1. I think its well-established that beta cells can regenerate, which is great for people with type 2, but the issue of autoimmunity remains a problem for eradication of type 1, which is why I'm convinced that any cure will have to consist of multiple treatments: one to arrest the immune system dysfunction, and another to regenerate beta cells. Lets see, we now have INGAP, exenatide (Byetta) and now gymnema sylvestre all proven to regenerate islets, yet we remain fairly short of practical treatments to address the issue of autoimmunity, so far, only Anti-CD3 monoclonal antibodies have any proven efficacy. Anyone care to resurrect Diapep 277 which was dumped by Sanofi Aventis?

Posted at 8:37AM on May 14th 2007 by Scott

2. You know what? I'm glad you keep publishing stories like this. More of us need to get angry about what is NOT being done for us diabetics. I'd be happy to get anything that makes my insulin work better for me, even if it's not a cure, even if it's not a working pancreas.

You hear me, science?! :)

Posted at 4:00PM on May 15th 2007 by Hannah

3. OK, so here's my question - does anybody have any thoughts on whether a "reverse spiral" is possible, i.e. is it possible that by reducing your weight, you could reduce your insulin dose, and by reducing dose and concurrently taking plant extracts such as gymmena sylvestra, that you could reduce insulin antibodies, thus giving the plant extracts time to help regenerate the beta cells, enough to reduce insulin use further, enough to increase beta cells, etc. and reverse the downward spiral? Does anybody out there think that it could be the insulin itself that's keeping us diabetic?
Kelly

Posted at 7:07PM on Jun 28th 2007 by Kelly

4. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's comment #3 relating to that blog..
http://www.thediabetesblog.com/2007/05/13/a-leaf-extract-lowers-insulin-requirements-in-iddm/#c5685596
"...to help regenerate the beta cells, enough to reduce insulin use further, enough to increase beta cells, etc. and reverse the downward spiral? Does anybody out there think that it could be the insulin itself that's keeping us diabetic? Kelly..."

Kelly ... assuming that it is possible to have perfectly healthy beta-cells without reducing weight and/or taking plant extracts ... Please discuss the role of HYPOglycaemia, in beta-cell regeneration, before and after diagnosis / insulin treatment of type 1 and/or type 2 Diabetics [with reference to the following]...
http://www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/1#c5614998

AND why


Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 22:51hrs SAT.30.JUN.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

Posted at 5:53PM on Jun 30th 2007 by Nicholas Dynes Gracey

5. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's comment #3 relating to that blog..
http://www.thediabetesblog.com/2007/05/13/a-leaf-extract-lowers-insulin-requirements-in-iddm/#c5685596
"...to help regenerate the beta cells, enough to reduce insulin use further, enough to increase beta cells, etc. and reverse the downward spiral? Does anybody out there think that it could be the insulin itself that's keeping us diabetic? Kelly..."

Kelly ... assuming that it is possible to have perfectly healthy beta-cells without reducing weight and/or taking plant extracts ... Please discuss the role of HYPOglycaemia, in beta-cell regeneration, before and after diagnosis / insulin treatment of type 1 and/or type 2 Diabetics [with reference to the following]...
http://www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/1#c5614998

AND what is the apparent relationship between 'HYPOglycaemia' and Men apparently having healthier hearts without the 'better numbers' and/or 'better control' that Women apparently have ...
http://www.thediabetesblog.com/2007/06/26/Diabetes-control-has-improved-dramatically-in-U.S./#c5653076

Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 23:33hrs SUN.01.JUL.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

Posted at 6:33PM on Jul 1st 2007 by Nicholas Dynes Gracey

6. Hi everyone,
It's great to see people thinking out there! Thanks for your responses.

In response to Nick ~ First, I need to digest your other piece you reference more thoroughly. I haven't thought much about HYPOglycemia and beta cell regeneration directly; but, here's my ramblings anyway.

Where my thinking is revolves around the following facts:
(1) When you take exogenous insulin, it suppresses your body's ability to secrete natural insulin. That much is clearly shown by the research. Your body basically says: "hey, why bother making insulin, there's plenty around." The more you take, the less you make. Hence, hypo's could logically suppress natural insulin secretion further, at least temporarily. It seems logical to me that, over time, this suppression, coupled with the creation of antibodies (which might be due not to the insulin itself, but the other impurities/additives in the insulin), might in and of itself generate a diabetic state via repetition - a state that wouldn't otherwise exist, or at least not exist as bad as it would have without exogenous insulin intervention.

(2) The testing of c-peptide levels can only tell us whether or not a pancreas is secreting insulin into the bloodstream - it can't tell us what the beta cell status is. Doctors will say that someone has no pancreatic function if their c-peptide is negligible, but that's inaccurate, particularly if they test you after you've taken a shot and are fasting (it should be a stimulated c-peptide test with no AM shot). All they can say is a pancreas isn't secreting insulin into the bloodstream - not whether the beta cells are present. You'd need a biopsy to assess that. The question rumbling around in my head is, why isn't that insulin being sent out into the bloodstream - what's turning the switch off in the beta cells telling them not to send it out? and what is the actual status of the beta cells? Could it be that the beta cell function is fine, suppressed but fine, but that the exogenous insulin and the antibodies that it creates over time, is sending the beta cells an electrical signal (and it is an electrical problem), to shut down?

On the question of hypo's and their impact on regeneration, it would seem to me possible that hypo's at least could temporarily heighten suppression of natural insulin. Same deal: the more you take the less you make. Since the trend always seems to be take more and more insulin as you gain weight and get more sedentary with age, it could be akin to just constantly pounding the pancreas into submission until it finally gives up....the proverbial "Uncle!"

On men having "healthier hearts" than women - I tried to find the article you mentioned, in the Chicago paper, but couldn't find it. In general, I doubt any and all reports like these until I can see the research for myself. Most of the research is seriously underpowered and funded by self-interested parties.

