Taking hgh while on keto

[David44]

Can you take hgh while being keto?
Without health issues?

 

[InjuredGorilla]

Look at Tristan Lee, the kid is a walking HGH Kit, if anything, Keto will help you avoid insulin resistance.

 

[Type-IIx]

Keto + rhGH will make GH insulin resistance effects more profound due to increased circulating fatty acids. Beneficial for fat loss, not so great for your health nor performance/gains.

 

[jJjburton]

Keto + rhGH will make GH insulin resistance effects more profound due to increased circulating fatty acids. Beneficial for fat loss, not so great for your health nor performance/gains.

So in this case pinning hgh as many times a day is more optimal for fat loss then a bolus dose?

 

[Pineapples4Puss]

So in this case pinning hgh as many times a day is more optimal for fat loss then a bolus dose?

To my understanding There is a refractory period in the cells which lipolysis occurs. So pinning more often doesn’t do anything if rest period is not over. It will just go to waste.

That is my view on it.

 

[Type-IIx]

So in this case pinning hgh as many times a day is more optimal for fat loss then a bolus dose?

Er no

 

[jJjburton]

Keto + rhGH will make GH insulin resistance effects more profound due to increased circulating fatty acids. Beneficial for fat loss, not so great for your health nor performance/gains.

Being this is what you said, wouldnt you want maximum amount of hgh in your system?

 

[Jin23]

So in this case pinning hgh as many times a day is more optimal for fat loss then a bolus dose?

You don't want carbs and you also don't want fats in your serum while GH is elevated. So meal timing is just as important while on keto or not keto.

Or were you also talking about just being in ketosis, being a problem for GH @Type-IIx ? So talking about a fasted state, obviously, but being in ketosis ...

Insulin resistance/elevated insulin could also be a problem on keto while doing GH, as you get more LDL B particles. But I have no idea what happens to insulin levels while on keto and doing GH ... Insulin probably stays at basal levels huh?

 

[jJjburton]

You don't want carbs and you also don't want fats in your serum while GH is elevated. So meal timing is just as important while on keto or not keto.

Or were you also talking about just being in ketosis, being a problem for GH @Type-IIx ? So talking about a fasted state, obviously, but being in ketosis ...

Insulin resistance/elevated insulin could also be a problem on keto while doing GH, as you get more LDL B particles. But I have no idea what happens to insulin levels while on keto and doing GH ... Insulin probably stays at basal levels huh?

Ahh ok got it. Thanks i misunderstood the fat loss aspect of hgh thats fasted vs ketosis.

Edit- for some reason i thought fasted and being in ketosis was same, but its not at all

 

[Type-IIx]

You don't want carbs and you also don't want fats in your serum while GH is elevated. So meal timing is just as important while on keto or not keto.

Or were you also talking about just being in ketosis, being a problem for GH @Type-IIx ? So talking about a fasted state, obviously, but being in ketosis ...

Insulin resistance/elevated insulin could also be a problem on keto while doing GH, as you get more LDL B particles. But I have no idea what happens to insulin levels while on keto and doing GH ... Insulin probably stays at basal levels huh?

Nope, supraphysiologic GH actually leads to increased insulin secretion. It's just not sufficient to make up for the net hyperglycemic effect.

High serum insulin combined with high serum FFAs potently suppresses hormone sensitive lipase: the rate-limiting step in hydrolysis of triglyceride (mobilization of adipose tissue stores).

On keto diets, though I doubt there's data on subjects that are keto + using rhGH clinically (not to mind supraphysiologically), it would follow that GH would increase insulin levels (likely defeating a primary aim of keto, to reduce insulin levels) & in combination with high serum FFAs (promoting insulin resistance) serve to eviscerate the purpose of keto dietary regimens. The primary purpose being to preferentially use FAs as energy substrates to reduce insulin-mediated fat storage. Though ketone bodies confer a protein sparing effect, drugs do this far better (and strength and hypertrophy - for the maintenance of muscle mass - proceed far more readily with carbohydrates in the diet).

Being in ketosis per se is healthy/fine, but the increased lipid intakes that are necessary to support ketosis cause increased FFAs in serum and aggravate rhGH-induced insulin resistance (and worsen its effects on fat loss).

Keto + rhGH would seem irrational to me.

A topic for another day is the community (bodybuilding) confusion of insulin resistance with hyperglycemia.

