Here is the complete list of current standard screenings for men over 50:
And, here’s a complete list of hormones on it: none.
Not testosterone, the one thing men's health has become synonymous with. Not SHBG, not estradiol, not anything upstream of either. The recommended panel covers blood pressure, cholesterol in some men, glucose in some men, and a handful of cancers and infections. That is the whole picture of male physiology as the guidelines see it.
More providers are correcting for this, though not by much. One hormone. Total testosterone, drawn whenever, which tells you almost nothing without SHBG and free testosterone beside it, and compares the result to a range that already treats decline as normal. PSA becomes the entire cancer conversation despite being at its weakest as a single value. Everything else is a metabolic panel and a lipid screen. Zero hormones by guideline, one by habit, and neither one assesses the whole person.
The result is a man in his fifties with rising visceral fat, flattening libido, poor recovery from workouts he used to handle easily, and a stack of results that read as unremarkable or borderline or “fine for his age.” Fine for his age is a comparison to a population that is itself getting sicker.
Part 1 covered labs I order in women. Most of that panel applies to men without modification, so I am not going to rewrite it here. What follows is what changes in men, what the numbers should be, and the tests that get skipped almost universally.
One note on how to read this. Labs measure physiology and hormone exposure, so everything below applies to anyone with testes, a prostate, or a testosterone-dominant hormonal environment. That includes trans women who have not had orchiectomy, nonbinary people on masculinizing therapy, and intersex people whose physiology sits outside either column. Where I write "men," I mean that physiology.
The core panel, with male thresholds
Fasting insulin. Same test, same reasoning, different urgency. Men store fat viscerally rather than subcutaneously, which means the same body weight carries more metabolic cost. A man with a normal BMI and a thickening waist can be profoundly hyperinsulinemic. I would like fasting insulin to be below 5. and typically order it with fasting glucose so we can calculate HOMA-IR. I’ve linked it, so you can check it out for yourself if you’ve had your fasting insulin drawn.
ApoB and NMR LipoProfile. Men develop coronary disease roughly a decade earlier than women. ApoB is the number that matters, not LDL-C. Under 80 mg/dL for primary prevention, under 60 for anyone with established disease, strong family history, or elevated Lp(a). The LP-IR score on the NMR gives you a second read on insulin resistance from the lipid side.
Lipoprotein(a). Get familiar with your risk ideally in your forties or earlier. Roughly one in five people carry an elevated level, and it is the single most common inherited driver of premature myocardial infarction in men who otherwise look low risk. And foundational in deciding whether we worry about your high cholesterol or not.
hsCRP. Above 1.0 mg/L gets my attention. Visceral fat is an active endocrine organ secreting inflammatory cytokines, and in men that fat is disproportionately visceral.
Ferritin with iron studies and transferrin saturation. This one shifts meaningfully in men. Without monthly menstrual iron loss, iron accumulates across a lifetime with no physiologic offload. Hereditary hemochromatosis is genetically equal between sexes but clinically expresses far more in men, and it presents as fatigue, joint pain, low testosterone, and elevated liver enzymes long before anyone thinks to check iron. Labs flag ferritin at 300 or 400. I start paying attention above 200, and transferrin saturation above 45% warrants HFE testing.
Homocysteine. Under 9. Cheap, actionable, and one of the better midlife predictors of cognitive decline.
Full thyroid panel. TSH, free T4, free T3, reverse T3, TPO and thyroglobulin antibodies. Thyroid disease is less common in men, which is exactly why it is missed for longer when it happens.
25-OH vitamin D. 60 to 80 ng/mL. Adiposity sequesters vitamin D, so heavier men need higher doses to reach the same serum level.
Plus the whole 9 yards
Total and free testosterone, LC/MS, morning draw
A random, Total testosterone alone tells you little. Free testosterone is what reaches the receptor and what correlates with symptoms, and the two diverge widely because of a Sex Hormone Binding Globulin (SHBG), which climbs steadily with age. A 60-year-old can have a total testosterone of 500 ng/dL and a free testosterone in the bottom decile, because SHBG has bound most of it.
Do the draw between 8 and 10 AM. Testosterone follows a diurnal rhythm and an afternoon draw can read 20 to 25% lower than your AM reading. Day-to-day variability is significant enough that a single low result should be confirmed on a second morning before anyone starts treatment. Specify that you want LC/MS draw, because this methodology provides high specificity, high sensitivity at low hormone ranges, and freedom from the chemical cross-reactivity that can occur with traditional immunoassays.