With warmest regards,

Kelly

Posted at 1:30AM on Jul 28th 2007 by Kelly

7. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's post @ 1:30AM on Jul 28th 2007 relating to Allie's other blog...
http://a.thediabetesblog.com/2007/07/21/less-insulin-longer-life/1#c6047829
"...In response to Nick ~ First, I need to digest your other piece you reference more thoroughly. I haven't thought much about HYPOglycemia and beta cell regeneration directly..."

In relation to 'indigestion' [excess blood glucose c/o eating too often] ... Kelly ... assuming that it is possible to have perfectly healthy beta cells without reducing weight and/or taking plant extracts [eg c/o insulin resistance ie 'adaptative insulin protection' eg c/o type 2 diabetes] ... Please discuss the role of HYPOglycaemia, in beta-cell regeneration, BEFORE and AFTER diagnosis / GM insulin treatment of type 1 and/or type 2 Diabetics [with reference to the following]...
www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/1#c5614998

"...(1) When you take exogenous insulin, it suppresses your body's ability to secrete natural insulin. That much is clearly shown by the research..."

Please cite just 1 just reference in relation to your 'insulin suppression' issue ... your abovementioned comment is in relation to, exogenous GM insulin, AFTER diagnosis of an above average/mean blood glucose level ... please discuss what is likely [forseeably] happening to downregulate the endogenous insulin secretion AND production BEFORE diagnosis ... ie the extraordinary challenges to the CNS [brain & spinal cord] of relative HYPOglycaemia and absolute HYPOglycaemia. For example, in the absence of priority-protective 'autoimmune downregulation' of the beta cells [yes type 1 diabetes is PROTECTIVE] in an ACUTELY-distressed-dehydrated-eating-to-often-Human [with above average/mean 'Juvenile' acute levels of HYPOglycaemia inducing growth hormone] ie a pre 'type 1' aka Juvenile onset Diabetic ... would VERY quickly succumb to HYPOglycaemia unawareness either temporary or permanent. Please compare the seconds / minutes / hours timeline of 'HYPOglycaemia distress' as compared to the days / weeks / months, of eating too often, that sometimes culminates in 'KETOacidosis distress'.
www.thediabetesblog.com/2007/07/10/hypoglycemia-and-the-brain/#c5936897

Pre 'type 1' diagnosis polyuria & polydipsia is a small price to pay for the remarkably protective 'adaptative homeostasis' that is 'type 1 diabetes' ...
http://www.thediabetesblog.com/2007/07/20/meager-data-on-benefits-of-diet-and-exercise-for-type-2s/#c6046706

"...(2) The testing of c-peptide levels can only tell us whether or not a pancreas is secreting insulin into the bloodstream - it can't tell us what the beta cell status is. Doctors will say that someone has no pancreatic function if their c-peptide is negligible, but that's inaccurate, particularly if they test you after you've taken a shot and are fasting (it should be a stimulated c-peptide test with no AM shot). All they can say is a pancreas isn't secreting insulin into the bloodstream - not whether the beta cells are present..."

Yes it's great news for the 'cure' for type 1 diabetes / Diabetics ... the beta-cell DNA & beta cells are there, ready & willing, 'right here & right now' to 'thermoelectrically' upregulate to produce all the insulin that is needed ... simply & sustainably remove the cause of the protective 'thermoelectrical' downregulation ... aka 'relative HYPOglycaemia distress' aka eating too often.

"...Since the trend always seems to be take more and more insulin as you gain weight and get more sedentary with age, it could be akin to just constantly pounding the pancreas into submission until it..."

Yes BUT that is a 'type 2', aka Adult onset, Diabetic scenario ie a CHRONICALLY-distressed-dehydrated-eating-to-often-Human [with below average/mean 'Juvenile' acute levels of HYPOglycaemia inducing growth hormone] in respect of which the pancreas simply produces more & more insulin and local homeostatic control increases at the insulin receptors aka life saving 'insulin resistance' and that is why UNdrugTREATED type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span ...
www.sciencemag.org/cgi/content/abstract/317/5836/369

AND it's great news for the 'cure' for type 2 diabetes / Diabetics ... the beta-cell DNA & beta cells are there, ready & willing, 'right here & right now' to 'thermoelectrically' control the production of all the insulin that is needed ... simply & sustainably choose to remove the cause of the protective average/mean blood glucose level ... aka 'relative HYPOglycaemia distress' aka eating too often.
www.thediabetesblog.com/2007/07/20/meager-data-on-benefits-of-diet-and-exercise-for-type-2s/1#c6044581

AND what is the apparent relationship between 'HYPOglycaemia' and Men apparently having healthier hearts without the 'better numbers' and/or 'better control' that Women apparently have >>> 3 clicks links to "...see the research..." ref via this ref >>>
http://www.thediabetesblog.com/2007/06/26/Diabetes-control-has-improved-dramatically-in-U.S./#c5653076

Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 13:15hrs SAT.28.JUL.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

www.thediabetesblog.com/2007/04/19/no-food-no-problem

Posted at 8:50AM on Jul 28th 2007 by Nicholas Dynes Gracey

8. Yikes, Nick, your "c/o eg" language is enough to make my head spin. In response, and my apologies in advance to those not interested in long posts:

(1) Nick, you stated: "In relation to 'indigestion' assuming that it is possible to have perfectly healthy beta cells without reducing weight and/or taking plant extracts" - In response, I'm not making that assumption. I tend to believe that, regardless of the type of diabetes present, the beta cell structure has likely been impacted negatively by something (an environmental trigger, like an infection or chemical exposure), which results in the development of the initial hyperglycemic symptoms. I further believe that the beta cell function may need help to repair itself (or it may not), but that can be increasingly difficult over time as body mass increases and there's an increasing burden of exogenous insulin present. What I'm also saying is, without a biopsy, a doctor who gives someone a c-peptide test which turns up with "undetected" levels can't say "your beta cells don't exist", or "you don't have any pancreatic function", they can only say that the pancreas isn't secreting insulin into the bloodstream. Doctors (including mine) often make assumptions/statements like these that aren't correct. Lastly, what I'm also saying is: "if you always do what you've always done, you'll always get what you've always got", i.e. if your habit is to take more and more insulin which suppresses your pancreatic function more and more, you'll likely continue to get the same results, i.e. decreased pancreatic function over time.

