Confirmatory blood-work analysis for the Core Restore liver-cleanse case study. Two Quest Diagnostics panels collected through Parsley Health:
🚺 Cycle phase confirmation: Lab 1 progesterone fell within the upper luteal-phase reference range, placing it in mid-luteal phase. Lab 2 was drawn during late luteal / menses transition (confirmed by WHOOP physiological signature). Cycle-phase confounding is named explicitly per marker below.
📊 Directional signage convention. This document preserves direction and magnitude without exposing personal numeric values. Raw lab PDFs are stored privately, not committed to this repo. Reference ranges shown to anchor the directional read.
The methylation cycle was restored. Three markers in that pathway moved in the favorable direction during the case-study window:
This is direct biochemical confirmation that the protocol’s intended mechanism — supporting Phase 2 conjugation pathways through methylation-cycle restoration — was occurring at the level of measurable bloodwork, not just wearable-derived autonomic data.
| Marker | Pre (Jan 2026) | Post (Apr 2026) | Direction | Mechanism |
|---|---|---|---|---|
| Homocysteine | Above reference range | Within range | ⬇⬇ | Elevated homocysteine = methylation cycle bottleneck = depleted SAMe = COMT cannot methylate 4-OH estrogens. Drop into range = restored Phase 2 capacity for estrogen detox.1 |
| Vitamin B12 | Low-normal | Mid-normal | ⬆ | Cofactor for methionine synthase. Low B12 elevates homocysteine. B12 ⬆ + homocysteine ⬇ = coherent methylation restoration. |
| Methylmalonic acid (MMA) | (not measured pre) | Within range | — | Functional B12 marker. In-range confirms B12 utilization at cellular level, not just serum availability. |
Why this matters for endometriosis specifically: estrogen is metabolized in the liver via Phase 1 (hydroxylation) and Phase 2 (methylation, sulfation, glucuronidation). The 4-hydroxy estrogen metabolites are reactive quinones that form DNA adducts and drive oxidative stress (Cavalieri & Rogan 2016).1 COMT methylates these dangerous metabolites into safer 2-methoxyestrogens. COMT requires SAMe (S-adenosylmethionine) as the methyl donor. SAMe is produced by the methylation cycle. When the methylation cycle is bottlenecked, homocysteine climbs, SAMe falls, and 4-OH estrogens accumulate — driving exactly the kind of inflammation that worsens endometriosis. The homocysteine drop documented here = direct evidence the protocol restored this pathway.
| Marker | Pre (Jan 2026) | Post (Apr 2026) | Direction | Notes |
|---|---|---|---|---|
| hs-CRP | Within optimal range | (not measured post) | (baseline only) | Already low-optimal — useful reference point for future panels. May et al. systematic review documents elevated hs-CRP in active endometriosis.2 |
| Sed rate (ESR) | Below reference, optimal | (not measured post) | (baseline only) | Confirms low systemic inflammation at baseline. |
| Apolipoprotein B | Above reference range | (not measured post) | (baseline only) | Cardiovascular risk marker. Elevated in endo populations.3 Worth retesting in future panel. |
| Ferritin | Within range | (not measured post) | (baseline only) | Iron stores and inflammation marker. Normal at baseline. |
| Marker | Pre (Jan 2026) | Post (Apr 2026) | Direction | Mechanism |
|---|---|---|---|---|
| Vitamin D, 25-OH | Low-optimal | Solid optimal | ⬆⬆ | Modulates immune function (regulatory T-cells, NK-cell activity), reduces inflammatory cytokines (IL-6, TNF-α), modulates aromatase expression. Documented therapeutic effect on pelvic pain in endometriosis RCT.4 Prospective cohort data also support inverse association between dietary vitamin D and endo risk.5 |
| Thyroid peroxidase antibodies | Negative | Negative | → | No thyroid autoimmunity (relevant context — endometriosis associated with elevated TPO antibody prevalence per Petta et al.).6 |
| Thyroglobulin antibodies | (not measured pre) | Below LOQ | — | No thyroid autoimmunity. |
| Gliadin antibodies (deamidated, IgG + IgA) | (not measured pre) | Negative | — | No celiac disease autoimmunity. |
| Tissue transglutaminase antibodies (IgG + IgA) | (not measured pre) | Negative | — | No celiac disease autoimmunity. |
| Marker | Pre (Jan 2026) | Post (Apr 2026) | Direction | Notes |
|---|---|---|---|---|
| TSH | High end of normal | Slightly above reference | ⬇ slightly worse | Likely cycle-phase confounded. TSH naturally elevates in late luteal phase (Lab 2 was drawn during late luteal / pre-menses). Estrogen increases thyroid binding globulin (TBG), which can elevate TSH feedback. Worth re-testing in follicular phase before drawing conclusions. May also reflect caffeine elimination during protocol (transient calorie restriction can nudge TSH). |
| Free T4 | Within range | Within range | → | Stable. |
| Free T3 | Within range | Slightly lower | ⬇ slightly | Could be cycle-phase or caloric effect. Within range both times. |
| Reverse T3 | (not measured pre) | Within range | — | Confirms healthy peripheral thyroid conversion at Lab 2. |
These were drawn during mid-luteal phase (cycle day ~22). Reference ranges below show why these values reflect the cycle moment, not a fixed personal baseline.
