The biomarkers Juno tracks.

ALMI = (arm LBM + leg LBM) / height². Sarcopenia-diagnostic threshold per EWGSOP2: <7.0 (M), <5.5 (F). GH-axis peptides and resistance-training adjuncts plausibly favorable; trial data sparse for ALMI specifically.

Ratio of trunk-region fat to hip-region fat. Higher values associate with metabolic-syndrome risk. GLP-1s shift A/G favorably alongside total fat loss. Sex-dependent baseline.

DEXA body-fat % is gold-standard relative to BIA / circumference methods. Range above is generic — actual optimal varies meaningfully by age and sex (30y M: ~10-15%, 30y F: ~18-23%, older adults: higher). GLP-1 agonists (tirzepatide, semaglutide, retatrutide), 5-amino-1MQ, AOD-9604 — all documented to lower body fat in trials. GH-axis peptides have mixed evidence.

Whole-body lean mass. GH-axis peptides (CJC-1295/ipamorelin, tesamorelin, MK-677) documented to increase LBM in trials. BPC-157 / TB-500 — no DEXA-confirmed effect. Tirzepatide / semaglutide can cause LBM loss alongside fat loss; recent retatrutide data suggests less LBM loss than semaglutide.

Trunk-region fat divided by leg-region fat. Independent cardiometabolic risk signal alongside A/G ratio.

Visceral adipose mass — distinct from subcutaneous fat. Tesamorelin is FDA-approved specifically for HIV-lipodystrophy-related VAT reduction. GLP-1 agonists also lower VAT in trials. Threshold of clinical concern varies by sex.

Femoral-neck BMD; canonical metric for hip-fracture risk. Tracks alongside T-score for trend context.

Absolute BMD value. T-score is derived from this. Trend over serial DEXAs is more clinically meaningful than the snapshot. Peptide context: GH-axis as above.

Whole-hip BMD aggregating multiple regions.

Same as tscore_lumbar — GH-axis peptides may favorably affect femoral BMD; trials sparse. Femoral neck T-score is the canonical metric for hip-fracture risk; track alongside lumbar for whole-body bone-health assessment.

Tesamorelin and GH-axis peptides (CJC-1295, ipamorelin, sermorelin, MK-677) have documented bone-density-favorable effects via IGF-1 elevation, though direct DEXA-confirmed BMD trials are limited. NAD+ precursors (NMN, NR) — no direct BMD evidence; mitochondrial-health framing is speculative for skeletal effects.

Total-hip T-score aggregates femoral-neck + trochanter + intertrochanteric. Used clinically as a backup when lumbar L1-L4 is degraded by arthritis / compression artifact. Peptide relevance: same GH-axis logic as tscore_lumbar.

Age-matched comparison for femoral neck. Most relevant in pre-menopausal women and men under 50 who have a DEXA. Same peptide context as tscore_femoral_neck.

Z-score compares against age-matched peers — different intervention threshold than T-score. Z-score < -2.0 in adults under 50 prompts secondary-cause workup. No specific peptide literature; same GH-axis context applies.

Age-matched comparison for total hip. Used alongside femoral-neck Z-score in younger adults to flag age-discordant bone loss.

ApoB counts every atherogenic lipoprotein particle (LDL, IDL, VLDL, Lp(a)) — for cardiovascular risk it's a more precise readout than LDL-C alone, especially when triglycerides are elevated or particles are small/dense. Targets vary by personal CV risk; lower is better for high-risk users (familial hypercholesterolemia, established CVD: <70). Same peptide interactions as LDL-C — GLP-1s modestly lower, GH-axis transiently raises during the first weeks, AAS (NOT peptides, common co-use) often increases. Track ApoB alongside LDL-C when LDL is borderline or particle-quality concerns are on the table.

Higher = better, generally. GLP-1 agonists (tirzepatide, semaglutide) modestly raise HDL-C (~2-5%, weight-loss driven). CJC-1295 + Ipamorelin: minimal documented effect. Anabolic-androgenic steroids (NOT peptides, often co-used) reliably SUPPRESS HDL — a 30-50% drop in HDL is a hallmark of cycling AAS, important to flag if the user discloses use. Tirzepatide trials show HDL gains modest relative to weight loss. Exercise (especially aerobic) is the strongest HDL-raising non-pharmacological lever — confounds peptide-attribution if user is also ramping cardio.

Sulfur-containing amino acid generated in methionine metabolism; elevated levels are an independent cardiovascular risk marker and a sensitive functional indicator of B12, folate, and B6 status. Treated by addressing the methylation cofactors (B12 methylcobalamin, methylfolate, B6) rather than directly. No direct peptide effects in common stacks. MTHFR polymorphisms (677TT homozygotes) often run higher and need methylated cofactors. NOTE: must be processed within 1h of draw — sample sitting at room temp falsely elevates due to RBC release. Order with the lab knowing this; many labs reject late samples.

