What My SHBG Number Was Telling Me About My Thyroid (I Had No Idea)

My SHBG was 72 nmol/L. I had run enough bloodwork at that point to know that was high – significantly high – and that it was almost certainly the reason my free testosterone was low despite total T that looked reasonable. What I could not figure out was why.

I wasn’t restricting calories. I wasn’t doing endurance training. My estradiol was not elevated. My liver enzymes were normal. I was eating enough protein. By every explanation I had read for why SHBG gets elevated, I should have been fine.

Then my wife – she’s a nurse practitioner and has been quietly more useful to this process than I give her public credit for – suggested we run a full thyroid panel alongside the next hormone draw.

What we found is the subject of this article. My TSH was 2.2, which most GPs including my semi-retired father would have told me was completely unremarkable. But free T3 was 2.4 pg/mL – low-normal – and reverse T3 was 26 ng/dL – elevated. The result was poor effective thyroid hormone action at the cellular level, which was driving SHBG production in my liver.

Over the following six months, with a protocol focused purely on supporting T4-to-T3 conversion, SHBG came down from 72 to 44 nmol/L. Free testosterone went from 9.2 to 17.2 pg/mL. I made no changes to my training, diet, or anything I was taking for testosterone directly.

The Short Version: Thyroid hormones directly regulate SHBG production in the liver. Suboptimal active T3 – even with a “normal” TSH – can sustain elevated SHBG and low free testosterone. If your SHBG is stubbornly elevated and the common explanations don’t fit, a full thyroid panel including free T3 and reverse T3 is worth running before you conclude the problem is something else.

The Baseline That Started This

I’ve been running quarterly bloodwork panels since I found Ron Males and the PowerandBulk.com framework about two years ago. Before that, I’d run bloodwork twice and both times looked at whatever my GP noted – TSH, CBC, a lipid panel, total testosterone. Both times he said everything looked fine. I walked out of a TRT consultation at 44 and decided there had to be a more rigorous approach to this.

The complete male hormone panel framework Ron laid out changed what I was ordering. Once I had full panels with SHBG, free T, free T3, reverse T3, and fasting insulin all in view simultaneously, patterns started emerging that had been invisible in the partial panels I was getting from my GP.

This panel was from my third comprehensive draw. I was 48, and I’d been working the protocol for several months. Sleep was consistently better. I was training correctly. My total T at 442 ng/dL was in a reasonable range. But free T at 9.2 pg/mL and SHBG at 72 nmol/L didn’t make sense given what I’d fixed.

Marker	Month 0 Value	Units	Context
Total Testosterone	442	ng/dL	Morning fasted draw, 7:45am
Free T (calc. Vermeulen)	9.2	pg/mL	Low-normal
SHBG	72	nmol/L	Elevated
Albumin-bound T (est.)	~152	ng/dL	Estimated, reasonable
Free Androgen Index	61	—	(T × 100) / SHBG
Estradiol (sensitive)	24	pg/mL	Normal range
Fasting Insulin	6.2	µIU/mL	Good – not the SHBG driver
ALT / AST	22 / 19	U/L	Normal liver function
TSH	2.2	mIU/L	Looks unremarkable
Vitamin D 25-OH	48	ng/mL	Adequate

Why the Standard Explanations Didn’t Fit

I’m an engineer. Before I accept a conclusion, I try to rule out the alternatives. SHBG elevation has a reasonably well-characterized set of drivers, so I worked through them methodically.

High estradiol raising SHBG: Estradiol was 24 pg/mL – mid-range, not elevated. This wasn’t the driver.

Caloric restriction: SHBG rises when the liver perceives inadequate nutrition. I was not restricting. Fasting insulin at 6.2 and albumin at normal range both indicated adequate nutritional status. Insulin and SHBG are inversely related – very low insulin (from restriction) pushes SHBG up. My insulin wasn’t particularly low.

Endurance training volume: High endurance training can drive SHBG elevation through cortisol and energy deficit signaling. I train three days a week, compound movement focused. Not the cause.

Aging: SHBG does trend upward with age – the aging and SHBG relationship is well-documented. At 48, some elevation is expected. But the magnitude of 72 nmol/L is higher than typical age-related drift, which tends to run in the 40s-50s for men my age who aren’t otherwise compromised.

Liver function: SHBG is produced by the liver, and liver dysfunction can alter SHBG production. My ALT, AST, and bilirubin were all normal. Liver function and SHBG didn’t explain it.

I’d been reading Ron’s SHBG overview carefully. It covered most of these drivers. There was one that I’d glossed over: thyroid hormones and SHBG. I had a TSH of 2.2 and assumed that meant my thyroid was fine. My wife had a different read on that assumption.