On your comments: (a) "Please discuss the role of HYPOglycemia in beta cell regeneration BEFORE and AFTER diagnosis/GM insulin treatment" and (b) "Please cite just 1 reference in relation to your 'insulin suppression' issue". In response, here's a short list of references:
(1) Insulin and glucagon secretion are suppresed equally during both hyper-and euglycemia by moderate hyperinsulinemia in patients with diabetes mellitus, journal of clinical endocrinology and metabolism, 1989, vol. 68, no. 5, 925-931.
(2) C-peptide suppression test: effects of gender, age and body mass index; implications for the diagnosis of insulinoma, journal of clinical endocrinology and metabolism, 1992, vol 74, no. 1, 204-210. (While on insulinoma, this paper has helpful information in the topic as well.)
(3) Lack of direct inhibition of insulin secretion by exogenous insulin in the canine pancreas, the journal of clinical investigation, vol 78, nov. 1986, 1193-1198. (Albeit somewhat morbid, this is a very good article on the topic.)
(4) C-peptide profiles in patients with non-insulin-dependent diabetes mellitus before and during insulin treatment, acta endocrinologica, 1992, vol. 126, 447-83.
(5) A study of serum free c-peptide responses to oral glucose load in diabetic patients: with special reference to types of diabetes and methods of treatment, Tohuku J. exp. med, 1984, vol 142, 249-260.

There are dozens of others in the reference lists from these 5 papers and many more to be pulled from PubMed. These 5 satisfied my own posing of the question ("Does exogenous insulin suppress endogenous insulin?" Answer: yes.") All can be obtained through your local university's health library.

In response to your post, yes, my comment was in relation to the taking of exogenous insulin, not just GM however, and not just after diagnosis of hyperglycemia, or for that matter, just in people with diabetes. Endogenous insulin secretion is suppressed in people without diabetes as well as those with. (Reference (5) above for references to 6 other papers on the topic.) Suppression of endogenous insulin is uniform in people taking exogenous insulin.

Next, you state: "please discuss what is likely [forseeably] happening to downregulate the endogenous insulin secretion AND production BEFORE diagnosis...ie the extraordinary challenges to the CNS [brain & spinal cord] of relative HYPOglycaemia and absolute HYPOglycaemia." In response, I believe the mechanism for the initial downregulation (as you call it) of endogenous insulin is different for different people and depends on the cause of the initial hyperglycemic event. In other words, I think the initial expression of hyperglycemia is due to different causes in different people - those who exhibit insulin antibodies as children, versus those who are overweight and have adult onset, versus those who fit no categorization cleanly, versus those who suffered a chemical exposure, may very well all be due to different causes. In addition, I don't think it's necessarily "downregulation" as you call it (at least before exogenous insulin is present). There may be plenty of insulin, but the body might not be able to access the insulin present, particularly in the case of chemical exposures. My current thinking is that no matter what the original insult was to the system that created the initial hyperglycemic event and the "type" of diabetes it caused, once exogenous insulin is in play, that may be the predominant and overriding factor that keeps someone diabetic and continues the downregulation.

On your statement of "polyuria & polydipsia being a small price to pay for the remarkably protective 'adaptative homeostatis' that is 'type 1 diabetes'": that's an interesting comment. The body is incredibly adaptive. In doing this research, I've learned that some 95-98% of people who are in the hospital with an infection are hyperglycemic. So how many of those people are subjected incorrectly to exogenous insulin to correct the hyperglycemia, whose bodies would have corrected just fine by themselves (thank you very much), but whose bodies then adapt to the taking of exogenous insulin by suppressing endogenous insulin secretion and then BECOME diabetic as a protective reaction to the taking of exogenous insulin? In essence, these are people who have become functionally dysfunctional in insulin regulation. And, my question - if this is right, can this spiral be reversed?

On your comment: "simply & sustainably remove the cause of the protective 'thermoelectrical' downregulation...aka 'relative HYPOglycaemia distress' aka eating too often" - I agree with you on several parts of your statement but not on others. I believe it is an electrical (neural connectivity) problem - the exogenous insulin acts to "turn off" the switch on sending insulin out into the bloodstream. (Reference (3) above is an interesting read on that topic.) I also believe that many if not most Type 2 diabetics could eliminate their condition if they were to exercise and lose excess weight, thus reducing unnecessary stress on their system. I haven't seen though that "eating too often" is the cause of the problem. Eating too much, yes. Eating too often, no. I haven't seen any research that would support that position. It seems more logical to me that eating small quantities frequently would help keep the glucose spikes (and corresponding insulin spikes) low and that would be beneficial. If you have some research on the topic, please point it out. That'd be interesting to read.

On your comment on my statement ("since the trend always seems to be to take more and more insulin as you gain weight and get more sedentary with age it could be akin to just constantly pounding the pancreas into submission until it cries 'Uncle!'") and your response "Yes BUT that is a 'type2', aka Adult onset." In response, I intended my comment for both, Type 1 and Type 2 and all other types. Over time, as we age, most of us become less fit, fatter, and more sedentary. This trend generally results in a Type 1 taking more exogenous insulin over time. Back to my comment of "the more you take the less you make" and at risk of being redundant, this trend to take more and more exogenous insulin would act to suppress endogenous insulin more and more. Over time, the downward spiral would worsen, potentially completely masking the original problem that created the original hyperglycemic event.

On your general comment - that "type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span", as I read it, the article you reference does not imply this is true. They, in fact, state the contrary: "As mammals age, compensatory hyperinsulinemia usually develops to maintain glucose homeostatis and prevent the progression toward life-threatening type 2 diabetes; however, increased circulating insulin might have negative effects on the brain that can reduce life span." Type 2 diabetics aren't adapted to live longer - it's a malfunction in the system, a dysfunctionality they're forcing their system to become functional with.

