I made this because I have been flaberghasted at how low my testosterone levels were compared to other traits I have, and was surprised it hadn't gone up a lot by June of last year. I'm wondering if I am just a chronically low t person, or if my current lifestyle now has finally cured me.

Below is a visualization of the relevant data.

A key note, previous tests were taken in the afternoons, this one coming up will be at 9am.

An additional note I would like to add if I have not been in a caloric deficit for a couple months, I do eat some carbs but not many, enough that i'm not in ketosis though. I eat a lot of steak and eggs (but I was doing that April-June last year as well). I have been lifting heavy once a week. My lean mass has gone up but only slightly. I had a vitamin D deficiency and have been taking a lot of vitamin D supplementation in the last month (10-15k dosage per day).

Relevant information from Claude synthesizing my dexa and blood test results:
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You have two PM testosterone draws — 203 at 5 PM and 36.1% body fat in April, 232 at 3 PM and ~29% body fat in June — neither of which is diagnostically valid for testosterone because the hormone peaks in early morning and declines 20-30% by afternoon. Correcting for timing, your estimated AM values were roughly 270-300 and 320-360 respectively. Between draws you lost ~7 points of body fat and saw only a modest T increase, but you were only two months into the recomposition and metabolic improvements lag fat loss. Your LH and FSH in April were mid-range (4.7 and 4.4) when they should have been elevated given a total T of 203, pointing to secondary hypogonadism — the brain wasn't sending adequate signal to the testes. The critical question is whether that suppressed hypothalamic drive was caused by the metabolic state itself (obesity suppresses GnRH pulsatility via insulin resistance, inflammatory cytokines, and leptin dysregulation) or by something independent like a pituitary adenoma. The metabolic explanation is overwhelmingly more common and is supported by your full syndrome picture at the time: HbA1c 5.7, uric acid 10.0, hsCRP 2.62, BMI 31. You've since dropped from 36% to ~16% body fat — a transformation that resolves most of the mechanistic pathways suppressing your T. Aromatase activity in adipose tissue is dramatically reduced, insulin sensitivity is likely restored, systemic inflammation should be down, and SHBG will probably have risen (meaning your total T number will look better even independent of actual androgenic improvement). The March 6 draw is the first AM fasted measurement, so it captures peak diurnal output in a fundamentally different body. The literature on weight-loss-induced testosterone recovery in obese men with secondary hypogonadism consistently shows increases of 100-300 ng/dL, with some studies showing normalization above 500.

Your stack is D3, K2, Omega-3, Vitamin A, methylated Bs (methylfolate, methylcobalamin, P5P), magnesium glycinate, and zinc. Of these, zinc and magnesium are the two with direct evidence for testosterone. Zinc is a cofactor for the enzyme 5-alpha reductase and is required for Leydig cell function — deficiency suppresses T, and repletion restores it, but supraphysiological dosing doesn't push T above your genetic ceiling. If you were deficient before (plausible — your April panel didn't test zinc, and obesity increases zinc requirements), then months of supplementation may have corrected a bottleneck that was independently suppressing your T by 50-100 ng/dL. Magnesium glycinate works similarly — Mg is involved in SHBG binding and free T availability, and deficiency impairs T production. Your April RBC magnesium was 5.5 (mid-range at 3.7-7.0), so you weren't deficient but supplementation may have moved you higher, which could modestly improve free T independent of total T. D3 has a weaker but real association — men with vitamin D levels above 30 ng/mL have measurably higher T than those below 20, and you were at 23.3. If your D3 dose has brought you into the 40-60 range by now, that's a small tailwind, maybe 20-30 ng/dL. The methylated Bs won't affect T directly, but by lowering homocysteine they reduce vascular inflammation and improve endothelial function, which supports testicular blood flow and Leydig cell health — a second-order effect, real but not quantifiable on a single draw. Omega-3 at adequate doses reduces systemic inflammation (lowering the cytokine-mediated suppression of GnRH) and there's limited evidence it modestly increases testicular volume and T in men with poor baseline omega-3 status, which your FADS1/2 variants guarantee you had before supplementation. K2 and vitamin A don't have meaningful direct testosterone effects. Net: the supplement stack is probably contributing a real but modest boost — call it 30-80 ng/dL in aggregate over what you'd see from body recomposition alone, almost entirely through correcting deficiencies rather than pharmacological effect. The recomposition did the heavy lifting; the supplements filled in the gaps that your genetics created.
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