My TSH Was 2.8 and My Doctor Said I Was Fine – What the Full Thyroid Panel Showed

My TSH was 2.8. My doctor looked at the number, said “that’s normal,” and moved on. He wasn’t wrong about the reference range. He was wrong about what the number meant for my testosterone, my energy, and the six years of slow decline I’d been chalking up to just being in my mid-40s.

TL;DR: A TSH of 2.8 is within the standard reference range. It is not within the functional optimal range for male hormone production. My free T3 was in the bottom third of range, my reverse T3 was elevated, and I had detectable TPO antibodies. Running the full panel changed everything. Here’s the data, the protocol, and what moved the numbers.

Some Background Before the Numbers

I’m David Nakashima, 48, aerospace engineer in suburban Seattle. My wife is a nurse practitioner – she works in primary care and orders my labs through her network, which means I get a more complete panel than most people can access through a standard GP visit. She’s also the person who first suggested, around the time I turned 44, that my thyroid was worth looking at more carefully. I’d dismissed it. My father was a GP before he semi-retired and had spent years telling me my thyroid was fine. I had two GPs telling me I was fine.

At 44, I walked into a TRT clinic. The consultation took about twelve minutes. They offered me testosterone cypionate based on a single total testosterone reading of 380 ng/dL. I walked out. Not because I was opposed to TRT categorically – I’d done enough reading to know it’s appropriate for some people – but because nobody had asked me a single question about thyroid, sleep, cortisol, diet, or anything else that might be suppressing my T. They went straight from “your number is low” to “here’s the prescription.”

I spent three months reading before I found Ron Males at PowerandBulk.com and decided his data-first approach was worth following. I was attracted specifically by his willingness to say “I got this wrong for two years” in his writing. I distrust certainty in this space. Ron’s approach matched mine: build from bloodwork, intervene conservatively, track the outcome.

I signed up for the Anabolic Alchemy program at 44, four months after the TRT clinic visit. I’ve been running some version of Ron’s protocols since.

The Baseline – What “Normal” Actually Looked Like

Thyroid Marker	My Result	Standard Range	Functional Optimal
TSH	2.8 mIU/L	0.4-4.0 mIU/L (in range)	1.0-2.0 mIU/L (optimal)
Free T4	1.1 ng/dL	0.8-1.8 ng/dL (in range)	1.2-1.6 ng/dL
Free T3	2.4 pg/mL	2.0-4.4 pg/mL (in range, low third)	3.2-4.0 pg/mL
Reverse T3	22 ng/dL	<25 ng/dL (barely in range)	<15 ng/dL
TPO antibodies	48 IU/mL	<35 IU/mL (elevated)	<10 IU/mL
TG antibodies	12 IU/mL	<20 IU/mL (in range)	<10 IU/mL

Testosterone Marker	My Result	Where I Wanted to Be
Total testosterone	380 ng/dL	550-750 ng/dL
Free testosterone	8.6 pg/mL	15-22 pg/mL
SHBG	68 nmol/L	20-45 nmol/L (high)
LH	4.2 mIU/mL	3-8 mIU/mL (mid-normal)
AM cortisol	19 mcg/dL	10-18 mcg/dL (slightly elevated)

Let me explain why these thyroid numbers mattered despite being “in range” on the standard panel.

TSH is a pituitary signal – it tells the thyroid to produce more hormone. A TSH of 2.8 means the pituitary is working moderately hard to push the thyroid to produce enough T3 and T4. TSH at 1.0-2.0 means the system is running efficiently without strain. 2.8 is not alarming. It’s a signal that something downstream may be underperforming.

My (free T3 – the active thyroid hormone that drives cellular metabolism, energy production, and downstream hormonal function including testosterone synthesis) at 2.4 pg/mL was in the bottom third of the reference range. Not deficient. Not optimal. Running sluggish.

The reverse T3 at 22 ng/dL was the more concerning number. (Reverse T3 is an inactive form of T3 that the body produces as a metabolic brake – high rT3 blocks T3 receptors, meaning your free T3 can be technically present but functionally blocked from doing its job). At 22 ng/dL, my rT3 was near the top of the “acceptable” range. In functional medicine terms, that level suggests my T4-to-T3 conversion was shunting too much toward the inactive rT3 pathway.

