily basis.

 

[Rolfe]

Since the glucose cannot get into the cells (due to the lack of insulin or insulin resistance), blood glucose concentration increases. The way the kdney works is that all the glucose presented to the proximal tubule is filtered, but then it all ought to be reabsorbed further down the system. However, the reabsorption system can only handle up to about 10mmol/l glucose in the blood (the renal glucose threshold). If blood glucose is higher than this, the capacity of the reabsorption is exceeded and the excess glucose spills over into the urine. The kidney isn't trying to excrete the glucose, it simply can't help it.

Then, the presence of all that glucose in the urine increases the osmolarity of the fluid. This interferes with the ability of the kidney to conserve water. Osmotic pressure created by the glucose pulls the water into the urine - osmotic diuresis. This tends to dehydrate the body, and of course the result is that the person feels thirsty and drinks to compensate.

This has always seemed to me to be the inevitable consequence of the fact that the system of filtration and reabsorption used by the kidney only works properly at fairly normal blood glucose concentrations. 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.

What is incomplete about that? What more do you want to know?

Rolfe.

 

[Kumar]

You mean WHY it happens? We don't really know for sure. There seems to be several possible triggers.

I am also thinking on "several possible triggers". pH imbalance, mucus/water blocks, menerals imbalance-calcium etc., inactivity( due to insulin excesses-natural or induced, higher levels, triggered due to food absorption disorders or its excretion), gulucotoxicity, accidental or progressive, or otherwise.

Can it be a result of progressive effect of persistent high BG/Insulin-natural, induced or medicated, anytime during lifetime or inhereted?

That is the type 2 situation. Kumar, it is highly embarrassing for you that you STILL haven't grasped the difference between type 1 and type 2.

Both type 1 & 2 can be due to inharent cause. Any such progression can still be taken as progressive effect.

Can it be caused due persistent exposure of weak acid/lactic acid to pancreas?

Whatever gave you THAT idea?

Acid is very toxic to cause any damage/mutation. I don't no about base/alkali effect.

 

[MRC_Hans]

No, no, and no.

Peobaby it may change un furthur understandings.

No.

Can lactic acidoses be an "acute candition"

It is aways an acute condition.


as arising from eg, metformin toxicity AND "chronic" condition arising from some other conditions-- MELAS (Mitochondrial myopathy, encephalopathy, lactacidosis, stroke)? We may be able to tollerate chronic condition for some time but acute condition can be immediat fatal.

There is no chronic condition.

Above that individual limit of fat store, ine may start getting IR condition.

Well, if I'm to be charitable; yes there is probably some individual limit where body fat becomes a risk factor.

Central obesity is thought to be more related to IR. HOW?

we don't know for sure.

Good, dynamic & different definitions. How you can say excess, if elevated BG level is there & it is still pending to be used but can't due to IR? Can we take it as excess, if total amount of insulin available in blood is higher that normal requirement to metabolize total sugar as present in blood?

Elevated insulin is what is needed to metabolize glucose in the face of insulin resistance, in other words to overcome IR.

Excess is more than that, which leads to hypo.

Read and UNDERSTAND Rolfe's post. You obviously haven't understood it. It answers your question.

No I understood it but it is not complete.

Yes, it is a complete answer to your question. You may not like the answer, but you'll have to live with that.

Hans

 

[MRC_Hans]

What is incomplete about that? What more do you want to know?

Rolfe.

Kumar is dissatisfied with your answer because you neclected to insert any bits and pieces he could pick out and reassemble to support his silliness.

Shame on you .

Hans

 

[Kumar]

I just logged on again to say the same thing, so now I needn't bother.

I think the words have no meaning for him. He's like a magpie picking up shiny jargon terms wherever he can find them and stuffing them randomly into his nest.

Let me complete the replies. Pls try to write in language understoodable to me, if it is for me..

Although I am very flexible to change & correct, What made you to think alike that?

 

[MRC_Hans]

I am also thinking on "several possible triggers". pH imbalance, mucus/water blocks, menerals imbalance-calcium etc., inactivity( due to insulin excesses-natural or induced, higher levels, triggered due to food absorption disorders or its excretion), gulucotoxicity, accidental or progressive, or otherwise.

Nonsense. Normally, I encourage people to think, but in your case, I'll make an exception: Don't think too much Kumar. Nothin good seems t ocome out of it.

Both type 1 & 2 can be due to inharent cause.

The term is "inherited vector". Both types have inherited vectors, although not necessarily the same.

Any such progression can still be taken as progressive effect.

A progression can be taken as a progressive effect? Where DO you get it from ?

Acid is very toxic to cause any damage/mutation.

No. SOME acids are poisonous. Not all acids.

I don't no about base/alkali effect.

Let's face it, Kumar, you don't no about anything much.

....

Don't worry everybody, I'm not going to keep being nasty to this poor wretch, I just need to blow some off steam, before he hits my ingore list for good. I think he deserves both.

Hans

 

[Kumar]

If you're trying to understand type 1 diabetes in this thread, why do you keep asking about insulin resistance? It has been repeatedly been pointed out to you that this occurs in type 2 diabetes, not type 1, and why type 1 diabetics do not develop insulin resistance.

Most of Type1 may be a later stage of type2/IR. Someone told me that natural & synthetic insulin is same, why then excess of synhetic insulin to type1/IDDM causes IR in him?