Systemlord
Member
Metformin cause an insane repetitive cough, it's like my body rejected it. All type 2 medicine caused problems with potassium within 24 hours except for Jardiance and Metformin.
Systemlord
Member
Jatenzo, oral T. I'm dropping weight fast, 7 pounds every week. The fat is just melting off with little effort since I got my glucose levels in the normal ranges.
I feel amazing on DHB, but I still don't know the long term effects, or the shit comes from China, the heavy metals etc. I'd love to feel like this just on TRT
I think since DHB doesn't bind to SHBG, and it's 2:1 anabolic androgenic, it's perfect for TRT
you mean diarrhea?
nodoctor
Active Member
Sh*ts, yes. And flatulence. Pretty well documented but was hoping I’d be the exception. I also remember something about it inhibiting growth hormone secretion but can’t recall the mechanism of action. Since supposedly it permanently improves your body’s ability to regulate blood sugar I decided it was worth a short term run and I think that was the right call. Hard to say though because that was right around when I went vegan, and likely all the fiber among other things improved my blood sugar.
I also have vague recollection of a Metformin recall possibly due to some carcinogenic concerns.
I also have vague recollection of a Metformin recall possibly due to some carcinogenic concerns.
Well, maybe. Im low shbg too, btw, and I struggle with trt.
However, thruout the years reading the boards Ive seen so many fucking guys with low shbg feeling great, they dont even "recognise" they have low shbg, they dont even understand why its a bad thing, they have great libido, energy, muscle, everything.
Just check out tnation, or the reddit boards, so so so many guys with shbg like 8 and shit feeling awesome.
So it must be some other mechanism at play, which we do not yet recognise.
Their low shbg is probably from TRT lowering it, people with low shbg pre-TRT are somehow doomed lol
Yes, maybe, Im not sure anymore. Again, Im low shbg myself and always struggled with trt, but u be surprised how many guys bloodworks ive seen now with like shbg of 10 (before trt), they jump on like 200mg once a week and life is great.
My close friend started trt a couple months ago, his shbg (pre trt) was 13, i was expecting shit result ... Hell no, couple weeks into 150mg a week and libido and energy is out of control.
So what the fuck is going on here.
Maybe people who hyper aromatize are the ones suffering, for me Estradiol is literally what's the motor behind how I feel. A lil too high or low and I feel like shit
Deleted member 43589
Well-Known Member
Here is a take from Mike Arnold on this subject:
Metformin has been found to increase AMPK activation which usually inhibits mTOR. AMPK doesn’t inhibit mTOR directly. Rather, it inhibits another protein that increases mTOR, so by manipulating those aspects of our physiology that interfere with this function, we can minimize AMPK’s negative effect on protein synthesis while continuing to receive its benefits.
In reality, a little AMPK activation isn’t going to have a noticeable impact on muscle growth. We already activate AMPK whenever we do cardio, yet cardiovascular exercise has proven to be a complement to our mass-building efforts, not a detriment.
Still, if we are going to be activating AMPK to a greater degree than normal, we should take steps to ensure mTOR continues exerting its anabolic effects at maximum capacity/near maximum capacity. Fortunately, mTOR can be activated in many different ways, and with bodybuilders already taking advantage of many of these on a continual basis, there is no danger of suppressing growth rate to a significant degree. Factors such as training, diet, drug use, and even the consumption of certain amino acids are all capable of activating mTOR to various degrees. When combined, they can provide a dramatic increase in mTOR that far exceeds the inhibitory influence of any insulin sensitizer, not to mention the positive effects that sensitizers themselves have on recover and growth via improved insulin sensitivity, increased Glut-4 expression, increased muscle glucose uptake, etc. There really is no need for concern. Real-world results confirm this, with innumerable bodybuilders having reaped the benefits of these products without any report of hindered growth.
Deleted member 43589
Well-Known Member
Here is another good study:
Burkhard L. Herrmann, Christian Berg, Elisabeth Vogel, Tanja Nowak, Katrin Renzing-Koehler, Klaus Mann, Bernhard Saller. Effects of a Combination of Recombinant Human Growth Hormone with Metformin on Glucose Metabolism and Body Composition in Patients with Metabolic Syndrome. February 2004 Hormone and Metabolic Research 36(1):54-61.
