Getbig.com: American Bodybuilding, Fitness and Figure
Getbig Main Boards => Gossip & Opinions => Topic started by: pupil B on February 19, 2020, 05:04:22 PM
-
editted in disclaimer: I was encouraged to post explaining this in another thread, and I am doing so very quickly and without much effort here to just get this concept out for research by you guys and to facilitate discussion. I have put only about 15 mins into this post, it is not very comprehensive or all encompassing, I am merely trying to get the ideas into your heads so you can think about this and help research it more to help give or take away its credibility and relevance to how insulin causes growth in bodybuilding. I have never seen this mentioned even once in all my time researching steroids/hormones/drugs or I would not be bothering to write a post about it myself.
I just got back from a long day of traffic, lab, and lectures and I am dead tired but i'll just write brief off the top of my head. I am a medical student and we learned something interesting about insulin some time ago and this is honestly way more likely to be the cause of insulins growth properties than simply shuttling nutrients. The professor was explaining that there is this concept in biochemistry called "spare receptors", where a specific cell has say, 100 receptors for a specific ligand, but only 10 of those are required for the full downstream effect to take place within the cell. Insulin is one of these ligands that "spare receptors" applies to. So whether you have 10 molecules of insulin bound to 10 receptors or 100 molecules bound to 100 (made up numbers obviously, you get the point), it does not matter, the maximum effect is achieved and the resulting downstream effect that results inside the cell is the same. It was further explained that many of these ligands (such as insulin) that have spare receptors often have secondary effects when present in large concentrations. Insulin is the example that was used throughout this discussion, and so it was explained how insulin in high concentrations actually binds to the IGF-1 receptor and causes growth this way, organs were mentioned as an example (think of the "hgh gut" people, makes perfect sense). And this is talking about relatively "high" concentrations in terms of normal people amounts. I would imagine their term "high" is absolutely nothing in comparison to actually astronomical amounts, such as... bodybuilders injecting hundreds of units of insulin per day).
In my full write up I was planning on doing, I would have done some research for each specific substances affinity for each receptor relevant to this discussion. Upon very very brief research in order to simply just get this concept out there for discussion,
"dose-dependent effects of GH and IGF-1 treatments on nitrogen metabolism, intestinal structure, and hepatic IGF-1-messenger RNA (mRNA) expression in postoperative parenterally fed rats"
"1 mg/kg/d of IGF-1 were equivalent to those of 0.66 IU/kg/d of GH"
One mole of IGF-1 weighs about 33.4% more than one mole of insulin, and one iu of insulin = 0.0347mg (numbers were googled very quickly and may be error prone I am dead tired and not putting much effort into this right now). So 1mg/kg/d of igf-1 = 0.75mg/kg/d of insulin or 21.6iu/kg/day. THIS IS NOT ACCOUNTING FOR THEIR INDIVIDUAL AFFINITY FOR THE IGF-1 RECEPTORS, THIS IS WHERE IT IS A WILD BASELESS ESTIMATE, but my point is not to give precise numbers, it is to show the general concept.
So take a 100kg bodybuilder. If we say that 1mg of igf-1 (keep in mind the price of this shit... people pay I think ~$130-180 for a ONE MILLIGRAM VIAL because of the results) = 0.75mg of insulin or 21.6iu... With the pros injecting insulin like water, let's say 300 (i have seen much more than this and this might even be a low estimate. no these doses of long acting insulin are not gonna kill them from hypo.), that's approximately the equivalent of 14mg igf-1 or like $2000 worth of shit each day?
Again the exact numbers are irrelevant and useless without somehow researching insulins affinity for every igf-1 receptor in the body, but this is the general point and I am sure you understand. This is not me pulling shit out of my ass this whole idea is due to what a ph.d in both molecular biology and biochemistry said regarding insulin and igf-1 receptors when teaching at a medical school. And you must admit that it makes much more sense than simply "pushing nutrients into cells". I am no ph.d but what else would the food do if not go into the muscles even without hundreds of units of insulin, stay in your blood stream to take a nice enjoyable bath, and then proceed to magically disappear without being used for either fat or muscle? It is also not as if the body doesn't produce insulin of its own when food is ingested (although obviously not in obscene BB amounts). It does not make much sense that the whole nutrient pushing thing is solely responsible for such massive growth, I believe this explanation is much more sensible and again it comes from a ph.d in molecular biology and biochemistry.
All the research I used here was found quickly on google I am sure I could get better and more concrete numbers/examples given time but I just wanted to get this out here quickly now so people could discuss it, and before I got too lazy to do it. I was intending this as a quick reply to a post in a thread where I said I would briefly explain it but I got slightly carried away and thought this deserves its own thread.
edit: no i will not show you the original medical school materials, I cannot risk being caught doing that especially on a forum about illegal drugs and ruin my life.
EDIT: PROOF I AM not pulling this out of my ass, again just short amounts of googling due to a PM request:
https://www.karger.com/Article/PDF/184146
https://www.karger.com/Article/ShowPic/184146/?image=000184146-1.jpg
... "Thus, stimulation of IGF-1 receptors may be obtained in vitro with high amounts of insulin."
-
You’re worse than fucking Matt.
-
You’re worse than fucking Matt.
Hahaha
-
You’re worse than fucking Matt.
surely fucking a specimen as sexy as matt can't be such bad thing ,,
-
editted in disclaimer: I was encouraged to post explaining this in another thread, and I am doing so very quickly and without much effort here to just get this concept out for research by you guys and to facilitate discussion. I have put only about 15 mins into this post, it is not very comprehensive or all encompassing, I am merely trying to get the ideas into your heads so you can think about this and help research it more to help give or take away its credibility and relevance to how insulin causes growth in bodybuilding. I have never seen this mentioned even once in all my time researching steroids/hormones/drugs or I would not be bothering to write a post about it myself.
I just got back from a long day of traffic, lab, and lectures and I am dead tired but i'll just write brief off the top of my head. I am a medical student and we learned something interesting about insulin some time ago and this is honestly way more likely to be the cause of insulins growth properties than simply shuttling nutrients. The professor was explaining that there is this concept in biochemistry called "spare receptors", where a specific cell has say, 100 receptors for a specific ligand, but only 10 of those are required for the full downstream effect to take place within the cell. Insulin is one of these ligands that "spare receptors" applies to. So whether you have 10 molecules of insulin bound to 10 receptors or 100 molecules bound to 100 (made up numbers obviously, you get the point), it does not matter, the maximum effect is achieved and the resulting downstream effect that results inside the cell is the same. It was further explained that many of these ligands (such as insulin) that have spare receptors often have secondary effects when present in large concentrations. Insulin is the example that was used throughout this discussion, and so it was explained how insulin in high concentrations actually binds to the IGF-1 receptor and causes growth this way, organs were mentioned as an example (think of the "hgh gut" people, makes perfect sense). And this is talking about relatively "high" concentrations in terms of normal people amounts. I would imagine their term "high" is absolutely nothing in comparison to actually astronomical amounts, such as... bodybuilders injecting hundreds of units of insulin per day).
