metformin + insulin

[candidizzle]

Basically yes.  GH is released during hypoglycemia to counteract the low blood sugar.  They work in opposition of each other, so a person taking GH is likely to have insulin insensitivity.   

yes and thats one of the reasons why you put insulin WITH gh for best gains

[G]

Basically yes.  GH is released during hypoglycemia to counteract the low blood sugar.  They work in opposition of each other, so a person taking GH is likely to have insulin insensitivity.   

actually Insulin is  a must when using more than 5 iu of gh, to keep the sugar levels stable

[Vet]

metformin icreases insulin receptors sensitivity, thus makes the body produce less insulin..it's stacked togather with slin to help get maximal effect from the slin without using very high doses of slin or increasing the dose after a few weeks of use

That makes no sense.  



From the Prescriber Information for metformin:
CLINICAL PHARMACOLOGY
Mechanism of Action

Metformin is an antihyperglycemic agent which improves glucose tolerance in patients
with type 2 diabetes, lowering both basal and postprandial plasma glucose. Its
pharmacologic mechanisms of action are different from other classes of oral
antihyperglycemic agents. Metformin decreases hepatic glucose production, decreases
intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral
glucose uptake and utilization.

http://www.fda.gov/cder/foi/label/2000/21202lbl.pdf


I'm going to post it again......  The primary action of metformin is by affecting liver glucose metabolism and glucose absorption.  The exact mechanism of this action is not known.  There is some thought that it will increase insulin sensitivity but that exact mechanism of action is also not kown.

[Vet]

yes and thats one of the reasons why you put insulin WITH gh for best gains

Candi, that goes back to what I've been preaching about insulin being something that has to be taken as a result of GH supplementation.    I'm willing to bet there are a large number of GH users who are "borderline" diabetic or type II diabetic. 

[G]

and improves insulin sensitivity by increasing peripheral
glucose uptake and utilization. [/b]

.

exactly..tahts the only use of metformin in bulk cycles, combined with slin. Heres a good article from anthony roberts about metformin.
http://steroidsprofiles.com/steroid/info/68

[candidizzle]

Candi, that goes back to what I've been preaching about insulin being something that has to be taken as a result of GH supplementation.    I'm willing to bet there are a large number of GH users who are "borderline" diabetic or type II diabetic. 

oh, no doubt, i 100% agree. 

[DIVISION]

is that why you dont have one that says "i dont know jackshit about steroids or how the endocrine system functions. " ? ..everybody already knows..?

 

I've been designing cycles for people for years.........through personal experience.

No google searches required.

You don't have to like it, but it's a fact.

I give out cycle advice via PM and have been doing so since before I was a Moderator here.

I'm not sure why you think you have either the knowledge or credibility to claim anything about me, but I do know a computer cowboy when I see one.

Your obsession with lashing out at anyone and everyone who disagrees with you, despite the fact that you really have no experience with AAS tells me that you have some severe inadequacies in your life.

You're trying to fill the gaps in your life with a false sense of power gained through your behaviour here.

Most people can see through it.

Personally, I think you have OCD/ADD or ADHD because your obsession with getting the last word, in whether you actually know anything pertaining to the subject or not, is legendary.

I don't have anything against you, but you've got to realize your meltdowns aren't endearing you to anyone.

I think it's great you read the journals, but reading something and actually seeing it through the course of your own experience are two completely different things.

Alot of guys on here have run many, many cycles and still don't have the "know it all" attitude that you bring to the table.

I think you should take this as constructive criticism because other people have tried to tell you the same thing.

People don't hate you (for the most part), but you're just making yourself look like an ass when you challenge people's opinions, people who have more knowledge and experience than yourself.

What exactly are you trying to gain from that?

You'd do yourself some good by more reading, and less posting.........and you'll learn alot more that way.



DIV

[candidizzle]

hey division, keep your long winded arrogant words to yourself. your "advice" is wasted here bro. i have no use for the opinions of some pathetic fuck with delsuions of grandeur and knowledge.

