What does metformin do exactly ?

[fitnessmuscle]

Guys just curious as to how and why people use metformin, does it give similar results to insulin? What have been your guys experience with metformin? Is it worth taking and can it be taken together with insulin or wouldn’t it be worth it ?

 

[qbkilla]

It increases insulin sensitivity. Gh can cause insulin resistance so people take it with that or berberine...even without gh. Better insulin sensitivity is good for body composition. Insulin is completely different people use various types of protocols to increase muscle mass. YouTube Justin Harris insulin for good info.

I use metformin. Never had a side or see any visible change but my a1c is very low even out of range so I'd assume it is beneficial to me.

 

[fitnessmuscle]

It increases insulin sensitivity. Gh can cause insulin resistance so people take it with that or berberine...even without gh. Better insulin sensitivity is good for body composition. Insulin is completely different people use various types of protocols to increase muscle mass. YouTube Justin Harris insulin for good info.

I use metformin. Never had a side or see any visible change but my a1c is very low even out of range so I'd assume it is beneficial to me.

Cool bro ,so in your opinion which one is better metformin or insulin , are gains and results similar or no ,with Hgh ? Btw bro ,what dose of metformin do you use and do you use it daily?

 

[fitnessmuscle]

Also would metformin be beneficial after an insulin cycle kinda like a pct or would it be better to take slin and metformin at the same time ?would that yield better results or be a waste ? sorry man I’m all over the place with questions but trying to learn the best way to utilize metformin or if at all ,thanks again guys

 

[slesh]

I’ll let @Type-IIx chime in but I can’t imagine taking them together is a good idea - sounds like a recipe to go hypo…

 

[fitnessmuscle]

I’ll let @Type-IIx chime in but I can’t imagine taking them together is a good idea - sounds like a recipe to go hypo…

Got ya , yeah I’m interested in hearing people’s results and opinions on this matter

 

[bg65]

I would be VERY careful using them together and unless you actually have type II diabetes i don't see any reason you should. As above, risk of hypoglycemia would be much higher taking metformin and insulin together. If you're bulking try insulin. So many ways... general rule of thumb is 10 grams of carbs for 1 unit of insulin. First time i tried it was pre-workout with a whey and waxy-maize type carb source, 5 units insulin and 50 units carbs. Limit fat as much as possible. I've since used it post work out with similar dose and carb amount, particularly on leg days. Some guys take it w meals, read Luki's thread..
If youre cutting then maybe try metformin, if bulking try insulin. Don't do them together.
Good dose for metformin would be 500mg in AM and 500 mg in PM

 

[qbkilla]

Cool bro ,so in your opinion which one is better metformin or insulin , are gains and results similar or no ,with Hgh ? Btw bro ,what dose of metformin do you use and do you use it daily?

I take 1g sustained release. To be honest I think you should research them more watch Justin Harris videos. They aren't similar. Asking which one you should use is like asking which you should do to get in shape... diet or training? Or which you should do to build muscle, bench press or dead lifts?

Both are tools but work in very different ways and can have consequences if not researched and used properly. Especially insulin.

 

[Fat]

I use 2000 mg every day to lower blood sugar and increase insulin sensitivity. It also lowers IGF1 which promotes longevity.

 

[DarrenH]

I use 2000 mg every day to lower blood sugar and increase insulin sensitivity. It also lowers IGF1 which promotes longevity.

Doesn't that lower gains?

 

[Fat]

Doesn't that lower gains?

Only if you're natural. Vigorous Steve said it lowers his strength but I've never felt that.

 

[qbkilla]

They talk about metformin here too..

 

[johnjuanb1]

I’ve been on 6-9ius HGH for a year. I felt it was time to do something to counteract the fasted glucose that must be high after a year at that dose. I haven’t had blood work in years but since adding metformin and Berberine my muscles are a lot more full and my fat loss is back on track. Nobody wants to get Palumboism from metabolic syndrome. I’m taking 500mg metformin sustained release at night and 600mg Berberine with my morning and noon meal.

 

[Type-IIx]

Metformin is a biguanide, a class of drugs that aid in glucose disposal. Metformin decreases blood glucose levels by reduced gluconeogenesis (liver), decreased glucose absorption (intestines), and increasing insulin sensitivity (liver) by increasing glucose uptake and utilization.