While I can't agree with you on your "no food no problem" position, I did appreciate your post.

Regards,

Kelly

Posted at 2:42PM on Aug 1st 2007 by Kelly

9. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's comment Posted at 2:42PM on Aug 1st 2007 relating to Allie's other blog...
http://a.thediabetesblog.com/2007/07/21/less-insulin-longer-life/1#c6047829
"...Yikes, Nick, your "c/o eg" language is enough to make my head spin ... And, my question - if this is right, can this spiral be reversed?"

YES.

Kelly ... my mind is in substantial agreement with substantially all of your comments and the references cited are acknowledged & most appreciated.

In relation to my "c/o eg" language ... follows is an attempt at distilling the 'diabetes' issue to a level of greater understanding...

WHAT CAUSES DIABETES...

Eating too often [for that particular Individual at that particular period of their life] causes relative HYPOglycaemia and relative HYPOglycaemia causes a reduction of beta cells/activity [especially type 1] and/or reduced insulin sensitivity aka insulin resistance [especially type 2].

WHAT CURES DIABETES...

(A) Maintain basal insulin [type 1 exogenous / type 2 endogenous] to prevent ketoacidosis.

(B) Eat Less Often ... specifically ... Eat ONLY clean water between meals and eat only when your blood glucose level, following your previous eat, has reduced to your chosen baseline blood glucose level [eg as related to the relative fuel demands of your particular activity level].

(C) Await beta cell recovery, sustainable, in respect of your increased reduction of relative HYPOglycaemia ie increasingly efficient reduction of the cause ... increasingly efficiently facilitates your beta cell & insulin sensitivity ... recovery ... ie the cure.

FOR MORE related info please follow the links via... http://www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217

Kelly ... in respect of the apparent fact & related comment that "type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span" please note that most type 2 Diabetics are ANYdrugTREATED and my comments relate to a discussion of an explanation relating the following parts of that research paper [www.sciencemag.org/cgi/content/abstract/317/5836/369] "... All the insulin-resistant mice displayed mild glucose intolerance ( Fig. 2D). However, diabetes did not develop in these mice because insulin concentrations increased to compensate for peripheral resistance, reaching the highest amount in old male bIrs2+/– and bIrs2–/– mice ( Fig. 2E). Consistent with the observed hyperinsulinemia, pancreatic islets were larger in old male bIrs2+/– and bIrs2–/– mice than in old controls ( Fig. 2F) ... however, long-lived brain-specific bIrs2+/– and bIrs2–/– mice are insulin resistant, hyperinsulinemic, and glucose intolerant. The mechanism responsible for this disparity is unknown. Regardless, our results point to the brain as the site where reduced insulin-like signaling can have a consistent effect to extend mammalian life span—as it does in C. elegans and D. melanogaster ( 1, 3)..."

WE MUST BE REGARDFULL.

Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 20:15hrs WED.01.AUG.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

http://www.thediabetesblog.com/2007/04/19/no-food-no-problem

Posted at 3:38PM on Aug 1st 2007 by Nicholas Dynes Gracey

10. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's comment Posted at 2:05AM on Aug 2nd 2007 relating to Allie's other blog...
http://a.thediabetesblog.com/2007/07/21/less-insulin-longer-life/1#c6047829
"...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"

WHAT CAUSES DIABETES...

Eating too often [for that particular Individual at that particular period of their life] causes relative HYPOglycaemia and relative HYPOglycaemia causes a reduction of beta cells/activity [especially type 1] and/or reduced insulin sensitivity aka insulin resistance [especially type 2].

A good starting reference to help with increasing your understanding about "WHAT CAUSES DIABETES" is to ponder upon 'relative temperature' ie the difference between going outside on a snowy day, after staying in a hot bath too long, vs going outside on a snowy day, having just had a quick cold bath; and this relative HYPOglycaemia reference...
http://www.alfediam.org/media/pdf/RevueBrunD&M5-2000.pdf

...'Relative HYPOglycaemia'... This situation was first evidenced by Harri who reported in 1924 five cases of hypoglycemia following a meal, that he called reactive hypoglycemia. Harris postulated that reactive hypoglycemia was some kind of counterpart to diabetes mellitus: while the latter was considered to result from hypoinsulinism, or at least impaired insulin action, hypoglycemia was expected to be due to hyperinsulinism or dysinsulinism. Symptoms fully similar to those occurring during insulin-induced hypoglycemia were observed at blood-glucose values below 0.7 g/100 l.

Later, this issue became for decades a matter of considerable controversy, due to a lack of consensus in definitions and to the unappropriate use of the oral glucose tolerance test. In addition, hypoglycemia has become a fashionable and overdiagnosed disorder in several countries, due to its popularization in the lay literature, so that a host of patients used to describe signs suggestive for hypoglycemia without any clinical evidence for low blood glucose, a situation that Cahill and Yager proposed to call "non-hypoglycemia". In agreement with them, Charles who found that such patients never exhibited hypoglycemia after a mixed meal concluded that this situation has no relation to glycemia and should rather be termed "post prandial idiopathic syndrome".

The number of terms applied to reactive hypoglycemia have added to the confusion: these included functional hyperinsulinism, essential hypoglycemia, functional hypoglycemia, dysinsulinism, hypoglycemic fatigue, insulinogenic hypoglycemia, and ... "relative HYPOglycaemia"...