Standard cardiovascular risk marker; targets depend on individual risk profile (lower for established CVD or familial hypercholesterolemia). GLP-1 agonists (tirzepatide, semaglutide) modestly lower LDL-C (~3-7% in trials, driven mostly by weight loss). CJC-1295 + Ipamorelin: GH axis activation can transiently raise LDL during the first weeks; longer-term effect is usually neutral or favorable as body composition improves. BPC-157 / TB-500: no documented effect. Anabolic-androgenic steroids (NOT peptides, sometimes co-used) often lower HDL and raise LDL. NOTE: Lp(a) and ApoB are more granular CV risk markers — track those when LDL is borderline or family history is concerning.

Largely genetic; one-time test is sufficient for most users unless reducing therapies (PCSK9 inhibitors, niacin in specific cases, future Lp(a)-specific therapies) are being trialed. Elevated Lp(a) is an independent CV risk factor that LDL-C and ApoB don't capture. No direct peptide effects documented in common stacks — peptides won't move this. NOTE: some labs report in mg/dL; conversion ≈ nmol/L × 0.4. Test once early, save the number, don't repeat unless on Lp(a)-targeted therapy.

Tightly coupled to recent diet and insulin sensitivity. GLP-1 agonists (tirzepatide, semaglutide) reliably lower triglycerides 15-30% in obesity/T2D trials. CJC-1295 + Ipamorelin: GH-axis activation typically lowers triglycerides via increased lipolysis and improved fasting metabolism. Tesamorelin: documented triglyceride-lowering effect in HIV-lipodystrophy trials. BPC-157 / TB-500: no documented effect. KEY CAVEAT: triglycerides require a true 12-hour fast for accurate reading — non-fasted readings can be 2-3× higher and don't reflect baseline. Recent alcohol (last 48h) elevates triglycerides substantially.

Percentage of blood volume occupied by red blood cells; tightly correlated with hemoglobin (HCT ≈ HGB × 3). Same peptide interactions as hemoglobin — TRT and AAS reliably raise HCT; values >52% in men or >48% in women often trigger therapeutic phlebotomy on TRT to reduce stroke risk. CJC-1295 / Ipamorelin: minimal effect. KEY CAVEAT: dehydration acutely raises HCT 2-5% — interpret in context of hydration status. Smoking chronically raises HCT (hypoxic stimulus). RANGES SHOWN ARE FOR ADULT MEN; women typically 34.9-44.5%.

Oxygen-carrying capacity. Low (anemia) screens for iron, B12, folate deficiencies, kidney disease (erythropoietin deficiency), bone marrow issues, or recent blood loss. HIGH hemoglobin in peptide users is a common finding worth flagging: testosterone (TRT) reliably raises hematocrit/hemoglobin via stimulated erythropoiesis — values >18 g/dL on TRT often trigger therapeutic phlebotomy. Anabolic-androgenic steroids (NOT peptides, common co-use) have an even stronger erythropoietic effect. CJC-1295 / Ipamorelin / Tesamorelin: minimal direct hematologic effect. GLP-1 agonists: occasionally cause mild iron-deficient anemia in users with rapid weight loss + low food intake. RANGES SHOWN ARE FOR ADULT MEN; women typically 12-15.5 g/dL.

Average red blood cell size. Low MCV (microcytic) = iron deficiency anemia, thalassemia, anemia of chronic disease (long-standing). High MCV (macrocytic) = B12 deficiency, folate deficiency, alcohol use, hypothyroidism, certain medications. Most common peptide-user pattern: high MCV from heavy alcohol use (paired with high GGT) or from B12/folate insufficiency. No direct peptide effects in common stacks. KEY INTERPRETATION: order MCV alongside iron studies + B12 + folate when investigating any anemia or fatigue presentation; MCV pattern narrows the differential dramatically.

Clotting factor count. Low platelets (thrombocytopenia) increase bleeding risk; very high (>500K) increase clotting risk. Some peptide users on long-term TRT or AAS run elevated platelets (mild increase rarely clinically significant). BPC-157 has documented hemostatic / wound-healing effects; not associated with platelet count changes in available human data. No direct effects from CJC-1295 / Ipamorelin / Tesamorelin / GLP-1 agonists. KEY CAVEAT: platelet clumping in the tube can falsely lower the reported count — if dramatically low without symptoms, redraw before assuming a real issue. NSAIDs + fish oil + aspirin reduce platelet FUNCTION (not count) — relevant to bleeding-risk decisions.

Measures variation in red blood cell size — broader distribution suggests mixed cell populations (recovering from anemia, dual deficiencies, hemolysis, marrow stress). RDW is a SENSITIVE early marker: it rises before MCV shifts and before hemoglobin drops, so an elevated RDW with otherwise-normal CBC can be the earliest detectable signal of iron or B12 deficiency. Some research links elevated RDW to all-cause mortality independent of anemia — it's a general marker of physiologic stress. No direct peptide effects in common stacks. KEY INTERPRETATION: rising RDW over serial readings is more informative than a single value.

Total white blood cell count — combined neutrophils, lymphocytes, monocytes, eosinophils, basophils. Always interpret alongside the WBC differential (separate report on a CBC). Elevated WBC: infection, acute inflammation, stress response, leukemia, recent intense exercise. Low WBC: viral infection, bone marrow suppression, autoimmune disease, certain medications. NORMAL is a wide range — within that range, lower is often better (chronic low-grade inflammation can drive the upper end of normal). No direct peptide effects in common stacks. BPC-157 has documented immunomodulatory effects in animal models — could shift WBC subset distribution; not consistently demonstrated in humans. KEY CAVEAT: WBC of 4-5 K/μL is functional optimal; values >8-9 chronically suggest inflammation worth investigating.