The TPO antibodies at 48 IU/mL told me there was an immune component. (Thyroid peroxidase antibodies indicate the immune system is producing antibodies against the thyroid enzyme responsible for making thyroid hormones – elevated TPO antibodies are the primary marker for Hashimoto’s thyroiditis, the autoimmune thyroid condition). My result wasn’t dramatically elevated, but 48 IU/mL above the 35 IU/mL cutoff is a positive finding. I had subclinical Hashimoto’s. My father, when I told him, said “hm, that’s interesting” in the way semi-retired GPs say things when they realize they missed something.

My SHBG at 68 nmol/L was the bridge between thyroid and testosterone. Thyroid hormones directly regulate SHBG production in the liver – when thyroid function is sluggish, SHBG typically runs high. My elevated SHBG was binding most of my testosterone, producing a free T of 8.6 pg/mL despite a total T of 380. Both numbers were low, but the SHBG-thyroid connection was the mechanism I needed to address.

What the Reference Ranges Miss

I want to spend a moment on this because it’s the point most people miss when they accept a “normal” TSH result.

Standard lab reference ranges are built from the central 95% of whoever the lab tested – which includes people with subclinical thyroid disease that hasn’t been diagnosed yet. The range doesn’t tell you where thyroid function is optimal for hormone production and male physiology. It tells you where you’re in the same range as 95% of tested samples, including the sample of people who have undiagnosed thyroid dysfunction. Ron covers this specific gap in his reference range vs optimal range article, and it applies to thyroid markers as much as it does to testosterone.

My GP saw 2.8 and stopped. Running the complete panel – adding free T3, reverse T3, and TPO antibodies to the standard TSH – changed the interpretation completely. If you order only TSH, you’ll often miss subclinical Hashimoto’s, poor T4-to-T3 conversion, and elevated rT3. All three of those were present in my results. The single-number TSH test missed all of them.

The Protocol – What I Changed

I want to be honest about the limitations of my approach. I was changing multiple variables simultaneously – this is not a controlled study, and I cannot isolate which intervention produced which result. What I can say is that my protocol was sequenced logically based on the deficiencies identified, and the bloodwork moved in the expected direction.

Selenium (selenomethionine) 200mcg daily: Selenium is required for the enzymatic conversion of T4 to active T3. The D1 deiodinase enzyme that performs this conversion is selenium-dependent. Inadequate selenium is one of the most common contributors to poor T4-to-T3 conversion and elevated rT3. I was likely suboptimal – my diet has never been particularly seafood-heavy despite living in the Pacific Northwest.

Zinc picolinate 30mg daily: Zinc is required for thyroid hormone synthesis and for the conversion of T4 to T3 at a different enzymatic step. My wife ordered a serum zinc alongside the thyroid panel – I came back at 72 mcg/dL, low-normal. Ron’s foundation stack already includes zinc; I hadn’t been taking it consistently. I got consistent.

Vitamin D3 5,000 IU with K2 MK-7: My 25-OH vitamin D came back at 31 ng/mL – technically sufficient, functionally suboptimal. Vitamin D receptor polymorphisms are associated with Hashimoto’s risk and autoimmune thyroid conditions more broadly. Getting into the 50+ ng/mL range is consistently associated with reduced TPO antibody levels in the literature, though causality is contested.

Eliminated gluten for 12 weeks: The autoimmune thyroid connection with gluten sensitivity – specifically molecular mimicry between gliadin proteins and thyroid tissue – is a mechanism that my wife flagged. It remains contested in the mainstream literature. I ran it for 12 weeks as an experiment. The TPO antibody result at week 12 was down meaningfully. I can’t prove the gluten elimination caused that. The correlation exists in my data.

Magnesium glycinate 400mg before bed: Magnesium is required for T4-to-T3 conversion at multiple enzymatic steps and for cortisol regulation. My slightly elevated AM cortisol was relevant here – chronic cortisol elevation promotes the rT3 shunting pathway, preferentially converting T4 to inactive rT3 rather than active T3.