While it seems a popular idea that Met increases skeletal muscle insulin sensitivity (which would be great for muscle anabolism), the primary site of its insulin sensitizing effects is the liver. Its actions on skeletal muscle is actually quite negative: it inhibits mTOR complex 1 (protein synthesis, translation) thereby reducing hypertrophy; it blocks the preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains); and blocks the endurance training (LISS, HIIT, cardio) enhancement of insulin sensitivity. When Metformin alone is compared to a progressive resistance training program alone in older sedentary people, its effects (on blood glucose levels & absorption, insulin sensitivity) are indistinguishable from the resistance training program alone; and Metformin + progressive resistance training does worse than either Metformin with no training and/or resistance training alone.

Insulin (exogenous) promotes the uptake & utilization of glucose from the blood into skeletal muscle, repleting glycogen, enhancing insulin sensitivity in skeletal muscle. Rather than blunting fat synthesis & promoting fat oxidation like Metformin (another of Met's effects), it does the opposite potently, and dramatically increases VLDL synthesis in the liver (increasing the most dangerous particles for cardiovascular risks). Over time at high doses, it worsens insulin sensitivity by diminished autophosphorylation of the IR & its downstream elements, thereby reducing this skeletal muscle uptake of glucose and logically (though it has not been demonstrated insofar as I am aware) the muscle protein anabolic effects. See Insulin’s effects and mechanisms in promoting skeletal muscle hypertrophy, November 17, 2022, Type-IIx MesoRx Article

While the two drugs (Met & slin) may be used in diabetic patients, it requires dose reductions, and this is further complicated by AAS (that increase insulin sensitivity in skeletal muscle). Since slin so potently overwhelms the effects of Met and they act oppositely in some key ways, this should be considered before combining the two. A potential very high severity outcome is hypoglycemic shock, coma, and death.

 

[slesh]

Metformin is a biguanide, a class of drugs that aid in glucose disposal. Metformin decreases blood glucose levels by reduced gluconeogenesis (liver), decreased glucose absorption (intestines), and increasing insulin sensitivity (liver) by increasing glucose uptake and utilization.

While it seems a popular idea that Met increases skeletal muscle insulin sensitivity (which would be great for muscle anabolism), the primary site of its insulin sensitizing effects is the liver. Its actions on skeletal muscle is actually quite negative: it inhibits mTOR complex 1 (protein synthesis, translation) thereby reducing hypertrophy; it blocks the preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains); and blocks the endurance training (LISS, HIIT, cardio) enhancement of insulin sensitivity. When Metformin alone is compared to a progressive resistance training program alone in older sedentary people, its effects (on blood glucose levels & absorption, insulin sensitivity) are indistinguishable from the resistance training program alone; and Metformin + progressive resistance training does worse than either Metformin with no training and/or resistance training alone.

Insulin (exogenous) promotes the uptake & utilization of glucose from the blood into skeletal muscle, repleting glycogen, enhancing insulin sensitivity in skeletal muscle. Rather than blunting fat synthesis & promoting fat oxidation like Metformin (another of Met's effects), it does the opposite potently, and dramatically increases VLDL synthesis in the liver (increasing the most dangerous particles for cardiovascular risks). Over time at high doses, it worsens insulin sensitivity by diminished autophosphorylation of the IR & its downstream elements, thereby reducing this skeletal muscle uptake of glucose and logically (though it has not been demonstrated insofar as I am aware) the muscle protein anabolic effects. See Insulin’s effects and mechanisms in promoting skeletal muscle hypertrophy, November 17, 2022, Type-IIx MesoRx Article

While the two drugs (Met & slin) may be used in diabetic patients, it requires dose reductions, and this is further complicated by AAS (that increase insulin sensitivity in skeletal muscle). Since slin so potently overwhelms the effects of Met and they act oppositely in some key ways, this should be considered before combining the two. A potential very high severity outcome is hypoglycemic shock, coma, and death.

@Type-IIx is the

 

[bg65]

And the liver, that's an organ in the body?

 

[qbkilla]

Metformin is a biguanide, a class of drugs that aid in glucose disposal. Metformin decreases blood glucose levels by reduced gluconeogenesis (liver), decreased glucose absorption (intestines), and increasing insulin sensitivity (liver) by increasing glucose uptake and utilization.

While it seems a popular idea that Met increases skeletal muscle insulin sensitivity (which would be great for muscle anabolism), the primary site of its insulin sensitizing effects is the liver. Its actions on skeletal muscle is actually quite negative: it inhibits mTOR complex 1 (protein synthesis, translation) thereby reducing hypertrophy; it blocks the preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains); and blocks the endurance training (LISS, HIIT, cardio) enhancement of insulin sensitivity. When Metformin alone is compared to a progressive resistance training program alone in older sedentary people, its effects (on blood glucose levels & absorption, insulin sensitivity) are indistinguishable from the resistance training program alone; and Metformin + progressive resistance training does worse than either Metformin with no training and/or resistance training alone.

