topology
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This is me spitballing, I haven't heard this discussed anywhere and I'm curious about other perspectives. The common myth is to actually TAKE more T4.
As we know, gigantism mostly occurs when a tumor forms on the pituitary gland, causing massive amounts of growth hormone to be released continuously. This skyrockets the baseline, making people dramatically taller among other things. A fair question is whether pulses would be superior to a constant baseline elevation. For normal people, yes, pulses are more efficient. But gigantism shows that if the baseline is high enough and sustained long enough, it overrides that advantage entirely. That distinction matters for what I'm about to argue.
From here on I'll refer to growth hormone as GH.
GH drives the production of new cartilage and bone material while thyroid hormone drives its conversion and maturation into actual bone. Think of GH as the person making sandwiches and thyroid hormone as the person selling them. The making is the harder and more limiting job, so allocating equal resources to both is inefficient. The bottleneck is on the production side.
Now, the chondrocyte "exhaustion timer" is commonly cited as the hard limit on height, roughly 40 replications before the cells wear out. I'd argue this is not the primary constraint. The bigger factor is simply time. Chondrocytes are mostly exhausted by how long they live and operate, not by hitting a replication ceiling. Gigantism actually demonstrates this. It forces growth to happen so rapidly that it functionally bypasses the exhaustion argument. If replication limit was the real ceiling, gigantism wouldn't work, nothing would.
So why doesn't more thyroid hormone make you taller? It should promote growth on the surface. The problem is you're deploying all your resources into selling when there isn't enough being made to keep up. Worse, research has only looked at extreme thyroid deficiency combined with GH administration in rodents. Nobody has studied the subtle range. Excess thyroid hormone accelerates growth plate ossification and closes the window faster, which is why it can actually make you shorter.
The key observation is this: a child injecting supraphysiological HGH doesn't get meaningfully taller. The growth plates are open, the GH is available, and the effect is smaller than it should be. That tells you the GH axis is not the rate-limiting step under normal physiological conditions. The only way GH overcomes this is at the extreme sustained levels seen in gigantism. Via elimination, the bottleneck sits at the chondrocyte level, and thyroid signaling is the primary driver of chondrocyte maturation and ossification rate.
Reducing thyroid signaling also reduces GH receptor sensitivity and IGF-1 production, so it can't be dropped significantly. The solution is modest suppression of thyroid activity -- whether through T4, T3, or both depending on the individual -- enough to slow ossification rate without meaningfully impairing the GH axis. The exact degree would vary by individual due to differences in thyroid sensitivity, and the window only matters while growth plates are still open. But The takeaway is that nobody actually reaches their true genetic height potential, and gigantism shows this. The ceiling isn't fixed, it's a timing problem. I don't think anyone has seriously explored this specific angle before, which is part of why I'm nervous I'm wrong or oversimplifying everything down to these three hormones. This also assumes estrogen is in check, since estrogen is its own major driver of growth plate closure and that variable needs to be controlled for any of this to hold.
Note that I simplified a lot and didn't go deep on many of the mechanisms, so there are likely gaps in how this is presented. If something seems off or underexplained, leave a comment. Any "Dnr" commentors will be promptly put on ignored.
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TLDR: Chondrocytes are time-limited, not replication-limited. Thyroid signaling is the primary driver of how fast that window closes -- for everyone, including gigantism cases where GH simply overwhelms the bottleneck rather than removes it. A modest reduction in thyroid activity slows ossification rate, preserves more of the growth window, and means most people never reach their true genetic height potential.
Inb4 BOTB.
@iblamexyz @Fridx @Scandicel @polonaecel @StyIix
As we know, gigantism mostly occurs when a tumor forms on the pituitary gland, causing massive amounts of growth hormone to be released continuously. This skyrockets the baseline, making people dramatically taller among other things. A fair question is whether pulses would be superior to a constant baseline elevation. For normal people, yes, pulses are more efficient. But gigantism shows that if the baseline is high enough and sustained long enough, it overrides that advantage entirely. That distinction matters for what I'm about to argue.
From here on I'll refer to growth hormone as GH.
GH drives the production of new cartilage and bone material while thyroid hormone drives its conversion and maturation into actual bone. Think of GH as the person making sandwiches and thyroid hormone as the person selling them. The making is the harder and more limiting job, so allocating equal resources to both is inefficient. The bottleneck is on the production side.
Now, the chondrocyte "exhaustion timer" is commonly cited as the hard limit on height, roughly 40 replications before the cells wear out. I'd argue this is not the primary constraint. The bigger factor is simply time. Chondrocytes are mostly exhausted by how long they live and operate, not by hitting a replication ceiling. Gigantism actually demonstrates this. It forces growth to happen so rapidly that it functionally bypasses the exhaustion argument. If replication limit was the real ceiling, gigantism wouldn't work, nothing would.
So why doesn't more thyroid hormone make you taller? It should promote growth on the surface. The problem is you're deploying all your resources into selling when there isn't enough being made to keep up. Worse, research has only looked at extreme thyroid deficiency combined with GH administration in rodents. Nobody has studied the subtle range. Excess thyroid hormone accelerates growth plate ossification and closes the window faster, which is why it can actually make you shorter.
The key observation is this: a child injecting supraphysiological HGH doesn't get meaningfully taller. The growth plates are open, the GH is available, and the effect is smaller than it should be. That tells you the GH axis is not the rate-limiting step under normal physiological conditions. The only way GH overcomes this is at the extreme sustained levels seen in gigantism. Via elimination, the bottleneck sits at the chondrocyte level, and thyroid signaling is the primary driver of chondrocyte maturation and ossification rate.
Reducing thyroid signaling also reduces GH receptor sensitivity and IGF-1 production, so it can't be dropped significantly. The solution is modest suppression of thyroid activity -- whether through T4, T3, or both depending on the individual -- enough to slow ossification rate without meaningfully impairing the GH axis. The exact degree would vary by individual due to differences in thyroid sensitivity, and the window only matters while growth plates are still open. But The takeaway is that nobody actually reaches their true genetic height potential, and gigantism shows this. The ceiling isn't fixed, it's a timing problem. I don't think anyone has seriously explored this specific angle before, which is part of why I'm nervous I'm wrong or oversimplifying everything down to these three hormones. This also assumes estrogen is in check, since estrogen is its own major driver of growth plate closure and that variable needs to be controlled for any of this to hold.
Note that I simplified a lot and didn't go deep on many of the mechanisms, so there are likely gaps in how this is presented. If something seems off or underexplained, leave a comment. Any "Dnr" commentors will be promptly put on ignored.
--------------
TLDR: Chondrocytes are time-limited, not replication-limited. Thyroid signaling is the primary driver of how fast that window closes -- for everyone, including gigantism cases where GH simply overwhelms the bottleneck rather than removes it. A modest reduction in thyroid activity slows ossification rate, preserves more of the growth window, and means most people never reach their true genetic height potential.
Inb4 BOTB.
@iblamexyz @Fridx @Scandicel @polonaecel @StyIix




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