Testosterone Isn’t Just a Male Hormone:
Why Total Testosterone Alone Doesn’t Tell You Enough

Testosterone gets filed away early as “the male hormone”, and oestrogen gets filed away as “the female one”. It’s a tidy story, and it’s wrong enough to cause real confusion when someone’s bloods come back and nobody can explain why they still feel the way they do.

Every woman’s ovaries and adrenal glands make testosterone throughout her life, and the tissue that responds to it doesn’t care what sex produced it. Muscle, bone, brain, skin and vaginal tissue all carry androgen receptors, which means testosterone is doing real, measurable work in a woman’s body long before menopause and well beyond it. It contributes to muscle strength and bone density, to mood stability and motivation, to cognitive sharpness, and to libido and sexual response. When it declines, and it does decline gradually from a woman’s late twenties onward, the result can look like plain fatigue, a flatter mood, a noticeably lower drive, or muscles that don’t respond the way they used to despite training just as hard.

In men, the same hormone is doing familiar work, but the framing usually stops at libido and muscle mass. It’s also central to energy, motivation, mood regulation, bone density and cognitive clarity, which is why a man with a testosterone level trending down over several years often describes it less as a sexual problem and more as a sense that his get-up-and-go has quietly gone missing.

The overlap matters. Fatigue, low mood, reduced muscle tone and a drop in libido show up on both sides of this hormone’s decline, which is exactly why testosterone deserves a place in the conversation whenever those symptoms turn up without an obvious explanation elsewhere. If you’ve already ruled out the usual explanations for persistent tiredness and testosterone hasn’t come up yet, it’s worth asking why not.

This is where most testosterone results stop telling the full story. A standard blood test usually reports total testosterone, which is every molecule of the hormone floating in the bloodstream regardless of what it’s doing there. The trouble is that most of it isn’t doing anything at all.

Roughly half of circulating testosterone is bound tightly to a protein called SHBG × (sex hormone binding globulin, the carrier protein that transports testosterone through the blood and controls how much of it is actually available to tissue). Most of the remainder is loosely attached to albumin. Only a small fraction, sometimes as little as one or two percent, circulates genuinely free and able to bind to a receptor and produce an effect. Total testosterone counts all of it, with no way of showing how much is locked up and unavailable versus how much is actually reaching a cell, which is exactly the gap I’m looking to close whenever a result and a symptom picture don’t seem to agree.

That distinction is the reason two people can have an identical total testosterone reading and feel completely different. If one of them has a high SHBG, more of their testosterone is bound and inactive, so the usable, free fraction is lower than the total number suggests, and the symptoms of low testosterone can be very real even while the total sits comfortably mid-range. If the other has a low SHBG, more testosterone is left unbound, so a total reading that looks unremarkable, or even slightly low, might still translate into a perfectly adequate free fraction, declining gradually in both sexes rather than failing suddenly in one and quietly in the other.

SHBG isn’t a fixed number. It rises and falls in response to what else is happening in the body, which is what makes it useful diagnostically rather than just a correction factor to apply and forget.

Thyroid function is one of the biggest drivers. An underactive thyroid tends to push SHBG down, while an overactive one pushes it up, so someone investigating unexplained fatigue alongside a testosterone concern is often looking at two connected threads rather than two separate problems. Insulin resistance works in the other direction: higher circulating insulin suppresses SHBG production in the liver, which is part of why conditions involving insulin resistance, including polycystic ovary syndrome, are so often accompanied by a low SHBG and a disproportionately high free androgen fraction even when total testosterone looks only mildly elevated. Liver function matters too, since SHBG is made in the liver and anything that impairs that production will shift the result. Oestrogen has the opposite effect to insulin, raising SHBG, which is why pregnancy, the combined oral contraceptive pill and oestrogen-based hormone therapy all tend to push SHBG upward and can mask a genuine testosterone deficiency underneath a total reading that looks acceptable. Body composition and age add another layer, with SHBG generally rising through midlife independent of anything else going on.