Insulin (exogenous) promotes the uptake & utilization of glucose from the blood into skeletal muscle, repleting glycogen, enhancing insulin sensitivity in skeletal muscle. Rather than blunting fat synthesis & promoting fat oxidation like Metformin (another of Met's effects), it does the opposite potently, and dramatically increases VLDL synthesis in the liver (increasing the most dangerous particles for cardiovascular risks). Over time at high doses, it worsens insulin sensitivity by diminished autophosphorylation of the IR & its downstream elements, thereby reducing this skeletal muscle uptake of glucose and logically (though it has not been demonstrated insofar as I am aware) the muscle protein anabolic effects. See Insulin’s effects and mechanisms in promoting skeletal muscle hypertrophy, November 17, 2022, Type-IIx MesoRx Article

While the two drugs (Met & slin) may be used in diabetic patients, it requires dose reductions, and this is further complicated by AAS (that increase insulin sensitivity in skeletal muscle). Since slin so potently overwhelms the effects of Met and they act oppositely in some key ways, this should be considered before combining the two. A potential very high severity outcome is hypoglycemic shock, coma, and death.

So based on this, metformin sounds like a hindrance to body composition?

 

[Muay Thai]

I take both SLIN and METFORMIN and am not currently taking GH with it, but when i did take GH with slin, results were way better (this was WITHOUT MET, just gh and slin)

 

[cmryan]

While it seems a popular idea that Met increases skeletal muscle insulin sensitivity (which would be great for muscle anabolism), the primary site of its insulin sensitizing effects is the liver. Its actions on skeletal muscle is actually quite negative: it inhibits mTOR complex 1 (protein synthesis, translation) thereby reducing hypertrophy; it blocks the preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains); and blocks the endurance training (LISS, HIIT, cardio) enhancement of insulin sensitivity. When Metformin alone is compared to a progressive resistance training program alone in older sedentary people, its effects (on blood glucose levels & absorption, insulin sensitivity) are indistinguishable from the resistance training program alone; and Metformin + progressive resistance training does worse than either Metformin with no training and/or resistance training alone.

This bit is new to me. Does metformin have any other deleterious effects on the outcome of those modes of training? As in, does it blunt any of the other adaptations one would expect to see from endurance training?

 

[OuchThatHurts]

Take the bad into consideration, but also take the good. I've been taking MET for years and I have only noted a slight drop in B12 (and related iron deficiency) on MET and BERB. Metformin not only reduces inflammation reducing cardiac events but is cardio protective, reduces kidney strain, and has neuroprotective effects that reduce cognitive decline, etc. It also is beneficial in regards to insulin resistance due to the traditional BBer high caloric intake - taking stress off beta cells and improved pancreatic function. It's important that we not look at MET as a PED.

I'm going to copy part of this well-referenced article here.
I highly recommend reading the full article:

Link: "Metformin: A Novel Weapon Against Inflammation"

"Beyond its consolidated role in T2D management, the pleiotropic actions of metformin have been extensively documented. Metformin can treat cardiovascular diseases by mechanisms distinct from its metabolic activities (Soraya et al., 2014; Liu et al., 2017; Dziubak et al., 2018). Metformin exerts nephroprotective effects in diabetic patients (Kawanami et al., 2020) and interferes with key immunopathological molecules involved in tumor progression (Ma et al., 2020). These findings, together with one particular breakthrough in metformin-induced longevity in microbes and mice (Cabreiro et al., 2013; Martin-Montalvo et al., 2013; Chen et al., 2017), provide the possibility of boosting its therapeutic potential in treating aging and age-related diseases (Storelli et al., 2013). Of note, emerging in vitro and in vivo evidence suggests that metformin can exert potent inflammation-inhibitory effects, irrespective of its capability of glucose control (Saisho, 2015; Bharath et al., 2020). Most recently, it is of great interest to find that metformin is able to dampen cytokine storms in patients who are infected with coronavirus disease 2019 (COVID-19). The use of metformin is significantly associated with reduced circulating levels of inflammatory markers (Cheng et al., 2020) and decreased in-hospital mortality (Hariyanto and Kurniawan, 2020; Kow and Hasan, 2020; Luo et al., 2020). It has become widely accepted that inflammation is a driving force behind various chronic diseases, including heart failure, atherosclerosis, diabetes, obesity, neurodegenerative disease, cancer, etc. The reduction in lifetime exposure to inflammation has contributed to the historical decline in old-age mortality (Finch and Crimmins, 2004; Couzin-Frankel, 2010)."