[DIVISION]

hey division, keep your long winded arrogant words to yourself. your "advice" is wasted here bro. i have no use for the opinions of some pathetic fuck with delsuions of grandeur and knowledge.

What's pathetic, the fact that I pegged you so easily or the fact that you take everything so personal?

I don't know you as a person off the forum, but your behavour on the forum dictates how people see you.

Is that pathetic?

It's just basic observation.



DIV

[candidizzle]

What's pathetic, the fact that I pegged you so easily or the fact that you take everything so personal?

I don't know you as a person off the forum, but your behavour on the forum dictates how people see you.

Is that pathetic?

It's just basic observation.



DIV

no, you as a person are pathetic.


your assessment of me is laughable. at best.

[Vet]

hey division, keep your long winded arrogant words to yourself. your "advice" is wasted here bro. i have no use for the opinions of some pathetic fuck with delsuions of grandeur and knowledge.

Its posts like this one (and the ones immediately before it) that make me think you are an idiot. 



Seriously dude, reread what you are posting.   Why?

[WillGrant]

Basically yes.  GH is released during hypoglycemia to counteract the low blood sugar.  They work in opposition of each other, so a person taking GH is likely to have insulin insensitivity.   

So when a diabetic is having a hypo would he be producing alot more GH?

[Vet]

So when a diabetic is having a hypo would he be producing alot more GH?

Yes....  Initially you have increased epinephrine production and glucagon release (this gives you a "shakey weak" feeling assocaiated with hypoglycemia), then if the hypoglycemia is prolonged, cortisol is released, then GH is released.  Typically the GH release is later in the hypoglycemic episode.    Basically if you would measure GH at the end of an "insulin reaction" in a diabetic, if the pituitary gland is functioning normally, there should be an elevation in GH levels because GH is one of the hormones released to counteract hypoglycemia (in addition to epinephrine and cortisol--which have much more detrimental effects than the GH will in terms of bodybuilding--which I'm guessing you are thinking about).   

This GH release (in conjunction with epinephrine and cortisol release) is associated with the Somogyi effect some diabetics have--where they have low blood glucose, and then have a rebound higher blood glucose that lasts for up to several hours after the hypoglycemic episode.

[WillGrant]

Yes....  Initially you have increased epinephrine production and glucagon release (this gives you a "shakey weak" feeling assocaiated with hypoglycemia), then if the hypoglycemia is prolonged, cortisol is released, then GH is released.  Typically the GH release is later in the hypoglycemic episode.    Basically if you would measure GH at the end of an "insulin reaction" in a diabetic, if the pituitary gland is functioning normally, there should be an elevation in GH levels because GH is one of the hormones released to counteract hypoglycemia (in addition to epinephrine and cortisol--which have much more detrimental effects than the GH will in terms of bodybuilding--which I'm guessing you are thinking about).   

This GH release (in conjunction with epinephrine and cortisol release) is associated with the Somogyi effect some diabetics have--where they have low blood glucose, and then have a rebound higher blood glucose that lasts for up to several hours after the hypoglycemic episode.

Interesting stuff mate 

[abc123]

Most people who post here on a regular basis know who Dizzle is....

No signature required.



DIV

Yes, but it's those that are new or only stop by infrequently that I worry about, should they take his advice.

[candidizzle]

Its posts like this one (and the ones immediately before it) that make me think you are an idiot. 



Seriously dude, reread what you are posting.   Why?

yo vet


guess what


i dont care what you think bro 

lol

[Van_Bilderass]

Candi, that goes back to what I've been preaching about insulin being something that has to be taken as a result of GH supplementation.    I'm willing to bet there are a large number of GH users who are "borderline" diabetic or type II diabetic. 

Yes and I think that's part of why they can stay lean year round. If you are insulin sensitive in fat cells you put on fat easy. Some degree of insulin resistance helps promote the lean look.

[4thAD]

Candi, that goes back to what I've been preaching about insulin being something that has to be taken as a result of GH supplementation.    I'm willing to bet there are a large number of GH users who are "borderline" diabetic or type II diabetic. 

Now would this be a permanent stop at diabetes door, or just while running the GH with out insulin? Is it something these users can recover from being that they had normal functioning bodies before GH?

