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metformin?

It's a medication used by type II diabetics to control blood sugar. It's considered a very safe medication with very few side effects (basically gastrointestinal upsets). Lactic acidosis is a very serious - but rare - side effect; if you're alcoholic or have kidney disease you should be careful.
 
Just started using it last week. Very effective for me at leveling out blood sugar after big meals= no lethargy...also feels a bit like keto, just bit depleted unless you're really taking in the carbs.

If you do a search you'll find it to be pretty well-liked and widely used.
 
Very common medication. I use to know a whole bunch about this but it seems as if I have forgot all of it, lol.

Anyways, I am having some insulin resistance with my GH/peptide use and am currently going over my options. I have been using Glucorell-r (R-ala with biotin) helps a little but not quite enough.

I will be putting in some heavy research again as things are different noe that I have cardiomyopathy.
 
Very common medication. I use to know a whole bunch about this but it seems as if I have forgot all of it, lol.

Anyways, I am having some insulin resistance with my GH/peptide use and am currently going over my options. I have been using Glucorell-r (R-ala with biotin) helps a little but not quite enough.

I will be putting in some heavy research again as things are different noe that I have cardiomyopathy.
Definitely let me know what you come up with. Acarbose (aka Glucobay aka Precose) is something you may want to look into. Just do a Google Scholar search and you'll pull up tons on it; supposedly it's quite effective for improving insulin resistance. For example:

http://edrv.endojournals.org/cgi/content/full/21/6/5853. Effect of -glucosidase-inhibitors on insulin sensitivity. Eight randomized placebo-controlled studies have been published examining the effect of -glucosidase inhibitors on insulin sensitivity in patients with IGT or type 2 diabetes mellitus (Table 2). In subjects with IGT, Chiasson et al. (206) demonstrated that acarbose (100 mg three times daily) for 4 months caused a 21% decrease in steady-state plasma glucose (SSPG) during an insulin suppression test using somatostatin, glucose, and insulin infusions. Similar results were obtained by Laube et al. (207), who reported that 12 weeks of acarbose treatment (100 mg three times daily) increased steady-state glucose infusion rate (SSGIR) by 45%. In addition, Shinozaki et al. (208) treated subjects with IGT with a different glucosidase inhibitor, voglibose (0.2 mg three times daily), for 12 weeks, and showed that SSPG levels decreased significantly after voglibose treatment. Thus, these data suggest that -glucosidase inhibitors improve insulin sensitivity in subjects with IGT and hyperinsulinemia possibly secondary to an amelioration of glucose-induced insulin resistance by reducing hyperglycemia in the postprandial period. In contrast to studies in subjects with IGT, studies examining the effect of -glucosidase inhibitors on insulin sensitivity in patients with type 2 diabetes showed no amelioration of insulin resistance despite decreased postprandial glycemia (209, 210, 211, 212, 213). Thus, these data are in support of the notion that -glucosidase inhibitors improve insulin sensitivity in subjects with IGT but have no effect on insulin sensitivity in subjects with overt type 2 diabetes.

I just ordered some and should have it within the week, so I'll be sure to let ya know how it goes.

Just started using it last week. Very effective for me at leveling out blood sugar after big meals= no lethargy...also feels a bit like keto, just bit depleted unless you're really taking in the carbs.

If you do a search you'll find it to be pretty well-liked and widely used.

Wow! Just goes to show how everyone is different. A few years ago, the most decent endo I ever had wrote me a script for it. Not only did it do nothing noticeable to help with my F'd up glucose/insulin, the GI sides and extreme lethargy where horrible. After a month of no improvement, I'd had enough and stopped taking it.
 
Would have been the perfect supplement if it didnt lower igf levels for 4hrs.
 
Another agent that may be of interest...

Acipimox (Olbetam) improves insulin resistance and increases blood levels of HGH/related peptides. However, being an antilipolytic, I'm not sure what the overall effect would be (re: fatloss)... then again, this drug is also VERY impressive in affects on both leptin and ghrelin, so I'm guessing it would be favorable for fatloss Here are a few interesting studies:

Reduction of Free Fatty Acids By Acipimox Enhances the Growth Hormone (GH) Responses to GH-Releasing Peptide 2 in Elderly Men -- Sytze van Dam et al. 85 (12): 4706 -- Journal of Clinical Endocrinology & Metabolism
GH release is increased by reducing circulating free fatty acids (FFAs). Aging is associated with decreased plasma GH concentrations. We evaluated GH releasing capacity in nine healthy elderly men after administration of GH-releasing peptide 2 (GHRP-2), with or without pretreatment with the antilipolytic drug acipimox, and compared the GHRP-2-induced GH release with the response to GHRH. The area under the curve (AUC) of the GH response after GHRP-2 alone was 4.8 times higher compared with GHRH alone (1834 ± 255 vs. 382 ± 78 µg/L·60 min, P < 0.001). Acipimox, which reduced FFAs from 607 µmol/L to 180 µmol/L, increased the GH AUC to 1087 after GHRH and to 2956 µg/L·60 min after GHRP-2 (P < 0.01). The AUC after acipimox/GHRP-2 were positively correlated with the AUC after GHRP-2 alone (r = 0.93, P < 0.01); this was also observed between acipimox/GHRH and GHRH alone (r = 0.73, P = 0.03). Significant negative correlations were observed between basal FFAs and AUC after GHRH or GHRP-2 after combining the data with and without acipimox (r = 0.58, P = 0.01 and r = 0.48, P = 0.04, respectively), and between basal FFAs and GH at t = 0 (r = -0.44, P = 0.001). Interestingly, GHRP-2 administration was followed by a significant early rise in plasma FFAs by 60% (P = 0.01), indicating an acute lipolytic effect. In conclusion, reduction of circulating FFAs strongly enhances GHRP-2-stimulated GH release in elderly men. The data indicate that the decreased GH release associated with aging can be reversed by acipimox and that the pituitary GH secretory capacity in elderly men is still sufficient.

