#1

A lot of the conversation around testosterone today is missing something important.

We focus almost entirely on serum levels—how high or low they are, whether they fall within a “normal” range. But the function of testosterone isn’t just about how much of it is floating around in the bloodstream.

What really matters is how well it works at the cellular level.

Two key but often overlooked factors: testosterone receptor density and receptor binding affinity.

You can have “normal” testosterone levels, but if your receptors are sparse or inefficient, the effects will be anything but optimal. On the other hand, you can have lower-than-ideal levels, but if your receptors are abundant and highly responsive, function may still be strong.

One example: L-carnitine supplementation can play a major role in improving androgen receptor density (paper linked below).

For some people on testosterone replacement therapy (TRT) who aren’t seeing the expected benefits, L-carnitine can be a game-changer—helping testosterone work more effectively at the cellular level.

Even for people not on TRT, L-carnitine supplementation can sometimes produce similar functional benefits by enhancing receptor activity, even if testosterone levels remain unchanged.

This is why a cellular perspective is so critical.

Physicians need to learn to think like cell biologists.

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#2

The AR gene contains CAG repeats, which affect androgen sensitivity:

  • Shorter CAG repeats → Higher AR sensitivity (stronger androgenic effects at lower testosterone levels)
  • Longer CAG repeats → Lower AR sensitivity (requires more testosterone to achieve the same effects)

Combing DNA can give some answers.

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#3

Do you have the link to that paper? The problem with oral carnitine supplementation is that it increases TMAO in the gut, which may increase risk of ASCVD.

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