In my full write up I was planning on doing, I would have done some research for each specific substances affinity for each receptor relevant to this discussion. Upon very very brief research in order to simply just get this concept out there for discussion,
"dose-dependent effects of GH and IGF-1 treatments on nitrogen metabolism, intestinal structure, and hepatic IGF-1-messenger RNA (mRNA) expression in postoperative parenterally fed rats"
"1 mg/kg/d of IGF-1 were equivalent to those of 0.66 IU/kg/d of GH"
One mole of IGF-1 weighs about 33.4% more than one mole of insulin, and one iu of insulin = 0.0347mg (numbers were googled very quickly and may be error prone I am dead tired and not putting much effort into this right now). So 1mg/kg/d of igf-1 = 0.75mg/kg/d of insulin or 21.6iu/kg/day. THIS IS NOT ACCOUNTING FOR THEIR INDIVIDUAL AFFINITY FOR THE IGF-1 RECEPTORS, THIS IS WHERE IT IS A WILD BASELESS ESTIMATE, but my point is not to give precise numbers, it is to show the general concept.
So take a 100kg bodybuilder. If we say that 1mg of igf-1 (keep in mind the price of this shit... people pay I think ~$130-180 for a ONE MILLIGRAM VIAL because of the results) = 0.75mg of insulin or 21.6iu... With the pros injecting insulin like water, let's say 300 (i have seen much more than this and this might even be a low estimate. no these doses of long acting insulin are not gonna kill them from hypo.), that's approximately the equivalent of 14mg igf-1 or like $2000 worth of shit each day?
Again the exact numbers are irrelevant and useless without somehow researching insulins affinity for every igf-1 receptor in the body, but this is the general point and I am sure you understand. This is not me pulling shit out of my ass this whole idea is due to what a ph.d in both molecular biology and biochemistry said regarding insulin and igf-1 receptors when teaching at a medical school. And you must admit that it makes much more sense than simply "pushing nutrients into cells". I am no ph.d but what else would the food do if not go into the muscles even without hundreds of units of insulin, stay in your blood stream to take a nice enjoyable bath, and then proceed to magically disappear without being used for either fat or muscle? It is also not as if the body doesn't produce insulin of its own when food is ingested (although obviously not in obscene BB amounts). It does not make much sense that the whole nutrient pushing thing is solely responsible for such massive growth, I believe this explanation is much more sensible and again it comes from a ph.d in molecular biology and biochemistry.
All the research I used here was found quickly on google I am sure I could get better and more concrete numbers/examples given time but I just wanted to get this out here quickly now so people could discuss it, and before I got too lazy to do it. I was intending this as a quick reply to a post in a thread where I said I would briefly explain it but I got slightly carried away and thought this deserves its own thread.
edit: no i will not show you the original medical school materials, I cannot risk being caught doing that especially on a forum about illegal drugs and ruin my life.
EDIT: PROOF I AM not pulling this out of my ass, again just short amounts of googling due to a PM request:
https://www.karger.com/Article/PDF/184146
https://www.karger.com/Article/ShowPic/184146/?image=000184146-1.jpg
... "Thus, stimulation of IGF-1 receptors may be obtained in vitro with high amounts of insulin."
This isn't a bad theory as to some of the mechanism of insulin growth.... But it doesn't explain the extra benefit when adding insulin in with already very high levels of igf present with gh and igf use, as is the case in pro bodybuilders..
One thing the phD doesn't think about is the overall physiological state of these bbers, they are not normal people, physiologically speaking, due to the cocktail of drugs they take....
The largest determination of the benefit found by a bber using insulin is their degree of insulin sensitivity. Large pro bbers use a large amount of growth hormone every day, this has been found to cause insulin resistance, so the bber using all this gh is no longer optimally utilising the nutrients he takes in, bber adds insulin all of a sudden he starts gaining a lot of muscle.....
This is further supported by the fact that aas users who do not use gh don't get great gains from adding insulin to their drug protocols because they are not insulin resistant from gh abuse (I experienced this myself when I have used insulin in the past). These observations support the theory that insulins main mechanism of growth is its ability to transport nutrients.
It's a nice theory though and could very well be adding some muscle gain benefits along with the main effect that insulin has... Imo.
-
Remember that a gh or igf using bber will have very high levels of igf hormones in their body already present and that these ligands bind their receptors in a dose dependent affinity to their receptor, so the fact that there are already very high levels of these hormones in these individuals mean that these receptors will be already heavily bound and that off target binding by adding insulin is made even less likely.....
It's true insulin may off target Bind to igf receptors due to the similar molecular structure of the two molecules but in cases where the actual molecule is present in high amounts (eg igf1) there will be likely very little off target binding of insulin to any igf receptors as the igf molecules already present in large amounts have a much greater affinity to their respective receptors....
-
A bit over my head but there is one point that resonated with me. The idea of pushing more nutrients into the muscle. Say you ingest 200 grams of carbs and take 20 ius of Humulin R. Yes, that insulin will help shuttle the glucose from those carbs into the cells (I'm not sure if it's just muscle cells) but my question is, so what? No matter how many carbs you consume, if you are healthy, your body is always going to produce enough insulin to shuttle those nutrients in any way. Does it really matter with muscle hypertrophy if it takes an hour (taking that 20ius) or two hours to do this? As posted, where are all these "extra" glucose going to go? As long as there is glucose in the blood at a specific level a healthy body is always going to produce enough insulin to shuttle it to the muscles or fat cells.
-
TL:DR:GFY
-
To me, it does make sense to use insulin prior to a workout so that you have it in your system working while training while at the same time you supply your body with predigested nutrients (amino acids, dextrose, creatine...). That way you are pumping nutrient-rich blood into the muscles cells instead of going into a catabolic state and having to "catch up" post workout.
As Milos explained it:
So here is rationale behind it. Men have about 5L of blood and women have about 4L distributed all over the body which is constantly circulating around. In a state of rest at maximum about 10 -12 % of that blood finds its way in to our skeletal muscles, as there is no real physiological demand at the time of a low physical activity period. However, when we become active, blood is sent to our working muscles… and that increased blood flow to exercising muscles (Hyperemia) can achieve an astonishing 60% increase in blood flow or more during weight training. This happens ONLY during the workout!
So as my father suggested, if I supply all the necessary anabolic nutrients in a pre-digested form (e.g; ATP, glucose, amino acids etc) into the blood stream right before training and then continue delivering more of the same nutrients during my training session whilst raising the most anabolic hormone in our body – insulin – I will create an immediate and maximal anabolic environment.
So instead of losing nutrients (protein degradation or catabolism) we are creating a greater nutritional uptake by our muscle cells (protein synthesis or anabolism) and simultaneously preventing anti-catabolism… everything we need to great the maximal results we are after. So we need to remember that we only have this opportunity during training, not before or after as blood will not be in the muscle to this extent.
It doesn’t make sense to send an empty plane from Sydney to LAX with no passengers on it does it? So why send empty blood through the working muscle, when you have a unique opportunity to insert all these nutrients into our cells?
-
Great post, very interesting.
You’re worse than fucking Matt.
Come on, he's not talking about slit or penile length ::)
-
A bit over my head but there is one point that resonated with me. The idea of pushing more nutrients into the muscle. Say you ingest 200 grams of carbs and take 20 ius of Humulin R. Yes, that insulin will help shuttle the glucose from those carbs into the cells (I'm not sure if it's just muscle cells) but my question is, so what? No matter how many carbs you consume, if you are healthy, your body is always going to produce enough insulin to shuttle those nutrients in any way. Does it really matter with muscle hypertrophy if it takes an hour (taking that 20ius) or two hours to do this? As posted, where are all these "extra" glucose going to go? As long as there is glucose in the blood at a specific level a healthy body is always going to produce enough insulin to shuttle it to the muscles or fat cells.