What the Thyroid Panel Showed

My wife ordered the expanded panel through her practice network – free T3, free T4, reverse T3, TPO antibodies, and TG antibodies alongside the standard TSH. I’ll note here that not everyone has this kind of lab access. Direct-pay lab services exist and are more accessible than most people realize – services like Marek Health or Discounted Labs allow you to order comprehensive panels without a physician’s order in most states.

When the results came back, the TSH of 2.2 looked normal, as expected. The rest of the picture looked different.

Thyroid Marker	My Value	Units	Lab Range	Functional Optimal
TSH	2.2	mIU/L	0.4 – 4.5	1.0 – 2.0 (debated)
Free T4	1.0	ng/dL	0.8 – 1.8	Upper half preferred
Free T3	2.4	pg/mL	2.3 – 4.2	Above 3.0 preferred
Reverse T3 (rT3)	26	ng/dL	9.2 – 24.1	Below 15 preferred
TPO Antibodies	18	IU/mL	<34 negative	Negative
TG Antibodies	<1	IU/mL	<4 negative	Negative

TPO and TG antibodies were negative, which ruled out Hashimoto’s thyroiditis as a cause. That’s the autoimmune thyroid condition I was somewhat concerned about given I’d run it as a differential possibility. No antibodies meant no autoimmune attack on the thyroid.

What was positive – if you can call it that – was the reverse T3 at 26 ng/dL, above the upper limit of the reference range, alongside a free T3 at the absolute floor of normal at 2.4 pg/mL. The ratio was off. Free T3 was barely in range; reverse T3 was out of range.

My wife explained what this pattern suggests: the body was converting T4 into reverse T3 (rT3 – an inactive mirror-image form of the active thyroid hormone T3, which blocks the same cellular receptors but produces no metabolic effect) at a higher rate than normal. The result was that even though my total thyroid hormone production looked adequate by TSH, the active hormone reaching my cells – free T3 – was competing with an excess of its inactive antagonist. Effective thyroid activity was lower than the headline numbers suggested.

This pattern is called subclinical hypothyroidism (inadequate thyroid hormone action at the cellular level, despite TSH remaining in the “normal” range), and my father – who spent 35 years as a GP and considers anything below TSH 4.0 acceptable – would not have caught it without the expanded panel. He still isn’t fully convinced the rT3 value is meaningful. We disagree on this.

The Connection I’d Completely Missed

The link between thyroid hormone status and SHBG production is direct and mechanistically well-established, though rarely discussed in general hormone optimization content.

SHBG is synthesized by hepatocytes (liver cells), and that synthesis is regulated in part by thyroid hormone signaling. Active T3 binds to thyroid hormone receptors in the liver that downregulate SHBG gene expression – essentially, adequate T3 suppresses SHBG production. When T3 action is impaired, either because T3 is genuinely low or because excess reverse T3 is blocking receptor sites, SHBG production increases. The liver is responding to what it perceives as suboptimal metabolic status by upregulating the binding protein that controls how much sex hormone is active.

The clinical implication: a man with subclinical hypothyroidism and elevated rT3 can have apparently normal total testosterone and estradiol, good dietary habits, appropriate body composition, and still have elevated SHBG and low free testosterone – because the regulatory signal to the liver to reduce SHBG output is not reaching its target. You can stack boron, nettle root, and every other SHBG intervention available and get limited results if the thyroid issue is unresolved.

I don’t claim I would have figured this out without Ron and without my wife’s clinical perspective. Ron had seen similar presentations in his client data – he references a client in the TSH article I wrote separately about the thyroid panel work. The SHBG angle specifically is what I want to document here because it’s the piece that wasn’t obvious.

One additional nuance worth stating: hyperthyroid SHBG elevation is also documented – in frank hyperthyroidism, excess T3 can actually drive SHBG very high through a different pathway. The relationship isn’t strictly linear. But for most men in the subclinical hypothyroid or poor T3 conversion pattern, improving T3 levels tends to bring SHBG down, not further up.

The Protocol

Ron Males designed this with me based on the thyroid picture. The goal was to support T4-to-T3 conversion and reduce reverse T3 production. This is Ron’s standard thyroid support protocol, detailed fully in the selenium, iodine, and zinc thyroid protocol piece. My specific implementation:

• Selenium selenomethionine 200mcg daily (critical for the deiodinase enzymes that convert T4 to active T3)
• Zinc picolinate 30mg daily (zinc and thyroid status are closely linked – zinc deficiency impairs thyroid hormone synthesis and conversion)
• Vitamin D3 5,000 IU + K2 200mcg daily (already partially in place, pushed from 48 to a target above 50 ng/mL)
• Magnesium glycinate 400mg before bed (magnesium deficiency impairs thyroid function; also important for cortisol-thyroid interaction management)
• Reduced refined carbohydrates and seed oils (inflammatory dietary patterns are associated with elevated rT3 production)
• Sleep priority: consistent 10:30pm lights-out, no change to existing habits

No thyroid medication. No iodine supplementation beyond what was naturally in my diet (I was not iodine-deficient based on dietary analysis, and excessive iodine supplementation in a euthyroid person can worsen thyroid function). No boron or SHBG-specific supplements added during this period – I wanted to see whether the thyroid protocol alone would move SHBG.