While insulin resistance is associated with hyperglycemia (and insulin resistance in skeletal muscle leads to hyperglycemia), exogenous insulin as (ab)used worsens (increases) systemic insulin resistance (even though it reduces blood glucose). This is because systemic insulin resistance is described as a function of blood levels of both glucose and insulin. HOMA-IR is defined as fasting serum insulin (μU/ml) * fasting plasma glucose (mmol/liter) / 22.5 & QUICKI as 1 / (log(fasting insulin μU/mL) + log(fasting glucose mg/dL)).

 

[Type-IIx]

Being in ketosis per se is healthy/fine, but the increased lipid intakes that are necessary to support ketosis cause increased FFAs in serum and aggravate rhGH-induced insulin resistance (and worsen its effects on fat loss).

This is wrong, sorry: increased FFAs in serum accelerate fat loss (due to increasing adipose tissue insulin resistance) but also reduce skeletal muscle insulin sensitivity: so energy balance controls - i.e., keto + rhGH gives accelerated fat loss in an energy deficit, at great expense for skeletal muscle (expect muscle loss) & in an energy surplus, is irrational.

The real question is the net effect of rhGH-induced increases to insulin levels in the presence of high serum FFAs: while insulin down-regulated HSL activity, it acts in opposition to GH in other ways.

I really want @PeterBond to attack this post above, because this is a simplified view of the system and there are a lot of moving parts (e.g., cAMP activity) and, while GH does increase insulin secretion, my instinct says that energy balance controls and that the increase to insulin levels is not controlling.

The way that I view it:
keto + rhGH (in a state of energy deficit) = accelerated fat loss vs. isocaloric non-keto (i.e., balanced) diet + rhGH
- slight favor to keto for fat loss because increased dietary fats increase serum FFAs, furthering insulin resistance in adipose tissue

keto + rhGH (in a state of energy surplus) = decreased skeletal muscle accretion vs. isocaloric non-keto (i.e., balanced) diet + rhGH
- due to increased skeletal muscle insulin resistance

IMO, keto (+ rhGH) is irrational due to:
- relative loss of skeletal muscle (due to decreased Akt/mTOR, strength loss due to insufficient energy availability, etc.) due to low carbohydrate
- superiority to body composition parameters with iscaloric non-keto diets + drugs (since we're already willing to use drugs)

Peter, could you disentangle this matter if you have time?

 

[Jin23]

Nope, supraphysiologic GH actually leads to increased insulin secretion. It's just not sufficient to make up for the net hyperglycemic effect.

High serum insulin combined with high serum FFAs potently suppresses hormone sensitive lipase: the rate-limiting step in hydrolysis of triglyceride (mobilization of adipose tissue stores).

On keto diets, though I doubt there's data on subjects that are keto + using rhGH clinically (not to mind supraphysiologically), it would follow that GH would increase insulin levels (likely defeating a primary aim of keto, to reduce insulin levels) & in combination with high serum FFAs (promoting insulin resistance) serve to eviscerate the purpose of keto dietary regimens. The primary purpose being to preferentially use FAs as energy substrates to reduce insulin-mediated fat storage. Though ketone bodies confer a protein sparing effect, drugs do this far better (and strength and hypertrophy - for the maintenance of muscle mass - proceed far more readily with carbohydrates in the diet).

Being in ketosis per se is healthy/fine, but the increased lipid intakes that are necessary to support ketosis cause increased FFAs in serum and aggravate rhGH-induced insulin resistance (and worsen its effects on fat loss).

Keto + rhGH would seem irrational to me.

A topic for another day is the community (bodybuilding) confusion of insulin resistance with hyperglycemia.

While insulin resistance is associated with hyperglycemia (and insulin resistance in skeletal muscle leads to hyperglycemia), exogenous insulin as (ab)used worsens (increases) systemic insulin resistance (even though it reduces blood glucose). This is because systemic insulin resistance is described as a function of blood levels of both glucose and insulin. HOMA-IR is defined as fasting serum insulin (μU/ml) * fasting plasma glucose (mmol/liter) / 22.5 & QUICKI as 1 / (log(fasting insulin μU/mL) + log(fasting glucose mg/dL)).

If gh does raise insulin beyond basal levels, on a ketogenic diet, then yes, that does indeed negate a lot of ketogenic diet's positive outcomes. If on topic of lipids, insulin increases inflammation in insulin resistant patients, and it increases oxidative stress which leads to more fat oxidization, which does lead to further inflammation, foam cells forming and then atherosclerotic plaque. Although linoleic acid seems to be the culprit here and not just cholesterol.