Basal body temperature monitoring: My wife suggested I track morning oral temperature before getting out of bed. The first two weeks averaged 96.9°F – below the 97.8-98.2°F range typically associated with adequate thyroid function. This confirmed the clinical picture. I tracked it throughout the protocol as a free daily proxy for thyroid status improvement.

Month 3 Check-In

Thyroid Marker	Baseline	Month 3	Change
TSH	2.8 mIU/L	1.9 mIU/L	-0.9 (trending optimal)
Free T3	2.4 pg/mL	3.1 pg/mL	+0.7
Reverse T3	22 ng/dL	16 ng/dL	-6 (-27%)
TPO antibodies	48 IU/mL	31 IU/mL	-17 (-35%)

Testosterone Marker	Baseline	Month 3	Change
Total testosterone	380 ng/dL	478 ng/dL	+98 (+26%)
Free testosterone	8.6 pg/mL	13.4 pg/mL	+4.8 (+56%)
SHBG	68 nmol/L	52 nmol/L	-16 (-24%)
AM cortisol	19 mcg/dL	14 mcg/dL	-5

Morning basal body temperature at month 3: averaging 97.6°F, up from 96.9°F.

The free T3 moving from 2.4 to 3.1 pg/mL, combined with rT3 dropping from 22 to 16 ng/dL, meant my thyroid hormone was becoming more available and less blocked. The SHBG dropping 16 points in three months – directly tied to improved thyroid function – drove most of the free testosterone improvement. My total T went up 98 points, but my free T nearly doubled because SHBG came down significantly.

TPO antibodies below 35 IU/mL for the first time: that was the result I found most interesting. Whether the gluten elimination, the vitamin D repletion, the selenium, or some combination drove that change, the autoimmune marker was moving in the right direction.

Month 6 – Final Results

Marker	Baseline	Month 3	Month 6	Total Change
TSH	2.8	1.9	1.6 mIU/L	-1.2 (optimal range)
Free T3	2.4	3.1	3.5 pg/mL	+1.1 (+46%)
Reverse T3	22	16	13 ng/dL	-9 (-41%)
TPO antibodies	48	31	22 IU/mL	-26 (-54%)
Total testosterone	380	478	568 ng/dL	+188 (+49%)
Free testosterone	8.6	13.4	18.2 pg/mL	+9.6 (+112%)
SHBG	68	52	42 nmol/L	-26 (-38%)
AM cortisol	19	14	12 mcg/dL	-7 (-37%)

Morning temperature at month 6: 97.9°F average. Within normal range for the first time in the four years I’d been occasionally measuring it informally.

Total testosterone from 380 to 568 ng/dL. Free testosterone from 8.6 to 18.2 pg/mL. SHBG from 68 to 42. The thyroid correction drove much of the SHBG normalization, which drove most of the free T improvement. This is the mechanism Ron describes in the complete male hormone panel article – thyroid function affects SHBG production, which determines how much of your total T is actually bioavailable. You can’t optimize free testosterone without addressing anything that’s driving SHBG abnormally high. In my case, that was the thyroid.

I want to be honest: this was not a simple n=1 intervention. I changed five variables at the same time and cannot cleanly isolate which drove which result. What I can say is that the bloodwork moved in the direction the mechanism predicts – thyroid function improving, SHBG coming down, free T going up, cortisol normalizing – over a six-month period of consistent protocol adherence.

What I Didn’t Need

I did not need levothyroxine. My numbers, while suboptimal in the functional sense, never reached the clinical hypothyroidism threshold (TSH above 4.0 with symptomatic presentation) that would warrant prescription thyroid medication. A TSH of 2.8 with mildly depressed free T3 and elevated rT3 is a different clinical picture from TSH of 6.2 with frank hypothyroid symptoms.

I also didn’t need NDT (natural desiccated thyroid – Armour, NP Thyroid) or T3 medication. Those are appropriate for people with more significant conversion problems or structural thyroid disease. My situation responded to nutritional support of the conversion pathways. I’d be cautious about anyone recommending prescription thyroid treatment to someone with a TSH in my range without first trying the nutritional approach for 3-6 months.

