Long term elevated GH→ igf-1 (intestinal epithelium contains igf-1 receptors)/associated insulin resistance development of metabolic syndrome may factor in (deposition of excess visceral adipose tissue).
It seems unlikely Mr Rogan/other professional bodybuilders would have diabetic neuropathy thus resulting in limb atrophy (i.e diabetic amyotrophy). For the majority of those afflicted, diabetic neuropathy is an extremely painful condition. In (2012?) the FDA approved taptendatol (synthetic opiate with dual action as u-opiate receptor agonist and norepinephrine reuputake inhibitor) to treat diabetic neuropathy… That’s how painful this condition is. Granted there are other alternatives and it’s unlikely opiates would be given as first line treatment given how prone they are to inducing dependence/addiction.
I’ve taken tapentadol (with a prescription) I can attest this medication is strong shit. If they’re giving someone tapentadol chances are they’re in quite a lot of pain.
Furthermore, exercising with diabetic neuropathy, particuarly intensive resistance training wouldn’t be an easy task. Particuarly when given muscles are numb/useless or unable to contract.
I don’t think we are going to get a whole lot of literature regarding ‘palumboism’. It isn’t a particuarly common medical ailment.
I’m no expert/doctor, only take my word with a grain of salt. God knows all the detrimental effects these concoctions of drugs have on the human body. These guys are using AAS, growth hormone (sometimes even synthetic igf-1), beta 2 agonists, thyroid hormones, occasionally stimulants, DNP… I’m sure I’m missing out on a few… Synthol? Insulin… One guy on here talked about a strongman competitor injecting pure epinephrine #edgy
@unreal24278 is correct on this score. Whereas GH abuse may well cause the habitus changes colloquially referred to as palumboism, the proposed mechanism of:
severe diabetic neuropathy–>
limb atrophy + abdominal distension 2ndry to gut dysmotility,
is simply incorrect.
Further, in the pics provided, Rogan’s face doesn’t manifest the coarsening of features that are the hallmark of acromegaly. It’s true that his appearance is different now that it was many years ago–but that’s true for all of us, for reasons that have nothing to do with supraphysiologic GH levels.
tl;dr Diabetic neuropathy does not cause palumboism, and Joe Rogan doesn’t have acromegaly.
There’s something to be said about the sheer volume of food one must intake to be 300lbs and single digit bodyfat such that it’s going to distend the gut, especially when done so on such a regular and consistent basis. The demands being placed on the body now are much more significant than they were in the 70s.
Yes however bloating induced via excess caloric intake should theoretically be reversible. Perhaps consistent excessive caloric intake could chronically increase intra abdominal pressure to the point wherein the “ab split” (diastasis recti) develops.
I’m shooting entirely unfounded/unresearched theories here. It’s unlikely this would be the case.
Certainly. Bodybuilding (say since the synthesis of dianabol ) hasn’t been the healthiest sport by a longshot at the top levels, but now it’s almost akin to a “death cult”. I guess one could say the same for most sport nowdays.
It’s unfortunate, our current approach of either “turning a blind eye” or harshly penalising those who happen to get caught doesn’t appear to be mitigating/minimising harm incurred either
It’s certainly reminiscent of pregnancy-induced diastasis, I’ll grant you that.
Speaking of pregnancy…The cause of palumboism-tummy might be something as simple as @T3hPwnisher’s ‘food baby’ hypothesis. But I have no special insight into the pathophysiology of this, so am reduced to hand-waving like everyone else here.
As an aside, it’s not obvious (to me) how a food baby could induce the limb changes that seem to accompany the abdominal-wall changes.
I mean… this is easily the dumbest, nonsensical theory I’ve ever put out on here but
Anabolic steroid use upregulates AR within skeletal muscle + induces the synthesis of new androgen receptors. Perhaps at a certain absurd dosage “super saturation” may occur, following prolonged use downregulation of existing androgen receptors will occur. At this point ever escalating dosages cease to exert a hypertrophic response, and perhaps the opposite could occur as androgen receptors would be “burnt out” (really getting in on the broscience BS here)
If one looks at the pathophysiology behind partial androgen insensitivity syndrome and/or lower motor neurone disease + PAIS combo (Kennedy’s disease) androgens either elicit a subpar (at physiologic dosages) or even theoretically a directly toxic effect towards skeletal muscle… if I recall androgens aren’t very effective at mitigating atrophy induced via lower motor neurone disease. Difficult to make a muscle bigger/stronger if there’s no viable motor units left/muscle can’t contract at all. But with Kennedy’s disease there’s something about genetic transcription being altered in a way not typical in response to anabolic steroid use, the hypothesised result = androgens inducing a dose dependent increase in the rate of muscular atrophy. This has been trialled within animal models (yea, metabolic pathways differ yadayadayada) and there’s one case report regarding testosterone administration resulting in reversible deterioration (human male with Kennedy’s disease).
Perhaps at a certain point genetic transcription mediated from anabolic steroid use deviates from the medically known/accepted “anabolic” response.
Super dumb theory, I mean these guys with palumbolism are still jacked. However proportions (i.e hip/shoulder ratio) etc are unaesthetic.
Perhaps there’s a toxic effect elicited towards skeletal muscle when certain concoctions of drugs are used. We know GH abuse, prolonged AAS abuse etc can have devastating effects regarding cardiovascular health.
Those afflicted with palumboism look as if they’ve had mass surgically removed from their limbs and said mass has been redistributed around the waist/stomach.
On an interesting note, not all competitors develop the diastasis/distended stomach look. Perhaps an element of genetic predisposition is at play.
Another theory, perhaps they’re extra terrestrial beings masquerading as humans (like invasion of the body snatchers). However they haven’t managed to conjure up a fully formed human frame, thus proportions remain slightly off.
Invasion of the bodybuilder snatchers
I’m running with this theory, there is no concrete data besides simple logic proving this to not be the case.
Have we considered simple nerve/muscle damage as the result of years spent lifting weights and accumulating injuries? In the similar way that Bas Rutten’s arms have severely atrophied as a result of nerve damage in his neck.
Atrophy would probably be asymmetrical (i.e localised atrophy in the region of injury).
As an example, I have nerve damage around my left ankle/calf, as a result I can’t contract my left calf properly/dorsiflex my left ankle adequately. My left calf is significantly smaller than my right and activities such as running result in significant pain/discomfort, there is nothing I can do about this.
It isn’t as if nerve damage in my left ankle has resulted in symmetric atrophy of both calves
At times an injury within a specific region can result in symmetric wasting (spinal trauma comes to mind), however it seems unlikely for injuries/nerve damage to result in symmetric wasting of the quadriceps, hamstrings, glutes, biceps, triceps, forearms, lats and upper back.
It’d be extremely, extremely rare for this to be the case, why is it that we see this exact pattern so frequently within bodybuilders