Yeah, there is a lot of emphasis on hyperglycemia but none on insulin resistance. A normal BG level is still achieved in the early stages of insulin resistance, it's just achieved through a higher insulin response ... it's a shame primary doctor care is fixated on fasting BG and not on fasting insulin. When your fasting BG is high it's already late ... But all of this is kinda a moot point I guess as nobody here really cares, seeing as they put their self in an insulin resistant state for months if not a year, years on end with using high amounts of exogenous gh. Especially in recent years, as there has been a shift in research, in regards of early cognitive decline and then dementia, AD, etc. towards brain glucose metabolism, ie. brain insulin resistance being a huge causal factor for these pathologies ...

 

[Type-IIx]

If gh does raise insulin beyond basal levels, on a ketogenic diet, then yes, that does indeed negate a lot of ketogenic diet's positive outcomes. If on topic of lipids, insulin increases inflammation in insulin resistant patients, and it increases oxidative stress which leads to more fat oxidization, which does lead to further inflammation, foam cells forming and then atherosclerotic plaque. Although linoleic acid seems to be the culprit here and not just cholesterol.

Yeah, there is a lot of emphasis on hyperglycemia but none on insulin resistance. A normal BG level is still achieved in the early stages of insulin resistance, it's just achieved through a higher insulin response ... it's a shame primary doctor care is fixated on fasting BG and not on fasting insulin. When your fasting BG is high it's already late ... But all of this is kinda a moot point I guess as nobody here really cares, seeing as they put their self in an insulin resistant state for months if not a year, years on end with using high amounts of exogenous gh. Especially in recent years, as there has been a shift in research, in regards of early cognitive decline and then dementia, AD, etc. towards brain glucose metabolism, ie. brain insulin resistance being a huge causal factor for these pathologies ...

Is there research data that demonstrates a nexus between rhGH use & cognitive decline and/or dementia?

I have seen data that shows the opposite exclusively. For example: the work of Grönbladh and colleagues shows that rhGH can reverse AAS-induced cognitive harms (e.g., visuo-spatial deficits); of course GH treatment in GHD patients improves psychological well-being, including energy, motivation, emotion, memory, and cognition; GH stimulates neurogenesis, positively influences learning and memory centers, protects the CNS, etc; and IGF-I similarly promotes cognitive function (e.g., acts as a neurotrophic factor, promotes neuron survival and growth, stimulates postnatal brain growth, etc.)

 

[Highly ecto]

This is wrong, sorry: increased FFAs in serum accelerate fat loss (due to increasing adipose tissue insulin resistance) but also reduce skeletal muscle insulin sensitivity: so energy balance controls - i.e., keto + rhGH gives accelerated fat loss in an energy deficit, at great expense for skeletal muscle (expect muscle loss) & in an energy surplus, is irrational.

The real question is the net effect of rhGH-induced increases to insulin levels in the presence of high serum FFAs: while insulin down-regulated HSL activity, it acts in opposition to GH in other ways.

I really want @PeterBond to attack this post above, because this is a simplified view of the system and there are a lot of moving parts (e.g., cAMP activity) and, while GH does increase insulin secretion, my instinct says that energy balance controls and that the increase to insulin levels is not controlling.

The way that I view it:
keto + rhGH (in a state of energy deficit) = accelerated fat loss vs. isocaloric non-keto (i.e., balanced) diet + rhGH
- slight favor to keto for fat loss because increased dietary fats increase serum FFAs, furthering insulin resistance in adipose tissue

keto + rhGH (in a state of energy surplus) = decreased skeletal muscle accretion vs. isocaloric non-keto (i.e., balanced) diet + rhGH
- due to increased skeletal muscle insulin resistance

IMO, keto (+ rhGH) is irrational due to:
- relative loss of skeletal muscle (due to decreased Akt/mTOR, strength loss due to insufficient energy availability, etc.) due to low carbohydrate
- superiority to body composition parameters with iscaloric non-keto diets + drugs (since we're already willing to use drugs)

Peter, could you disentangle this matter if you have time?

Hey Type-llx, l have a chronic shoulder problem that has not responded well to multiple cortisone injections and 9 months of constant physio. l have started trying BPC-157 and TB-500 on it and wanted to add GH to the protocol. l have been eating carnivore for over 6 years and do really well on it. l know from a bodybuilding point of view carnivore with GH is pointless. Would you think GH would still be of any benefit from solely a healing point of view while eating like l do.

