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LANTUS to improve insulin sensitivity - "experiment"

Awesome, thank you. I have a meter that is not very accurate and sometimes gives me readings that are 20 points off from what I get in the labs.
It happened to my friends mom all the time ...She thought she had her diabetes under control,,but when she would go
for blood tests they would come back wayyyy higher ...Now she got that meter and shes adjusted her meds and much better ...
 
yes everything was the same

as for the second one, I think that with 350g of carbs lantus it is totally unnecessary because your pancreas does not need to be relieved from the outside with such a small amount it will cope on its own without any problems
No hypoglycemia? I love lantus dieting but post lift I get the cold sweats and dizziness some, usually resolved with whey, but along with being muscular you’re pretty fucking tall too correct?
 

Here’s a cool study for some insight
The sad part is the machines that Passed the test we're by the old standards of the FDA 25 percent variance...Again criminal.... How is it possible that they think it's OK?
I mean everyone on this board pretty much hates the FDA for their stupidity and banning things that they should not..
Making things prescriptions that they should not.. I think we are the only country left or maybe one or two other countries that you need a prescription for met Forman everywhere else is over the counter..
I remember they were going to be in NAC and make a prescription completely preposterous... So they're so hard on all kinds of drugs
I when it to comes to money in vaccinations and bad glucometers they simply don't acknowledge it....
Corruption is so ridiculous
 
@luki7788, when you say (lantus) at night before bedtime, do you mean right before you go to sleep with or without food?
I eat my last meal right before bed so then I gave lantus but it doesn't really matter because lantus doesn't have peaks and you have no chance of getting hypoglycemia from it
 
Thank you for these words and the sentiment, b-boy! I'd never call you an idiot because I at least try to be in the right neighborhood when I make a judgment like that (an unkind one).

Luki's not one either by any stretch of the imagination even though I disagree vehemently with his posts, like here, that seek to demonstrate that insulin improves insulin sensitivity. Rather than stupid, luki's posts on this topic are merely stubborn (because they refuse to flex or bend in the face of reason), ignorant (because he is motivated by animus rather than valuing factual information on the basis of obviously adequate & pertinent education and experience), and egotical (because he presumes that any reader should "of course" view insulin as totally harmless if not healthy because of his own risk tolerance).

I feel like I've been beating this drum here on ProM for a while now, that insulin (slin; exogenous insulin) inherently worsens insulin sensitivity (increases insulin resistance). But I will use the rest of this reply to try to explain it clearly and simply for anybody that cares to read or understand this:

It can be very confusing to those familiar with these concepts from bodybuilding discussions that hyperglycemia (elevated blood glucose) is but one factor that is associated with insulin resistance, but is not actually synonymous with insulin resistance (hyperglycemia =/= insulin resistance). Yes, reducing blood glucose to normal levels is very important in order to improve insulin sensitivity while using exogenous growth hormone (rhGH) because glucose is toxic to the pancreatic β cells.

Insulin Sensitivity is multifactorial & comprises systemic (e.g., QUICKI) and peripheral (e.g., GLUT-4) components, and is regulated centrally by GLP-1 & GIP. Hyperglycemia, i.e., high blood glucose, is but one factor (the other being insulin) that serves as a proxy for systemic Insulin Resistance (the reciprocal of insulin sensitivity). There are other aspects, including carbohydrate tolerance, etc.

Exogenous insulin reduces blood glucose and thereby prevents this glucotoxicity but actually causes insulin resistance.

Endogenous insulin is secreted in a pulsatile (quick bursts) fashion to regulate growth and metabolism, unlike testosterone that is secreted in a more steady-state fashion (gradual release into the blood; but subject to diurnal variations, e.g., more secretion in the morning than midday/evening). Chronic insulin elevations, e.g., those that are germane to the release profile of a daily low dose of insulin glargine (Lantus), possess a relatively large area-under-the-curve (AUC) due to the release profile (high concentrations on long time frames) vs. normal-healthy endogenous insulin release profiles (comparable to regular insulin pharmacokinetics, e.g., Actrapid, Novolin or HumuLin -R). That large AUC of Lantus and/or moderately-high & frequent exogenous regular insulin doses are described as chronic hyperinsulinemia.

This resistance does not occur by negative feedback at the β cell level.

Instead, what occurs with chronic hyperinsulinemia that causes insulin resistance is multifactorial and includes:
1. Increasing HOMA-IR & decreasing QUICKI (biochemical measures of insulin resistance)
2. Impaired insulin signal transduction due to receptor (IR) dysfunction & diminished autophosphorylation of the IR, thereby blocking GLUT-4 translocation to the cell surface in muscle & fat cells, meaning more glucose in blood:
View attachment 179201

3. Increasing sn-1,2-diacylglycerol (DAG) levels and activity due to de novo synthesis.


I believe they touch on insulin increasing insulin resistance
 

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