Abstract
Abdominal obesity and insulin resistance are central findings in metabolic syndrome. Since treatment with recombinant human growth hormone (rhGH) can reduce body fat mass in patients with organic GH deficiency, rhGH therapy may also have favourable effects on patients with metabolic syndrome. However, due to the highly increased risk for type 2 diabetes in these patients, strategies are needed to reduce the antagonistic effect of rhGH against insulin. We conducted a 18-month randomised, double-blind, placebo-controlled study to assess the effect of rhGH in combination with metformin (Met) in patients with metabolic syndrome. 25 obese men (55 +/- 6 years, BMI 33.4 +/- 2.9 kg/m (2)) with mildly elevated fasting plasma glucose (FPG) levels at screening (6.1-8.0 mmol/l) were included. All patients received metformin (850 mg twice daily) either alone or in combination with rhGH (daily dose 9.5 microg/kg body weight). An oGTT was performed at baseline, after 6 weeks, and after 3, 6, 12, and 18 months of therapy. Glucose disposal rate (GDR) was measured by euglycemic hyperinsulinemic clamp at 0 and 18 months and body composition was measured by DEXA every 6 months. In the Met + GH group, IGF-I increased from 146 +/- 56 microg/l to 373 +/- 111 microg/l (mean +/- SD) after 3 months and remained stable after that. BMI did not change significantly in either group during the study. Total body fat decreased by -4.3 +/- 5.4 kg in the Met + GH group and by -2.7 +/- 2.9 kg in the Met + Placebo group (differences between the two groups: p = n. s.). Waist circumference decreased in both groups (Met + GH: 118 +/- 8 cm at baseline, 112 +/- 10 cm after 18 months; Met + Placebo: 114 +/- 7 cm vs. 109 +/- 8 cm; differences between the two groups: p = 0.096). In the Met + GH group, FPG increased significantly after 6 months (5.9 +/- 0.7 vs. 6.7 +/- 0.4 mmol/l; p = 0.005), but subsequently decreased to baseline levels (18 months: 5.8 +/- 0.2 mmol/l). FPG remained stable in the Met + Placebo group until 12 months had elapsed, and then slightly decreased (baseline: 6.2 +/- 0.3, 18 months: 5.5 +/- 0.6 mmol/l, p = 0.02). No significant changes were seen in either group regarding glucose and insulin AUC during oGTT or HbA (1c) levels. GDR at 18 months increased by 20 +/- 39% in Met + GH-group and decreased by -11 +/- 25% in the Met + Placebo group (differences between the two groups: p = 0.07). In conclusion, treatment of patients with metabolic syndrome and elevated FPG levels did not cause sustained negative effects on glucose metabolism or insulin sensitivity if given in combination with metformin. However, since our data did not show significant differences between the two treatment groups with respect to body composition or lipid metabolism, future studies including larger numbers of patients will have to clarify whether the positive effects of rhGH on cardiovascular risk factors that have been shown in patients with GH deficiency are also present in patients with metabolic syndrome, and are additive to the effects of metformin.
Summary
* Both groups received 850 mg Metformin/twice daily
* In the Met + hGH group, IGF-I increased, stabilized after 3 months, the Metformin + placebo group did not change
* Total body fat decreased in both groups, almost double in the hGH group
* Waist circumference decreased in both groups (more in the HGH group)
* After 18 months total muscle mass increased by 0.5 +/- 3.7 kg in the Met+GH group (range -4.6 to 3.7) and decreased by -2.4 _/- 2.9 in the
Met+Placebo group (range –5.7 to 2.2)
* Serum total testosterone levels significantly increased in both groups after 18 months
* Insulin levels did not significantly differ between those patients receiving only metformin and those receiving metformin and hGH
Burkhard L. Herrmann, Christian Berg, Elisabeth Vogel, Tanja Nowak, Katrin Renzing-Koehler, Klaus Mann, Bernhard Saller. Effects of a Combination of Recombinant Human Growth Hormone with Metformin on Glucose Metabolism and Body Composition in Patients with Metabolic Syndrome. February 2004 Hormone and Metabolic Research 36(1):54-61.