The conventional cutoff for hypogonadism is a total testosterone below 300 ng/dL. I treat symptomtomatically alongside numbers. This is “off label use” and is not FDA approved.
SHBG
Low SHBG in a man predicts type 2 diabetes and metabolic syndrome more strongly than low testosterone does, even after adjusting for testosterone. It is one of the more useful single markers on this list. High insulin suppresses SHBG. Falling SHBG in a man with a growing waist is metabolic dysfunction announcing itself two ways at once.
Labs report a range somewhere around 10 to 57 nmol/L in men, which is wide enough to be nearly useless. Ideally I am looking for SHBG to be between 30 to 50 nmol/L. Below 20 is a metabolic red flag regardless of how the rest of the panel looks. Above 60 is why a man with a reasonable total testosterone value feels like he has none. Read it alongside free testosterone and fasting insulin, because SHBG earns its keep as a triangulation point rather than a standalone number.
When SHBG is low
I think of low SHBG as a liver finding. SHBG is made in the liver, and a liver busy making fat makes less of it. Fructose drives that fat production harder than glucose does, which is why it lowers SHBG faster. A low SHBG in a man with central adiposity means hepatic fat until proven otherwise. I check ALT, AST, GGT, and ferritin alongside it, then go further when those move: ultrasound, elastography by FibroScan or FibroTouch, or an Enhanced Liver Fibrosis score. Also, Rule out hypothyroidism, and review any exogenous androgens or glucocorticoids, both of which suppress SHBG on their own.
The intervention here is healing the liver and the insulin, rather than the hormone. Cut fructose specifically rather than carbohydrate generally, cut out alcohol, build muscle, and treat the insulin resistance directly. Berberine and metformin both have a place depending on the patient.
Best part? SHBG climbs as hepatic fat falls. That makes it an inexpensive way to track whether your liver is actually responding, months before imaging would show you anything.
When SHBG is high.
Typically high SHBG is a bioavailability problem. Total testosterone reads adequate, free testosterone is low normal, but you feel like shit. This is the single most common missed diagnosis I see in men over sixty.
High SHGB is a bane of my existence.
I cannot overstate the importance of looking for the cause before reaching for a supplement or another intervention. SHBG rises with age, with hyperthyroidism, with liver disease, with chronic caloric restriction and inadequate protein, with endurance overtraining, with celiac disease, with anticonvulsants such as phenytoin and carbamazepine, and with estrogen containing medication or exposures. To name a few.
Beyond that, the evidence thins out... but here’s what we do know:
Boron at 10 mg daily lowered SHBG roughly 9% within six hours and raised free testosterone about 28% at one week, in a small short study.
Magnesium appears to reduce testosterone binding to SHBG, though that work is in vitro.
Zinc can often have an inverse relationship with SHBG. Men with highest dietary intake of zinc (above 25 mg daily), had about 22% lower SHBG. Reasonable to add 15 to 30 mg daily.
Nettle root can be used
The practical point matters more than any of the supplements. If SHBG stays high and free testosterone stays low with symptoms, testosterone therapy gets dosed against free testosterone rather than total. Men with high SHBG frequently need higher or more frequent Testosterone dosing to reach the same free level, and dosing to a normal total testosterone leaves them exactly where they started.
Estradiol
Turns out, men need estradiol, just like women need testosterone. It drives bone mineral density in men more directly than testosterone does, and it governs libido, joint comfort, lipid handling, and cognition. Below roughly 15 pg/mL, men develop joint stiffness, bone loss, and worsening lipids.
This is where I see the most iatrogenic harm in men’s health. Anastrozole gets prescribed reflexively alongside testosterone to men whose estradiol was never actually high, and they end up with aching joints, no libido, and accelerating bone loss while being told their hormones are optimized. Use the sensitive LC/MS assay, because standard immunoassay is unreliable at male concentrations. I aim for 20 to 40 pg/mL in men on therapy.
LH and FSH
LH and FSH determine whether the problem is testicular or central, and that distinction can change the entire landscape. High LH and FSH with low testosterone means primary testicular failure. Low or inappropriately normal LH and FSH with low testosterone means the signal from the pituitary is the problem, which requires investigation rather than a prescription. Obesity, opioids, chronic stress, sleep apnea, and pituitary pathology all produce that pattern, and treatment at the source.
Prolactin
Order prolactin in anyone with low testosterone and low or normal LH. Elevated prolactin in that setting means prolactinoma until imaging says otherwise. It is uncommon, and can be missed for years. Treatment is straightforward once identified.