FOR MORE related info please follow the links via... www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217

Kelly ... in respect of the apparent fact & related comment that "type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span" please note that most type 2 Diabetics are ANYdrugTREATED and my comments relate to a discussion of an explanation relating the following parts of that research paper [www.sciencemag.org/cgi/content/abstract/317/5836/369] QUOTE: "... All the insulin-resistant mice displayed mild glucose intolerance (Fig. 2D). However, diabetes did not develop in these mice because insulin concentrations increased to compensate for peripheral resistance, reaching the highest amount in old male bIrs2+/– and bIrs2–/– mice (Fig. 2E). Consistent with the observed hyperinsulinemia, pancreatic islets were larger in old male bIrs2+/– and bIrs2–/– mice than in old controls ( Fig. 2F) ... however, long-lived brain-specific bIrs2+/– and bIrs2–/– mice are insulin resistant, hyperinsulinemic, and glucose intolerant. The mechanism responsible for this disparity is unknown. REGARDLESS, our results point to the brain as the site where reduced insulin-like signaling can have a consistent effect to extend mammalian life span—as it does in C. elegans and D. melanogaster (1, 3)..."

WE MUST BE REGARDFULL because virtually every Peer reviewed research paper contains a paradox. By focussing on the paradox it is a relatively straightforward process to make the next scientific breakthrough. Most Scientists simply continue the dogma by carrying on REGARDless of the paradox. Diabetes type 1 & type 2 can be cured quite easily by sustainably reducing and then removing the cause and the major step to achieve that cure is a desire to be free from diabetes rather than carry on REGARDless ... being REGARDmore is too small a step. We need to be 'REGARDFULL'.

Warm thanks; Nick

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

http://www.thediabetesblog.com/2007/04/19/no-food-no-problem

Posted at 4:00PM on Aug 2nd 2007 by Nicholas Dynes Gracey

11. Hi Allie, Scott, Hannah & Kelly;

re Allie's blog & Kelly's 'Gymena Sylvestre' post @ 4:46PM on Jul 29th 2007 commenting upon Allie's other blog...
http://www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6415853
"...but to possibly resolve the hyperglycemic condition entirely. The research you mentioned in another piece on Gymena Sylvestre shows regeneration is possible. I've also read that research and am now taking the herb as a result to test it on myself...'

Kelly ... one challenge with being ANYdrugTREATED, including the adoption of a "herb" as a drug, is the degree to which there is a REDUCTION of the CAUSE [aka the major contributory factor(s)] that led to the apparent 'lack of health' in the first place.

(a) To what degree was your type 1 hyperglycaemic condition caused by a deficiency of 'Gymena Sylvestre'?; and (b) By adding a drug like herb Gymena Sylvestre, to your diet, to what degree has your behaviour or lifestyle been modified to reduce/remove the cause of your type 1 hyperglycaemic condition?; and (c) What is the degree of sustainability of achieving a 'cure' by adding a drug like herb Gymena Sylvestre to your habit of eating too often [ie 'eating again' before your blood glucose has reduced to 'normal' levels]?

Edema is a protective process whereby the body is protecting certain cells, especially certain nerve cells, from water STARVATION aka dehydration...

HYPERglycaemia is a protective process whereby the body is protecting certain cells, especially certain nerve cells, from HYPOglycaemic STARVATION due to too fast dropping levels of glucose. Relative HYPOglycaemia aka dropping levels of glucose = localised cellular 'STARVATION warning' ... so the body protects against that potential localised cellular glucose STARVATION with all manner of methods to prevent/reduce that danger ... including priority-protective 'autoimmune down-regulation' of the beta cells.

To help understand the abovementioned process please understand the following imaginary example...

... Administration of Gymena Sylvestre is apparently following a conventional belief that type 1a diabetes is a 'disease' [aka the body got it all wrong ... here comes the ANYdrugTREATED 'fixit'] rather than seeing the life-saving inflammatory response that apparently protects pre type 1a from the potential extraordinary consequences of sudden HYPOglycaemic unawareness.

... Cells are being recycled all day long ... cells that are potential sources of HYPOglycaemia aka beta cells eg may make a 100 renewed cells every hour and 100 recycled cells every hour ... when healthy ... BUT with 'eating too often' acute HYPOglycaemic distress can shift the renewed:recycled ratio to eg 99:101 so there is less potential for relative HYPOglycaemia or absolute HYPOglycaemia ... the safety effect is cumulative and if the acute HYPOglycaemic distress is prolonged then a 99:101 renewed:recycled ratio can lead to life-saving HYPERglycaemia [eg transient supernormal glycaemia in response to a meal] 'slowly but surely'' OR eg if the acute HYPOglycaemic distress is 'short & sweet' then a 75:125 ratio can bring about life-saving HYPERglycaemia [eg TSG in response to distress] relatively quickly ... either way the body is in priority-protection mode from acute HYPOglycaemic distress caused by 'eating too often' because 'eating too often' blocks the natural balancing 'cure' which should be achievable c/o 'eating less often'.

... How sure is it that Gymena Sylvestre is curing type 1a or removing HYPERglycaemic symptoms ie overriding the safety-net of the autoimmune downregulation of beta cells and potentially creating a physiological state of delicate HYPOglycaemic unawareness (?) together with 'good numbers' & 'good control'. [If You bang your hand repeatedly with a hammer You can 're-educate' pain receptors, to stop Yourself moving your hand, if You cut the sensory nerve that goes back to your brain ... BUT how well are You cured?].

Any 'HYPOglycaemic drug', including Gymena Sylvestre, which may reduce the 'priority-protective HYPERglycaemic state' ... should carefully address the potential consequence of localised cellular glucose STARVATION aka HYPOglycaemia, especially the 'glucose flow' to localised delicate nerve cells, especially in the CNS [brain & spinal cord] ... because of the "HYPOglycaemia unawareness" that is a foreseeable consequence of inappropriate removal of such a vital source of fuel/glucose.

In relation to your description of a "hyperglycemic condition" aka 'indigestion' [aka excess blood glucose c/o 'calling upon HYPOglycaemic responses' too often c/o eating too often] ... Kelly ... assuming that it is possible to have perfectly healthy beta cells without reducing weight and/or taking plant extracts [eg c/o insulin resistance ie 'adaptative insulin protection' eg c/o type 2 diabetes] ... Please discuss the role of localised cellular glucose STARVATION aka HYPOglycaemia, in beta-cell regeneration, BEFORE and AFTER diagnosis / GM insulin treatment of type 1 and/or type 2 Diabetics [with reference to the following]...
www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/1#c5614998

Kelly also re your '1:30AM on Jul 28th 2007' comment @ www.thediabetesblog.com/2007/05/13/a-leaf-extract-lowers-insulin-requirements-in-iddm/#c6415789
"...(1) When you take exogenous insulin, it suppresses your body's ability to secrete natural insulin. That much is clearly shown by the research..."