^ you said it "if the body is healthy"... pro bodybuilders that abuse gh become insulin resistant and don't optimally utilise nutrients they consume...
Also I think there is a benefit to ramming nutrients with greater than normal physiological doses of insulin as anyone that eats 100gram's of carbs constantly or in a single meal there is going be added insulin resistance on that front also that insulin use can overcome.
-
^ you said it "if the body is healthy"... pro bodybuilders that abuse gh become insulin resistant and don't optimally utilise nutrients they consume...
Also I think there is a benefit to ramming nutrients with greater than normal physiological doses of insulin as anyone that eats 100gram's of carbs constantly or in a single meal there is going be added insulin resistance on that front also that insulin use can overcome.
Don't you think it matters what kind of carbs you eat? If you are eating complex carbs you don't get the insulin spike that you do with simple carbs. The difference between eating jelly beans versus oatmeal. The complex carbs are more "time released" and give you a more sustained energy release and no insulin spike.
Also, what do you think of Milos' theory about supplying nutrients, predigested nutrients, that go right into your bloodstream and into your muscle while you are training since that's the only time when the muscles get such a large influx of blood supply and using insulin to shuttle it in there fast when you most need it?
-
Don't you think it matters what kind of carbs you eat? If you are eating complex carbs you don't get the insulin spike that you do with simple carbs. The difference between eating jelly beans versus oatmeal. The complex carbs are more "time released" and give you a more sustained energy release and no insulin spike.
Also, what do you think of Milos' theory about supplying nutrients, predigested nutrients, that go right into your bloodstream and into your muscle while you are training since that's the only time when the muscles get such a large influx of blood supply and using insulin to shuttle it in there fast when you most need it?
When talking about nattys i don't think it matters as much because you don't have that anabolic environment from super high androgens, gh igf and insulin..... so really spiking insulin then in natural amounts, I don't know that you are really getting that big anabolic response you are when your jacked up on everything.
I'm not a fan of milos, I think his attitude is just take more and more insulin and it's the answer for everything.... His "scientific" explanations are always full of errors.
The big takeaway imo is that whilst there are drug protocols that generally speaking we can all more or less follow, the same is not true of nutrition. We all make different amounts of different enzymes and have substantial differences metabolically, so what works great for one will not work so great for the next guy, this means unfortunately we all have to try different things nutritionally and see what works in our bodies.
This is a reason nutritional research is so hit and miss and not really great for individuals, as they average the data from a large group of people who all have different responses to whatever they are testing. Stats are good for working through data and estimating large groups, (like giving general guidelines for a population), but cannot predict an individual response.
-
When talking about nattys i don't think it matters as much because you don't have that anabolic environment from super high androgens, gh igf and insulin..... so really spiking insulin then in natural amounts, I don't know that you are really getting that big anabolic response you are when your jacked up on everything.
I'm not a fan of milos, I think his attitude is just take more and more insulin and it's the answer for everything.... His "scientific" explanations are always full of errors.
The big takeaway imo is that whilst there are drug protocols that generally speaking we can all more or less follow, the same is not true of nutrition. We all make different amounts of different enzymes and have substantial differences metabolically, so what works great for one will not work so great for the next guy, this means unfortunately we all have to try different things nutritionally and see what works in our bodies.
This is a reason nutritional research is so hit and miss and not really great for individuals, as they average the data from a large group of people who all have different responses to whatever they are testing. Stats are good for working through data and estimating large groups, (like giving general guidelines for a population), but cannot predict an individual response.
Very thoughtful and informative posts. You seem very well educated on this subject. I'd like to get VanB on here as this is right up his alley.
-
Very thoughtful and informative posts. You seem very well educated on this subject. I'd like to get VanB on here as this is right up his alley.
Cheers mate
-
thanks pupil, i got the idea now
but to me it doesn't resonate with the claims you made first
"insulin is not the reason for larger muscle through nutrient shuttling"
insulin is (in great part) responsible for shuttling nutrients in muscle cells
the texts and info you provided offer additional information as to what else is or can be done with insulin when it's "spilling over"
and that's good stuff, so thanks
-
Also I think there is a benefit to ramming nutrients with greater than normal physiological doses of insulin as anyone that eats 100gram's of carbs constantly or in a single meal there is going be added insulin resistance on that front also that insulin use can overcome.
i don't think you can treat insulin resistance by adding in more exogenous insulin
-
Don't you think it matters what kind of carbs you eat? If you are eating complex carbs you don't get the insulin spike that you do with simple carbs. The difference between eating jelly beans versus oatmeal. The complex carbs are more "time released" and give you a more sustained energy release and no insulin spike.
Also, what do you think of Milos' theory about supplying nutrients, predigested nutrients, that go right into your bloodstream and into your muscle while you are training since that's the only time when the muscles get such a large influx of blood supply and using insulin to shuttle it in there fast when you most need it?
digestion and the time it takes to digest carbs is what will determine the rate at which glucose is released
the milos theory works in practice
but i do believe large amounts of slin will also increase gut swelling..
-
The big takeaway imo is that whilst there are drug protocols that generally speaking we can all more or less follow, the same is not true of nutrition. We all make different amounts of different enzymes and have substantial differences metabolically, so what works great for one will not work so great for the next guy, this means unfortunately we all have to try different things nutritionally and see what works in our bodies.
This is a reason nutritional research is so hit and miss and not really great for individuals, as they average the data from a large group of people who all have different responses to whatever they are testing. Stats are good for working through data and estimating large groups, (like giving general guidelines for a population), but cannot predict an individual response.
i think the opposite regarding the drug protocol part
i think most people will have a very different reaction to a similar drug protocol
for example a 10mg dbol pill a day can do wonders for some and nothing for others
i think it's all very individual, the training, the food, the drugs, the everything
-
TL:DR:GFY
this...
-
A lot could be said about insulin but even though igf-1
probably plays a part in its pro-anabolic effects it's not like igf is responsible for the massive and quick weight gain. It's water. Neither IGF nor GH causes massive muscle gain , by themselves they build virtually no muscle. No one is gaining 30lbs of muscle in a month due to insulin cross-reacting with IGF receptors.
I think the main beneficial effects of insulin from a bodybuilder's POV is the water volumization, simply a cosmetic effect, which is no small thing for a competitive bb. Anyone who has used it knows you can put on a bunch of pounds overnight and it goes away just as fast when you stop. It's like filling a balloon with water.
It fixes the insulin resistance from gh or more correctly puts a band-aid on it. It's very anti-catabolic and long term I would guess this is its main benefit for real muscle growth. Milos' idea of using it before workouts does make sense especially if one does very catabolic giant set marathon workouts. Increased blood flow to muscle while having aminos in the blood may be beneficial for muscle growth and apart from the workout insulin itself increases blood flow. Since we are constantly breaking down and building muscle, if we can reduce breakdown we end up with more muscle.
What many don't know about insulin is the main mechanism behind the blood glucose lowering effect, and it may be worth knowing. It is not by opening up the cells so they accept glucose. Insulin stops glucose release from the liver. From what I remember reading diabetics who skip their insulin keep storing glucose but since there is no break to stop liver glucose production BG skyrockets.