IGF-1
IGF-1 a proxy for growth hormone axis function. It is produced mainly in the liver under growth hormone signaling. It promotes cell survival, inhibits apoptosis, and mediates exercise-induced neurogenesis in the hippocampus. Protein intake is the main dietary lever on circulating levels in humans, and protein restriction lowers it. That same anti-apoptotic signaling is why high IGF-1 tracks with cancer risk, which is what makes it a marker worth reading in both directions.
Low IGF-1 goes along with sarcopenia (muscle loss), poor recovery, central adiposity, and declining bone density.
High IGF-1 is a different conversation. Men in the highest category of circulating IGF-1 carry roughly 38% higher prostate cancer risk than men in the lowest. Every growth hormone secretagogues (examples are Sermorelin, Ipamorelin, and Ibutamoren (MK-677)) sold in a longevity clinic work by raising IGF-1. If you were to start any of these peptides, I want the baseline number, and in a man with a prostate cancer history I want a real discussion before he does.
DHEA-S
DHEA is marker of adrenal reserve. Measure the sulfated form rather than DHEA itself, because it has a long half-life and stays steady across the day, while DHEA swings hour to hour and gives you a random number and no-one knows what it actually means.
DHEA-S peaks in the mid-twenties and falls roughly 2 to 3% a year after that. Alas. Labs report age-stratified ranges, which means the decline is built into the reference range and a 60-year-old can be flagged normal at a level that would have been alarming at 30. I aim for roughly 300 to 450 mcg/dL in men, which is the range of a healthy man in his late 20ties and 30ties. I do not chase the top of the range, because there is no evidence that a higher is better however there is real evidence that pushing androgen precursors has negative implications.
When DHEA-S is low.
Sorry to use a cop out answer here, but normal aging decline does account for a lot of the decline. Beyond that, the causes worth ruling out are exogenous glucocorticoids, which suppress ACTH and take DHEA-S down with it. These medications include oral, inhaled, and topical steroids. Opioids can do the same thing. So do chronic caloric restriction, overtraining, untreated sleep apnea, chronic kidney disease, insulin resistance, and any significant illness or surgery.
A low DHEA-S with fatigue, low blood pressure, salt craving, or hyponatremia is a reason to evaluate for adrenal insufficiency rather than to reach for a supplement. Morning cortisol and ACTH first, cosyntropin stimulation if the picture warrants it. Then rule out “adrenal fatigue” with a salivary cortisol curve.
You might have heard of “Pregnenolone Steal” an argument that chronic stress diverts pregnenolone away from DHEA toward cortisol. I am skeptical of that model, because adrenal steroid production is compartmentalized by zone and enzyme rather than drawing on one shared pool. Chronic stress does track with low DHEA-S. The mechanism is probably not the one commonly described.
In naturopathic medicine, removing the obstacles to cure is always Step 1. So, if able, taper the unnecessary steroids with whoever prescribed them, address the opioids, treat the apnea, eat enough, and fix the insulin resistance. Next, reasonable to start with 25 to 50mg of DHEA daily and recheck DHEA-S along with total and free testosterone, estradiol, and PSA at eight to twelve weeks. Through years of practice, I have found that OTC DHEA is not equivalent to compounded form and sustained release micronized capsule is best.
DHEA is a precursor to both androgens and estrogens, and men aromatize it. It is important to watch the downstream numbers.
One caution that matters for this audience: in men with prostate cancer, particularly anyone on ADT, supplemental DHEA supplies substrate for androgen synthesis and does not belong in the plan. The same logic applies to any hormone-sensitive malignancy. DHEA is also banned in competitive sport.
When DHEA-S is high.
Look at your supplements first! DHEA usually turns up under another name or buried in a blend: prasterone, dehydroepiandrosterone, pregnenolone, androstenedione, adrenal glandulars, adrenal cortex extract, and most products sold as testosterone boosters, adrenal support, cortisol support, libido formulas, or anti-aging stacks.It is far and away the most common cause, and most elevations resolve on a recheck four weeks after stopping.
If it stays high, the differential is worth taking seriously. Non-classic congenital adrenal hyperplasia is the one people miss, so check 17-hydroxyprogesterone. ACTH-dependent Cushing syndrome raises DHEA-S, while adrenal Cushing typically lowers it, which makes DHEA-S a useful discriminator when cortisol is the question.
A markedly elevated DHEA-S, particularly above 700 mcg/dL or climbing on serial draws, warrants adrenal imaging. Adrenal tumors, including carcinoma, secrete DHEA-S, and this is one of the few times a single lab value should move directly to a CT. Milder elevations in a man with insulin resistance and high stress load usually track back to those, and treating them can be a slow process, because it took decades to get here.