Abstract
Abdominal obesity and insulin resistance are central findings in metabolic syndrome. Since treatment with recombinant human growth hormone (rhGH) can reduce body fat mass in patients with organic GH deficiency, rhGH therapy may also have favourable effects on patients with metabolic syndrome. However, due to the highly increased risk for type 2 diabetes in these patients, strategies are needed to reduce the antagonistic effect of rhGH against insulin. We conducted a 18-month randomised, double-blind, placebo-controlled study to assess the effect of rhGH in combination with metformin (Met) in patients with metabolic syndrome. 25 obese men (55 +/- 6 years, BMI 33.4 +/- 2.9 kg/m (2)) with mildly elevated fasting plasma glucose (FPG) levels at screening (6.1-8.0 mmol/l) were included. All patients received metformin (850 mg twice daily) either alone or in combination with rhGH (daily dose 9.5 microg/kg body weight). An oGTT was performed at baseline, after 6 weeks, and after 3, 6, 12, and 18 months of therapy. Glucose disposal rate (GDR) was measured by euglycemic hyperinsulinemic clamp at 0 and 18 months and body composition was measured by DEXA every 6 months. In the Met + GH group, IGF-I increased from 146 +/- 56 microg/l to 373 +/- 111 microg/l (mean +/- SD) after 3 months and remained stable after that. BMI did not change significantly in either group during the study. Total body fat decreased by -4.3 +/- 5.4 kg in the Met + GH group and by -2.7 +/- 2.9 kg in the Met + Placebo group (differences between the two groups: p = n. s.). Waist circumference decreased in both groups (Met + GH: 118 +/- 8 cm at baseline, 112 +/- 10 cm after 18 months; Met + Placebo: 114 +/- 7 cm vs. 109 +/- 8 cm; differences between the two groups: p = 0.096). In the Met + GH group, FPG increased significantly after 6 months (5.9 +/- 0.7 vs. 6.7 +/- 0.4 mmol/l; p = 0.005), but subsequently decreased to baseline levels (18 months: 5.8 +/- 0.2 mmol/l). FPG remained stable in the Met + Placebo group until 12 months had elapsed, and then slightly decreased (baseline: 6.2 +/- 0.3, 18 months: 5.5 +/- 0.6 mmol/l, p = 0.02). No significant changes were seen in either group regarding glucose and insulin AUC during oGTT or HbA (1c) levels. GDR at 18 months increased by 20 +/- 39% in Met + GH-group and decreased by -11 +/- 25% in the Met + Placebo group (differences between the two groups: p = 0.07). In conclusion, treatment of patients with metabolic syndrome and elevated FPG levels did not cause sustained negative effects on glucose metabolism or insulin sensitivity if given in combination with metformin. However, since our data did not show significant differences between the two treatment groups with respect to body composition or lipid metabolism, future studies including larger numbers of patients will have to clarify whether the positive effects of rhGH on cardiovascular risk factors that have been shown in patients with GH deficiency are also present in patients with metabolic syndrome, and are additive to the effects of metformin.
Summary
* Both groups received 850 mg Metformin/twice daily
* In the Met + hGH group, IGF-I increased, stabilized after 3 months, the Metformin + placebo group did not change
* Total body fat decreased in both groups, almost double in the hGH group
* Waist circumference decreased in both groups (more in the HGH group)
* After 18 months total muscle mass increased by 0.5 +/- 3.7 kg in the Met+GH group (range -4.6 to 3.7) and decreased by -2.4 _/- 2.9 in the
Met+Placebo group (range –5.7 to 2.2)
* Serum total testosterone levels significantly increased in both groups after 18 months
* Insulin levels did not significantly differ between those patients receiving only metformin and those receiving metformin and hGH
nodoctor
Active Member
carcinogen: NDMA--not the only reason, but one of the reasons I dropped metformin. Worth noting that not ALL metformin formulations contained the NDMA (and NDMA is in a ton of stuff, but it's a confirmed carcinogen and they yanked Zantac because of it, so still seems like an issue. ) Here's a source:
Deleted member 43589
Well-Known Member
Here is a list of all the companies the FDA found NDMA in. To date, all of these companies have recalled the products and solved the problem. Very few companies even had issues. The brand I use none was detected.
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