My father’s comment at the six-month mark: “The selenium finding is interesting. We didn’t run those panels in practice routinely.” That felt like progress.

The Protocol Priority List

Tier 1 – Test First, Always

• Full thyroid panel before assuming TSH alone tells the story: TSH, free T3, free T4, reverse T3, TPO antibodies, TG antibodies
• Add serum zinc and 25-OH vitamin D to that same draw
• If you have access to one, track basal body temperature for two weeks before and during the protocol – it’s free and it correlates with thyroid function

Tier 2 – Nutritional Support (run for at least 12 weeks)

• Selenium as selenomethionine 200mcg daily – the form matters, selenomethionine absorbs better than selenite
• Zinc picolinate 25-30mg daily with food
• Vitamin D3 5,000 IU with K2 MK-7, daily with a fatty meal
• Magnesium glycinate 400mg elemental before bed – required for T4-to-T3 conversion

Tier 3 – Consider for Autoimmune Component

• If TPO antibodies are elevated (above 35 IU/mL), a 12-week strict gluten elimination is worth running and retesting – the mechanism is plausible, the cost is low, and your own data will tell you if it’s relevant for you
• Stress management: the cortisol-thyroid interaction runs both ways. Chronic cortisol elevation promotes the rT3 shunting pathway. Any protocol that addresses cortisol will also tend to improve T4-to-T3 conversion efficiency

Tier 4 – Only If Nutritional Approach Fails

• Prescription thyroid medication (levothyroxine or T3) – only if TSH is above 4.0 with symptoms or if nutritional intervention fails to move free T3 after 6 months
• This is a conversation for a physician or endocrinologist, not something to self-prescribe based on internet research

What You’re Probably Thinking Right Now

My doctor said my TSH is fine. Should I push back?

Ask for the complete panel: free T3, reverse T3, and TPO antibodies in addition to TSH. If your doctor says “TSH is sufficient screening,” they may be right for population-level screening. They may not be right for someone trying to understand why their free testosterone is low despite an apparently normal total T. The additional markers are inexpensive and the information they provide is materially different from TSH alone.

Is Hashimoto’s a big deal?

Subclinical Hashimoto’s – TPO antibodies present but thyroid function not yet severely impaired – is more common than most people realize. It exists on a spectrum. Managing it through the nutritional and dietary approaches I described can sometimes slow or stabilize progression. Some people with detectable TPO antibodies never develop overt hypothyroidism. Others do. The answer is to track it and address the factors known to influence the autoimmune component, not to ignore it because it’s “subclinical.”

How do I know my free T3 is “low” if it’s within the reference range?

Because the reference range includes people with undiagnosed subclinical thyroid dysfunction. A free T3 in the bottom third of the range – in my case, 2.4 pg/mL against an upper bound of 4.4 pg/mL – represents roughly half the hormonal output of someone at the top of the range. The lab isn’t wrong to call it “normal.” It’s not wrong for you to call it “suboptimal” and address it. These are different questions.

What if selenium doesn’t move my numbers?

Run the protocol for at least 12 weeks with consistent supplementation before concluding it’s not working. Thyroid panel changes are slow. If at 12 weeks your free T3 is unchanged and rT3 is unchanged, the T4-to-T3 conversion problem either isn’t selenium-driven or isn’t the primary variable. That’s when the conversation with a knowledgeable physician about other causes becomes warranted.

Where to Start

Order the full thyroid panel. Not just TSH. If your doctor won’t add free T3, reverse T3, and TPO antibodies, use a direct lab service and pay for it yourself – it’s not expensive and the information is worth significantly more than the cost.

If your TSH is above 2.0, your free T3 is in the bottom third of range, or your TPO antibodies are above 35 IU/mL, you have something to work with nutritionally before concluding you need a prescription or that the problem is inevitable aging.

My T at 44 was 380 ng/dL and I had a TRT consult booked. My T at 48 is 568 ng/dL with a free T of 18.2 pg/mL. The thyroid was the variable that had been quietly suppressing everything else, and a single TSH test had missed it for years.

The thyroid panel you need is not the one your GP automatically orders. Ask for the full picture before concluding the picture is normal.