Completes the hepatic panel alongside ALT (existing), AST, and GGT. ALP is produced by liver, bone, intestine, and placenta — elevation patterns: hepatocellular = ALT/AST up, ALP normal; cholestatic = ALP + GGT up; bone = ALP up with normal GGT (Paget's, vitamin D deficiency, bone tumors, healing fractures, growing adolescents). No direct peptide effects in common stacks. GROWTH-HORMONE-AXIS NUANCE: CJC-1295 + Ipamorelin + Tesamorelin can transiently raise ALP via bone remodeling (especially in younger users); persistent elevation warrants a fractionated ALP to separate liver vs bone origin.

BPC-157 has shown hepatoprotective effects in animal models — could lower ALT or prevent rises. Tirzepatide / Semaglutide reduce ALT in NAFLD/MASH patients (subset of SURMOUNT-MASH trial). CJC-1295 + Ipamorelin: no consistent ALT effect documented. KEY CONFOUNDERS: intense eccentric training in last 48-72h raises ALT 2-5x transiently (muscle origin, not liver); alcohol; statins (rare); high-dose acetaminophen. Anabolic-androgenic steroids (NOT peptides but often co-used) can elevate ALT substantially.

Read alongside ALT (existing entry) — together they characterize hepatic vs. extrahepatic causes of elevation. AST is less liver-specific than ALT: muscle injury, intense exercise, and red blood cell turnover all raise AST. AST/ALT ratio >2 with high MCV suggests alcohol; ratio <1 with both elevated suggests metabolic-associated steatotic liver disease (MASLD). BPC-157 has shown hepatoprotective effects in animal models — may lower or prevent rises. GLP-1 agonists lower AST modestly in NAFLD/MASH patients. KEY CONFOUNDERS: eccentric training in last 48-72h, statins (rare), AAS (NOT peptides, common co-use).

Most abundant plasma protein; reflects liver synthesis capacity AND systemic inflammation (negative acute-phase reactant — falls during inflammation). Low albumin suggests advanced liver disease, kidney protein loss (nephrotic syndrome), severe malnutrition, or chronic inflammation. Used in the free testosterone calculation (Vermeulen equation) and free-cortisol estimation. No direct peptide effects in common stacks. KEY CAVEAT: dehydration falsely elevates albumin; over-hydration falsely lowers. Healthy adult range is narrower than the standard lab range suggests — values <4.0 g/dL in an otherwise healthy adult warrant a look at protein intake or chronic inflammation. Long-term low-calorie dieting (common in peptide users on cuts) can subtly lower albumin.

Hemoglobin breakdown product; cleared by the liver. Elevation can be hepatic (liver dysfunction), pre-hepatic (hemolysis — increased RBC breakdown), or post-hepatic (biliary obstruction). Gilbert's syndrome (benign genetic variant affecting ~5-10% of population) elevates total bilirubin mildly (1.0-2.5 mg/dL) without disease — easily mistaken for liver problems. Fasting and dehydration also acutely raise total bilirubin in Gilbert's carriers. No direct peptide effects in common stacks. AAS (NOT peptides, common co-use) can elevate bilirubin in users developing cholestatic injury. KEY INTERPRETATION: if total bilirubin is elevated, order direct (conjugated) bilirubin to fractionate — mostly indirect bilirubin suggests Gilbert's or hemolysis; mostly direct suggests hepatic or biliary cause.

Sensitive marker for biliary/hepatobiliary disease, alcohol use, and certain medications (anticonvulsants, NSAIDs). Most useful as the third hepatic enzyme alongside ALT + AST to distinguish hepatocellular injury (ALT/AST up, GGT normal) from cholestatic/alcohol patterns (GGT and ALP up). No direct peptide effects in common stacks. AAS use (NOT peptides, common co-use) frequently elevates GGT alongside ALT/AST. KEY CONFOUNDERS: alcohol in last 2-4 weeks is the dominant signal; chronic drinkers run high baselines that take weeks to normalize after stopping.

Marker of ovarian reserve in women — declines progressively from the mid-20s, near-undetectable after menopause. PCOS often elevated (>4-5 ng/mL). Reasonably stable across the menstrual cycle so cycle-day timing isn't critical. No direct peptide effects documented in common stacks; AMH is genuinely a passive readout of remaining ovarian follicles. STRONGLY age-dependent — interpret with age in mind (women 20-25: ~3-4; women 30-39: ~1.5-2.4; women 40+: <1). RANGES SHOWN ARE FOR ADULT WOMEN IN REPRODUCTIVE AGE; men can have AMH but it's typically tested for fertility-window awareness in women only.

