Diabetes Fast Weight Loss

Diabetes Fast Weight Loss .
Andre Willers
8 Apr 2011

Synopsis :
Mice whose insulin and glucagon mechanisms have been knocked out , do NOT get diabetes(ie hyperglycemia)
See NewScientist 26 Feb 2011 p10 "Insulin toppled as ruler of diabetes"

Discussion :

Weight loss .
If you are overweight , rapid weight-loss will ensue , together with diarrhea . The GLP-1 system activates and excretes surplus energy stores . Monitoring is advisable , especially electrolytes . See below .

Overview :
The efficient Insulin-Glucagon system to control blood-glucose levels is finicky , as it is tied to the so many feedback-loops . Especially the nervous system .

Glucagon seems to be the major diabetes-culprit .
Stress , and repeated peaks of stress, causes glucagons to signal fight-or-flight signals to the system to have lots of energy glucose around .
The insulin system tries to keep up , but repeated peaks of stress leads to continual high insulin levels . The system learns insulin resistance just to be able to keep functioning .

The old GLP-1 system remains as default backup (Plan B)

Mice whose insulin and glucagon mechanisms have been knocked out , do NOT get diabetes(ie hyperglycemia)

1.Why not ?
Glucagon-like peptide-1(GLP-1) is manufactured in the gut . This seems to take over the regulatory functions of the glucose levels .
But the level of control is crude and a lot of energy goes to waste (see para 2 below)
The Insulin-Glucagon system is much more efficient .

2.Where does the surplus glucose go ?
Still under study .
But probably put into the body's general storage (lipid capsules) and excreted .

Three items to consider here :

2.1 Atkins high-fat , high protein diet does control diabetes II

2.2 Intralipid should have a major effect .

2.3 The operation that connects the stomach to the duodenum also stabilizes blood-sugar levels even in diabetic patients . Mechanism unknown , but suggestive of a trigger-signal that the more sophisticated Insulin-Glucagon system has failed and to go to Plan B . Note that the introduction of stomach acids into the duodenum would probably stimulate increased GLP-1 secretion (See Appendix A below)

3.Diabetes II (Insulin resistance)
Experiments with leptin (which suppresses glucagon) is underway
I would suggest combining this with Intralipid and/or a high-fat diet .

Unlearning :
Once insulin resistance as been learned , it is not so easy to unlearn .
Aspects of the amygdala and blood-circulation are involved .
General stress has to be unlearned .

See previous posts .

A useful general aid is Chocolate .
Specifically , 5-10 gm of cacao mass per day .
This reduces venous stress by associating endorphin production (theobromine) with erasure of the previous memory of stress in the vein musculature .
Something like propranolol in the cacao mass combined with an endorphin promoter .

So , taking a beta-blocker along with the chocolate will help .
Not just for diabetes , but general stress and Bad Memories (PTSD)

The point is to break the feedback loops without breaking the organism .

Warning :
Taking a beta-blocker together with chocolate should be monitored , especially initially . Hypoglycemia might occur . Especially if insulin or insulin promoters or alcohol is simultaneously being used .

Critical period :
Note the quick breakdown of GLP-1 (2 minutes) . This is the critical period . Notice the correlation with Long-Term-Potentiation .
The beta-blocker has to be taken simultaneously with the chocolate .
Grind the beta-blocker pill up and sprinkle it over the chocolate .

Weight loss .
If overweight , rapid weight-loss will ensue , together with diarrhea . The GLP-1 system activates and excretes surplus energy stores . Monitoring is advisable , especially electrolytes .

A Complete Cure for Diabetes
This is now at least in sight .
In the meantime , you can at least get thinner and de-stressed .

Chocolates , ho !

Andre .

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Appendix A
From Wiki
Glucagon-like peptide-1(GLP-1) is derived from the transcription product of the proglucagon gene. The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-1 as a gut hormone. The biologically active forms of GLP-1 are: GLP-1-(7-37) and GLP-1-(7-36)NH2. Those peptides result from selective cleavage of the proglucagon molecule.
GLP-1 secretion by ileal L cells is dependent on the presence of nutrients in the lumen of the small intestine. The secretagogues (agents that cause or stimulate secretion) of this hormone include major nutrients like carbohydrate,protein and lipid. Once in the circulation, GLP-1 has a half life of less than 2 minutes, due to rapid degradation by the enzyme dipeptidyl peptidase-4. It is a potent antihyperglycemic hormone, inducing glucose-dependent stimulation of insulin secretion while suppressing glucagon secretion. Such glucose-dependent action is particularly attractive because when the plasma glucose concentration is in the normal fasting range, GLP-1 no longer stimulates insulin to cause hypoglycemia. GLP-1 appears to restore the glucose sensitivity of pancreatic β-cells , with the mechanism possibly involving the increased expression of GLUT2 and glucokinase. GLP-1 is also known to inhibit pancreatic β-cell apoptosis and stimulate the proliferation and differentiation of insulin-secreting β-cells. In addition, GLP-1 inhibits gastric secretion and motility. This delays and protracts carbohydrate absorption and contributes to a satiating effect.
Physiological functions
GLP-1 possesses several physiological properties that make it (and its analogs) a subject of intensive investigation as a potential treatment of diabetes mellitus.[1][2][3] The known physiological functions of GLP-1 include:
§ increases insulin secretion from the pancreas in a glucose-dependent manner.
§ decreases glucagon secretion from the pancreas by engagement of a specific G protein-coupled receptor.
§ increases insulin-sensitivity in both alpha cells and beta cells
§ increases beta cells mass and insulin gene expression, post-translational processing and incretion.
§ inhibits acid secretion and gastric emptying in the stomach.
§ decreases food intake by increasing satiety in brain.
§ promotes insulin sensitivity.
As a proof of the physiological role of GLP-1 in post-prandial insulin secretion, it has been shown that an oral dose of glucose triggers a much higher peak in plasma insulin concentration compared to an intravenous dose.
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