So yeah, maybe "nutrient shuttling" isn't the major reason it seems to "work" for bodybuilders.
-
i don't think you can treat insulin resistance by adding in more exogenous insulin
You can, this is well established medical fact.... If you couldn't type two diabetics would all die from the condition.
I don't think you have a great understanding here.
-
digestion and the time it takes to digest carbs is what will determine the rate at which glucose is released
the milos theory works in practice
but i do believe large amounts of slin will also increase gut swelling..
Gut swelling?
-
TL,DR,FO
-
i don't think you can treat insulin resistance by adding in more exogenous insulin
??? ??? ???
-
??? ??? ???
You can, this is well established medical fact.... If you couldn't type two diabetics would all die from the condition.
I don't think you have a great understanding here.
willl can correct me if misunderstood, but I think he is talking about what I meant by putting a band-aid on insulin resistance. Adding more insulin to an insulin resistant state doesn't reduce the resistance, it likely makes it worse. Obviously. Fixing insulin resistance is done by not bombarding the cells with glucose and insulin constantly. Endogenous insulin is increased by GH use too, but it's not enough sometimes to keep BG in check. Here exogenous insulin can help protect your organs but in the long term it's hardly an ideal situation.
-
Yep I see what your saying, of course insulin resistance cannot be treated itself by adding more insulin, the elevated blood glucose caused by the resistance to endogenously produced insulin can be treated by adding exogenous insulin.
In cases where we consider health, such as type 2 diabetes, it is the elevated blood glucose that drives the diseases these people experience, much more so than elevated insulin levels.. That's why type 2 patients may need to add insulin to control their BGL, this has a positive health effect in these patients.
-
Yep I see what your saying, of course insulin resistance cannot be treated itself by adding more insulin, the elevated blood glucose caused by the resistance to endogenously produced insulin can be treated by adding exogenous insulin.
In cases where we consider health, such as type 2 diabetes, it is the elevated blood glucose that drives the diseases these people experience, much more so than elevated insulin levels.. That's why type 2 patients may need to add insulin to control their BGL, this has a positive health effect in these patients.
Yes it's the glucose that can be directly toxic, not the insulin. 20 years ago Milos said that insulin use could protect people from disease and diabetes itself, by protecting the pancreas and most were like wtf is he saying? But he had somewhat of a point in certain situations. I know a few years ago there was debate in the medical community on whether it might be a good idea to put some type 2s on insulin sooner instead of persisting with the oral agents. I haven't followed the debate so I don't know what the cutting edge is nowadays.
-
willl can correct me if misunderstood, but I think he is talking about what I meant by putting a band-aid on insulin resistance. Adding more insulin to an insulin resistant state doesn't reduce the resistance, it likely makes it worse. Obviously. Fixing insulin resistance is done by not bombarding the cells with glucose and insulin constantly. Endogenous insulin is increased by GH use too, but it's not enough sometimes to keep BG in check. Here exogenous insulin can help protect your organs but in the long term it's hardly an ideal situation.
^^
btw type 2 can be dealt with (cured) very efficiently without any meds at all
-
I think the main beneficial effects of insulin from a bodybuilder's POV is the water volumization, simply a cosmetic effect, which is no small thing for a competitive bb. Anyone who has used it knows you can put on a bunch of pounds overnight and it goes away just as fast when you stop. It's like filling a balloon with water.
What many don't know about insulin is the main mechanism behind the blood glucose lowering effect, and it may be worth knowing. It is not by opening up the cells so they accept glucose. Insulin stops glucose release from the liver. From what I remember reading diabetics who skip their insulin keep storing glucose but since there is no break to stop liver glucose production BG skyrockets.
agree on the water
i didnt know the liver release part of insulin mechanism, interesting, thanks
-
So yeah, maybe "nutrient shuttling" isn't the major reason it seems to "work" for bodybuilders.
without this nutrient shuttling (glucose primarily), there would be no exceptional water retention within the muscle, don't you think?
-
thanks pupil, i got the idea now
but to me it doesn't resonate with the claims you made first
"insulin is not the reason for larger muscle through nutrient shuttling"
insulin is (in great part) responsible for shuttling nutrients in muscle cells
the texts and info you provided offer additional information as to what else is or can be done with insulin when it's "spilling over"
and that's good stuff, so thanks
I mean again IMO whether it's one mechanism or the other basically boils down to anyones speculation, it just simply makes more sense in my head that this is responsible for more growth than the nutrient shuttling thing, not that the nutrient shuttling is useless. My main point was simply to get the idea out there like you said, not really argue that nutrient shuttling in itself is useless. I don't know either way (no one does). My goal was to introduce the fact that there is another pathway for growth besides the nutrient shuttling and to get people talking about it. It is ONLY my personal opinion that it seems to make more sense that the IGF-1 receptor binding plays a greater part, I am not claiming otherwise. That is why I want people to get the idea and research/think about it and discuss it, so maybe we can get to the bottom of this.
EDIT: God damn it is so weird to be posting here and seeing all these famous old names posting in my thread, after reading old getbig gh15 era threads for years and years... Van bilderass and pellius posting in my thread, who would have imagined.
-
From what I remember reading diabetics who skip their insulin keep storing glucose but since there is no break to stop liver glucose production BG skyrockets.
The rest of your posts are good but I had to nitpick with this statement here - Most of the body's cells require insulin for glucose uptake. Diabetics who dont take their insulin go into ketosis because the glucose is unable to be utilized
-
The rest of your posts are good but I had to nitpick with this statement here - Most of the body's cells require insulin for glucose uptake. Diabetics who dont take their insulin go into ketosis because the glucose is unable to be utilized
Well, take a look at this article.
https://bjanaesthesia.org/article/S0007-0912(17)37337-3/fulltext
Current dogma would have us believe that administration of insulin to somebody with severely deranged diabetes suddenly and miraculously allows the cells in the body to breathe again and be restored to their former healthy state.
...
Indeed, rather than stimulating glucose uptake in tissues such as muscle, insulin in fact reduces glucose uptake. This is because the main factor driving glucose uptake is the ‘mass action’ effect of hyperglycaemia and the concentration gradient between the extracellular and intracellular glucose concentrations. Glucose transporters are not rate limiting under these conditions, even in the face of severe insulin deficiency.
...
Insulin produced an immediate reduction of 50% in hepatic glucose production (Ra); this was the only change leading to the decrease in glucose during the low-dose study.
...
The results are very much in keeping with Schafer's concept of a primary role of insulin in regulating blood glucose concentration through control of hepatic glucose storage
If you have some issue or comment on what the authors claim let me know. I didn't really read it very closely but they claim that insulin's main action wrt to BG is the hepatic effect like I said.
I mean again IMO whether it's one mechanism or the other basically boils down to anyones speculation, it just simply makes more sense in my head that this is responsible for more growth than the nutrient shuttling thing, not that the nutrient shuttling is useless. My main point was simply to get the idea out there like you said, not really argue that nutrient shuttling in itself is useless. I don't know either way (no one does). My goal was to introduce the fact that there is another pathway for growth besides the nutrient shuttling and to get people talking about it. It is ONLY my personal opinion that it seems to make more sense that the IGF-1 receptor binding plays a greater part, I am not claiming otherwise. That is why I want people to get the idea and research/think about it and discuss it, so maybe we can get to the bottom of this.