Please discuss what is likely [forseeably] happening to downregulate the endogenous insulin secretion AND production BEFORE diagnosis ... ie the extraordinary challenges to the CNS of relative HYPOglycaemia and absolute HYPOglycaemia. For example, in the absence of priority-protective 'autoimmune downregulation' of the beta cells [yes type 1 diabetes is PROTECTIVE] in an ACUTELY-distressed-dehydrated-eating-too-often-Human [with above average/mean 'Juvenile' acute levels of HYPOglycaemia inducing growth hormone] ie a pre 'type 1' aka Juvenile onset Diabetic ... would VERY quickly succumb to HYPOglycaemia unawareness either temporary or permanent. Please compare the seconds / minutes / hours timeline of 'HYPOglycaemia distress' as compared to the days / weeks / months, of eating too often, that sometimes culminates in 'KETOacidosis distress'.

www.thediabetesblog.com/2007/07/10/hypoglycemia-and-the-brain/#c5936897

Pre 'type 1' diagnosis polyuria & polydipsia is a small price to pay for the remarkably protective 'adaptative homeostasis' that is 'type 1 diabetes' ...
http://www.thediabetesblog.com/2007/07/20/meager-data-on-benefits-of-diet-and-exercise-for-type-2s/#c6046706

Kelly further re your additional '1:30AM on Jul 28th 2007' comments @ www.thediabetesblog.com/2007/05/13/a-leaf-extract-lowers-insulin-requirements-in-iddm/#c6415789
"...(2) The testing of c-peptide levels can only tell us whether or not a pancreas is secreting insulin into the bloodstream - it can't tell us what the beta cell status is. Doctors will say that someone has no pancreatic function if their c-peptide is negligible, but that's inaccurate, particularly if they test you after you've taken a shot and are fasting (it should be a stimulated c-peptide test with no AM shot). All they can say is a pancreas isn't secreting insulin into the bloodstream - not whether the beta cells are present..."

Yes it's great news for the 'cure' for type 1 diabetes / Diabetics ... the beta-cell DNA & beta cells are there, ready & willing, 'right here & right now' to 'thermoelectrically' up-regulate to produce all the insulin that is needed ... simply & sustainably remove the cause of the protective 'thermoelectrical' down-regulation ... aka 'relative HYPOglycaemia distress' aka eating too often.

"...Since the trend always seems to be take more and more insulin as you gain weight and get more sedentary with age, it could be akin to just constantly pounding the pancreas into submission until it..."

Yes BUT that is a 'type 2', aka Adult onset, Diabetic scenario ie a CHRONICALLY-distressed-dehydrated-eating-too-often-Human [with below average/mean 'Juvenile' acute levels of HYPOglycaemia inducing growth hormone] in respect of which the pancreas simply produces more & more insulin and local homeostatic control increases at the insulin receptors aka life saving 'insulin resistance' and that is why UNdrugTREATED type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span ...
www.sciencemag.org/cgi/content/abstract/317/5836/369

AND it's great news for the 'cure' for type 2 diabetes / Diabetics ... the beta-cell DNA & beta cells are there, ready & willing, 'right here & right now' to 'thermoelectrically' control the production of all the insulin that is needed ... simply & sustainably choose to remove the cause of the protective above average/mean blood glucose level ... aka 'relative HYPOglycaemia distress' aka eating too often.
www.thediabetesblog.com/2007/07/20/meager-data-on-benefits-of-diet-and-exercise-for-type-2s/1#c6044581

AND what is the apparent relationship between localised cellular glucose STARVATION aka 'HYPOglycaemia' and Men apparently having healthier hearts without the 'better numbers' and/or 'better control' that Women apparently have >>> 3 clicks links to "...see the research..." ref via this ref >>>
http://www.thediabetesblog.com/2007/06/26/Diabetes-control-has-improved-dramatically-in-U.S./#c5653076

Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 13:23hrs SAT.04.AUG.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

www.thediabetesblog.com/2007/04/19/no-food-no-problem

Posted at 8:41AM on Aug 4th 2007 by Nicholas Dynes Gracey

12. Hi Allie, Scott, Hannah & Kelly;

This is a re-posted copy of my comment, in reply to Kelly, previously posted at 5:50am [your time] Aug 6th 2007 [which was registered on www.thediabetesblog.com until approx 10am your time].

re My reply above Posted at 4:00PM on Aug 2nd 2007 in reply to Kelly's comment [#10 above] Posted at 2:05AM on Aug 2nd 2007 ["...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"] which has recently been deleted [by/for Kelly?] and then re-posted above as Kelly's 'new' comment #12 Posted at 10:37PM on Aug 5th 2007 ["...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"]; and in regard to my associated post...
http://www.thediabetesblog.com/2007/08/03/food-for-happy-thoughts/1#c6562860

WHAT CAUSES DIABETES...