[IAMTHEGAME]

yo vet


guess what


i dont care what you think bro 

lol

The sad truth of this statement is until he said anything negative about you, you were all on his jock, so obviously you do care...IMO

[candidizzle]

The sad truth of this statement is until he said anything negative about you, you were all on his jock, so obviously you do care...IMO

dude, i honestly appreciate you dedicating this "iamthegame" acount to me. whoever you are operating this. much thanks bro; really make feel special 

[IAMTHEGAME]

dude, i honestly appreciate you dedicating this "iamthegame" acount to me. whoever you are operating this. much thanks bro; really make feel special 

How does it feel to really be loathed here???  Just asking....lol

[Vet]

Yes and I think that's part of why they can stay lean year round. If you are insulin sensitive in fat cells you put on fat easy. Some degree of insulin resistance helps promote the lean look.

I disagree with that completely.   

There is some thought that fat cells as an organ are more sensitive to the effects of insulin.  This is why fat cells secrete Resistan, that causes insulin resistance.  This goes along  with the though that Insulin resistance actually leads to higher bodyfat levels because there is higher circulating amount of insulin in an attempt for the body to keep blood glucose levels "normal".    Because the fat is "more sensitive" it will continue to take up nutrients in instances where insulin may be too low for other organs---ie muscle tissue and continue to inhibit insulin activity, leading to more insulin being secreted and more nutrient uptake.  And if the body isn't so insulin insensitive that it slides towards ketoacidosis, fat may not be burned (as in subclinical insulin insensitivity where the only abnormality may be a slightly elevated AM blood glucose after an evening carbohydrate load or shifting fructosamine levels).  This leads to fat accumulation, not depression of bodyfat. 

Supposedly the omental fat (which contains intrabdominal fat bodies) are especially susceptable to this.  I personally think that is part of the reason we are seeing so many bodybuilders with "GH" gut.   Its not "intestinal or liver enlargement" or "organ bloating" like so many internet guru's claim secondary to GH use.   It makes more sense for accumulation of fat within the omental fat bodies, leading to abdominal  distension than "organs growing".    This is brought on by GH causing insulin insensitivity.
  Think in terms of central adiposity with Type II diabetics.  Its very similar in my mind. 

[Van_Bilderass]

I disagree with that completely.   

There is some thought that fat cells as an organ are more sensitive to the effects of insulin.  This is why fat cells secrete Resistan, that causes insulin resistance.  This goes along  with the though that Insulin resistance actually leads to higher bodyfat levels because there is higher circulating amount of insulin in an attempt for the body to keep blood glucose levels "normal".    Because the fat is "more sensitive" it will continue to take up nutrients in instances where insulin may be too low for other organs---ie muscle tissue and continue to inhibit insulin activity, leading to more insulin being secreted and more nutrient uptake.  And if the body isn't so insulin insensitive that it slides towards ketoacidosis, fat may not be burned (as in subclinical insulin insensitivity where the only abnormality may be a slightly elevated AM blood glucose after an evening carbohydrate load or shifting fructosamine levels).  This leads to fat accumulation, not depression of bodyfat. 

Supposedly the omental fat (which contains intrabdominal fat bodies) are especially susceptable to this.  I personally think that is part of the reason we are seeing so many bodybuilders with "GH" gut.   Its not "intestinal or liver enlargement" or "organ bloating" like so many internet guru's claim secondary to GH use.   It makes more sense for accumulation of fat within the omental fat bodies, leading to abdominal  distension than "organs growing".    This is brought on by GH causing insulin insensitivity.
  Think in terms of central adiposity with Type II diabetics.  Its very similar in my mind. 

Well, how do you explain the extremely lean bodybuilders then, especially since you say many of them are severely insulin resistant? With the use of GH they stay much leaner throughout the off-season nowadays, even despite using lots of insulin too.

GH leads to higher insulin levels. Doesn't translate to higher bodyfat, so apparently the increase in insulin isn't enough to override the fat burning effects. Research shows that if you block the raise in FFA's you improve insulin sensitivity. The fat burning effects of GH are what leads to insulin resistance.

