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HOW(?) & WHY(?) Liquid-Eating & Intermittent-Fasting can be so beneficial to your Health...
Tuesday, 11 March 2008
DISTRESS causes HYPOglycemia RELATIVE to the Relative NORMOglycemia before that DISTRESS ...HOW ?
"Every Day And In Every Way I Am Getting Better And Better"...
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Relative HYPOglycemia persists if ... 'HYPOglycemia effectors' such as DISTRESS persists and/or HYPOglycemia FOOD administration persists and/or HYPOglycemia DRUG administration persists ... each/any 'HYPOglycemia effector' persisting ... irrespective of the INITIAL onset of HYPOglycemia relative to a previous Relative NORMOglycemia ... for Any particular Individual at that particular time of their LIFE. Such a physiological state may reasonably be referred to as:-
Relative-HYPOglycemia-Distress "RHOD" ...WHY ?
Francine Kaufman's 'Distress-HYPOthesis' [please click on the 2 links above].
Hi AnyOne, also re the above... ARE 'INSULIN INFUSIONS' GENERALLY ASSOCIATED WITH SIMULTANEOUS GLUCOSE INFUSIONS? Warm thanks; Nick
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Are 'insulin infusions' generally associated with simultaneous glucose infusions?
I'm not certain what you mean by each, but in practice, I do not believe this to be the case, except in a hospital setting, when surgical patients may have both dextrose and insulin in their IV drip. But patients' daily practice, the basic idea is to dose insulin in proportion to carbohydrate consumption in order to ensure those digested carbohydrates are able enter the cells for fuel.
Unfortunately, it is largely an estimate and the medical profession has done very little to deliver plasma glucose regulated insulin replacement. The time course of the glucose-lowering actions of subcutaneously injected insulin, even the shortest acting insulin analogues, is measured in hours whereas that of endogenous insulin in non-diabetic individuals is measured in minutes.
With regard to one of the elements you have included here, let me respond to one: "There's certainly a strong belief that significant stress can bring out diabetes," she [Dr. Francine Kaufman] said.
However, I would add the the theory dubbed the "Accelerator Hypothesis" has also suggested something along these lines. In essence, the "Accelerator Hypothesis" predicts earlier diabetes onset in heavier people -- without necessarily a change in risk, but the theory views type 1 and type 2 diabetes as essentially the same disorder of insulin resistance, set against different genetic backgrounds.
Unfortunately, many pediatric endocrinologists are reporting an increase in the incidence of T1DM in young children, and this is occurring on a worldwide basis (across continents, in Asia, Australia, North and South America, and Europe). Of course, as noted by the authors, many registries do not track adults along with children. But the theory posits that if the age of diagnosis is becoming lower, there must be a reason; hence, the Accelerator Hypothesis. Early weight gain and increasing BMI of young children may lead to increased insulin resistance and an earlier destruction of pancreatic beta cells in a person who may be genetically predetermined to develop T1DM. Unfortunately, the authors acknowledge that relatively few of the children in their sample were overweight, as well as numerous other shortcomings. The study has a number of provocotive thoughts, but was nevertheless useless.
http://care.diabetesjournals.org/cgi/content/full/26/10/2865
However, one potentially valuable excerpt may be taken away from this, and that is that increased stress, whether it is derived from insulin resistance induced by the physical stress of increased body mass, or psychological stress induced by external, environmental incidents such as earthquakes could accelerate the onset of T1DM among people who are already likley to develop the disease anyway. So what? This does not establish a link between autoimmunity and insulin resistance (which, by the way, I would add is distinctly different from what I refer to as "insulin interference" -- a temporary rather than a chronic condition which may be caused by competition for the cell receptors due to the presence of other hormones. But unlike a chronic insulin resistance, this has a very clear cause and is immediately resolved when the interference is gone)
My response: Uh duh! OF COURSE stress can induce type 1 diabetes, as it places additional burden on an endocrine system already operating at full capacity because of autoimmune destruction of an increasingly smaller number of beta cells, thus the last remaining beta cells are forced to produce additional insulin induced by stress, which ultimately causes cell aptosis. This is common sense, not science. Unfortunately, there are also too many problems with the basic theory, many of which had already been proven (and proven again) by countless researchers, and the many holes in this theory seem to be quite far from "air tight".
I would go back to Brent Hoadley's basic issue, which is that science is about asking the RIGHT question, and usually results in MORE questions than correct answers. My basic argument is that theories must be replicated by other scientists in order to be proven, and it is important for those to incorporate as much of the published works as possible (not selectively excluding those factual elements that work against the author's theory) to be accepted as established truth.
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