MRC_Hans said:
Sorry, you have taken it like that & felt. Since there were confusions & backlog due to so many posting, I just refreshed. Moreover, in view of many things still unknown to you/scince--we can speculate/think differently & dynamically to add. Look at one of your reply;
Should I take it as final & absolute, whatever told by you or can still think differently?
Mojo said:
I now think IR is just a "persistant hyperglycemia" either due to excess absorption of sugar or due to lesser loss in urine. It will cause high insulin secretions, whether this higher insulin persist in system or not & how it can be catabolized--we may still have to see? In view of Rolfe's replies, it looks "renal thresholds & urine losses" are not related to persistant hyperglycemia (althought we may also have to assess it by considering, total sugar loss per day and total loss without medications).
Now we can check any predisposed impression resulting into more craving of sugar/fatty foods & their excess digestion/exess absorption. Can there any normal limit to digestion & absorption which may be effected due to predisposed or aquired impressions?
A "genetically predisposed pancreas defect", huh? You, sir, are a moron. I mentioned 2 predispositions, and neither was a "genetically predisposed pancreas defect." If you won't bother reading answers, then don't bother asking questions.Kumar said:
"I think." Means the whole paragraph is one huge series of idiotic assertions. And it is. You don't understand diabetes and you don't understand genetics or inheritance, and yet you keep on making up theories about both.
Yes, because our "natural" habitat is a hyperbaric chamber. Idiot.
Mojo
Mostly harmless
Kumar said:
No, I was not making fun of you on this occasion. I was pointing out that glycosuria is caused by high blood sugar levels, not low insulin levels. In anyone with functioning beta cells, high blood sugar levels will always be accompanied by increased insulin production. The insulin level does not have any effect on the level of glucose in the urine.
ETA: I reserve the right to make fun of you in the future.
Rolfe
Adult human female
This is complete and total nonsense.Kumar said:
Kumar runs true to form. He's been told it like it is several times by several differnt people, but simply ignores their explanations in favour of his own fanciful inventions.
I recall that this is the guy who thinks that homoeopathy can alter water structure to give H<SUB>3</SUB>O<SUB>6</SUB> and H<SUB>4</SUB>O<SUB>8</SUB> and so on, and at the same time suggested that different forms of H<SUB>2</SUB>O might also exist, such as H-H-O and the (presumably subtly different) O-H-H.
Kumar, if you have no interest in learning from the discoveries of the people who have carefully studied these subjects before you, why post?
Rolfe.
Rolfe said:
And I always thought you were quite bright
Mojo
Mostly harmless
Well, it's a pretty dreadful place, but I doubt he's ever been there.Rolfe said:
Oh, the perils of Caps Lock!
Mojo
Mostly harmless
Kumar, as I told you on the last page, the low pH in the stomach is to enable the digestion of proteins there. It has nothing to do with carbohydrate digestion.Kumar said:
Mojo said:
But high blood sugar will normally be possible when low insulin is there in blood. High & excess insulin levels can be there in IR condition.
Anyway, do you people want to say that in IR condition, there can't be unutilized insulin, if hyperglycemia is also there.?Means, all the secreted or injected insulin will be utilized which is still not sufficient to metabolize all the available glucose in blood, so hyperinsulinemia happens? Do you want to say that there can't be hyperinsulinemia when glucose level is still higher? If yes, what is then the meaning of IR?
Can you tell me about cycle of insulin in normal & in IR condition?
Mojo
Mostly harmless
Only in insulin-dependent diabetics. In anyone who has functioning beta cells, high blood sugar will cause the beta cells to produce insulin, thus increasing the level of insulin in the blood. Blood sugar, above a certain level, will cause glucosuria. In untreated insulin-dependent diabetics, the high blood sugar may be a result of hypoinsulinaemia, but in anyone who isn't (i.e. healthy people and non-insulin dependent type 2 diabetics) elevated blood sugar will be accompanied by elevated blood insulin.Kumar said:
No. The high blood insulin level in insulin resistant diabetics is a result of the high blood sugar level.
In a healthy person, elevated blood glucose causes the beta cells to produce more insulin. The insulin causes cells to take up glucose from the blood, thus reducing the blood glucose level. As a result of the reduced blood glucose level the beta cells produce less insulin, and the blood insulin level falls again.
In insulin resistant diabetics, raised blood glucose causes the beta cells to produce more insulin, as in a healthy person. Because their body's cells are insulin resistant, this does not cause the cells to absorb glucose adequately, so the blood glucose level remains high. Because the blood glucose level remains high, the beta cells continue to produce insulin. This is what causes the elevated blood insulin level.
Of course not, you idiot! High blood glucose levels cause hyperinsulinaemia!
People have been doing this for a couple of years now, but you haven't taken the slightest bit of notice, have you?
Go read a book.
MRC_Hans
Penultimate Amazing
- Joined
- Aug 28, 2002
- Messages
- 24,967
*sigh* If there's a heaven, I hope I'll be rewarded for my patienceKumar said:
Anyway, there just might be an angle here that has not been crystal clear so far, so let's remedy that:
Kumar, assume you are charged with throwing pepples through a home in the wall. For some reason, you aim is only so good, and with no room for improvement (quite appropriate for you, in fact
). Now, as long as the hole is big, you can hit it virtually every time. But now suppose the hole is made smaller; now, only half the pepples you throw actually go through the hole, the rest are wasted. Lets assume the hole is made even smaller, so only one in ten go through. So for each pepple you get through the hole, you need to throw 10.Get it?
Now, consider insulin. Insulin can be seen as a key that opens the cell to clucose. In an oversimplification, you can say that each insulin molecule lets a glucose molecule through.
