Bro-Science Myth #2: “Insulin protects the pancreas by giving the pancreatic islet β-cell a break”
False:
Low-dose insulin glargine (e.g., Lantus) may stave off or slow the progression from prediabetes (impared fasting glucose or impaired glucose tolerance) or early diabetes to type 2 diabetes mellitus (insulin-resistant; T2DM), characterized by total pancreatic islet β-cell failure; but hyperinsulinemia worsens insulin sensitivity. Exogenous insulin in healthy adults worsens insulin sensitivity by increasing HOMA-IR (defined as [fasting values] serum insulin (μU/ml) * plasma glucose (mmol/liter) / 22.5; optimal range 0.5 – 1.4) & worsening QUICKI (defined as 1 / (log(insulin μU/mL) + log(glucose mg/dL))). In healthy adults, Bouche et al. conducted an experiment using an isoglycemic-hyperinsulinemic clamp (mimicking exogenous insulin in healthy adults) and found that pre-exposure to hyperinsulinemia increased insulin secretion by ~40% (21). [
27].
In a study authored by Owens, D. R. [
27] that is often touted as evidentiary support for the practice of training-day low dose insulin glargine (e.g., Lantus) to promote pancreatic β-cell “rest,” in healthy bodybuilders, the data, rather than supporting this practice, argues for initiating insulin treatment in prediabetes and/or early T2DM before the current observed worldwide clinical practice of initiation of insulin therapy after a duration of T2DM of approximately 10 years x mean HbA1c > 9%. [
27].
The study [
27] proposed that three (3) groups of individuals are particularly suitable for early intensive insulin therapy:
- Treatment-naive (i.e., no prior exposure to exogenous insulin) patients who present with marked hyperglycemic symptoms with HbA1c > 8.5%
- Latent autoimmune diabetes of adults (type 1.5 diabetics; LADA) patients… characterized by the presence of islet autoantibodies (i.e., treatment initiation indicated when glutamic acid decarboxylase > 20 U/mL) & low C-peptide secretion
- Patients possessing elevated cardiovascular risk factors (e.g., hyperlipidemia, hypertension)…. but the data does not bear out the purported rationale for this practice…
The purported “multifaceted benefits of insulin” that include ostensible anti-inflammatory & antioxidant effects that may protect endothelial function & vascular function is eviscerated by the bodybuilding practice of supra-physiologic anabolic-androgenic steroids that increase ROS (reactive oxygen species) production [
31] and deleteriously alter endothelial cell function, particularly those that inhibit 11β-HSD2 (e.g., fluoxymesterone, oxymetholone, testosterone), or alternately inhibit cortisol oxidation and exert MR action (e.g., trenbolone) [
30] and combined rhGH use (increasing serum IGF-I) reduces eNOS (endothelial nitric oxide synthase) activity. [
32].
These purported benefits are, further, not materialized in any of the large scale studies that measured cardiovascular risk (from ACCORD to ADVANCE to VADT) (29, 30, 31) [
27] . In the most relevant and well-powered study, the ORIGIN trial (Outcome Reduction with an Initial Glargine Intervention; a long-term, prospective, large scale, randomized-controlled trial [n=12,537]) in prediabetes and early T2DM patients, patients followed up with at a median of 6.2 years showed no effect on:
- nonfatal myocardial infarction (MI; heart attack)
- nonfatal stroke
- death from cardiovascular causes
- revascularization, or
- hospitalization for heart failure [27]
Indeed, the common bodybuilding use of short & rapid-acting insulin preparations is strongly associated with increased cardiovascular risk.
The crux of the argument that exogenous insulin use promotes “β-cell rest” is rooted in a small (n=7), 2.5 page, 1976 study in diabetic patients that postulated that overcoming glucotoxicity (by exogenous insulin) in turn allows a store of readily available endogenous insulin to be accumulated for early release to a nutrient challenge, thereby, enhancing β-cell function. [
29]. See [
27] citing Turner, et al. (
18). Naturally, the expansion of this logic is inapposite healthy adult bodybuilders using high dose rhGH (i.e., increasing HSL activity, thereby increasing circulating free-fatty acids, inducing insulin resistance).
.gif "IP Gear")
)
. What is really more likely, be logical… that the change in season/some sudden iron deficiency he developed in ONE MONTH caused this drastic change in A1c… or the lantus. Luki is incredibly regimented with diet, just read his log. He is very consistent, this is not some sudden change with folic acid or vitamin E, do not be ridiculous. We know that with liver disease (although not exactly what Luki was experiencing), if anything we see a falsely low A1c… and since luki has been recovering wouldnt we if anything see it raise if the liver issues were giving it a false reading?