My wife ordered all labs and reviewed the results with me at each checkpoint. All interpretation was done in consultation, not by me independently. I want to be clear about that.

Month 3 – First Checkpoint

Marker	Month 0	Month 3	Change
Total Testosterone (ng/dL)	442	458	+16 (+3.6%)
Free T – calc. (pg/mL)	9.2	13.8	+4.6 (+50.0%)
SHBG (nmol/L)	72	54	-18 (-25.0%)
Free Androgen Index	61	85	+24 (+39.3%)
Estradiol (pg/mL)	24	26	+2 (within variance)
TSH	2.2	2.4	Slight increase (expected)
Free T3 (pg/mL)	2.4	2.9	+0.5 (+20.8%)
Reverse T3 (ng/dL)	26	19	-7 (-26.9%)

The TSH increasing slightly was expected and not a concern – as T4-to-T3 conversion improved, the hypothalamus adjusted signal slightly. This is normal negative feedback behavior in the axis.

SHBG dropped 18 points. Free T moved from 9.2 to 13.8. I had not added a single SHBG-specific supplement. I had added selenium, zinc, and adjusted D3 and magnesium. The intervention was entirely thyroid-directed.

Reverse T3 dropping from 26 to 19, alongside free T3 rising from 2.4 to 2.9, suggested the conversion pathway was responding. The cortisol-thyroid interaction is worth noting here: cortisol stress drives rT3 production by shunting T4 toward the inactive form. Magnesium and sleep improvement both reduce chronic cortisol load, which may have partially contributed to the rT3 improvement alongside the selenium and zinc work.

I was not tempted to draw strong conclusions yet. Three months is one data point. I continued the protocol unchanged.

Month 6 – Final Results

Marker	Month 0	Month 3	Month 6	Net Change (0→6)
Total Testosterone (ng/dL)	442	458	468	+26 (+5.9%)
Free T – calc. (pg/mL)	9.2	13.8	17.2	+8.0 (+87.0%)
SHBG (nmol/L)	72	54	44	-28 (-38.9%)
Albumin (g/dL)	4.5	4.6	4.5	Stable
Free Androgen Index	61	85	106	+45 (+73.8%)
Estradiol (pg/mL)	24	26	25	Stable
TSH	2.2	2.4	2.4	Stable
Free T3 (pg/mL)	2.4	2.9	3.4	+1.0 (+41.7%)
Reverse T3 (ng/dL)	26	19	14	-12 (-46.2%)
Free T3:Reverse T3 ratio	0.09	0.15	0.24	+167% (directionally correct)

SHBG went from 72 to 44. Calculated free testosterone went from 9.2 to 17.2 pg/mL – essentially doubled. The free androgen index moved from 61 to 106.

The thyroid picture normalized substantially: free T3 at 3.4 pg/mL is now in the upper half of reference range, reverse T3 at 14 ng/dL is well within range, and the free T3 to reverse T3 ratio improved from 0.09 to 0.24, which is the direction every functional medicine framework I’ve read suggests it should move.

Total testosterone moved only 5.9%. This is consistent with the mechanism: the intervention wasn’t stimulating T production, it was removing the SHBG suppression that was hiding the testosterone I already had. The bioavailable testosterone that was functionally accessible to my tissues improved dramatically even though the production didn’t change much.

Subjectively: the change was noticeable. I’m cautious about subjective reports because I know they’re confounded by expectation. But my wife noticed changes in my energy and mood before I told her the month 6 results, which I take as a more reliable signal than my own self-assessment.

I Want to Be Honest About the Limitations

This is one person’s experience over six months. I cannot prove causality. Six months includes seasonal variation, possible diet changes I didn’t track perfectly, one period of elevated work stress, and my son’s baseball tournament schedule that disrupted sleep for about three weeks in month 4.

The calculated free T I’m reporting is the Vermeulen formula estimate, not a directly measured value. Direct measurement by equilibrium dialysis or LC-MS/MS would be more accurate. For within-person comparison it’s useful; as an absolute number, it has meaningful error margins.

