russian grey
𝐋𝐃𝐀𝐑 𝐢𝐬 𝐚 𝐜𝐡𝐨𝐢𝐜𝐞
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During puberty, a caloric deficit isn't just "cutting" — it literally switches off the growth signal. The key mediator here is leptin, not just GH and IGF-1.
How Leptin works with bone
Leptin acts directly on the growth plates, not through intermediaries like GH. There are leptin receptors in the cartilage tissue of endochondral ossification zones — and when leptin binds to them, it triggers chondrocyte proliferation. This was proven back in 2002: at a concentration of 0.5–1.0 µg/mL, leptin expanded the growth plate by up to +64%.
Furthermore, leptin doesn't just "permit" growth; it amplifies the IGF-1 signal. It upregulates IGF-I receptor expression on chondrocytes, meaning it makes them more sensitive to the very hormone everyone obsesses over. And most importantly, in mouse experiments, leptin restored bone length even when IGF-1 was suppressed. It acts as an independent growth factor, separate from the GH/IGF-1 axis.
How was this proven? In an experiment, mice were put on 60% of their normal caloric intake (a 40% deficit) — their growth slowed down. Then they were injected with leptin. The result: bone length fully recovered, even though blood IGF-1 remained suppressed (70% below normal).
Leptin is not just a satiety hormone that happens to affect bones. It's a fully-fledged skeletal growth factor, working through its own receptor system on the chondrocytes of the growth plates.
Dose-dependency: The inverted U-shape effect
It's not "the more, the better." Leptin has an inverted U-shaped curve:
· At a concentration of 0.5–1.0 µg/mL: stimulation of chondrocyte proliferation (up to +64%).
· Above 1.0 µg/mL: the effect is inhibited. This means that obesity with chronically high leptin also stunts growth — not because there's too little leptin, but because the receptors for it become desensitized.
You need a normal level, not a maximum.
Why a caloric deficit kills your growth
The chain is simple:
Caloric deficit ---> drop in leptin.
Low leptin ---> "starvation" signal to the hypothalamus.
HPG axis is suppressed ---> less GnRH ---> less testosterone.
The liver responds worse to GH ---> IGF-1 drops.
Growth plates receive fewer proliferation signals.
And the key point: Leptin stimulates growth independently of IGF-1. So even if GH and IGF-1 are normal, but leptin has dropped — the growth signal weakens.
What does this mean in practice?
Leptin stimulates chondrocytes in the growth plates — that's proven. It upregulates IGF-1 receptor expression — also proven. A caloric deficit kills leptin — proven. And in mice, leptin restored growth even during starvation — proven too.
But this doesn't mean you should inject yourself with leptin. The regulation is complex, the dose-dependency is inverted, and if you overdo it just a bit, the receptors shut down: growth doesn't accelerate, it gets suppressed.
What actually works is eating enough. Leptin rises from food, especially with a normal amount of calories.
CONCLUSION
Leptin is one of the few hormones that works directly on the growth plates. And it's basically free, since leptin rises from food, especially when you're eating enough calories.
If you're in a caloric deficit during puberty, you're shutting down your growth plates by crashing your leptin. It's not because "there are too few calories", it's because the "satiated" signal disappears, and the brain chooses to "survive" rather than grow.
Eat. Sleep. Don't starve.
@Nkq. @bozenka @trav @grind
@aspiringpslgodess
How Leptin works with bone
Leptin acts directly on the growth plates, not through intermediaries like GH. There are leptin receptors in the cartilage tissue of endochondral ossification zones — and when leptin binds to them, it triggers chondrocyte proliferation. This was proven back in 2002: at a concentration of 0.5–1.0 µg/mL, leptin expanded the growth plate by up to +64%.
Furthermore, leptin doesn't just "permit" growth; it amplifies the IGF-1 signal. It upregulates IGF-I receptor expression on chondrocytes, meaning it makes them more sensitive to the very hormone everyone obsesses over. And most importantly, in mouse experiments, leptin restored bone length even when IGF-1 was suppressed. It acts as an independent growth factor, separate from the GH/IGF-1 axis.
How was this proven? In an experiment, mice were put on 60% of their normal caloric intake (a 40% deficit) — their growth slowed down. Then they were injected with leptin. The result: bone length fully recovered, even though blood IGF-1 remained suppressed (70% below normal).
Leptin is not just a satiety hormone that happens to affect bones. It's a fully-fledged skeletal growth factor, working through its own receptor system on the chondrocytes of the growth plates.
Dose-dependency: The inverted U-shape effect
It's not "the more, the better." Leptin has an inverted U-shaped curve:
· At a concentration of 0.5–1.0 µg/mL: stimulation of chondrocyte proliferation (up to +64%).
· Above 1.0 µg/mL: the effect is inhibited. This means that obesity with chronically high leptin also stunts growth — not because there's too little leptin, but because the receptors for it become desensitized.
You need a normal level, not a maximum.
Why a caloric deficit kills your growth
The chain is simple:
Caloric deficit ---> drop in leptin.
Low leptin ---> "starvation" signal to the hypothalamus.
HPG axis is suppressed ---> less GnRH ---> less testosterone.
The liver responds worse to GH ---> IGF-1 drops.
Growth plates receive fewer proliferation signals.
And the key point: Leptin stimulates growth independently of IGF-1. So even if GH and IGF-1 are normal, but leptin has dropped — the growth signal weakens.
What does this mean in practice?
Leptin stimulates chondrocytes in the growth plates — that's proven. It upregulates IGF-1 receptor expression — also proven. A caloric deficit kills leptin — proven. And in mice, leptin restored growth even during starvation — proven too.
But this doesn't mean you should inject yourself with leptin. The regulation is complex, the dose-dependency is inverted, and if you overdo it just a bit, the receptors shut down: growth doesn't accelerate, it gets suppressed.
What actually works is eating enough. Leptin rises from food, especially with a normal amount of calories.
CONCLUSION
Leptin is one of the few hormones that works directly on the growth plates. And it's basically free, since leptin rises from food, especially when you're eating enough calories.
Don't confuse "eating enough" with "eating goyslop". Leptin rises from calories, but if it's fast food and sugar, you'll just get fat instead of growing. You need real food for growth, not garbage.
Eat. Sleep. Don't starve.
@Nkq. @bozenka @trav @grind
@aspiringpslgodess
Nutritionally-Induced Catch-Up Growth - PMC
Malnutrition is considered a leading cause of growth attenuation in children. When food is replenished, spontaneous catch-up (CU) growth usually occurs, bringing the child back to its original growth trajectory. However, in some cases, the CU growth ...
www.ncbi.nlm.nih.gov