Eating too often [for that particular Individual at that particular period of their life] causes relative HYPOglycaemia aka HYPOglycaemic distress and HYPOglycaemic distress causes [especially in type 1] a reduction of beta cells/activity and/or [especially in type 2] reduced insulin sensitivity aka insulin resistance aka carbohydrate resistance aka carbohydrate allergy aka glucose mediated inflammation aka glucose fever [which is an acute protective response that protects brain related cells from HYPOglycaemic distress]...
http://diabetes.diabetesjournals.org/cgi/content/full/55/12/3238

A good starting reference to help with increasing your understanding about "WHAT CAUSES DIABETES" is to ponder upon 'relative temperature' ie the difference between going outside on a snowy day, after staying in a hot bath too long, vs going outside on a snowy day, having just had a quick cold bath; and this relative HYPOglycaemia reference...
http://www.alfediam.org/media/pdf/RevueBrunD&M5-2000.pdf

...'Relative HYPOglycaemia'... This situation was first evidenced by Harri who reported in 1924 five cases of hypoglycemia following a meal, that he called reactive hypoglycemia. Harris postulated that reactive hypoglycemia was some kind of counterpart to diabetes mellitus: while the latter was considered to result from hypoinsulinism, or at least impaired insulin action, hypoglycemia was expected to be due to hyperinsulinism or dysinsulinism. Symptoms fully similar to those occurring during insulin-induced hypoglycemia were observed at blood-glucose values below 0.7 g/100 l.

Later, this issue became for decades a matter of considerable controversy, due to a lack of consensus in definitions and to the unappropriate use of the oral glucose tolerance test. In addition, hypoglycemia has become a fashionable and overdiagnosed disorder in several countries, due to its popularization in the lay literature, so that a host of patients used to describe signs suggestive for hypoglycemia without any clinical evidence for low blood glucose, a situation that Cahill and Yager proposed to call "non-hypoglycemia". In agreement with them, Charles who found that such patients never exhibited hypoglycemia after a mixed meal concluded that this situation has no relation to glycemia and should rather be termed "post prandial idiopathic syndrome".

The number of terms applied to reactive hypoglycemia have added to the confusion: these included functional hyperinsulinism, essential hypoglycemia, functional hypoglycemia, dysinsulinism, hypoglycemic fatigue, insulinogenic hypoglycemia, and ... "relative HYPOglycaemia"...

FOR MORE related info please follow the links via... www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217

Kelly ... in respect of the apparent fact & related comment that "type 2 Diabetics are superior to mere Mortals that is how UNdrugTREATED type 2 Diabetics are adapted to live longer than the average/mean Human life-span" please note that most type 2 Diabetics are ANYdrugTREATED and my comments relate to a discussion of an explanation relating the following parts of that research paper [www.sciencemag.org/cgi/content/abstract/317/5836/369] QUOTE: "... All the insulin-resistant mice displayed mild glucose intolerance (Fig. 2D). However, diabetes did not develop in these mice because insulin concentrations increased to compensate for peripheral resistance, reaching the highest amount in old male bIrs2+/– and bIrs2–/– mice (Fig. 2E). Consistent with the observed hyperinsulinemia, pancreatic islets were larger in old male bIrs2+/– and bIrs2–/– mice than in old controls (Fig. 2F) ... however, long-lived brain-specific bIrs2+/– and bIrs2–/– mice are insulin resistant, hyperinsulinemic, and glucose intolerant. The mechanism responsible for this disparity is unknown. REGARDLESS, our results point to the brain as the site where reduced insulin-like signaling can have a consistent effect to extend mammalian life span—as it does in C. elegans and D. melanogaster (1, 3)..."

WE MUST BE REGARDFULL because virtually every Peer reviewed research paper contains a paradox. By focussing on the paradox it is a relatively straightforward process to make the next scientific breakthrough. Most Scientists simply continue the dogma by carrying on REGARDless of the paradox. Diabetes type 1 & type 2 can be cured quite easily by sustainably reducing and then removing the cause and the major step to achieve that cure is a desire to be free from diabetes rather than carry on REGARDless ... being REGARDmore is too small a step. We need to be 'REGARDFULL'.

Warm thanks; Nick

... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.
www.thediabetesblog.com/2007/04/19/no-food-no-problem

ps FOR MORE related info please follow the links via...
www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217

Posted at 3:19PM on Aug 6th 2007 by Nicholas Dynes Gracey

13. Hi Allie & Anyone else who is REGARDFULL to the extraordinary re-re-posting of Kelly's most recent comment...

My reply above Posted at 4:00PM on Aug 2nd 2007 was in reply to Kelly's comment [#10 above] Posted at 2:05AM on Aug 2nd 2007 ["...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"] which was subsequently [by/for Kelly?] then re-posted above as Kelly's 'new' comment #12 Posted at 10:37PM on Aug 5th 2007 ["...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"]; which was subsequently [by/for Kelly?] then re-re-posted above as Kelly's 'new' comment #12 Posted at 03:16PM on Aug 6th 2007 ["...Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?"]; Subsequently my re-posted copy of my comment, in reply to Kelly, was Posted at 3:19PM on Aug 6th 2007.

Warm thanks; Nick

... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

http://www.thediabetesblog.com/2007/04/19/no-food-no-problem

ps FOR MORE related info please follow the links via...
http://www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217
http://www.thediabetesblog.com/2007/05/25/tv-causes-elevated-glucose-in-children/1#c6581479

Posted at 4:37PM on Aug 6th 2007 by Nicholas Dynes Gracey

14. Interesting. In follow up, Nick, do you have some references to direct me to to learn more about your "WHAT CAUSES DIABETES" statements above?

Also, I don't get the WE MUST BE REGARDFULL sentence. Care to elaborate?

Kelly

Posted at 6:24PM on Aug 6th 2007 by Kelly

15. In response, Nick,

I read the article you cited, but I didn't find it particularly relevant to the "cause" and "cure" you presented (that eating in and of itself causes diabetes). The point of the paper, a review, is to lend itself to diagnosing postprandial hypoglycemia - those who experience hypoglycemia following a meal. This effectively rules out all Type 1's and likely most Type 2's. And while the "cure" they present for this particular condition is avoidance of carbs, this "cure" doesn't apply to the rest of the diabetic population, who doesn't suffer from this condition.

In keeping with the papers Bev and Allie posted, I do think in the case of Type 1 diabetes that cellular inflammation is a key to the problem - that the inflammation has to be allieviated before beta cell regeneration can occur, either on its own or with help (e.g. from herbs like Gymnema Sylvestre). I believe that with Type 1's, given that the inflammation is resolved, that beta cell regeneration can occur on its own, but I believe Gymnema Sylvestre, and other herbs, can play a role in helping this along. Gymnema Sylvestre has clearly been shown to regenerate beta cells, and with Type 1's, my belief is that healing is likely to be a long, natural process once the inflammation has been removed.