I am not a clinician. My wife is, which gave me better access than most men will have to this kind of collaborative interpretation. The complete male hormone panel guidance and the reference range versus optimal range framework are a starting point, but if your thyroid panel looks unusual, work with a knowledgeable practitioner before deciding on a protocol. The cortisol-thyroid interaction is real and complex. Reverse T3 elevation can have multiple causes, not all of which are fixed by selenium and zinc alone.

I also want to note: some of my improvement may reflect the general protocol work I was doing during this period – sleep consistency, training, the magnesium and D3 work that predated the thyroid protocol. I tried to isolate the thyroid-focused additions as the new variable, but I can’t fully separate them from the baseline program.

The Honest Breakdown

Tier 1 – Know your numbers first (costs only the bloodwork):

• Run a full hormone panel. If your SHBG is above 50 and you can’t explain it by the standard drivers (high E2, caloric restriction, endurance overtraining), add a complete thyroid panel to your next draw.
• The thyroid panel that matters: TSH, free T4, free T3, reverse T3, TPO antibodies. Not just TSH. TSH alone tells you almost nothing about conversion efficiency.
• Calculate your free T3 to reverse T3 ratio. A ratio below 0.20 is a reasonable threshold to investigate further.

Tier 2 – Foundation interventions (low cost, broad benefit):

• Selenium selenomethionine 200mcg daily. This is the rate-limiting cofactor for the deiodinase enzymes that convert T4 to active T3. Selenomethionine is the form with best absorption – not selenite, not inorganic selenium.
• Zinc picolinate 30mg daily. Zinc deficiency directly impairs thyroid hormone synthesis and T4-to-T3 conversion. If you’re not sure about your zinc status, RBC zinc is a more accurate test than serum zinc.
• Magnesium glycinate 400mg before bed. Addresses both cortisol-related rT3 elevation and the direct magnesium-free T connection.
• D3 5,000 IU + K2. Get your 25-OH vitamin D above 40 ng/mL before adding anything else.

Tier 3 – Consider after Tier 2 runs for 8-12 weeks:

• Dietary inflammatory load reduction – refined carbohydrates and seed oils. Not a dramatic protocol, just a meaningful reduction. The impact on rT3 production is real.
• Sleep consistency. Chronic sleep disruption drives rT3 elevation through cortisol. Getting this right amplifies everything else.

Tier 4 – SHBG-specific supplementation (after thyroid is addressed):

• Boron citrate 9mg daily, run for 60-90 days with bloodwork monitoring. Most useful once the thyroid-SHBG driver is resolved, as you’re then addressing any residual SHBG elevation directly.

Before You Ask

Do I need T3 medication to fix this?
In my case, no. The selenium, zinc, and dietary changes were sufficient to improve conversion enough that the rT3 dropped and free T3 rose meaningfully. T3 medication (Cytomel/liothyronine) is a more aggressive intervention that bypasses the conversion issue entirely – but it also requires careful dosing and monitoring to avoid overshooting. My wife’s view was that we try nutritional support first and reassess at 6 months. That approach worked for me. For someone with a more severe conversion deficit, the answer might be different.

How common is this pattern?
I don’t have data on prevalence, and I’d be making things up if I gave you a number. What I can say is that elevated rT3 alongside low-normal free T3 in an otherwise “normal” TSH panel is not rare in men presenting with low free testosterone and SHBG above 50. It’s simply not routinely tested, so most men never know it’s there.

My doctor only tested TSH and said everything was fine. Should I push for the full panel?
That’s a personal decision about how you engage with your healthcare provider. What I’ll say is that the thyroid picture my GP would have reported – TSH 2.2, everything looks normal – and the thyroid picture that actually mattered were completely different. The reference range versus optimal range problem is particularly acute with thyroid markers. If your free T is low and you can’t explain it, the full panel is worth the cost.

Is this specific to men over 45?
The aging and SHBG relationship makes this pattern more likely with age – SHBG trends up and thyroid conversion efficiency tends to decrease in older men. But I’ve seen discussion of elevated rT3 in younger men with high stress loads, chronic dieting, and sleep disruption. The mechanism doesn’t require age.

What does Ron say about this?
Ron has seen this pattern enough times that it’s part of his standard diagnostic approach now. The Anabolic Alchemy program includes thyroid assessment as part of the root cause evaluation for men whose SHBG doesn’t respond to standard interventions. His perspective is that the thyroid-SHBG link is one of the most consistently missed connections in natural hormone optimization work.

Where I Am Now

Six months of data, four bloodwork panels, an uncomfortable number of spreadsheet tabs. SHBG went from 72 to 44. Free testosterone went from 9.2 to 17.2. The intervention was entirely thyroid-directed. If your SHBG is elevated and you’ve run through the obvious explanations without resolution, consider what your T4-to-T3 conversion looks like. The number worth knowing is reverse T3 – and most hormone panels don’t include it unless you ask.