EDIT: God damn it is so weird to be posting here and seeing all these famous old names posting in my thread, after reading old getbig gh15 era threads for years and years... Van bilderass and pellius posting in my thread, who would have imagined.
The insulin/igf-1 connection has been talked about for decades in these circles. Not only the cross-reactivity but the fact that insulin can elevate endogenous igf-1. Apparently there seems to be a difference between different synthetic insulins in their ability to stimulate igf-1. From what I remember Lantus was supposed to be particularly effective. More igf-1 is likely beneficial for muscle growth but guys are putting on tons of weight on it very quickly and that can only be due to water shifts.
^^
btw type 2 can be dealt with (cured) very efficiently without any meds at all
Sure, just losing weight could cure a type 2. Of course only few patients are ready for a radical lifestyle change even in the face of severe health issues so damage control becomes important. Shit, I work with a dude who is even too lazy to take his Metformin.
-
This is shaping up to be a great thread, I much prefer this to the boring political baiting spewed in this board. Great posts Van_Bilderass.
-
its amazing, all this science ant yet 99.9% of the people who use it look like shit...
-
its amazing, all this science ant yet 99.9% of the people who use it look like shit...
Because meat heads don't care for understanding and leveraging the science! ;D
-
its amazing, all this science ant yet 99.9% of the people who use it look like shit...
How very True.
Then the same can be said for the vast majority using Steroids & or GH.
How many lads do we Here in the gym talking about what there taking or going to take
To Get HUGE & RIPPED - Yet very very few do.
Look how they Train or Rather Don’t Train & Their lives outside of the Gym.
If They Concerned Themselves Less with Taking this & that & Just Got On with some simple
Basic exercises, Worked hard at them, Food & Rest.
Just Keep it Simple.
-
its amazing, all this science ant yet 99.9% of the people who use it look like shit...
Sure most who use it look like shit, but then again most who use steroids also look like shit. Or GH or anything.
To be honest, there isn't that much science actually in our hobby, the really sharp minds are few and far between. Even I can see that, and I only give half a shit about all this stuff.
Anyway, yesterday I did a google on the Lantus/IGF-1 connection I've seen mentioned in the past, and from my 10 second glance at an abstract it appears as though the reason Lantus is thought to enhance IGF-1 levels is because Lantus has *low* affinity for IGF-1 receptors. Insulins which have higher affinity will *lower* IGF-1 as well as GH. Makes sense right? So would a bodybuilder want to use an insulin with high affinity in megadoses as sort of a poor man's IGF-1 or something like Lantus which may increase endogenous IGF? Ultimately I think this mechanism is probably not behind most benefits bodybuilders feel from it so it probably doesn't matter.
Seems like IGF-1 use isn't that popular anymore, most just noticed better pumps and vascularity. Part of it may be because the doses of the research chems are too low but even those who were able to use Increlex noticed it wasn't magic.
My training partner back in like 98 or 99 got ahold of one or two milligrams of LR3 from a scientist at a university and he told me it put 20lbs of muscle on him overnight. He was like 320lbs lean but even back then I told him it probably wasn't the IGF-1 that did it, it was probably the insulin he started at the same time :D But it was hard to get and extremely expensive so he thought it was magic :D
-
Sure most who use it look like shit, but then again most who use steroids also look like shit. Or GH or anything.
To be honest, there isn't that much science actually in our hobby, the really sharp minds are few and far between. Even I can see that, and I only give half a shit about all this stuff.
Anyway, yesterday I did a google on the Lantus/IGF-1 connection I've seen mentioned in the past, and from my 10 second glance at an abstract it appears as though the reason Lantus is thought to enhance IGF-1 levels is because Lantus has *low* affinity for IGF-1 receptors. Insulins which have higher affinity will *lower* IGF-1 as well as GH. Makes sense right? So would a bodybuilder want to use an insulin with high affinity in megadoses as sort of a poor man's IGF-1 or something like Lantus which may increase endogenous IGF? Ultimately I think this mechanism is probably not behind most benefits bodybuilders feel from it so it probably doesn't matter.
Seems like IGF-1 use isn't that popular anymore, most just noticed better pumps and vascularity. Part of it may be because the doses of the research chems are too low but even those who were able to use Increlex noticed it wasn't magic.
My training partner back in like 98 or 99 got ahold of one or two milligrams of LR3 from a scientist at a university and he told me it put 20lbs of muscle on him overnight. He was like 320lbs lean but even back then I told him it probably wasn't the IGF-1 that did it, it was probably the insulin he started at the same time :D But it was hard to get and extremely expensive so he thought it was magic :D
Why use all these PEDs to look like Crap. ( not saying you do )
Why not just have a clean diet & Simple & Effective Training routine
And look much better being lean & Muscular.
If all the parameters aren’t in check & Of a reasonably low body fat it’s to damn hard
To know what’s doing what. Just Guess work.
I’m not bothered with working with / helping anyone that’s fat & has a Shotgun approach
To what they do & Take.
-
Why use all these PEDs to look like Crap. ( not saying you do )
Why not just have a clean diet & Simple & Effective Training routine
And look much better being lean & Muscular.
If all the parameters aren’t in check & Of a reasonably low body fat it’s to damn hard
To know what’s doing what. Just Guess work.
I’m not bothered with working with / helping anyone that’s fat & has a Shotgun approach
To what they do & Take.
I look like absolute shit, always did really. I just find this stuff mildly interesting for whatever reason. I don't do a lot of gear anymore. HRT for the most part.
I don't know how far you got in bodybuilding and what you have taken but I'm guessing there's been plenty of gear use :D Have you used insulin? GH? Tren? IGF-1?
Guys here think even Mr Olympias are absolute retards for taking so many drugs, so how stupid are all of us who are virtual nobodies? :D We all have our reasons, as stupid as they may seem to everyone else.
-
I look like absolute shit, always did really. I just find this stuff mildly interesting for whatever reason. I don't do a lot of gear anymore. HRT for the most part.
I don't know how far you got in bodybuilding and what you have taken but I'm guessing there's been plenty of gear use :D Have you used insulin? GH? Tren? IGF-1?
Guys here think even Mr Olympias are absolute retards for taking so many drugs, so how stupid are all of us who are virtual nobodies? :D We all have our reasons, as stupid as they may seem to everyone else.
I really doubt you look like absolute shit
Maybe not a high calibre look but I bet you looked moderately decent
And do you agree that certain fellas respond differently to different compounds? For example one can respond very well to say deca but have near zero response to anadrol, and if so why is this? (Assuming all gear taken is legit and not bunk)
-
I really doubt you look like absolute shit
Maybe not a high calibre look but I bet you looked moderately decent
And do you agree that certain fellas respond differently to different compounds? For example one can respond very well to say deca but have near zero response to anadrol, and if so why is this? (Assuming all gear taken is legit and not bunk)
Different guys definitely respond differently to drugs, but I would probably say it's more that some don't seem to get much out of any steroid. Or maybe some just don't have the number of muscle fibers or nice muscle bellies genetically to begin with, so even if the response is what could be expected the end result is still a relatively crap physique. Just a little bigger. Some may look so good naturally with full muscle bellies and so on that even a modest response makes them look like a million bucks.