Regards,

Kelly

Posted at 10:43PM on Aug 6th 2007 by Kelly

16. Continued, in response, to Nick's last post.

To (a) above: I'll offer first an analogy: Lack of oranges, specificallly, didn't cause scurvy; however, eating them did cure it. Would you postulate that eating oranges, since they weren't specifically the cause of the problem, then can't be the cure? The analogy is the same. While the mechanism behind why Gymnema Sylvestre (GS) promotes regeneration of beta cells may not be known, it does, in fact, regenerate them.

To (b): As shown in the paper Bev cited, alleviating inflammation appears to be a key to solving the Type 1 diabetes problem. Without doing this as a part of the therapy, efforts to cure the problem didn't work. GS may work by alleviating the inflammation to allow the beta cells to regenerate naturally. It might not. While the path may be different, the end is the same.

To (c): by relieving the inflammation, it could be that the beta cells are being allowed to do their own healing. If that's the case, the mechanism is true healing, and thereby, also self-sustaining.

One item that hasn't been talked about at all is the issue of autoimmunity. How does your theory survive the idea that some Type 1's exhibit antibodies to insulin before being put on exogenous insulin? Care to bat that one around?

Regards,

Kelly

Posted at 11:32PM on Aug 6th 2007 by Kelly

17. Hi Allie, Scott, Hannah, Kelly & Anyone else who is interested in the CAUSE, CURE & PREVENTION of type 1a 'diabetes mellitus'; and in regard to my associated post in relation to relative HYPOglycaemia aka HYPOglycaemic distress...
http://www.thediabetesblog.com/2007/05/25/tv-causes-elevated-glucose-in-children/1#c6581479

Kelly re your comment, apparently above, Posted at 11:32PM on Aug 6th 2007...
"...One item that hasn't been talked about at all is the issue of autoimmunity. How does your theory survive the idea that some Type 1's exhibit antibodies to insulin before being put on exogenous insulin? Care to bat that one around?..."

In reply ... the key foundation of my opinion is that the "autoimmunity", referred to, is protective in controlling the HYPOglycaemic effects of endogenous insulin, at the time, as described in your question.

WHAT CAUSES DIABETES...

Eating too often [for that particular Individual at that particular period of their life] causes relative HYPOglycaemia aka HYPOglycaemic distress and HYPOglycaemic distress causes [especially in type 1a] a reduction of beta cells/activity and/or [also in type 1] reduced insulin sensitivity aka insulin resistance aka carbohydrate resistance aka carbohydrate allergy aka glucose mediated inflammation aka glucose fever [which is an acute protective response that protects brain related cells from HYPOglycaemic distress]...
http://diabetes.diabetesjournals.org/cgi/content/full/55/12/3238

Endogenous insulin [and the associated insulin:glucagon ratio] needs to be very carefully kept under homeostatic control especially in conditions of HYPOglycaemic distress eg precipitated by certain antibiotics, foods or psychological pressures. One such method is autoimmunity. Another is insulin resistance. 'Autoimmunity' + 'carbohydrate/insulin' resistance = substantial 'increased' protection from the extraordinary challenges of HYPOglycaemic distress.

What is likely [forseeably] happening to down-regulate the endogenous insulin secretion AND production BEFORE diagnosis ... ie the extraordinary challenges to the CNS of relative HYPOglycaemia and absolute HYPOglycaemia. For example, in the absence of priority-protective 'autoimmune down-regulation' of the beta cells [yes type 1 diabetes is PROTECTIVE] in an ACUTELY-distressed-dehydrated-eating-too-often-Human [with above average/mean 'Juvenile' acute levels of HYPOglycaemia inducing growth hormone] ie a pre 'type 1' aka Juvenile onset Diabetic ... would VERY quickly succumb to HYPOglycaemia unawareness either temporary or permanent. Please compare the seconds / minutes / hours timeline of 'HYPOglycaemia distress' as compared to the days / weeks / months, of eating too often, that sometimes culminates in 'KETOacidosis distress'.

... Cells are being recycled [c/o 'autoimmunity'] all day long ... cells that are potential sources of HYPOglycaemia aka beta cells eg may make a 100 renewed cells every hour and 100 recycled cells every hour ... when healthy ... BUT with 'eating too often' acute HYPOglycaemic distress can shift the renewed:recycled ratio to eg 99:101 so there is less potential for relative HYPOglycaemia or absolute HYPOglycaemia ... the safety effect is cumulative and if the acute HYPOglycaemic distress is prolonged then a 99:101 renewed:recycled ratio can lead to life-saving HYPERglycaemia [eg transient supernormal glycaemia in response to a meal] 'slowly but surely'' OR eg if the acute HYPOglycaemic distress is 'short & sweet' then a 75:125 ratio can bring about life-saving HYPERglycaemia [eg TSG in response to distress] relatively quickly ... either way the body is in priority-protection mode from acute HYPOglycaemic distress caused by 'eating too often' because 'eating too often' blocks the natural balancing 'cure' which should be achievable c/o 'eating less often'.

Kelly ... What's your opinion for the appearance of [above average] endogenous insulin 'autoimmunity' + above average/mean blood glucose aka HYPERglycaemia aka type 1a diabetes?

Warm thanks; Nick

... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

http://www.thediabetesblog.com/2007/04/19/no-food-no-problem

ps FOR MORE related info please follow the links via...

www.thediabetesblog.com/2007/07/25/early-prevention-of-type-1-diabetes-human-trials/1#c6436217

www.thediabetesblog.com/2007/08/03/food-for-happy-thoughts/1#c6562860

www.thediabetesblog.com/2007/04/03/the-honeymoon-period#c5589475

Posted at 4:27PM on Aug 7th 2007 by Nicholas Dynes Gracey