Single morning (7-9 AM) draw is the simplest cortisol assessment — captures the diurnal peak. Low values (<6 μg/dL) screen for adrenal insufficiency; very high (>25) for Cushing's or recent stress. For richer adrenal-axis assessment, 4-point salivary diurnal cortisol (separate test) tracks the curve through the day. No direct peptide effects in common stacks. KEY CAVEATS: must be morning (7-9 AM); avoid recent acute stress, biotin >5mg/day, exogenous glucocorticoid use. Hormonal birth control elevates total cortisol (raises cortisol-binding globulin) — free cortisol is unaffected. CJC-1295 + Ipamorelin: GH axis activation modestly raises cortisol via cross-talk; not clinically significant in most users.

Adrenal androgen precursor; stable surrogate for DHEA production (sulfated form has longer half-life). Strongly age-dependent — declines by ~10%/decade after age 25, so older users will read lower regardless of any intervention. No direct peptide effects documented for the common stack peptides (BPC-157, TB-500, CJC/Ipamorelin, Tesamorelin, GLP-1s). DHEA supplementation (not a peptide) raises both DHEA and downstream androgens including testosterone — often used alongside peptide stacks but tracked separately. RANGES SHOWN ARE BROAD ADULT MALE; reference labs band by age (men 30-49 ~280-640, men 70+ ~40-325) and sex (women ~150-410 at 30, ~20-200 at 70+).

More potent androgen than testosterone, produced from T via 5α-reductase in skin, hair follicles, prostate. Elevated DHT drives androgenetic alopecia and benign prostatic hyperplasia in susceptible users. Most relevant to users on TRT (TRT raises DHT alongside T), users on AAS, and users on hair-loss medications (finasteride/dutasteride SUPPRESS DHT — reading DHT confirms 5α-reductase inhibition is working). No direct peptide effects in common stacks. KEY CAVEATS: LC-MS/MS strongly preferred over immunoassay for accuracy; morning draw when paired with T. RANGES FOR ADULT MEN; women typically <10 ng/dL.

Most relevant for users on exogenous testosterone (TRT, anabolic-androgenic steroids) where aromatization raises E2 — aromatase inhibitors (anastrozole) are sometimes used in response. CJC-1295 + Ipamorelin: no consistent direct effect on E2; weight loss from any source modestly lowers E2 in men via reduced aromatase substrate. Tirzepatide / Semaglutide: weight loss can lower E2 in men with obesity. BPC-157 / TB-500: no documented E2 effect. RANGES SHOWN ARE FOR ADULT MEN. Premenopausal women have cycle-dependent E2 (roughly 30-400 pg/mL with ovulatory peak); postmenopausal women <30 pg/mL. The 'sensitive' (LC-MS/MS) assay is required for accurate low-level readings (men, postmenopausal women).

Pituitary gonadotropin. In men, FSH stimulates Sertoli cell function and spermatogenesis. In women, FSH stimulates ovarian follicle growth — rises sharply in perimenopause and menopause (>25 mIU/mL postmenopausal). Exogenous androgens (TRT, AAS) suppress FSH via negative feedback — low FSH + low LH on TRT is expected. Kisspeptin (a peptide) directly stimulates GnRH → LH/FSH release; one of the few peptides with documented HPG axis effects. CJC-1295 + Ipamorelin: minimal FSH effect. RANGES SHOWN ARE FOR ADULT MEN; women have cycle-dependent values (follicular ~3-10, menopausal >25).

Biologically active thyroid hormone — symptoms correlate with T3 more than T4. Low T3 with normal T4 can indicate poor T4→T3 conversion (selenium / zinc deficiency, chronic stress, low-calorie dieting, illness). Common in users doing aggressive cuts or fasting. Tirzepatide / Semaglutide may slightly lower T3 during rapid weight loss (adaptive thermogenesis). No direct peptide effects from the standard stack peptides documented. Reverse T3 (rT3) is the inactive isomer — order alongside if poor conversion is suspected.

The thyroid's primary output; converted to active T3 peripherally. Read with TSH for thyroid status: high T4 + low TSH = hyperthyroidism; low T4 + high TSH = primary hypothyroidism; low T4 + low TSH = central / pituitary hypothyroidism (rare). No direct peptide effects in common stacks. Exogenous T4 (levothyroxine) elevates free T4 and suppresses TSH. CJC-1295 + Ipamorelin: no documented thyroid axis effect.

The biologically active fraction of testosterone — the part not bound to SHBG or albumin. Most clinically reliable when CALCULATED from total testosterone + SHBG + albumin (Vermeulen equation) rather than measured by direct immunoassay (the latter is notoriously inaccurate). Equilibrium dialysis is the gold standard but rarely ordered. Symptoms of low T correlate better with free T than total T, especially when SHBG is at the extremes. Same peptide interactions as total testosterone — exogenous androgens (TRT, AAS) raise it; CJC-1295 + Ipamorelin don't directly affect HPG axis but improving body composition can modestly lift free T via lower SHBG. RANGES SHOWN ARE FOR ADULT MEN; women typically <2 pg/mL.

Most directly affected biomarker for GH-axis peptides. CJC-1295 + Ipamorelin: IGF-1 typically rises 20-40% within 4-6 weeks of consistent dosing. Tesamorelin (FDA-approved GHRH analog): IGF-1 elevation documented in HIV-lipodystrophy trials. Sermorelin: similar but milder effect. BPC-157 / TB-500: no documented IGF-1 effect. Range above is for adult 30-49; falls naturally with age — older users should expect lower baseline.