| Marker | Pre (Jan 2026) | Cycle-phase context | Notes |
|---|---|---|---|
| Estradiol | Within luteal range | Mid-luteal range: 56–214 pg/mL | Consistent with mid-luteal phase. |
| Progesterone | High end of luteal range | Luteal range: 2.6–21.5 ng/mL | Peak luteal — confirms functional ovulation. Healthy mid-luteal value. The cycle-phase anchor for all subsequent analysis. |
| Estrone | Within luteal range | Luteal: 16–173 pg/mL | Normal. |
| DHEA-S | Within range | — | Adrenal androgen status normal. |
| Testosterone (total + free) | Within range | — | Within age-appropriate female range. |
| Insulin (fasting) | Within range, well below upper | — | Insulin sensitivity is good. |
| Group | Status | Notes |
|---|---|---|
| Comprehensive metabolic panel (glucose, BUN, creatinine, eGFR, electrolytes, calcium, protein, albumin, bilirubin, liver enzymes ALT/AST/ALP) | All within range | Fasting glucose within range. ALT/AST low-normal — no liver enzyme elevation. eGFR within range — normal kidney function. |
| CBC with differential | All within range except hematocrit slightly above (likely hydration-related) | WBC, RBC, hemoglobin, platelets all normal. Hematocrit slightly elevated is most often dehydration. |
| Lipid panel (Lipoprotein(a)) | Optimal | Lp(a) very low — cardiovascular risk marker, optimal at baseline. |
| Magnesium RBC | Mid-range | Cellular magnesium status adequate — important context because magnesium is a cofactor for methylation. |
What it does establish: multiple biomarkers moved in the direction predicted by the protocol’s underlying mechanism, with the homocysteine improvement being mechanistically aligned with the case study’s central thesis about Phase 2 estrogen clearance. That’s not proof — but it’s evidence.
Honest scope-setting before discussing the parallel microbiome data: this case study is a hepatic Phase 2 case report. It documents biomarker shifts (homocysteine ⬇⬇, B12 ⬆, vitamin D ⬆⬆) that reflect restored hepatic methylation cycle and Phase 2 capacity. It does not directly characterize whether microbiome-driven β-glucuronidase activity was simultaneously attenuating those effects.
Specifically, the following measurements were NOT performed during the case-study window and would be required to test the integrative microbiome × estrogen-clearance thesis directly:
| Not measured | Why it would matter |
|---|---|
| β-glucuronidase enzyme activity (urine or stool) | Would quantify whether bacterial deconjugation was actually occurring at clinically meaningful levels during the protocol, vs. just being theoretically present based on species composition |
| DUTCH Complete urine hormone metabolite panel | Would show whether 2-OH / 4-OH / 2-MeO estrogen ratios shifted in directions consistent with Phase 2 improvement; could indicate whether the COMT methylation pathway was effectively delivering substrate |
| Vaginal microbiome retest during or immediately after Core Restore | Would show whether the protocol itself shifted the vaginal community composition; the most recent Evvy data is from ~17 months before the Core Restore (May / Nov 2024) |
| Gut microbiome characterization | Would show whether gut estrobolome composition could account for any residual estrogen recirculation; gut β-glucuronidase activity is the larger-magnitude estrobolome effect in most populations |
| Serum free estrogen + estrogen-binding-globulin status | Would help separate “more conjugated, less free” (Phase 2 working) from “less conjugated, more free” (microbiome reactivating) |
The author’s vaginal microbiome characterization (Study 001 pilot data, May 2024 + Nov 2024 retest) shows a CST-IV dysbiotic pattern with roughly half the community composition having β-glucuronidase and/or sulfatase enzymatic potential (Gardnerella spp., Prevotella spp., Atopobium / Fannyhessea, Megasphaera, Sneathia). On published mechanism, these species’ enzymes deconjugate cleared estrogens in vitro.
Whether they were actively doing so in this author’s body during the Core Restore protocol — and at what magnitude — is not measured by this case study.
That distinction matters for two reasons:
For the full discussion of the integrative thesis, what the published research supports separately for each axis, why the integrative cohort research is sparse, and what specific future measurements would test the framework — see microbiome-estrogen-axis.md. That document explicitly frames the dual-axis thesis as hypothesis-generating, with concrete recommendations for the empirical research design that would move it to hypothesis-confirming.
For anyone considering similar tracking, the highest-yield additions would be:
See ../../research/ for the full consolidated bibliography across the repo.
Cavalieri EL, Rogan EG. “Depurinating estrogen-DNA adducts, generators of cancer initiation: their minimization leads to cancer prevention.” Clin Transl Med. 2016;5(1):12. PMID: 27060235 ↩ ↩2
May KE, Conduit-Hulbert SA, Villar J, Kirtley S, Kennedy SH, Becker CM. “Peripheral biomarkers of endometriosis: a systematic review.” Hum Reprod Update. 2010;16(6):651-674. PMID: 20462942 ↩
Melo AS et al. “Endometriosis and lipid profile: a cross-sectional study.” (Verify exact citation; multiple studies document dyslipidemia in endo cohorts.) ↩
Mehdizadehkashi A et al. “The effect of vitamin D supplementation on chronic pelvic pain of patients with endometriosis: a randomized, double-blind, placebo-controlled trial.” Gynecol Endocrinol. 2021;37(7):640-645. ↩
Harris HR, Chavarro JE, Malspeis S, Willett WC, Missmer SA. “Dairy-food, calcium, magnesium, and vitamin D intake and endometriosis: a prospective cohort study.” Am J Epidemiol. 2013;177(5):420-430. PMID: 23380045 ↩
Petta CA, Arruda MS, Zantut-Wittmann DE, Benetti-Pinto CL. “Thyroid autoimmunity and thyroid dysfunction in women with endometriosis.” Hum Reprod. 2007;22(10):2693-2697. ↩