"Every Day And In Every Way I Am Getting Better And Better"...
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The GlucoNeoGenic INHIBITING behavior illustrated above TREATS ... in a sometimes SUSTAINABLE, sometimes non-SUSTAINABLE way ... HYPOglycemia and/or treats, in a sometimes SUSTAINABLE, sometimes non-SUSTAINABLE way ... Relative-HYPOglycemia-Distress aka "RHOD" (?)
What GlucoNeoGenic behavior CURES ... in a substantially SUSTAINABLE way ... HYPOglycemia and/or cures in a substantially SUSTAINABLE way ... Relative-HYPOglycemia-Distress aka "RHOD" (?) and thereby avoids and/or PREVENTS the 'HYPOglycemia-STATES' ...WHY ?
BECAUSE an example of a 'HYPOglycemia-STATE' is a form of 'pre-diabetes' so barely distinguishable from 'pre-Type 1A' diabetes that One could reasonably suppose that the 'distress' referred to, way back in 1994/95, by Francine Kaufman as associated with CAUSING diabetes 'during an earthquake' ... may well amount to Relative-HYPOglycemia-Distress being the main avoidable CAUSE of T1A diabetes ...
EG ... "Autoimmune HYPOglycemia" aka pre-T1A diabetes ?
...Associated with the development of circulating anti-insulin antibodies as per T1A diabetes.
The development of anti-insulin antibodies has been reported in over 200 patients most of whom had medical issues with a gland, associated with DISTRESS adaption, called the "thyroid gland".
...The autoimmune HYPOglycemia is associated with eating and/or eating too OFTEN and occurs 3-4 hours after meals following an initial postprandial HYPERglycemic phase that is due to the antibodies interfering with the exit of insulin from the plasma to reach its target tissues. Later, after most of the meal is absorbed, inappropriate high levels of insulin dissociate from this antibody-bound compartment, resulting in HYPOglycemia. Insulin levels in excess of 1000 pmol/L are observed at time of HYPOglycemia, and these persons have high titers of insulin auto-antibodies aka pre-T1A diabetes (?) ... {so may this be an associated DISTRESS that leads to T1A diabetic 'HYPERglycemic compensation' (?)}.
Endocrinol Metab Clin North Am. 1999 Sep; 28(3): 603-18, vii.
Redmon JB, Nuttall FQ.
> 0999 www.tinyurl.cOM/3cr4ds {Redmo001@maroon.tc.umn.edu ~ Autoimmune HYPOglycemia}
Department of Medicine, University of Minnesota Medical School, Minneapolis, USA.
GlucoNeoGenesis is the generation of glucose from non-sugar carbon substrates like pyruvate, lactate, glycerol, and glucogenic amino acids.
The vast majority of GlucoNeoGenesis takes place in the liver and, to a smaller extent, in the cortex of kidneys. This process occurs during periods of INTERMITTENT... fasting, starvation, or intense exercise and is highly endergonic.
GlucoNeoGenesis is often associated with ketosis.
The short-term treatment of HYPOglycemia is the oral or intravenous administration of glucose. If the patient is unable to take carbohydrate by mouth, 25 to 50 g of glucose (in the form of a 50% glucose solution) should be given by intravenous injection immediately after drawing a sample for glucose determination and a sample to be saved for additional diagnostic studies. Glucagon (1.0 mg intramuscularly), which promotes hepatic glucose release, can be used when immediate glucose administration is impractical. However, the effect of glucagon is transient and exogenous glucose administration should be started as soon as possible.
The plasma glucose concentration is monitored to ensure that HYPOglycemia does not recur; continuous glucose infusions may be required to prevent recurrent HYPOglycemia in some disorders.
After initial treatment the mechanism of HYPOglycemia should be determined. Drug-induced HYPOglycemia can be treated with glucose infusion and drug withdrawal.
Hi AnyOne, also re CAUSES of HYPOglycemia ... WHAT DO YOU DO or WHAT SHOULD YOU DO or WHAT DO YOU SUGGEST FOR every day 'GlucoNeoGenic FITTENING' the HUMAN BODY'S CAPACITY for NATURAL GlucoNeoGenesis? Warm thanks; Nick
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