Pituitary gonadotropin. In men, LH stimulates Leydig cell testosterone production. In women, LH triggers ovulation. Pulsatile secretion — single draw is a snapshot. Exogenous androgens (TRT, AAS) suppress LH — low LH + low T = primary hypogonadism vs central; LH paired with T distinguishes the two. Kisspeptin (a peptide) directly stimulates GnRH → LH. Gonadorelin (a peptide) and hCG (NOT a peptide, often co-used) mimic LH signaling to maintain testicular volume during TRT. CJC-1295 + Ipamorelin: minimal LH effect. RANGES FOR ADULT MEN; women have cycle-dependent values with mid-cycle peak 25-80.

In women, progesterone is produced by the corpus luteum after ovulation — a mid-luteal value (~7 days before expected period) >5 ng/mL confirms ovulation occurred; >10 ng/mL is optimal. Postmenopausal women run <0.5 ng/mL. In men, progesterone is normally <1 ng/mL — elevation can indicate exogenous progestational AAS, certain testicular tumors, or extreme stress (cortisol pathway crossover). RANGES SHOWN ARE FOR REPRODUCTIVE-AGE WOMEN; men should be <1. Timing critical — draw 7 days before expected next period for ovulation confirmation. No direct peptide effects in common stacks.

Elevated prolactin (>15-20 ng/mL in men, >25 ng/mL in non-pregnant women) can indicate pituitary adenoma, hypothyroidism, drug effect (antipsychotics, opioids, some antidepressants), or recent stress/nipple stimulation. Suppresses libido and fertility in both sexes. PEPTIDE INTERACTIONS: 19-nor-progestational AAS (NOT peptides, common co-use) like nandrolone are notorious for raising prolactin — flagged for users disclosing AAS use. PT-141 and oxytocin (peptides) transiently raise prolactin around dosing. Kisspeptin can transiently raise prolactin in some studies. CJC-1295 + Ipamorelin: minimal effect. KEY CAVEATS: morning fasting draw; avoid stress, exercise, and nipple stimulation in the prior hour. Cabergoline is the standard treatment for elevated prolactin.

The metabolically inactive isomer of T3; T4 is converted to either active T3 or inactive rT3 depending on physiologic state. Elevated rT3 with normal/low free T3 indicates the body is shunting T4 toward the inactive pathway — common during caloric restriction, intense training, chronic stress, illness, or low T3 syndrome. The free-T3-to-rT3 ratio is more informative than rT3 alone (ratio >20 typically considered healthy, <10 suggests poor T4 → T3 conversion). No direct peptide effects in common stacks. Tirzepatide / Semaglutide can modestly raise rT3 during aggressive weight loss (adaptive thermogenesis pattern). KEY CAVEATS: low calories, low carbs, and overtraining all elevate rT3 acutely — interpret in the context of recent diet + training load.

SHBG binds testosterone and estradiol — without it you cannot interpret total testosterone correctly. High SHBG (often from hyperthyroidism, low calories, or aging) lowers free T even when total T looks fine. Low SHBG (from insulin resistance, obesity, or androgen use) inflates free T. Exogenous androgens including TRT suppress SHBG within 4-8 weeks; CJC-1295 + Ipamorelin have no documented SHBG effect. Tirzepatide / Semaglutide raise SHBG modestly as weight drops (insulin sensitivity improvement). RANGES SHOWN ARE FOR ADULT MEN; adult women are typically 20-130 nmol/L.

The primary autoantibody marker for autoimmune thyroid disease — Hashimoto's thyroiditis (most common cause of hypothyroidism) and Graves' disease both show elevated TPO Abs. Positive TPO Abs predict future hypothyroidism even with currently-normal TSH; worth tracking if family history of autoimmune thyroid disease or if TSH is trending upward. No direct peptide effects in common stacks. Test ONCE if negative — antibody levels rarely fluctuate meaningfully day-to-day; recheck only if symptoms or TSH change. POSITIVITY is more important than the absolute number. Thyroglobulin antibodies (Tg Abs) are the companion test for full autoimmune thyroid screening — order both for a complete autoimmune workup.

Pituitary signal to the thyroid — high TSH indicates the thyroid is being asked to produce more (hypothyroidism); low TSH indicates suppression (hyperthyroidism or exogenous thyroid). No direct peptide effects in stack peptides. Tirzepatide / Semaglutide can cause modest weight-loss-driven TSH shifts. KEY INTERACTIONS: biotin supplements above 5mg/day skew TSH assays — pause biotin 48-72h before draw. Acute illness suppresses TSH (non-thyroidal illness syndrome) — wait 2-4 weeks after recovery for accurate reading.

BPC-157 + TB-500 have no documented effect on testosterone in human studies. CJC-1295 + Ipamorelin (GHRP) modestly raise IGF-1 but no consistent testosterone effect. Tesamorelin is a GHRH analog (IGF-1 axis, not HPG axis). Tirzepatide / Semaglutide (GLP-1) — modest fat loss can raise free testosterone in men with obesity; total T effect is variable. Direct exogenous testosterone (TRT) elevates total T and may suppress LH/FSH; not a peptide. Range above is for adult males 30-49; adult females and older men have different reference bands.