Of course different guys could have different responses to specific drugs and everyone has their favorites. But let's say someone gets little out of say Dianabol, how likely is it he will respond like crazy to another steroid? Or if you don't get much of anything out of test, how likely is it that you will blow up on Deca? I mean most pros stacks probably look fairly similar. Like test as a baseline. It always seems to "work" as expected.
Anadrol is actually a funny case. Some say they don't always feel it and others think it's "instant muscle" as Duchaine said. I don't know why that is. I thought it was shit the first times I tried it, thought maybe it was all fake. Later on I liked it. The best for strength out of all steroids.
Just some thoughts. :)
-
I look like absolute shit, always did really. I just find this stuff mildly interesting for whatever reason. I don't do a lot of gear anymore. HRT for the most part.
I don't know how far you got in bodybuilding and what you have taken but I'm guessing there's been plenty of gear use :D Have you used insulin? GH? Tren? IGF-1?
Guys here think even Mr Olympias are absolute retards for taking so many drugs, so how stupid are all of us who are virtual nobodies? :D We all have our reasons, as stupid as they may seem to everyone else.
I’ve used AAS . I’ve worked with many that have used GH / Insulin.
I won 2 British Powerlifting Champs Before using anything - More Fool Me.!!
Then swapped over To Bodybuilding & competing for U.K. & Doing Very Well again
On a National Level - Yes I used AAS.
My point was that all these Wonderful exotic Drugs aren’t Necessary to Have a Decent
Physique- No we can’t all be Mr U.K. / Sweden But we can look half decent with diet & Training.
If looking like a Blob / Fat Bulky Man is where their at - How & why waste good Money on
What are Supposedly Physique Enhancing Drugs - When No Enhancement is Visible.
Then again to each there own - If It Makes Them Happy.
You can afford them & want to use them that’s fine by Me.
-
Sure most who use it look like shit, but then again most who use steroids also look like shit. Or GH or anything.
To be honest, there isn't that much science actually in our hobby, the really sharp minds are few and far between. Even I can see that, and I only give half a shit about all this stuff.
Anyway, yesterday I did a google on the Lantus/IGF-1 connection I've seen mentioned in the past, and from my 10 second glance at an abstract it appears as though the reason Lantus is thought to enhance IGF-1 levels is because Lantus has *low* affinity for IGF-1 receptors. Insulins which have higher affinity will *lower* IGF-1 as well as GH. Makes sense right? So would a bodybuilder want to use an insulin with high affinity in megadoses as sort of a poor man's IGF-1 or something like Lantus which may increase endogenous IGF? Ultimately I think this mechanism is probably not behind most benefits bodybuilders feel from it so it probably doesn't matter.
Seems like IGF-1 use isn't that popular anymore, most just noticed better pumps and vascularity. Part of it may be because the doses of the research chems are too low but even those who were able to use Increlex noticed it wasn't magic.
My training partner back in like 98 or 99 got ahold of one or two milligrams of LR3 from a scientist at a university and he told me it put 20lbs of muscle on him overnight. He was like 320lbs lean but even back then I told him it probably wasn't the IGF-1 that did it, it was probably the insulin he started at the same time :D But it was hard to get and extremely expensive so he thought it was magic :D
If insulin, at varying levels, lowers gh/igf, why was it that when I was given an insulin sensitivity test there was an inverse relationship between when I was injected with insulin which immediately lowered blood glucose levels my gh level went up. And when I was injected with dextrose my gh level immediately began to drop.
Since it seems that low blood sugar is one the mechanism that stimulates gh production why would it be that insulin, in any form, would lower gh production?
-
I have heard taking "slin" around workouts gives one the craziest pump
-
I have heard taking "slin" around workouts gives one the craziest pump
Well, hopefully not just slin. Need some dextrose to keep from passing out. And, as Milos recommends, all those predigested nutrients being shuttled into the muscles from the blood flow due to the workout. That's what gives you the pump. Through in some Viagra or Cialis and watch the veins bulge.
-
If insulin, at varying levels, lowers gh/igf, why was it that when I was given an insulin sensitivity test there was an inverse relationship between when I was injected with insulin which immediately lowered blood glucose levels my gh level went up. And when I was injected with dextrose my gh level immediately began to drop.
Since it seems that low blood sugar is one the mechanism that stimulates gh production why would it be that insulin, in any form, would lower gh production?
I would guess that while acute hypoglycemia increases GH some long acting insulins in diabetics show a trend of lowered IGF-1 over time due to your body thinking there is a lot of IGF-1 around. In the abstract I glanced at they asked whether this GH lowering effect might be beneficial in a diabetic context. So insulin can do both.
-
Sure most who use it look like shit, but then again most who use steroids also look like shit. Or GH or anything.
To be honest, there isn't that much science actually in our hobby, the really sharp minds are few and far between. Even I can see that, and I only give half a shit about all this stuff.
Anyway, yesterday I did a google on the Lantus/IGF-1 connection I've seen mentioned in the past, and from my 10 second glance at an abstract it appears as though the reason Lantus is thought to enhance IGF-1 levels is because Lantus has *low* affinity for IGF-1 receptors. Insulins which have higher affinity will *lower* IGF-1 as well as GH. Makes sense right? So would a bodybuilder want to use an insulin with high affinity in megadoses as sort of a poor man's IGF-1 or something like Lantus which may increase endogenous IGF? Ultimately I think this mechanism is probably not behind most benefits bodybuilders feel from it so it probably doesn't matter.
Seems like IGF-1 use isn't that popular anymore, most just noticed better pumps and vascularity. Part of it may be because the doses of the research chems are too low but even those who were able to use Increlex noticed it wasn't magic.
My training partner back in like 98 or 99 got ahold of one or two milligrams of LR3 from a scientist at a university and he told me it put 20lbs of muscle on him overnight. He was like 320lbs lean but even back then I told him it probably wasn't the IGF-1 that did it, it was probably the insulin he started at the same time :D But it was hard to get and extremely expensive so he thought it was magic :D
When they say "affinity" they are talking about how much of a molecular connection the hormone (eg lantus) has for the particular receptor (the receptor is located on the cell surface and transmits, via a binding induced shape change to its hormone, a signal that activates it's function within the cell [eg glucose uptake through the cell membrane])... The reason insulin and the igf hormones have this interplay between each other's receptors is because they have similar molecular structures..
If lantus has a lower affinity for the igf receptors this does not mean it's use will enhance igf production it only means lantus off target binding to igf receptor will be reduced and that extra igf activation is not there...
Lantus or whatever insulin cannot preferentially bind the igf receptors over igf itself (when igf is present), this is because the igf is the perfect molecular "fit" for its receptor, whereas insulin sort of fits the igf receptors due to the structural similarity. This is my main point from earlier in the thread, if igf is super high due to gh use or igf use (as it is in all pro bodybuilders) the off target effects of insulin binding the igf receptors are nullified, insignificant.
-
I would guess that while acute hypoglycemia increases GH some long acting insulins in diabetics show a trend of lowered IGF-1 over time due to your body thinking there is a lot of IGF-1 around. In the abstract I glanced at they asked whether this GH lowering effect might be beneficial in a diabetic context. So insulin can do both.
This is a good question for non bodybuilders, how potent is the insulin in activating the igf negative feedback loop by binding the igf receptor?
but as I mentioned in the other posts, in a bodybuilder that is using a heap of gh igf it doesn't matter as the body's own production is meaningless.
