Body Fat at 28% to 17% – What Every Bloodwork Marker Did During the Recomposition

TL;DR: I went from 28% body fat to 17% over 11 months while tracking a full hormone panel every 8 weeks. Testosterone went from 310 to 626 ng/dL. But the marker that moved fastest and most consistently was estradiol – it dropped nearly in half before testosterone had moved much at all. Here is every number, every checkpoint, and what I learned about the fat-hormone relationship.

Some context before the data. At 41, I ran a brutal 18-month stretch that wrecked my numbers – a bad merger at work, my closest friend’s divorce, a parent’s terminal diagnosis, all compressed into the same window. My testosterone crashed from 720 to 310 ng/dL. I have written about the stress and recovery arc separately. What I have not published until now is the body composition data that ran alongside that recovery – because the fat loss was a major part of why the testosterone came back, and I did not understand that clearly until the bloodwork told me.

I found Ron Males and PowerandBulk.com during a 2am research session when I was reading everything I could about natural T recovery before committing to TRT. Ron’s framework was the one that made the most mechanistic sense. He was direct about the fat-estrogen-testosterone relationship in a way most content glossed over. I signed up for Anabolic Alchemy and started tracking everything.

Why Body Fat Matters More Than Most T-Optimization Content Admits

Adipose tissue – body fat – is not inert storage. It produces aromatase (the enzyme that converts testosterone into estradiol, the primary estrogen in men). The more body fat you carry, especially visceral fat around the organs, the more aromatase activity you run, and the more testosterone gets converted to estrogen before it can do anything useful. This is not a fringe theory – it is basic endocrinology that most gym-based hormone content ignores because it does not sell supplements.

At 28% body fat I was running a significant aromatase load. My estradiol was elevated relative to my testosterone. My SHBG was suppressed because my fasting insulin was high. My free testosterone was therefore lower than my already-low total testosterone would suggest. The cascade was complete: fat drove aromatase, aromatase drove estrogen, estrogen and insulin suppressed SHBG, and the compounded effect was free testosterone that was functionally low even in a man who was theoretically in the “normal” range.

Understanding this changed how I tracked the recovery. Bodyweight was the least informative number. Waist circumference was more informative. But the bloodwork – specifically estradiol, SHBG, and fasting insulin tracked against fat loss – told the real story.

The Baseline – Month 0

I use a Whoop band and had been tracking HRV for about four months before the protocol started. My HRV at baseline was 31 ms – very low for my age and consistent with the chronic sympathetic activation that Ron identified as the primary driver of my hormonal collapse. My wife had told me I needed to do something. She was not wrong.

Marker	Month 0	Units
Bodyweight	208	lbs
Body fat % (estimated, calipers)	28	%
Waist circumference	40	inches
Total testosterone	310	ng/dL
Free testosterone (calculated)	6.8	pg/mL
SHBG	18	nmol/L
Estradiol	48	pg/mL
IGF-1	141	ng/mL
Fasting insulin	14	uIU/mL
HbA1c	5.7	%
Cortisol (AM)	24	mcg/dL
Whoop HRV (7-day avg)	31	ms

The estradiol at 48 pg/mL on a total T of 310 is the number that jumps out. The ratio was badly skewed. In a man with a T of 310, estradiol in the 20s would be expected. At 48, the aromatase activity was running well above what my fat mass alone would predict – the chronic cortisol elevation from the stress period was also upregulating aromatase directly. Two separate inputs driving the same problem.

The Protocol – What I Actually Changed

Ron sequenced this deliberately. Stress management and sleep first. Deficit and fat loss second. Training third.

Months 1-2: No caloric deficit. Focus on sleep quality (Whoop tracking), breathwork, alcohol eliminated completely, morning sunlight protocol. This was harder to follow than it sounds because my instinct was to cut calories immediately. Ron held the line – until my HRV was out of the 30s, adding a caloric deficit would add cortisol to an already-cortisol-dominated system and impede fat loss rather than accelerate it.

Month 3 onward: Slow deficit of 250-300 kcal below maintenance. Protein floor of 175g per day. Three strength sessions per week – squat, press, pull – kept simple and progressive. Walking 10,000+ steps daily, which I tracked on Whoop.

Month 4 onward: Added zinc bisglycinate 25mg and magnesium glycinate 400mg at bedtime. Vitamin D3 5,000 IU with K2. No T-specific supplements until month 6 when Ron added boron 9mg. No Tongkat ali, no Fadogia, nothing exotic until the lifestyle foundation was established.