This is context rather than a checklist to work through item by item. A high SHBG in someone with an underactive thyroid tells a different story to a high SHBG in someone on hormonal contraception, even though the number on the page looks identical, which is usually where I start asking what else is going on before deciding what the SHBG result actually means. The same reasoning applies to oestrogen metabolism × Oestrogen Metabolism after oestrogen has been used by the body, it needs to be broken down and cleared through several pathways before elimination. and the stress response more broadly, an area covered in more depth in the COMT gene and how it shapes stress response and oestrogen clearance, and it’s a useful reminder that hormone results rarely make sense read in isolation from the rest of the picture.

In Men:
Testosterone production in men comes overwhelmingly from the testes, under instruction from a signalling pathway that runs from the brain down through the pituitary gland. It peaks in early adulthood and then declines gradually, typically losing roughly one to two percent a year from the thirties onward, a slope gentle enough that most men attribute the early symptoms to simply getting older rather than to a specific, measurable hormonal shift.

The symptoms that eventually prompt someone to get tested tend to cluster around energy, mood, libido and erectile function, alongside a loss of muscle mass and strength that doesn’t respond the way it once did to the same training. Bone density also depends on adequate testosterone, so a man with an unexplained drop in bone density is one of the situations where testing testosterone properly, rather than assuming it’s simply age, earns its place.

In Women:
The trajectory is different, and it starts earlier than most women expect. Testosterone production in women declines steadily from the late twenties, long before any of the more familiar signs of perimenopause appear, which means the hormone has often been quietly falling for fifteen or twenty years by the time other symptoms bring someone in for a broader hormonal picture.

Menopause itself, meaning the drop in oestrogen and progesterone from the ovaries, has surprisingly little direct effect on testosterone. Age is the bigger driver. After menopause, the adrenal glands become the more significant relative source of testosterone as ovarian contribution winds down, which is one reason adrenal health and stress physiology deserve a place in the conversation whenever testosterone comes up for a woman in her forties or fifties. The symptoms attributed to declining testosterone in this life stage include persistent fatigue, reduced libido and sexual response, low mood, brain fog, muscle weakness and declining bone density, many of which overlap heavily with the symptoms attributed to falling oestrogen, which is exactly why untangling which hormone is actually driving which symptom benefits from looking at more than one marker at a time.

Getting a useful answer means testing three things together rather than one in isolation: total testosterone, SHBG, and a calculated free testosterone derived from the other two.

Total testosterone establishes the baseline, the raw amount the body is producing. SHBG shows how much of that total is bound up and unavailable. Free testosterone, calculated from the two together using a validated equation rather than measured directly, is the figure that actually reflects what’s reaching tissue and driving symptoms. Direct immunoassay tests that claim to measure free testosterone on their own are notoriously unreliable, particularly in women, where testosterone circulates at a fraction of male concentrations and most standard assays weren’t built with that range in mind. The calculated approach, using total testosterone and SHBG together, remains the more clinically defensible way to get to that number.

Timing adds another layer worth understanding rather than following blindly. Testosterone follows a daily rhythm in men, peaking in the morning and declining through the day, which is why a fasting, early-morning sample gives a more representative picture than an afternoon one. In women who are still cycling, testosterone and SHBG both shift across the menstrual cycle, so a result taken on day three looks different to one taken during the luteal phase purely as a function of timing rather than anything pathological. Getting the timing right isn’t about chasing a perfect number so much as making sure the number you eventually get actually means something before anyone tries to interpret it.

Once total testosterone, SHBG and calculated free testosterone are sitting in front of you alongside a genuine symptom picture, thyroid function, insulin sensitivity, and where someone is in their reproductive life stage, a testosterone result stops being a single flag to react to and becomes a piece of evidence that either supports or contradicts the story the symptoms are already telling.

That’s a very different exercise to glancing at one number against a reference range and deciding whether it’s normal, and it’s the exercise I want someone going through before they draw any conclusions about their hormones from a single line on a lab report. A total testosterone that looks fine can still leave someone under-androgenised if their SHBG is high enough to lock most of it away. A total testosterone that looks low can still be functionally adequate if SHBG is low enough to leave plenty free. The symptoms, not the single number, are what decide which of those situations is actually in front of you, and the three results together are what let you tell them apart with any confidence.

If fatigue, low libido, mood changes, or unexplained muscle or bone loss have you wondering whether testosterone is part of your picture, a consultation looks at total testosterone, SHBG and calculated free testosterone together, alongside your thyroid function, insulin sensitivity and broader symptom history, rather than reacting to a single number in isolation.