-
This is a good question for non bodybuilders, how potent is the insulin in activating the igf negative feedback loop by binding the igf receptor?
but as I mentioned in the other posts, in a bodybuilder that is using a heap of gh igf it doesn't matter as the body's own production is meaningless.
Yeah it doesn't matter in that situation. I haven't done enough reading to come to real conclusions on what is going on. In vitro Lantus has a high affinity for IGF receptors so in theory Lantus should lower GH and IGF but in diabetics it actually raises IGF so either it has low affinity at the pituitary specifically or it causes better glycemic control which leads to GH surges. I don't know.
There is someone on this forum running MK-677, and while IGF rose a lot his BG is also creeping upwards and he was debating adding some Lantus. So it would be interesting to see if the addition of Lantus further enhances IGF.
I know there have been a bunch of guys on the forums running high doses of Lantus and some getting their IGF tested but I haven't been interested enough to know their results. In the real world knowing about all this stuff won't make a big difference so it's only mildly interesting :D
Bodybuilders will keep experimenting and keeping what works and discarding what doesn't.
-
Lantus or whatever insulin cannot preferentially bind the igf receptors over igf itself (when igf is present), this is because the igf is the perfect molecular "fit" for its receptor, whereas insulin sort of fits the igf receptors due to the structural similarity. This is my main point from earlier in the thread, if igf is super high due to gh use or igf use (as it is in all pro bodybuilders) the off target effects of insulin binding the igf receptors are nullified, insignificant.
This is completely false, look up the concept of competitive inhibitors. A higher affinity compound (or the natural one that is a "perfect fit") being present does not somehow prevent the lower affinity one from binding at all. If this was true almost no drugs at all in existence would work, only giving people the natural substances (like testosterone) would work... any relative difference in affinities, even massive ones, can be overcome through one substance outcompeting another.
-
Yeah it doesn't matter in that situation. I haven't done enough reading to come to real conclusions on what is going on. In vitro Lantus has a high affinity for IGF receptors so in theory Lantus should lower GH and IGF but in diabetics it actually raises IGF so either it has low affinity at the pituitary specifically or it causes better glycemic control which leads to GH surges. I don't know.
There is someone on this forum running MK-677, and while IGF rose a lot his BG is also creeping upwards and he was debating adding some Lantus. So it would be interesting to see if the addition of Lantus further enhances IGF.
I know there have been a bunch of guys on the forums running high doses of Lantus and some getting their IGF tested but I haven't been interested enough to know their results. In the real world knowing about all this stuff won't make a big difference so it's only mildly interesting :D
Bodybuilders will keep experimenting and keeping what works and discarding what doesn't.
Yeah your right, that mk677 especially would be interesting....
-
This is completely false, look up the concept of competitive inhibitors. A higher affinity compound (or the natural one that is a "perfect fit") being present does not somehow prevent the lower affinity one from binding at all. If this was true almost no drugs at all in existence would work, only giving people the natural substances (like testosterone) would work... any relative difference in affinities, even massive ones, can be overcome through one substance outcompeting another.
I've got a degree in molecular cell biology, basics of competitive inhibition is a first year subject. Let me try explain to you where your misunderstanding here.
A drug works to competitively inhibit via binding the active binding site on a given receptor, this prevents the normal hormone substrate from binding it's active site, simple enough. What I think you are trying to argue is that in drug use etc when the concentration of the drug (inhibitor) is greater than that of the normal substrate it will bind at a greater rate therefore achieving greater levels of inhibition.
What you miss here is that chemical inhibitors (your average drug) are very small chemical molecules much much smaller than a protein, with a very basic one dimensional structure, that align electrochemically to only to a small specific area of the protein receptor at the active site, thus they can have a great affinity to that site and outcompete the much larger more complex natural protein hormone.
In the case we are speaking of here we are talking about much larger more complex molecules, proteins (insulin and igf proteins) Protein structure is much more complex with four stages of structure (you have probably covered tertiary quaternary etc) this means that these molecules affinity for each other's receptors active sites is much more regulated by their structures, much more than a tiny chemical (typical drug) that can bind freely to a receptor active site and easily outcompete the natural hormone due to its simplicity in structure, an advantage that the less than optimised insulin does not have over igf proteins when binding the igf receptors.
So as I said the structural optimisation of the igf hormone for its receptor in addition to its very high concentrations in pro bodybuilders will likely negate the great majority off target binding of insulin to igf receptors, there will still be some binding but the degree to which this occurs will likely be drastically reduced for these reasons.
-
I have heard taking "slin" around workouts gives one the craziest pump
I remember taking it once and getting a crippling forearm pump from squeezing the handles on the leg press :D
-
I've got a degree in molecular cell biology, basics of competitive inhibition is a first year subject. Let me try explain to you where your misunderstanding here.
A drug works to competitively inhibit via binding the active binding site on a given receptor, this prevents the normal hormone substrate from binding it's active site, simple enough. What I think you are trying to argue is that in drug use etc when the concentration of the drug (inhibitor) is greater than that of the normal substrate it will bind at a greater rate therefore achieving greater levels of inhibition.
What you miss here is that chemical inhibitors (your average drug) are very small chemical molecules much much smaller than a protein, with a very basic one dimensional structure, that align electrochemically to only to a small specific area of the protein receptor at the active site, thus they can have a great affinity to that site and outcompete the much larger more complex natural protein hormone.
In the case we are speaking of here we are talking about much larger more complex molecules, proteins (insulin and igf proteins) Protein structure is much more complex with four stages of structure (you have probably covered tertiary quaternary etc) this means that these molecules affinity for each other's receptors active sites is much more regulated by their structures, much more than a tiny chemical (typical drug) that can bind freely to a receptor active site and easily outcompete the natural hormone due to its simplicity in structure, an advantage that the less than optimised insulin does not have over igf proteins when binding the igf receptors.
So as I said the structural optimisation of the igf hormone for its receptor in addition to its very high concentrations in pro bodybuilders will likely negate the great majority off target binding of insulin to igf receptors, there will still be some binding but the degree to which this occurs will likely be drastically reduced for these reasons.
There is no way inhibitors must arbitrarily be small... it is very very typical for agonists or antagonists to have a structure almost identical to the original substance for the very reasons you stated, the complexity of receptors overall structure, obviously disregarding ones that bind to regulatory sites (as in other than the one the original substance binds to) on a protein such as allosteric sites.
In fact go look up acetylcholinesterase inhibitors... they are much larger/bulkier than acetylcholine itself... structural optimization is simply another word for... wait for it... "AFFINITY"
There are many substances in existence with higher affinities for given receptors than the original/intended substance. Take trenbolone for example, studies in rats show it binds to androgen receptors in rat prostates with 5x as much affinity as testosterone. Which btw is what androgenic ratings for steroids mean. Like trenbolones rating of "500" is relative to testosterones base affinity that they used for androgen receptor binding in rats, or "100". If something binds rat prostate androgen receptors with 5x as much affinity as testosterone, it's given a 500. If it's 1/5, then it's given 20, so on and so forth. (I am not saying this in regards to what you're saying about the original substance being a "perfect fit" for it's receptor... simply untrue)
-
There is no way inhibitors must arbitrarily be small... it is very very typical for agonists or antagonists to have a structure almost identical to the original substance for the very reasons you stated, the complexity of receptors overall structure, obviously disregarding ones that bind to regulatory sites (as in other than the one the original substance binds to) on a protein such as allosteric sites.