 

[Type-IIx]

Hey Type-llx, l have a chronic shoulder problem that has not responded well to multiple cortisone injections and 9 months of constant physio. l have started trying BPC-157 and TB-500 on it and wanted to add GH to the protocol. l have been eating carnivore for over 6 years and do really well on it. l know from a bodybuilding point of view carnivore with GH is pointless. Would you think GH would still be of any benefit from solely a healing point of view while eating like l do.

First, you're asking for advice on self-treatment of a medical condition. For that, I posit to you that your medical practitioners would be very happy to use these hormones if they actually demonstrably worked (and were relatively safe). The fact that your doctors/physiotherapists/etc. are not giving you a peptide treatment option sort of indicates these are not regarded as having therapeutic value.

Theoretically, any effect of rhGH depends on the site of injury, the specific tissue. Chronic shoulder pain could be rooted in the joint, bone, bursa, tendon sheaths, etc. While rhGH may be effective for musculotendionous healing (i.e., minor muscle tears; or in certain tendinopathies), it is ineffective for acute healing or for use postoperatively; and may worsen prognosis. Think scar tissue accrual.

You would not want to attempt any specialized injection procedure yourself into the soft tissue (or joint!) as it is just too risky. Further, with rhGH what you are likely to see is deposition of collagen or necrotic tissue accrual. While collagen deposition by rhGH could be potentially beneficial with injection directly into the tendon, you - as mentioned - don't want to attempt to perform this technique yourself.

I'd steer far clear of the rhGH; consider surgery if indicated; and mention my intentions to try BPC-157 (and I suppose TB-500, whatever that one does I'm clueless) to my doctors.

You mentioned a tendency to overdo your training despite pain that led to your condition. Now I note a tendency to overdo your recovery with drugs that could lead to its becoming even worse.

 

[Highly ecto]

First, you're asking for advice on self-treatment of a medical condition. For that, I posit to you that your medical practitioners would be very happy to use these hormones if they actually demonstrably worked (and were relatively safe). The fact that your doctors/physiotherapists/etc. are not giving you a peptide treatment option sort of indicates these are not regarded as having therapeutic value.

Theoretically, any effect of rhGH depends on the site of injury, the specific tissue. Chronic shoulder pain could be rooted in the joint, bone, bursa, tendon sheaths, etc. While rhGH may be effective for musculotendionous healing (i.e., minor muscle tears; or in certain tendinopathies), it is ineffective for acute healing or for use postoperatively; and may worsen prognosis. Think scar tissue accrual.

You would not want to attempt any specialized injection procedure yourself into the soft tissue (or joint!) as it is just too risky. Further, with rhGH what you are likely to see is deposition of collagen or necrotic tissue accrual. While collagen deposition by rhGH could be potentially beneficial with injection directly into the tendon, you - as mentioned - don't want to attempt to perform this technique yourself.

I'd steer far clear of the rhGH; consider surgery if indicated; and mention my intentions to try BPC-157 (and I suppose TB-500, whatever that one does I'm clueless) to my doctors.

You mentioned a tendency to overdo your training despite pain that led to your condition. Now I note a tendency to overdo your recovery with drugs that could lead to its becoming even worse.

Thank you for your response. Yes you are right l am being impatient because of the 9 months of doing exactly what l have been told by doctor and physio for very little improvement. My doctor and physio have never even heard of BPC-157 when l mentioned it to them. l might also have given you the wrong impression of my intensions and plans of use of GH. All l have been doing is putting 0.5mg of BPC and 0.5mg TB under the skin once a day as close to the injury site as possible. As a 54 year old my intension with the GH was to use just 2iu a day sub q for 6 or so months to try and give me more youthful levels in the hope of helping the healing process along a little bit. l did test my GH levels a few months ago and they were only 0.2 (range <5.0), my lGF levels were below mid range as well. l never had intensions of jabbing needles into my shoulder joint. it was more about using a replacement type dose.

