Low Testosterone: Do You Need TRT or Is There Something to Try First
Testosterone is made through a chain, and when levels are low, the only question that matters is where in that chain the breakdown happened.
The chain works like this. Your brain releases a hormone called GnRH, which tells your pituitary gland to release two hormones called LH and FSH. Those two hormones travel through your bloodstream to your testicles and tell them to produce testosterone. When testosterone levels rise high enough, the brain detects this and dials back GnRH, which dials back LH and FSH, which dials back production. It is a loop with a built-in thermostat.
When testosterone is low, the loop broke somewhere. Either the brain stopped sending the signal, or the testicles stopped responding to it. These are two completely different problems, and they require two completely different solutions.
The way you find out which one you have is a morning blood draw that checks LH and FSH alongside your total testosterone. Most men with low T only get their testosterone checked. That tells you the output is low. It does not tell you why.
If your testosterone is low and your LH and FSH are also low or in the normal range, you have what is called secondary hypogonadism, which means the signal from the brain is absent or insufficient. The testicles in this case are not broken. They are just not receiving the command. This is a signaling problem, not a hardware problem.
If your testosterone is low and your LH and FSH are high, you have what is called primary hypogonadism, which means the brain is already sending the signal as hard as it can and the testicles still cannot respond. The command is there. The hardware is the problem.
That distinction changes everything about what happens next.
For secondary hypogonadism, the goal is to restore the signal. Two tools get used here. The first is something called clomiphene citrate, which is a selective estrogen receptor modulator that blocks estrogen's feedback signal to the brain. Because the brain reads low estrogen as low testosterone, blocking that signal causes the brain to release more LH and FSH, which drives the testicles to produce more testosterone on their own. A 2025 systematic review across 10 randomized controlled trials and 819 patients found that clomiphene produced a mean testosterone increase of 273.76 ng/dL. That is a meaningful increase coming entirely from the body's own system.
There is also a version of this called enclomiphene, which is the active isomer of clomiphene without the inactive isomer that causes most of the side effects. A 2024 study of 66 men found that enclomiphene produced a median testosterone increase of 166 ng/dL with side effects in only 13.8 percent of men, compared to 47 percent with standard clomiphene. The testosterone increase was somewhat lower, but for many men the side effect profile makes it the better starting point.
The second tool for secondary hypogonadism is HCG, something called human chorionic gonadotropin, which structurally mimics LH and directly stimulates the testicles in the same way the pituitary signal would. This is particularly useful for men who want to preserve fertility while addressing their low testosterone, because both clomiphene and HCG keep the testicles active rather than bypassing them.
For primary hypogonadism, where the testicles cannot respond regardless of the signal, external testosterone, meaning TRT, is most likely the appropriate path. The signaling system is already working. There is nothing to unlock or restore. The body simply cannot produce what it needs, and replacing it externally is what fills that gap.
The one concern men raise most often when considering TRT is fertility. Exogenous testosterone suppresses LH and FSH because the brain detects high testosterone levels and shuts down the signal, which means the testicles stop receiving stimulation for sperm production. This is where HCG becomes important again. A 2005 study found that 500 IU of HCG every other day was enough to maintain intratesticular testosterone at baseline levels in men whose LH and FSH had been suppressed by exogenous testosterone. Maintaining intratesticular testosterone is what keeps sperm production going. So TRT plus HCG at that dose can address the hormone replacement while preserving testicular function.
Before any of this, there is a more fundamental question worth asking. Low LH and FSH can point to secondary hypogonadism, but they can also reflect lifestyle-driven suppression. Chronic sleep deprivation, significant caloric restriction, high body fat, and heavy alcohol use all reduce the brain's output of GnRH, which in turn reduces LH and FSH and drops testosterone. In this case, the chain is intact. The whole system is just operating at a lower set point because of the inputs it is receiving.
No drug corrects a lifestyle-driven signal suppression in any lasting way. The lab numbers may shift, but the underlying driver stays in place and typically reasserts itself. This is why confirming that sleep, nutrition, and body composition are addressed before attributing a low LH picture to a physiological disorder matters. The two can look identical on a lab panel.
The entire framework collapses to something simple. Low testosterone with low or normal LH and FSH means the signal is the problem, and you work with the signaling system first. Low testosterone with high LH and FSH means the hardware is the problem, and TRT is the appropriate tool. One lab panel with three numbers answers the question that most men spend months trying to work out through symptoms alone.
The version of this that almost never gets discussed is that many men who end up on TRT for decades would have responded just as well to a two-dollar clomiphene prescription, because nobody checked LH and FSH before writing the script. That is not a criticism of TRT. It is just a measurement problem. One extra lab value prevents it entirely.
References
- 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
- 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
- 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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