Other diet drugs used by bodybuilders can cause insulin resistance as well: the beta agonists and T3.

You are also looking at sedentary type II diabetics, not hard training bodybuilders. Bodybuilders make their muscles sensitive constantly by training hard. This will help drive glucose into muscle preferentially. Mild insulin resistance IMO is correlated with an extremely lean bodybuilder look - a disease state like actual type II diabetes is another matter.

[Van_Bilderass]

Vet, take a look at this piece by Lyle McDonald from his forum. Explains it beautifully. Candidizzle, you read this too, very good stuff. 

I received this email at my bodyrecomp adress and the sender said he didn't mind (and sort of wanted me to) if I adressed it in the forum so here goes.

***

I was extremely shocked to see you writing that during dieting, it would be actually
GOOD to be insulin resistant. You argued that Clen/ephedrin actually cause insulin
resistance (IR), sort of implying that that's one of the mechanisms via which they
work whereas I always thought that they worked DESPITE that effect.

the thing to realize is what insulin resistance actually implies. Insulin is a storage hormone, stimulating nutrient uptake in many tissues (including liver, muscle, and fat cells). This is especially true for glucose.

So what happens when fat cells are insulin resistant? It means that insulin can't inhibit lipolysis (fat breakdown). Nor can it activate nutrient storage. This is part of why severely insulin resistannt individuals get increased blood levels of glucose, fatty acids and cholesterol, insulin is unable to either limit release from the cell or stimulate uptake. Since muscle is full (see below), they either get stored in inappropriate places (beta-cells of the liver) or float around in the bloodstream.

What about in muscle? An insulin resistant muscle cell is unable to uptake glucose. Without glucose to use for fuel, the cell has to find an alternative source. In this case, that alternative source is fatty acids.

So when fat cell insulin resistance is high, fatty acids are easier to mobilze. When muscle cell insulin resistance is high, glucose isn't used for fuel and fatty acids are. So in a caloric deficit, this means you use more fat for fuel b/c they are coming out of fat cells more easily and muscle is usingg them preferentially for fuel.

this is part of how things like clen, EC and GH work. By mobilizing fatty acids at a high rate and making the muscle cell insulin resistant, muscle has to forego glucose for fuel and use the mobilized fatty acids instead (note: this also spares protein in a carb insufficient state). A recent study on GH found that the fatty acid mobilizing effect of GH was THE key to its protein sparing effects: block the increase in fatty acids and you get the same amount of protein loss.

On that note, you should realize that studies examining predisoposition to obesity (for example, in the Pima indians) find that insulin sensitivity predicts weight gain and insulin resistance predicts weight loss or stability.

Insulin resistance develops with obesity and can be thought of as a way for the body trying to prevent further weight gain. Note that this is different in growing individuals such as children or pregnant women. More below.

Well I always thought IR was extremely bad in all situations (gaining weight, losing
weight, fat guy, skinny guy).

To be even more accurate to what I wrote above you need to differentiate muscle insulin resistance from whole body insulin resistance. In general, the body will develop insulin resistance in this order:

liver then muscle then fat cell

There are some weird genetic exceptions but the above would be a typical progression with diet induced insulin resistance.

Now, when muscle becomes insulin resistant, this shuttles more calories to the fat cells preferentially. In that sense, localized (muscular) insulin resistance causes more fat to be gained for a given caloric load. It's negative calorie partitioning. Note that this isn't only local, there are central (brain effects) controlling these processes as well.

This makes perfect sense: if the muscle is plenty full of nutrients and there is still a surplus, they should get pushed into storage as effectively as possible. So the msucle stops accepting nutrients and the rest go to the fat cells. The best way to prevent this is not to overeat and to deplete muscular fuel stores with exercise. In modern society, we do both: eat too much and don't exercise often enough. So muscle gets full of nutrients, becomes insulin resistant, and the excess calroeis go to fat cells post haste.