Companion autoantibody marker to TPO Abs for complete autoimmune thyroid disease screening. Either antibody being positive is consistent with autoimmune thyroid disease (Hashimoto's most commonly); both positive strengthens the case. Tg Abs can also interfere with thyroglobulin measurement in thyroid cancer follow-up — relevant if user has a history. No direct peptide effects in common stacks. Test once if negative; recheck only if new symptoms or worsening TSH. POSITIVITY matters more than the absolute number — even a 10 IU/mL value is meaningful if measured by a sensitive assay.

Stores body iron AND functions as an acute-phase reactant — elevated ferritin can mean iron overload OR inflammation, and the two situations need totally different responses. Read alongside transferrin saturation and hs-CRP to disentangle. Low ferritin (<30 ng/mL) is the most sensitive marker for early iron deficiency, often present before hemoglobin drops. Female users in menstruating years frequently run low without realizing. No direct peptide effects in common stacks. INTERPRETATION: optimal range above assumes the user is not iron-loaded; users with hereditary hemochromatosis or chronic transfusion targets are different. Track alongside saturation when iron status matters.

BPC-157 has anti-inflammatory effects in animal models — could lower CRP. Tirzepatide / Semaglutide reduce CRP in obese patients (driven mostly by weight loss). CJC-1295 + Ipamorelin: no consistent CRP effect. KEY CONFOUNDERS: any acute infection in last 2 weeks can raise CRP 10-100x; intense training in last 48h raises CRP 2-5x; obesity is a baseline elevator; smoking; recent surgery or injury.

Reflects both kidney function AND protein intake / hydration / muscle catabolism. BUN/creatinine ratio adds context: >20 suggests dehydration or upper GI bleeding; <10 suggests low protein intake or hepatic dysfunction. High-protein diets (common among peptide users targeting recomp or muscle gain) routinely elevate BUN above the standard range without indicating kidney disease — interpret in context. Dehydration acutely raises BUN more than creatinine. No direct peptide effects in common stacks. GH-axis peptides (CJC-1295 / Ipamorelin / Tesamorelin / MK-677) can transiently raise BUN via increased nitrogen turnover; not clinically significant if creatinine + eGFR are normal.

Standard kidney function marker, but muscle-mass-dependent — heavily muscled users often run high creatinine without kidney disease (use cystatin C as a confirmation marker if available). Eat-and-drink before draw normally; avoid intense eccentric training in last 48h (transiently raises creatinine via muscle breakdown). No direct peptide effects in common stacks. GH-axis peptides (CJC/Ipamorelin, MK-677, tesamorelin) can modestly raise creatinine via increased lean mass over months. KEY CAVEAT: dehydration falsely elevates; over-hydration falsely lowers. Cystatin C is the better marker for users with extreme body composition (very muscular or sarcopenic).

Muscle-mass-independent kidney function marker — preferred over creatinine-based eGFR for users with extreme body composition (heavily muscled OR sarcopenic). Cystatin C-based eGFR is more accurate in these populations and identifies early CKD that creatinine-based formulas miss. Order alongside creatinine when the user is very muscular (otherwise creatinine reads high without disease) or very lean elderly (creatinine reads low and hides disease). No direct peptide effects documented in common stacks; cystatin C is a passive kidney readout. KEY CAVEAT: glucocorticoid use, thyroid disease, and high-cell-turnover states (cancer, autoimmune) can affect cystatin C independent of GFR — context matters.

Derived from creatinine + age + sex + (historically race, now removed in CKD-EPI 2021); <60 sustained over 3+ months defines chronic kidney disease. NO direct peptide effects in common stacks but the eGFR formula's creatinine-dependency means heavily muscled users can show artificially LOW eGFR even with normal kidney function. Modern formulas (CKD-EPI 2021) drop the race coefficient. Cystatin C-based eGFR is the muscle-mass-independent alternative when creatinine-based eGFR is questionable. Order eGFR alongside creatinine routinely — the derivation is automatic at any modern lab.

Mean leukocyte telomere length — a proxy for cellular aging. NO HARMONIZED REFERENCE RANGE — labs (Life Length, TeloYears, Repeat Diagnostics) report results in different formats: absolute kilobases (kb), percentile vs age-matched cohort, or 'telomere age' (age your telomeres look like). Most relevant for tracking epitalon (Russian-developed peptide claimed to support telomerase activity) — the strongest peptide-relevance use case in this library. Also relevant to general longevity intervention tracking (caloric restriction, exercise, NAD precursors). KEY CAVEAT: high intra-individual variation between draws (10-15% noise) requires 6-12+ month retest intervals to detect signal; single readings are uninformative. Test once for a baseline; retest annually at most. The 'longer = better' framing is an oversimplification — extremely long telomeres carry their own cancer risk.