 

[Type-IIx]

Thank you for your response. Yes you are right l am being impatient because of the 9 months of doing exactly what l have been told by doctor and physio for very little improvement. My doctor and physio have never even heard of BPC-157 when l mentioned it to them. l might also have given you the wrong impression of my intensions and plans of use of GH. All l have been doing is putting 0.5mg of BPC and 0.5mg TB under the skin once a day as close to the injury site as possible. As a 54 year old my intension with the GH was to use just 2iu a day sub q for 6 or so months to try and give me more youthful levels in the hope of helping the healing process along a little bit. l did test my GH levels a few months ago and they were only 0.2 (range <5.0), my lGF levels were below mid range as well. l never had intensions of jabbing needles into my shoulder joint. it was more about using a replacement type dose.

Systemic replacement GH increases markers of collagen metabolism suggesting net deposition of certain types of collagen (e.g., in bone, tendon) but I wouldn't view this as anything more than a waste of money for injury rehabilitation or prevention.

I truly am sorry to hear that so far treatment has been unsuccessful. I wouldn't give up on modern medicine for the use of some grey market peptides, as these almost certainly offer little in the way of real treatment. I acknowledge the anecdotes from people experiencing pain reduction in soft tissue injuries that are best described as minor discomforts that they had for years.

Those anecdotes seem quite apart from your severe pain and still acute injury, real physical limitations, and perhaps even limb immobilization/atrophy. Just be careful not to fall for any false hope/quick fix as there are a lot of hucksters out there preying on this.

 

[Type-IIx]

I'll just sum up my thoughts on this matter:

Keto (without drugs; for naturals): good for longevity and for fat loss (especially dieting down to low body fat levels) but incompatible with optimal/maximal muscular strength and muscle mass gains due to insufficient glycolytic pathway energy substrates to sustain high intensity muscular contractions; and due to reduced Akt/mTOR activity (controls muscle protein synthesis, translation); ketone bodies additionally serve to confer a protein sparing effect to claw back some retention of muscle loss: well-designed cyclical regimens best support all of these aims.

Keto (with rhGH): accelerates fat loss in energy deficit (due to increased insulin resistance in adipocytes). In fact, GH increases hormone-sensitive lipase (HSL) activity; direct oxidation of FFAs; and suppresses the lipoprotein lipase (LPL) in adipose tissue. But, the increase in blood levels of FFAs (attendant to increased dietary fat intakes) decreases adipose tissue HSL activity, thus reducing hydrolysis of "trapped" triglyceride, despite the insulin resistant effects on the adipocyte (preventing storage of new triglyceride therein)... expect circulating FFAs to be very high. Now, GH likely prevents muscle catabolism by its anticatabolic effects (i.e., net retention of LBM and protein stores during fasting; N, Ca, K retention, though largely in the extracellular matrix).
- But increases to muscular size and strength in an energy surplus (keto) will be relatively slowed relative to an isocaloric balanced or high carbohydrate diet due mostly to lack of glycolytic substrates (again, necessary to support intense resistance training). RhGH use will promote some muscle anabolism by IGF-I-mediated Akt/mTOR activity (again sort of "clawing back" some anabolic potency despite somewhat reduced insulin levels vs. higher carbohydrate intakes).

You could certainly make the argument without looking foolish whatsoever that keto is rational with rhGH for fat loss and even recomp (energy deficit, or at maintenance).

I do, however, believe many of the rationales underpinning keto are eviscerated, at least partly, by rhGH use: i.e., maintaining low insulin levels (increased by rhGH) to promote FA liberation by the utilization of MCTs and ketone bodies to support such; protein sparing by ketone bodies (considering the far more profound effects of rhGH/AAS to effect anticatabolism); and the very fact that rhGH serves lipolytic, recomp, and growth functions better than keto does on an isocaloric moderate-high carbohydrate diet (with improved muscular strength and size increases) renders keto+rhGH suboptimal.

Now, the use of some principles from cyclical keto dietary regimens (e.g., titrating carbohydrate intakes around training; maintaining insulin sensitivity with low carbohydrate/higher dietary fat intakes - without actually entering or maintaining a state of ketosis) apply almost universally to enhanced bodybuilders.

But rhGH+keto would seem quite different (and less logical) vs. keto for a natural bodybuilder.

None of this is to say that rhGH+keto does not support increased muscle size/strength, but rather that it is suboptimal versus a moderate/high carbohydrate intake diet with the use of rhGH.

 

[Jin23]

Is there research data that demonstrates a nexus between rhGH use & cognitive decline and/or dementia?