But as fat cells get filled up, problems start. The fat cell starts releasing a lot of hormones such as leptin, TNf-alpha, resistin (may only be relevant in rats) and others that prevent further nutrient storage (you can also get an increase in fat cell number). Now you're developing full body insulin resistance.

Once full body insulin resistance develops (with obesity), this acts to LIMIT further weight gain. Note that insulin resistance also means higher basal levels of insulin (there are also higher levlels of leptin as you get this fat). Both insulin and leptin *should* act to signal the brain to make you stop eating but the system isn't very sensitive to that. Additionally, it serves to push nutrients towards oxidation when you diet for the reasons above.

It's interesting to note that individuals without fat cells (lipodystrophy), which mimicks full body insulin resistance are protected against weight gain. First their muscles and liver fill up with nutrients, then they develop severe hyperglycemia, hypercholesterolemia and all the rest. Individuals with severe genetic insulin resistance have the same effect occur: they don't gain weight. They get a bunch of other health problems if you overfeed them but the severe genetic insulin resistance makes it so tnutrients can't be stored in their cells.

Also consider that insulin sensitivity improves as you lose weight. And the single time you are most prone to gain wight is at the end of the diet: when you are most insulin SENSITIVE.

As above, insulin sensitivity predicts weight gain, insulin resistance (full body) weight/fat loss.

Basically insulin resistance isn't always BAD. Quite in fact, it can be adaptive.

Now, in the context of excess calories/carbs and no activity (i.e. weight gain), insulin resistance is a bad thing to have. If you have muscular insulin resistance, more calories go to fat cells. If you have ful lbody insulin resistance, excess calories either sit in the bloodsream or get stored in the wrong spots, causing cell death.

Actually, if the goal is muscle gain with limited fat gain, it'd be wonderful to have fat cells resistant to nutrient storage and locally increase muscular insulin sensitivity. This would cause preferential nutrient partitioning to muscle. The question is how to do it. I have an idea but it's not fully fleshed out. For fatter individuals who begin an exercise program, this occurs naturally which is (IMO) one reason they can lose fat and gain muscle at the same time. The exercise preferentially improves muscular insulin sensitivity, the fat cells are releasing fat like nobody's business and you get calorie partitioning until the point that it all starts to balance out.

When you're dieting and not eating enough carbs (by definition, on a diet, carbs are reduced), insulin resistance is adaptive. By making muscle rely on fatty acids for fuel, glucose is spared for the brain and other tissues which require it.

Note that most of the current insulin sensitizing medications (especially the TZD drugs) cause further weight gain. Obesity docs don't care becuse they just want to see blood glucose and the rest levels go down.

As above, whole body insulin resistance develops in an effort to both limit further fat/weight gain and ensure that the body burns the fat off (sparing muscle) when you diet. This would have been adaptive in the context of our evolutionary dieting pattern, it's maladptive in our current environment.

I've been avoiding caffeine like the plague since I read it causes IR - should I now
start getting in massive amounts again? And acquire ephedrine which I haven't used
in years?

ONLY if you're going to diet.

Should I also NOT get my fish oil in?

Fish oils are interesting, in rats at least (I have yet to see this studied in humans and I don't consider the rat research conclusive except for the fact taht humans demonstrate similar end effects) they decrease fat cell insulin sensitivity and improve muscle cell insulin sensitivity. They also improve fat oxidation and a host of other stuff but the net results is nutrient partitioning aways fomr fat cells and towards muscle cells.

And should I NOT try to acquire
Glugophage from the doc? If I should try to get a prescription for something, what
would you recommend?? . I am 29yrs old, 5' 11", weight around 300 lbs with fat%
around 32%.

Riht before his death, Dan Duchaine commented that adding insulin sensitizersr to a diet seemed to increase muscle loss.

However, if you're at the point medically that you need to control blood glucose, you need to listen to your doctor, not me. Getting your diet and exercise program in order and losing bodyfat should be your primary goal as that alone will improve insulin sensitivity.

Lyle

[candidizzle]

Van, thank you for posting that. very good read.

on a side note.. the whole article as i was reading i was thinking about the fish oil question... thinking i was royally fucking myself... lol..   damn what a relief when he said it was the exception..