Standard metabolic screen. Pre-diabetes: 100-125; diabetes: ≥126 on two separate fastings. Pairs with fasting insulin for HOMA-IR (existing entry). GLP-1 agonists (tirzepatide, semaglutide) reliably lower fasting glucose 10-30 mg/dL in T2D / obese patients. CJC-1295 + Ipamorelin + Tesamorelin: GH-axis activation transiently raises insulin resistance, so fasting glucose can edge upward during the first 4-8 weeks — usually stabilizes thereafter as body composition improves. MK-677: known to raise fasting glucose 5-15 mg/dL within weeks — flag for users with pre-existing impaired glucose tolerance. 5-amino-1MQ: animal data suggests improved insulin sensitivity; no consistent human data. KEY CAVEATS: must be true 10-12h fast; recent illness (especially viral) acutely raises glucose; stress / dawn phenomenon affect AM readings.

Fasting insulin paired with fasting glucose is the most sensitive readout for insulin resistance (HOMA-IR derived = fasting insulin × fasting glucose / 405). GLP-1 agonists (tirzepatide, semaglutide) typically lower fasting insulin within 8-12 weeks as insulin sensitivity improves. GH-axis peptides (CJC-1295, ipamorelin, tesamorelin, MK-677): GH transiently increases insulin resistance, so fasting insulin can RISE while on these — opposite direction of GLP-1s. 5-amino-1MQ may improve insulin sensitivity in animal models; no consistent human data. KEY CAVEATS: fast 10-12h before draw, no exercise in prior 24h (transient insulin sensitivity drop), and recent illness skews readings.

Tirzepatide reduces HbA1c by ~2.0% over 40 weeks in T2D patients (SURPASS trials). Semaglutide reduces by ~1.5% (SUSTAIN trials). Liraglutide ~1.0%. Both classes are GLP-1 agonists with concentration-dependent effect on insulin secretion + glucagon suppression + delayed gastric emptying. CJC-1295 / Ipamorelin: GH effects can transiently INCREASE insulin resistance and modestly raise HbA1c in some users — opposite direction of GLP-1 agonists. BPC-157: no documented HbA1c effect.

Anaerobic metabolism end-product; widely considered the most accessible proxy for mitochondrial efficiency. Elevated resting lactate suggests inadequate oxidative phosphorylation (mitochondrial dysfunction, severe illness, sepsis); low optimal range suggests efficient mitochondrial function. Post-exercise lactate clearance rate is more informative than resting value alone — slow clearance = poor mitochondrial capacity. Mitochondrial peptides like SS-31 (elamipretine) and MOTS-c are theorized to improve lactate handling but human data is limited. CJC-1295 / Ipamorelin / Tesamorelin: GH-axis activation modestly improves mitochondrial biogenesis over months; effect on resting lactate is small. KEY CAVEAT: must be drawn at rest (sit 15+ min before draw); recent exercise, anxiety, or breath-holding during venipuncture elevate lactate transiently 2-4x. Tourniquet time matters: prolonged tourniquet > 1 min falsely elevates.

Neural growth factor critical for neuroplasticity, memory formation, and synaptic function. NO HARMONIZED REFERENCE RANGE — different ELISA assays and labs report wildly different values (some report 8-46 ng/mL, others 1-20 ng/mL, others normalize to platelet count since platelets are the primary BDNF reservoir). Useful for tracking the effects of nootropic / neural peptides: selank, semax, dihexa, P21, cerebrolysin, NSI-189 — all theorized to raise BDNF. Cerebrolysin has the strongest documented effect. Exercise (especially aerobic) is the strongest non-peptide BDNF elevator. KEY INTERPRETATION: track CHANGE over time within the same assay/lab rather than absolute values; cross-lab comparisons are meaningless without method standardization. Order from specialty labs (Boston Heart, certain reference labs) — not in standard wellness panels.

Primary copper-binding protein in plasma; 95%+ of plasma copper is bound to ceruloplasmin. Low ceruloplasmin with high plasma copper is the classic Wilson's disease pattern (rare). Low both = copper deficiency. Acute-phase reactant — rises with inflammation, so an elevated ceruloplasmin with normal copper may just reflect chronic inflammation. No direct peptide effects in common stacks. KEY INTERPRETATION: order alongside copper and zinc routinely when investigating mineral status; alone, ceruloplasmin is hard to interpret.

Essential mineral; paired with zinc for proper interpretation (zinc:copper ratio ~10:1 to 15:1 optimal). High-dose zinc supplementation over months can deplete copper, causing anemia and neurological symptoms — track copper alongside zinc when supplementing. Low copper sometimes seen in post-bariatric surgery, malabsorption, or Wilson's disease (where copper is incorrectly excluded from ceruloplasmin and accumulates in tissues). Plasma copper alone is incomplete — ceruloplasmin is the binding protein and should be ordered together. No direct peptide effects in common stacks. GHK-Cu (a peptide) contains copper as a structural element; topical use is unlikely to shift systemic copper meaningfully.

