Low Testosterone: Do You Need TRT or Is There Something to Try First

Testosterone levels don't tell you very much on their own. They tell you that something is off, but not where the problem is, and the where is everything when it comes to deciding what to do next.

Your body makes testosterone through a chain. Your hypothalamus in your brain sends a signal to your pituitary gland, which then releases two hormones called LH and FSH, which stands for luteinizing hormone and follicle-stimulating hormone, and those hormones travel through your bloodstream to your testicles and tell them to produce testosterone. That's the whole pathway. Brain signals pituitary, pituitary signals testicles, testicles produce testosterone.

Now when testosterone is low, the breakdown is somewhere in that chain. And the only way to know where it is, is to look at LH and FSH alongside your testosterone in a morning blood draw.

Most guys never get that explained to them. They get a total testosterone number, maybe a free testosterone number, and then a recommendation. But without LH and FSH, you're missing the part that actually tells you what's going wrong.

Think of it this way. If a factory isn't producing anything, you need to know whether the workers aren't getting orders, or whether they're getting orders but physically can't do the job. Same problem on the surface. Completely different fixes.

Low testosterone with low or normal LH and FSH means the signal is the problem. Your pituitary isn't sending the command loudly enough, or at all, and your testicles are sitting there capable of working but not being told to. This is called secondary hypogonadism, meaning the failure is upstream, secondary to the testicles themselves. In most cases, the testicles are fine.

Low testosterone with high LH and FSH means the opposite. Your brain is already screaming the signal as loud as it can and the testicles simply aren't responding. That's called primary hypogonadism, and it means the failure is in the testicles themselves.

These two situations look the same on a basic testosterone panel. They require completely different treatment. That's why the LH and FSH numbers matter so much.

If you're in the secondary category, where your signal is low and your testicles are capable, there are options worth trying before committing to testosterone replacement therapy. One of them is something called clomiphene citrate, which is a medication that blocks estrogen receptors in the hypothalamus and pituitary, and that blockade tricks your brain into thinking estrogen is low, which causes it to ramp up LH and FSH, which then tells your testicles to produce more testosterone. You're not adding testosterone from the outside. You're turning up the volume on a signal your body already knows how to make.

A 2025 systematic review and meta-analysis covering ten randomized controlled trials and 819 patients found that clomiphene produced a mean testosterone increase of around 274 ng/dL. That's a meaningful shift in most men who start in the low range, and it's achieved without suppressing the body's own production the way exogenous testosterone does.

A related compound called enclomiphene, which is a purified version of the active component in clomiphene, showed a median testosterone increase of 166 ng/dL in a 2024 study of 66 men, and the difference from regular clomiphene worth knowing about is the side effect profile. In that study, clomiphene produced side effects in about 47 percent of men compared to 13.8 percent with enclomiphene, largely because regular clomiphene contains both an active and an inactive isomer, and the inactive one appears to be responsible for most of the estrogenic side effects including mood changes and visual disturbances.

Another option in the secondary category is something called HCG, or human chorionic gonadotropin, which is a hormone that mimics LH directly at the testicle. Rather than working upstream like clomiphene does, HCG delivers the signal straight to where it needs to go. Both approaches can be effective. Which one makes more sense depends on the specifics of the case.

The reason these options matter is that they preserve the body's natural production and they preserve fertility. When you add testosterone from the outside, your pituitary detects that the levels are adequate and shuts off its own LH and FSH signal, which tells the testicles to stop working, which stops sperm production. For men who want to have children or who want to preserve that option, this is worth taking seriously.

If you're in the primary category, where LH and FSH are already high and the testicles aren't responding, those upstream interventions aren't going to help. You can't turn up a signal that's already at maximum. TRT is the appropriate path here because the only way to get testosterone into that body is to bring it in from the outside.

For men on TRT who want to maintain fertility, a 2005 study found that adding HCG at 500 IU every other day was enough to maintain intratesticular testosterone at baseline levels even while exogenous testosterone was suppressing LH. Sperm production requires testosterone inside the testicle specifically, not just in the bloodstream, and HCG keeps that local environment intact.

Before any of this, the foundations have to be there. Sleep deprivation measurably suppresses testosterone. Excess body fat increases aromatase activity, which is an enzyme that converts testosterone into estrogen, pulling levels down further. Chronic stress elevates cortisol, which competes with testosterone at a hormonal level. No intervention, pharmaceutical or otherwise, is going to overcome a body that isn't sleeping, is carrying significant visceral fat, and is under chronic stress. The drug becomes a patch over conditions that are actively working against it.

But once those foundations are solid and levels are still low, this is the question that determines the path: where in the chain is the breakdown? Because TRT is the right answer for some men and it's the wrong first step for others, and the only thing that separates those two groups is a lab result that most of them have never had explained to them.

The difference between replacing something your body can still make and replacing something it cannot is worth one additional blood draw.

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References

1. Souza et al. 2025. "Clomiphene or enclomiphene citrate for the treatment of male hypogonadism: a systematic review and meta-analysis of randomized controlled trials." Archives of Endocrinology and Metabolism. 10 RCTs, 819 patients, mean increase 273.76 ng/dL. Source
2. Coviello AD et al. 2005. "Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression." JCEM. 500 IU EOD maintained intratesticular testosterone at baseline. Source
3. Saffati et al. 2024. "Safety and efficacy of enclomiphene and clomiphene for hypogonadal men." Translational Andrology and Urology. 66 men, enclomiphene median increase 166 ng/dL, side effects 13.8% vs 47% with clomiphene. Source

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