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Metaformin

Lizard King

Lizard King

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Sep 9, 2010
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I read once about some cognitive longevity affects... I don’t remember the details, anybody ever hear this? Slows the aging of the brain and I think there was some research that suggested it might be helpful in preventing or at least slowing down stuff like Alzheimer’s
Guess you didnt click the link Mike posted.
 
tommyguns2

tommyguns2

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Dec 25, 2010
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GI issues usually go away in a few weeks, at least it did for me. One side effect to be careful about, sometimes when taking a pee will result in an unwanted bowel movement. There is sometimes no control over the poop coming out.....

You mean it gets worse? I've "sharted" a few times in the past year or so. A relatively new phenomena....
 
FlyingDragon

FlyingDragon

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Nov 4, 2010
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Doesnt get worse, just have to remain on guard that it could happen. For me it happens a few times a month, almost always when I am out in public....

You mean it gets worse? I've "sharted" a few times in the past year or so. A relatively new phenomena....
 
Mike_RN

Mike_RN

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The shart probability increases by a power of 10!
 
Bigtex

Bigtex

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Aug 14, 2012
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Now you guys know why I take it. Here is something you definitely need to be aware of it you take it, especially if you are also taking a drug like prilosec with it.

Metformin is known to interfere with the absorption of B12, increasing the risk of vitamin B12 deficiency. Low B12 levels contribute to higher concentrations of artery-clogging homocysteine—an independent risk factor for cardiovascular disease. The tiny amounts of vitamin B12 and other B-vitamins found in commercial supplements is usually not enough to offset this problem. Individuals using metformin should ensure that they are taking higher doses of B-vitamins (at least 300 mcg of methylcobalamin, the active form of vitamin B12) and checking their homocysteine levels to ensure proper protection.
 
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Bigtex

Bigtex

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Gregory M. Fahy Robert T. Brooke James P. Watson Zinaida Good Shreyas S. Vasanawala Holden Maecker Michael D. Leipold David T. S. Lin Michael S. Kobor, and Steve Horvath. Reversal of epigenetic aging and immunosenescent trends in humans. Volume18, Issue6, December 2019. https://doi.org/10.1111/acel.13028

Researchers recently published data showing how low-dose growth hormone (hGH) DHEA combined with metformin (or possibly Berberine) can actually slow down biological aging and restore the size of the thymus gland.
 
Bigtex

Bigtex

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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

So in this study those doing hGH and Metformin actually increased IGF-levels those who only did Metformin had no change in IGF-1 levels.
 
Bigtex

Bigtex

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Here is the study Palumbo mentioned

R. Grace Walton et al. Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: A randomized, double‐blind, placebo‐controlled, multicenter trial: The MASTERS trial. Aging December 2019. Volume18, Issue6 e13039

Abstract
Progressive resistance exercise training (PRT) is the most effective known intervention for combating aging skeletal muscle atrophy. However, the hypertrophic response to PRT is variable, and this may be due to muscle inflammation susceptibility. Metformin reduces inflammation, so we hypothesized that metformin would augment the muscle response to PRT in healthy women and men aged 65 and older. In a randomized, double‐blind trial, participants received 1,700 mg/day metformin (N = 46) or placebo (N = 48) throughout the study, and all subjects performed 14 weeks of supervised PRT. Although responses to PRT varied, placebo gained more lean body mass (p = .003) and thigh muscle mass (p < .001) than metformin. CT scan showed that increases in thigh muscle area (p = .005) and density (p = .020) were greater in placebo versus metformin. There was a trend for blunted strength gains in metformin that did not reach statistical significance. Analyses of vastus lateralis muscle biopsies showed that metformin did not affect fiber hypertrophy, or increases in satellite cell or macrophage abundance with PRT. However, placebo had decreased type I fiber percentage while metformin did not (p = .007). Metformin led to an increase in AMPK signaling, and a trend for blunted increases in mTORC1 signaling in response to PRT. These results underscore the benefits of PRT in older adults, but metformin negatively impacts the hypertrophic response to resistance training in healthy older individuals. ClinicalTrials.gov Identifier: NCT02308228.

1. There was a trend for blunted strength gains in metformin that did not reach statistical significance. Note- the blunted strength gains were not considered statistically significant.
2. Metformin did not affect fiber hypertrophy, or increases in satellite cell or macrophage abundance with Progressive Resistance Training (PRT).
3, In the full study with PRT, metformin does not affect fiber hypertrophy, but inhibits increased type I fiber frequency, without significantly affecting satellite cell expansion.
4. Metformin led to an increase in AMPK signaling, and a trend for blunted increases in mTORC1 signaling in response to PRT.

Limitations of this study which are very important to consider, this trial did not include sedentary control groups. Therefore, we are unable to draw conclusions regarding the effects of metformin alone on muscle mass and strength in generally healthy older adults. The effects of metformin in frail elderly, alone or in combination with resistance exercise, need further study. Although metformin appears to preserve lean mass in sedentary diabetic patients (Lee et al., 2011),it would be important to know whether metformin affects muscle mass and strength gains with PRT in older diabetic patients. Our study was not designed to address these issues, and the majority of our cohort was nonobese and free from metabolic disease. Another thing to consider is what happens when you include testosterone and hGH? We do know that testosterone administration greatly decreases AMPK signaling and increases mTORC1 signaling. Increases in hGH and IGF-1 also do the same.

So for those who are doing steroids and even hGH, how significant would metformin negatively impact the hypertrophic response to resistance training?
 
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