In fact go look up acetylcholinesterase inhibitors... they are much larger/bulkier than acetylcholine itself... structural optimization is simply another word for... wait for it... "AFFINITY"
There are many substances in existence with higher affinities for given receptors than the original/intended substance. Take trenbolone for example, studies in rats show it binds to androgen receptors in rat prostates with 5x as much affinity as testosterone. Which btw is what androgenic ratings for steroids mean. Like trenbolones rating of "500" is relative to testosterones base affinity that they used for androgen receptor binding in rats, or "100". If something binds rat prostate androgen receptors with 5x as much affinity as testosterone, it's given a 500. If it's 1/5, then it's given 20, so on and so forth. (I am not saying this in regards to what you're saying about the original substance being a "perfect fit" for it's receptor... simply untrue)
Have you ever used bioinformatics resources?
What year are you?
-
Have you ever used bioinformatics resources?
have you considered you are saying things that do not make any sense... a college degree does not make one an expert in something.
i am a medical student i am not in college... we have been covering pharmacology and biochemistry surprisingly in depth...
-
have you considered you are saying things that do not make any sense... a college degree does not make one an expert in something.
i am a medical student i am not in college... we have been covering pharmacology and biochemistry surprisingly in depth...
I'm a part of a research team that maps protein structure via x Ray crystallography.... So I am well informed.
My sister is a MD, there is not a great need for medical doctors to have a deep understanding of cell signalling so the teaching level is in accordance (single subject study).
Arguing about competitive inhibition generally is just ego bullshit and off from the topic at hand, I've made my points on insulin and igf and given my thoughts on the subject, you think what I have said makes no sense, that's okay with me.
Cheers.
-
I'm a part of a research team that maps protein structure via x Ray crystallography.... So I am well informed.
My sister is a MD, there is not a great need for medical doctors to have a deep understanding of cell signalling so the teaching level is in accordance (single subject study).
Arguing about competitive inhibition generally is just ego bullshit and off from the topic at hand, I've made my points on insulin and igf and given my thoughts on the subject, you think what I have said makes no sense, that's okay with me.
Cheers.
I said specific things you said made no sense like antagonists having to be very small, and the natural ligand being a perfect fit for receptors, because that makes no sense and made you come across as not knowing what you were talking about in this context. I was not addressing your points specifically
cheers
-
i like your skepticism and the way you approach this, pupil
-
Well, take a look at this article.
https://bjanaesthesia.org/article/S0007-0912(17)37337-3/fulltext
i took the time to read the whole article
a lot of great info on there, excellent find
-
i took the time to read the whole article
a lot of great info on there, excellent find
So did I - And
No doubt we’ll have several pro calibre Physiques & at least 1 Mr Olympia
Winner on here with that information.
Endocrine Pharmacology & In Fact all the Biological actions is Fascinating,
How our Bodies do what they do is Outstanding.
-
i like your skepticism and the way you approach this, pupil
I am skeptical about everything, being biased is pointless. I don't care to flaunt my cock trying to be "right", I just wanna find out what is actually right, generally speaking.
edit: in fact i really don't ever want to touch insulin ever, lol. I tried it once at I think 30iu fast acting post workout while on 8iu hgh for two? weeks at most, and eh. The recovery and fullness was absolutely retarded but after reading a lot about it on here, I don't want to get a gigantic gut and fuck up my physique in other ways, and I simply don't have the time or will to base my eating so much around insulin and having to inject it so much.
-
So did I - And
No doubt we’ll have several pro calibre Physiques & at least 1 Mr Olympia
Winner on here with that information.
Endocrine Pharmacology & In Fact all the Biological actions is Fascinating,
How our Bodies do what they do is Outstanding.
no doubt, but the article provides another insight (new for me) on insulin (outside of bbing) and i appreciate that kind of information
-
I am skeptical about everything, being biased is pointless. I don't care to flaunt my cock trying to be "right", I just wanna find out what is actually right, generally speaking.
edit: in fact i really don't ever want to touch insulin ever, lol. I tried it once at I think 30iu fast acting post workout while on 8iu hgh for two? weeks at most, and eh. The recovery and fullness was absolutely retarded but after reading a lot about it on here, I don't want to get a gigantic gut and fuck up my physique in other ways, and I simply don't have the time or will to base my eating so much around insulin and having to inject it so much.
How many carbs did you eat after injecting that much insulin? I think the gut comes from abuse. Milos never had a gut and Wolf would get some off season distension but never a full on bubble gut and I think it was stated that he use insulin every day with every meal.
-
30iu fast acting for your first shot ever? or did you build that up...?
-
I ate uhh I think 210g carbs and I did one or two 10iu shots first to get a feel for it then went to 30. Was doing 7g carbs/iu. I didn't personally experience bad sides or anything but it's too much of a pain in the ass for me to use consistently (timing it injecting it and eating/drinking the specific food with it every day or multiple times is annoying). Plus I want to avoid potential gut like I said.
-
I ate uhh I think 210g carbs and I did one or two 10iu shots first to get a feel for it then went to 30. Was doing 7g carbs/iu. I didn't personally experience bad sides or anything but it's too much of a pain in the ass for me to use consistently (timing it injecting it and eating/drinking the specific food with it every day or multiple times is annoying). Plus I want to avoid potential gut like I said.
I always thought the 10 grams per iu was a bit much. Do you think it makes sense as Milos stated about using insulin just prior to training with enough dextrose and aminos, creatine sipped during training to shuttle more nutrients into the muscle at a time when it is getting the most blood supply.
-
I always thought the 10 grams per iu was a bit much. Do you think it makes sense as Milos stated about using insulin just prior to training with enough dextrose and aminos, creatine sipped during training to shuttle more nutrients into the muscle at a time when it is getting the most blood supply.
;D
-
I am skeptical about everything, being biased is pointless. I don't care to flaunt my cock trying to be "right", I just wanna find out what is actually right, generally speaking.
edit: in fact i really don't ever want to touch insulin ever, lol. I tried it once at I think 30iu fast acting post workout while on 8iu hgh for two? weeks at most, and eh. The recovery and fullness was absolutely retarded but after reading a lot about it on here, I don't want to get a gigantic gut and fuck up my physique in other ways, and I simply don't have the time or will to base my eating so much around insulin and having to inject it so much.
If this was true you wouldn't be hammering your angle on this like you are somehow in the know, after a brief question to a phD and doing one pharmacology subject, you think you reinvented the wheel... Lol.
Rookie :D
-
I always thought the 10 grams per iu was a bit much. Do you think it makes sense as Milos stated about using insulin just prior to training with enough dextrose and aminos, creatine sipped during training to shuttle more nutrients into the muscle at a time when it is getting the most blood supply.
I mean I guess the basic premise makes sense but I cant claim to know how much specifically of a difference that one protocol would make over another. I doubt it would be noticeable given at that level, everyone’s on so much of everything under the sun anyway, but again that’s just personal conjecture with no basis.
-
You’re worse than fucking Matt.
;D ;D ;D
I'm starting to think the scientific method is worse than me. How the fuck can we have something like insulin that we apparently know so much about and yet not even understand its mechanism for growth? ???
I understand it hasn't been primarily researched in that area, but regardless - you'd think science would be more settled on this...