Month 2 Checkpoint

Marker	Month 0	Month 2	Change
Bodyweight	208 lbs	204 lbs	-4 lbs
Waist	40 in	39 in	-1 in
Total testosterone	310 ng/dL	328 ng/dL	+18
SHBG	18 nmol/L	22 nmol/L	+4
Estradiol	48 pg/mL	40 pg/mL	-8
Fasting insulin	14 uIU/mL	11 uIU/mL	-3
Cortisol (AM)	24 mcg/dL	19 mcg/dL	-5
Whoop HRV (7-day avg)	31 ms	38 ms	+7

The estradiol moved before the testosterone did. This is the pattern I see throughout the entire 11-month arc – estradiol leads, testosterone follows. The mechanism is logical: estradiol is downstream of aromatase activity, which is downstream of fat mass and cortisol. Reduce the drivers, estradiol falls first. Testosterone recovers into the improved environment second. The lag between estradiol improvement and testosterone improvement was consistently about 4-6 weeks across every checkpoint.

The SHBG moving from 18 to 22 – in the right direction – as fasting insulin dropped was textbook. Hyperinsulinemia suppresses hepatic SHBG production. As insulin normalizes, SHBG normalizes. Higher SHBG in this context is not bad – it was moving from a suppressed state toward the middle of the range, which improves the testosterone-to-estradiol ratio even before total T has fully recovered.

Month 4 Checkpoint

Marker	Month 0	Month 2	Month 4	Change M0→M4
Bodyweight	208	204	197	-11 lbs
Waist	40 in	39 in	37 in	-3 in
Body fat % (est.)	28%	26%	23%	-5%
Total testosterone	310	328	442	+132 ng/dL
Free testosterone	6.8	7.6	10.4	+3.6 pg/mL
SHBG	18	22	31	+13 nmol/L
Estradiol	48	40	32	-16 pg/mL
IGF-1	141	148	174	+33 ng/mL
Fasting insulin	14	11	7	-7 uIU/mL
HbA1c	5.7%	—	5.4%	-0.3%
Cortisol (AM)	24	19	16	-8 mcg/dL
Whoop HRV	31 ms	38 ms	48 ms	+17 ms

Month 4 was when my wife noticed the change before I did. She mentioned it casually on a Tuesday evening and I was not sure what to say. The testosterone jump from 328 to 442 between months 2 and 4 was the largest single-checkpoint gain in the arc. It coincided with the period when visceral fat loss was accelerating, cortisol was finally in normal range, and SHBG was climbing back toward the reference range.

Free testosterone nearly doubled from baseline to month 4 – from 6.8 to 10.4 pg/mL. This is the number I care about most subjectively. Free testosterone is what the body actually uses. At 6.8 I felt like a different person than I do at 10.4. The energy, the mental clarity, the recovery from exercise – all of these track more closely with free T than with total T in my experience.

Month 6 Checkpoint

This was a significant milestone for me psychologically because month 6 was when Ron had originally suggested we would have a meaningful conversation about whether TRT was still on the table. It was clearly not on the table.

Marker	Month 0	Month 4	Month 6	Change M0→M6
Bodyweight	208	197	191	-17 lbs
Waist	40 in	37 in	35 in	-5 in
Body fat % (est.)	28%	23%	20%	-8%
Total testosterone	310	442	531	+221 ng/dL
Free testosterone	6.8	10.4	13.2	+6.4 pg/mL
SHBG	18	31	36	+18 nmol/L
Estradiol	48	32	26	-22 pg/mL
IGF-1	141	174	196	+55 ng/mL
Fasting insulin	14	7	5	-9 uIU/mL
Cortisol (AM)	24	16	14	-10 mcg/dL
Whoop HRV	31 ms	48 ms	58 ms	+27 ms

Estradiol at 26 pg/mL on a total T of 531 ng/dL is a healthy ratio. At baseline, estradiol was 48 on a T of 310 – nearly 15% of total T by a rough equivalency measure. At month 6, it was 26 on a T of 531. The aromatase load had come down dramatically as visceral fat came off and cortisol normalized.