Hematocrit and CBC
If you are on testosterone therapy of any kind, your provider will get this tested and track it. Red cell mass rises with testosterone, and erythrocytosis is the most common adverse effect. Above 50% warrants investigation. Above 54%, hold therapy until it normalizes, then restart at a lower dose. Therapeutic phlebotomy works, and if you are phlebotomizing repeatedly, recheck ferritin, because you will drive it into depletion.
One thing I would like to point out — since the question comes up in nearly every consult — is the erythrocytosis and cardiovascular risk question. The TRAVERSE trial randomized over 5,000 hypogonadal men with cardiovascular disease or high cardiovascular risk to testosterone gel or placebo. Testosterone was noninferior to placebo for major adverse cardiac events, with no increase in prostate cancer incidence. The FDA removed the boxed warning language about cardiovascular risk from testosterone labeling in February 2025.
PSA as a starting point
A single PSA value in isolation is a weak test. Used well, it is a strong one.
Get a baseline in your forties. Baseline PSA measured between 40 and 50 is one of the strongest available predictors of lifetime prostate cancer mortality. A man with a PSA under 1.0 at 45 has a very different thirty-year trajectory than a man at 1.5, and neither number triggers anything on a standard report.
Track velocity. The rate of change carries more information than any single value. This requires that someone is actually looking at the trend, which requires that the values are in one place.
Free PSA percentage. In the 4 to 10 ng/mL range, a free PSA at or below 25% shifts probability toward cancer, while above 25% points toward benign prostatic hyperplasia. This is cheap and very useful test!
PSA density. PSA divided by prostate volume from MRI or ultrasound. PSA density above 0.15 is meaningful, in a bad way, and it is the single best tool for distinguishing a large benign prostate from a concerning one.
Pre-biopsy markers. The Prostate Health Index, 4Kscore, SelectMDx, and ExoDx all reduce unnecessary biopsies in the gray zone. As does a multiparametric MRI, arguably more accurate that anything else. So if the response to your PSA is "get a biopsy" with no imaging and no secondary marker, ask why.
If you are on gender-affirming hormone therapy. Estrogen and androgen blockade suppress PSA profoundly. In a cohort of trans women on estrogen, median PSA was 0.02 ng/mL, roughly fiftyfold lower than in similarly aged cisgender men. The 95th percentile in that cohort was 0.6 ng/mL, and the single highest value recorded was 2.2. Apply the conventional 4.0 ng/mL threshold to that physiology and essentially nobody crosses it, cancer or no cancer, so a clinically significant tumor can hide under the cutoff for years. A 2025 systematic review in BJU International examined the available reference intervals and the working proposal is an upper limit closer to 1.0 ng/mL. Vaginoplasty does not remove the prostate. If the prostate is present, it needs a plan, and that plan cannot run on cisgender reference ranges.
If you are on androgen deprivation therapy
If you are on androgen deprivation therapy ADT is designed to make you hypogonadal on purpose, and everything that comes with that arrives simultaneously and with speed. By year one, you would have lost muscle, accumulated both subcutaneous and visceral fat, be measurably more insulin resistant, and lose bone at the lumbar spine at rates far exceeding normal aging. Cardiovascular risk rises alongside all else.
There’s a general consensus for monitoring all of this, but to no one’s surprise population-level data published in 2025 found that adherence to those recommendations is poor, with large proportions of men on ADT never receiving baseline lipid, glycemic, or bone density assessment at all. You, by virtue of reading this, are here to help close the gap.
Here’s a list for every man on ADT:
Fasting insulin, fasting glucose, and hA1c at baseline and every 6 mo. Insulin resistance on ADT develops fast and precedes any change in hA1c.
Full lipid panel with ApoB at baseline and annually.
DEXA at baseline and every one to two years, with FRAX scoring. Bone loss on ADT starts immediately.
25-OH vitamin D, calcium, and consideration of a bone turnover marker such as CTX
Estradiol. ADT collapses it alongside testosterone, and that collapse drives the hot flashes and much of the bone loss.
Obviously, CBC.
Serum testosterone by LC.MS to confirm castrate level. A meaningful subset of men on LHRH agonists never reach adequate suppression, and breakthrough testosterone predicts worse oncologic outcomes. Roughly 7% of men fail to stay under 50. Against the 20 target, 41% fail. Standard immunoassay cannot measure that low anyways. If nobody is measuring it, nobody knows, and men absorb every side effect of ADT for less suppression
hsCRP, because the inflammatory environment matters for both cardiovascular and oncologic trajectories
And highest impact interventions get breezed over: resistance exercise and optimal lean protein consumption. Every man starting ADT should leave that appointment with a strength training and a meal plan.