**broken link removed**
Objective: The regulation and function of systemic ghrelin levels appear to be associated with food intake and energy balance rather than GH. Since GH, in turn, acutely induces lipolysis and insulin resistance in skeletal muscle, we aimed to study the isolated and combined effects of GH, free fatty acids (FFAs) and insulin sensitivity on circulating ghrelin levels in human subjects.

Design: Seven GH-deficient patients (aged 37 ± 4 years (mean ± S.E.)) were studied on four occasions in a 2 x 2 factorial design with and without GH substitution and with and without administration of acipimox, which lowers FFA levels by inhibition of the hormone-sensitive lipase, in the basal state and during a hyperinsulinemic euglycemic clamp.

Results: Serum FFA levels decreased with acipimox administration irrespective of GH status. The GH-induced reduction in insulin sensitivity was countered by acipimox. Fasting ghrelin levels decreased insignificantly during GH administration alone, but were reduced by 33% during co-administration of GH and acipimox (Aci) (in ng/l): 860 ± 120 (–GH – Aci), 711 ± 130 (–GH + Aci), 806 ± 130 (+GH – Aci), 574 ± 129 (+GH + Aci), P < 0.01. The clamp was associated with a further, moderate lowering of ghrelin. GH and acipimox induced a reciprocal 25% increase in serum leptin levels (µg/l): 11.2 ± 4.4 (–GH – Aci), 11.7 ± 4.4 (–GH + Aci), 11.5 ± 4.4 (+GH – Aci), 13.9 ± 4.2 (+GH + Aci), P = 0.005.

Conclusion: Our data suggest that antilipolysis via suppression of the hormone-sensitive lipase in combination with GH administration is associated with significant and reciprocal changes in ghrelin and leptin.

**broken link removed**
Obesity is commonly associated with elevated plasma free fatty acid (FFA) levels, as well as with insulin resistance and hyperinsulinemia, two important cardiovascular risk factors. What causes insulin resistance and hyperinsulinemia in obesity remains uncertain. Here, we have tested the hypothesis that FFAs are the link between obesity and insulin resistance/hyperinsulinemia and that, therefore, lowering of chronically elevated plasma FFA levels would improve insulin resistance/hyperinsulinemia and glucose tolerance in obese nondiabetic and diabetic subjects. Acipimox (250 mg), a long-acting antilipolytic drug, or placebo was given overnight (at 7:00 P.M., 1:00 A.M., 7:00 A.M.) to 9 lean control subjects, 13 obese nondiabetic subjects, 10 obese subjects with impaired glucose tolerance, and 11 patients with type 2 diabetes. Euglycemic-hyperinsulinemic clamps and oral glucose tolerance tests (75 g) were performed on separate mornings after overnight Acipimox or placebo treatment. In the three obese study groups, Acipimox lowered fasting levels of plasma FFAs (by 60-70%) and plasma insulin (by approximately 50%). Insulin-stimulated glucose uptake during euglycemic-hyperinsulinemic clamping was more than twofold higher after Acipimox than after placebo. Areas under the glucose and insulin curves during oral glucose tolerance testing were both approximately 30% lower after Acipimox administration than after placebo. We conclude that lowering of elevated plasma FFA levels can reduce insulin resistance/hyperinsulinemia and improve oral glucose tolerance in lean and obese nondiabetic subjects and in obese patients with type 2 diabetes.

[Improvement of insulin sensitivity associated wit... [Rev Med Chil. 1994] - PubMed result
Insulin sensitivity was estimated in a morbidity obese, insulin-resistant, glucose-intolerant patient before and after 4 weeks of treatment with Acipimox (250 mg t.i.d), an orally-administered, long-acting antilypolitic drug. The ensuing fall in circulating levels of fasting free fatty acids was associated with a clear amelioration of insulin resistance, as assessed by a minimal model analysis of a frequently sampled intravenous glucose tolerance test as well as by an oral glucose tolerance test. Similarly, this treatment brought about a reappearance of GH response to oral stimulation with clonidine. The evidence showing Acipimox-induced amelioration of insulin resistance in this patient without diet, exercise or weight loss should encourage exploring the potential utility of this drug in this type of patients.
 
Acarbose

Definitely let me know what you come up with. Acarbose (aka Glucobay aka Precose) is something you may want to look into. Just do a Google Scholar search and you'll pull up tons on it; supposedly it's quite effective for improving insulin resistance.

I just ordered some and should have it within the week, so I'll be sure to let ya know how it goes.
Won't even need to wait a few days! Desite excellent diet and rigorous exercise, my Hemoglobin A1c was [sill] elevated (surprise, surprise! :rolleyes: ); so my GP finally took matters into his own hands and wrote me a script for this. I'll be trying it with my first meal today (~4:00-5:00) and definitely be sure to let y'all know how it goes... (hopefully a lot better than metformin, lol!)

It's about an hour after my first meal with the Acarbose... just 440 calories :) Typically my first meal is 1,000-1,300 cals, (anything <1,000 is EXCELLENT), so it goes w/o saying, this is a HUGE improvement for the better! I feel completely satisfied; no shakes/dizziness/nausea/blurred vision (=> no urges to raid the fridge)! Oh ya, an no GI upset like with that G-damn metformin! :p
 
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