The IGF-1 climb to 196 ng/mL surprised me. I had not expected protein optimization and sleep recovery to drive IGF-1 that far. Ron explained it as a combined effect – sleep architecture improving (which drives GH pulsatility and downstream IGF-1), protein adequacy increasing (which supports hepatic IGF-1 synthesis), and the reduced cortisol burden (which had been actively suppressing the GH axis). All three were moving simultaneously. The IGF-1 reflected all three at once.

Final Results – Month 11

The last three months (months 8-11) were slower progress on fat loss – I was running the standard 0.5 lb/week pace as I approached 17% body fat, which is normal. The hormonal improvement continued tracking the fat loss closely.

Marker	Month 0	Month 6	Month 11	Total Change
Bodyweight	208 lbs	191 lbs	182 lbs	-26 lbs
Waist	40 in	35 in	32 in	-8 in
Body fat % (est.)	28%	20%	17%	-11%
Total testosterone	310	531	626	+316 ng/dL
Free testosterone	6.8	13.2	16.8	+10.0 pg/mL
SHBG	18	36	40	+22 nmol/L
Estradiol	48	26	22	-26 pg/mL
IGF-1	141	196	218	+77 ng/mL
Fasting insulin	14	5	4	-10 uIU/mL
HbA1c	5.7%	—	5.1%	-0.6%
Cortisol (AM)	24	14	12	-12 mcg/dL
Whoop HRV	31 ms	58 ms	68 ms	+37 ms

316 ng/dL of total testosterone recovered. Estradiol cut nearly in half. HRV more than doubled. Every single marker I tracked moved in the right direction across 11 months. I did not start at 310 because of some genetic or medical condition that required pharmaceutical intervention. I started at 310 because excess body fat, chronic cortisol, and a collapsed recovery system were actively suppressing a hormonal axis that was otherwise functional. Remove the suppressors and the axis recovered.

What the Bloodwork Timeline Taught Me

The sequencing of which markers moved when is the most useful finding for anyone trying to understand this process.

First to move (months 1-2): Cortisol, HRV, fasting insulin. These responded to behavioral changes – sleep improvement, alcohol elimination, stress management – before any meaningful fat loss had occurred. This is why Ron insisted on the nervous system work before the deficit. The cortisol needed to come down before the fat loss would produce its full hormonal benefit.

Second to move (months 2-4): Estradiol and SHBG, tracking the early fat loss and insulin improvement. Estradiol is the fastest-moving marker in the testosterone-estrogen system. It responds to aromatase activity changes within weeks. SHBG follows insulin sensitivity with a similar lag.

Third to move (months 3-6): Total testosterone and free testosterone, following the improved hormonal environment. The body does not immediately upregulate testosterone production when estradiol drops – the HPT axis (the communication chain from hypothalamus to pituitary to testes that controls testosterone production) takes time to recalibrate. The testosterone climbed steadily as the suppressive inputs were removed.

Last and most sustained (months 4-11): IGF-1, which continued improving throughout and was still trending upward at the final measurement. This makes sense – IGF-1 is downstream of GH pulsatility, sleep architecture, protein nutrition, and general metabolic health, all of which were still improving at month 6 and beyond.

The Part That Was Harder Than the Data Shows

I am a finance person. I like clean data. The 11-month arc looks orderly in a table. It did not feel orderly. Month 3 was a flat patch where nothing on the scale moved for three weeks and I almost called Ron to say the protocol was not working. Month 7 was a second plateau that lasted two weeks. The psychological work of staying in a slow protocol when progress is not visible is the part that the tables do not capture.

The flat patches were real. The progress through them was also real, just happening at a level the scale could not measure. The bloodwork always showed movement even when the scale did not. Ron’s instruction every time I hit a flat: pull the bloodwork, not the rip cord. The bloodwork told me to hold. I held.

Ron Males described the body composition and hormone relationship in the fat loss and testosterone piece and in the body recomposition protocol in ways that I wish I had read before starting rather than during. If you have not read those, they explain the mechanism behind what I just showed in tables. Read those, then come back to this data. The numbers will make more sense.

One Thing to Take Away

If you are at 25%+ body fat and your testosterone is in the 200s-400s, the most impactful thing you can do is not find the right supplement. It is lose the fat slowly, without destroying the cortisol-sleep system in the process. The bloodwork will follow the fat loss with a 4-6 week lag on each marker. Estradiol first, then SHBG, then testosterone, then IGF-1. Trust the sequence. Pull labs every 8 weeks so you can see it happening even when the scale is lying to you. The process is slower than you want it to be and more effective than most people believe it can be.