Now, in a healthy person (no IR), the "keyholes" are large and plentiful, so a given amount of insulin in the blood-stream quickly and effectively lets the available glucose through the cell walls and make it available for the metabolism. Thus, the amount of insulin effectively regulates the BG level; more insulin, the BG falls, less insulin, it rises. So when you eat, glucose enters the bloodstream from the digestive system. Sensing the rising BG, the pancreas releases insulin, so the glucose can go into the cells and be metabolized. After a while, the BG falls back towards quiscent level, and the insulin secretion slows down acoordingly, maintaining equlibrium.
This is how it works in a non-diabetic person. One more thing you need to know to know is that insulin is short-lived; once released into the blood-stream, it only exists for a limited time, then it is broken down, whether it is used or not.
Now. let's look at the type 1 patient: Herethe pancreas is not able to produce enough insulin (in some cases virtually none at all is produced), so when this person eats, and the BHG rises, little or no extra insulin is released. So the glucose stays in the blood-stream (and glucose is NOT short-lived) where it is only removed slowly by whatever insulin IS released, plus whatever can be removed through the urine. The effect on the patient is that BG is high, but cells are lacking energy.
Over to the (early stage) type 2 patient: Here the pancreas is able to react to the increased BG after eating, and therefore the insulin level in the blood rises with the BG. Unfortnately, due to IR, the "key holes" are small and reduced in numbers, so even though a lot of insulin is present and there is plenty glucose around, only a limited amount is getting through. Like with the pepples, a lot have to be thrown to get a few through the hole in the wall. At a later stage, the insulin production also falls, but that's another story.
This should explain why I make a distinction between elevated insulin and excess insulin. And it is not relevant to talk about unutilized insulin, because even though it does not all get to let glucose into cells, it is all needed to create a sufficiently high concentration, so that SOME glucose gets through.
...
Well, I tried
.Hans
Rolfe said:This is complete and total nonsense.
How?
I recall that this is the guy who thinks that homoeopathy can alter water structure to give H<SUB>3</SUB>O<SUB>6</SUB> and H<SUB>4</SUB>O<SUB>8</SUB> and so on, and at the same time suggested that different forms of H<SUB>2</SUB>O might also exist, such as H-H-O and the (presumably subtly different) O-H-H.
That was not an illustration, telling or true chemical equation but just was shown for example sake. Read my comments in that post. If you can't understand my intention behind that, that is only your problem or....
Kumar runs true to form. He's been told it like it is several times by several differnt people, but simply ignores their explanations in favour of his own fanciful inventions.
Kumar, if you have no interest in learning from the discoveries of the people who have carefully studied these subjects before you, why post?
Because many explainations/aspects are still not complete, not yet known and not yet "absolute". Therefore I am trying to learn, learning & learned. Why you people become irritating after some time....commonly? Are you tired/exhausted? This thread was going pretty well but also started spoiling by TTTT.
Rolfe
Adult human female
I AM NOT A "BRIGHT"!!!!Darat said:And I always thought you were quite bright
Oh, that's not what you meant.... Er.... Sorry....
Rolfe.
Rolfe
Adult human female
Because we are completely frustrated by explaining things carefully to you, and having these explanations consistently ignored or misrepresented.Kumar said:
It's not true to say that you only want to learn. If you wanted to learn, you would now be quite knowledgeable about diabetes and its various complications, from all the good and correct information you have been given. And you would take the advice of so many posters and go and read a few books.
You don't want to learn. You want to find some way which will allow you to claim that reality is the way you want it to be. When told anything that seems to argue against the explanation you want, you ignore it, or contradict it, or imply that the poster doesn't know what they're talking about.
This becomes very wearing after a while.
For example, I have told you several times that glycosuria is simply an inevitable side-effect of the blood glucose concentration rising above the renal threshold. For any reason at all, not only in diabetes. And irrespective of what the insulin is doing. And that no matter how much glucose is lost in the urine, it doesn't make any practical difference to the blood glucose level. And that this is not a regulatory system, but merely a by-product of the way the kidney works.
And then you simply come along and say totally stupid things such as
This is absolute proof that you don't want to learn, you just want to imagine your own (wrong) explanations.
Kumar, as I said to you the first day you came on this forum, diabetes is one of the most extensively studied conditions in all medicine. An enormous amount is known about it. It is vanishingly improbable that you have discovered something that all these armies of specialist diabetologists around the world have missed. And the only way to see if you're right, is to learn what is already known about diabetes, and see if there is a rational explanation for your observations there.
But no. You want to stick to your ignorant explanation of what you think you've seen going on, so you have to reject all the knowledge that is being given to you and try to pretend that it means something else.
Well, I've had it. Again. There are only so many times I'm prepared to post the same explanation and have it twisted out of all recognition to suit your fantasies. Same as with the hours I spent trying to explain the Cori cycle to you, or the differences between ions and salts and elements, and intracellular and extracellular fluid. All a waste of time.
And you can call this TTT is you like, but I'm sick of seeing your pathetic little ego insist that you are the only pure-motived person here, and contribute so much, while we are only vested interests and closed minds. You're unteachable.
Rolfe.
Mr. Hans,
Thanks & well explained by translating in simple/my language with good example.
In case of type2 with IR: when sugar is not able to go in cells, will this not result into hypoglycemic type episodes & weakness/death of cells due to less available glucose to them due to IR inspite of hyperglycemia?
Whether this codition of IR remains persistant in type2 patients for whole of their balance life or can be reversed?
Thanks & well explained by translating in simple/my language with good example.
In case of type2 with IR: when sugar is not able to go in cells, will this not result into hypoglycemic type episodes & weakness/death of cells due to less available glucose to them due to IR inspite of hyperglycemia?
Whether this codition of IR remains persistant in type2 patients for whole of their balance life or can be reversed?