Muscle is your largest site of glucose disposal, so building it lowers fasting insulin, pulls fat out of the liver, and raises SHBG from the liver side. Loading bone is also the only non-pharmacologic intervention that reliably holds bone density, which matters most in exactly the men who lose it fastest, those on ADT and those post-gonadectomy. Two to three sessions weekly, progressive load, compound movements.
Inadequate protein raises SHBG, lowers IGF-1, and costs lean mass, and men who train hard while eating the way they did at twenty-five hit all three at once. I want 1.2 to 1.6 g/kg of body weight daily, toward the higher end on ADT or in survivorship, spread across meals at roughly 30 to 40 g each rather than loaded into dinner.
A few more!
GGT. The earliest marker of hepatic fat and oxidative stress, an independent predictor of diabetes and cardiovascular events, and an honest reflection of alcohol intake.
ALT. Labs flag it around 50. In men, anything sustained above 30 deserves a look at hepatic fat.
Uric acid. An independent metabolic and cardiovascular risk marker that rises years before a first gout flare and tracks tightly with insulin resistance and fructose intake.
Omega-3 index. Below 4% carries meaningfully elevated cardiac mortality risk.
Cystatin C. Catches early kidney decline before creatinine-based eGFR moves. Particularly relevant in muscular men, in whom creatinine overestimates dysfunction.
AM cortisol. Chronic stress physiology drives visceral fat, suppresses the gonadal axis, and erodes bone.
Sleep apnea screening. Not a lab, but an important screening tool. Untreated apnea suppresses testosterone, raises hematocrit, worsens insulin resistance, and drives hypertension. Treating it moves more numbers on this list than any supplement will.
The complete list:
Fasting insulin with fasting glucose. Insulin below 5 uIU/mL, glucose below 90 mg/dL, HOMA-IR below 1.5.
ApoB and NMR LipoProfile with LP-IR score. ApoB below 80 mg/dL, below 60 with established disease, strong family history, or elevated Lp(a). LP-IR below 45.
Lipoprotein(a). Below 75 nmol/L, or below 30 mg/dL. Once in a lifetime.
hsCRP. Below 1.0 mg/L.
Ferritin with iron, TIBC, and transferrin saturation. Ferritin 50 to 150 ng/mL. Transferrin saturation 20 to 45%. Above 45% warrants HFE testing.
Total and free testosterone, LC/MS, drawn 8 to 10 AM. Total 600 to 900 ng/dL. Free in the upper third of the reference range. Symptoms carry equal weight.
SHBG. 30 to 50 nmol/L. Below 20 is a metabolic red flag, above 60 explains a man who feels nothing from an adequate total testosterone.
Estradiol, sensitive LC/MS assay. 20 to 40 pg/mL. Below 15 costs you bone, joints, and libido.
LH and FSH. No target. These are read against testosterone to tell you whether the problem is testicular or central.
Prolactin, if testosterone is low and LH is not elevated. Below 15 ng/mL.
IGF-1. Mid-range for your age, not the top quartile.
DHEA-S. 300 to 450 mcg/dL.
CBC with hematocrit. Below 50%. Investigate above 50, hold testosterone above 54.
Homocysteine. Below 9 umol/L.
Full thyroid panel. TSH 0.5 to 2.0 mIU/L, free T4 mid-range, free T3 in the upper third, reverse T3 low, TPO and thyroglobulin antibodies negative.
25-OH vitamin D. 60 to 80 ng/mL.
PSA, tracked over time. Under 1.0 ng/mL at 45 is a favorable baseline. Velocity matters more than any single value. Add free PSA percentage if the value falls between 4 and 10, where above 25% favors benign prostatic hyperplasia.
Bonus: GGT below 25 U/L. ALT below 30 U/L. Uric acid below 5.5 mg/dL. Omega-3 index above 8%. Cystatin C with an eGFR above 90. AM cortisol 10 to 18 mcg/dL drawn between 7 and 9 AM.
Ksenia Malarkey, ND is a naturopathic physician specializing in integrative oncology, hormones, and metabolic health.
She provides medical care for Washington residents and offers global health coaching.
To schedule a free 15-minute consult, visit drkseniamalarkey.com
Thank you for this information. To reduce the SHBG, what kinds of magnesium and zinc are needed and in what dosages? Thank you
Ah, I've been wearing pants with waist=38" for ... too long.
Maybe I better not toss those 36" pants!?
Comprehensive info here.
Thank you so much.
I shall print this and add it to my file.