I have seen data that shows the opposite exclusively. For example: the work of Grönbladh and colleagues shows that rhGH can reverse AAS-induced cognitive harms (e.g., visuo-spatial deficits); of course GH treatment in GHD patients improves psychological well-being, including energy, motivation, emotion, memory, and cognition; GH stimulates neurogenesis, positively influences learning and memory centers, protects the CNS, etc; and IGF-I similarly promotes cognitive function (e.g., acts as a neurotrophic factor, promotes neuron survival and growth, stimulates postnatal brain growth, etc.)

For sure, both GH and IGF are potent neurotrophic and neuroprotective factors in the brain. RhGH was even shown, in mice that were injected with the Aβ-peptide, in order to simulate AD, to have broad effects in ameliorating a lot of AD's negative effects. And AD and Parkinson's patients both have lowered IGF levels, right? GH is suma sumarum also very anxiolytic, reducing inflammation, so I'd say it's use with aas is for sure of some help in reducing aas induced depressive state, hyperactive amygdala, etc. Imho, rhGH is a good idea as an addon to a aas cycle, purely for the reason of neuro health.

Now, the question is; do all the positive effects of GH when combined with the negatives of insulin resistance it causes, lead to a net positive outcome in regards to loss of dopaminergic neurons? Idk how up to date you are on insulin and dementia, AD, PD, .. but this is imo a great summation on the topic: The Relevance of Insulin Action in the Dopaminergic System

Be interested in hearing your thoughts on long term supraphysiological dosages of rhGH, for bodybuilding purposes, and it's potential negatives, specifically attributed to insulin resistance. I'd assume it's positives can't negate it's negatives in a longer run? Especially in a hypercaloric, carb heavy diet ...

For me personally, being an add person with GAD, I can't run normal aas dosages without a low dose ssri. But the ssri worsens my adhd so much, that I can't even read 3 sentences, without switching to 10 different thought processes while trying to focus on the task at hand. So, I stick to low, trt+ dosages. Also, aas really worsen my impulsivity and novelty seeking behavior. Which got me thinking, do aas upregulate D2 signaling? I know there's a bimodal relationship between dopamine and test, just not quite sure how that works up all together ...

Anyway, I wanted to add, that the aas using population is heavy in drug addictive personalities, ie. it's heavy with users who have problems in their reward systems and thus don't have the most stable brain chemistry as is. Statistics show, for instance, that adhd patients are much much more likely to end up abusing rec drugs which also means aas for that matter. So I always wanted to do more research and present a workflow on how to ameliorate aas detrimental effects on brain chemistry. But the vast majority of aas using population really aren't biohackers but are on much more self destructive path and idk if they really do care. But I bet that people would start caring if they were made clear, how disruptive aas really are for their personalities and brain health. Anyway, I'm rambling, long day ...

 

[Highly ecto]

Systemic replacement GH increases markers of collagen metabolism suggesting net deposition of certain types of collagen (e.g., in bone, tendon) but I wouldn't view this as anything more than a waste of money for injury rehabilitation or prevention.

I truly am sorry to hear that so far treatment has been unsuccessful. I wouldn't give up on modern medicine for the use of some grey market peptides, as these almost certainly offer little in the way of real treatment. I acknowledge the anecdotes from people experiencing pain reduction in soft tissue injuries that are best described as minor discomforts that they had for years.

Those anecdotes seem quite apart from your severe pain and still acute injury, real physical limitations, and perhaps even limb immobilization/atrophy. Just be careful not to fall for any false hope/quick fix as there are a lot of hucksters out there preying on this.

l was actually told by the doctor and physio that because of the damage to the rotator cuff, cartilage separation, inflammation in the bursa and frozen shoulder this was a serious injury and would not respond quickly to treatment if at all, and quite possibly need surgery to improve the situation. This was the key word the doctor used IMPROVE the situation. He told me it would be highly unlikely that even surgery would return my shoulder to 100% like before the injury. He also said me continuing to aggravate the injury with weight training and cricket for nearly 12 months has certainly made things worse than they needed to be.
Because of some of the stories you read of people using BPC, TB, HGH and even DECA having such good results with there long term injuries, l was taking the attitude, what have l got to lose. Hence why l started BPC-157/TB-500 treatment. That is why l was also considering safe doses of HGH and even considering 100-200mg a week of DECA. l know l am probably grasping at straws looking for improvement in the shoulder, but the surgery route was an expensive route with no guarantee anyway. Even though this is of no use to me now this situation has shown me that continuing to aggravate certain injuries can cause irreversible damage.
l also do get what your saying about the comparison of injuries in these anecdotes its not always comparing apples with apples.