Critical for methylation, DNA synthesis, and red blood cell formation. Paired with B12 — folate deficiency masks B12 deficiency in CBC by 'fixing' the macrocytosis, hiding the neurological B12 issue. Always interpret folate alongside B12 + homocysteine. Folic acid (synthetic) vs methylfolate (active) matters for MTHFR polymorphism carriers — homozygous 677TT users may have suboptimal conversion and benefit from methylfolate over folic acid. No direct peptide effects documented in common stacks. KEY CAVEATS: serum folate reflects recent intake; RBC folate (separate test) is the better long-term marker but rarely ordered. Folic acid fortification in US grain products keeps most users above the deficiency floor.

Red blood cell magnesium reflects intracellular magnesium status — far more useful than serum magnesium (which the body tightly regulates and which only drops when reserves are severely depleted). Insufficient magnesium is one of the most common nutritional shortfalls in adults and contributes to muscle cramps, sleep issues, glucose intolerance, and elevated blood pressure. No direct peptide effects in common stacks. Magnesium supplementation (glycinate, malate, or threonate forms — NOT oxide, which is poorly absorbed) is often a low-cost win for peptide users running aggressive protocols. KEY INTERPRETATION: serum magnesium is uninformative for early deficiency; RBC is more sensitive. Functional magnesium status also reflects in red cell distribution width (RDW), neuromuscular irritability, and pulse rate variability.

Essential trace mineral; component of glutathione peroxidase (key antioxidant enzyme) and required for thyroid hormone deiodination (T4 → T3 conversion). Selenium deficiency is one of the underappreciated drivers of suboptimal T4→T3 conversion — pair with rT3 and free T3 when investigating poor conversion patterns. Brazil nut soils variably high in selenium (one Brazil nut per day is often sufficient supplementation; more is not better, selenium has a narrow therapeutic window). No direct peptide effects in common stacks. KEY CAVEAT: high-dose selenium supplementation (>400 μg/day chronically) is associated with adverse outcomes — track to avoid over-supplementation as much as deficiency.

Snapshot of iron in circulation — must be interpreted alongside ferritin (storage), TIBC (binding capacity), and transferrin saturation (utilization) for a meaningful iron-status picture. Single serum iron alone is uninformative. Highly diurnal (peaks late morning) and affected by recent dietary iron — fasting morning draw recommended. Recent iron supplementation falsely elevates. Female users in reproductive years frequently run low. No direct peptide effects documented in common stacks. KEY INTERPRETATION: low iron + low ferritin = deficiency; low iron + high ferritin = anemia of chronic disease (inflammation); high iron + high ferritin + high saturation = potential iron overload (consider hemochromatosis screen).

Calculated from serum iron + TIBC: (serum iron / TIBC) × 100. The single most sensitive marker for iron overload — saturation >45% in men or >35% in women warrants hemochromatosis workup. Saturation <20% with low ferritin confirms iron deficiency. No direct peptide effects documented in common stacks. KEY INTERPRETATION: order this and ferritin together routinely; saturation distinguishes 'storage' iron (ferritin) from 'utilization' iron (saturation). Hereditary hemochromatosis affects ~1 in 200-300 Caucasians (homozygous); testing transferrin saturation catches asymptomatic cases before liver damage develops.

Critical for methylation, red blood cell formation, neurological function, and energy metabolism. Standard reference range floor (200 pg/mL) is too low — clinical symptoms often present at 200-400 pg/mL despite 'normal' lab reading; functional medicine targets >500 pg/mL with methylmalonic acid (MMA) as the functional confirmation marker. Vegetarians and vegans, users on metformin, users with H. pylori or post-bariatric anatomy, and older adults run higher deficiency rates. No direct peptide effects in common stacks. Cyanocobalamin oral supplementation is unreliable for some users; methylcobalamin or hydroxocobalamin (injectable or sublingual) are better absorbed if MMA is elevated. Methylcobalamin is also one of Juno's library entries — Tier 3 standalone.

No direct peptide effects documented for any of the common stack peptides (BPC-157, TB-500, CJC/Ipamorelin, Tesamorelin, GLP-1 agonists). Vitamin D affects many other things (immune function, bone density, mood, testosterone synthesis indirectly), so a deficient or low-optimal value is worth surfacing as a baseline-health item. Seasonal variation is expected (lower in winter at higher latitudes). Supplementation typically needed at 1000-5000 IU/day to reach optimal range.

Essential mineral for testosterone synthesis, immune function, wound healing, and ~300 enzymes. Plasma zinc is the most accessible assessment but a poor reflector of total body zinc — short-term intake heavily influences the reading. RBC zinc and zinc-deficiency functional markers (alkaline phosphatase activity, taste threshold testing) are more informative for chronic status but rarely ordered. Common shortfall in vegetarians, heavy sweaters (athletes), and users on long-term PPIs. Supplementation should be paired with copper at ~10:1 ratio — high-dose zinc displaces copper over months. No direct peptide effects in common stacks but zinc status affects testosterone production and wound healing (relevant to BPC-157 / TB-500 user expectations).

8-hydroxy-2'-deoxyguanosine — urinary marker of oxidative DNA damage. NO HARMONIZED REFERENCE RANGE — values depend on assay method (ELISA, HPLC-MS) and normalization (per mg creatinine to control for urine concentration). Most labs report typical ranges 1-15 ng/mg creatinine. Useful as a longitudinal marker of oxidative stress reduction interventions: glutathione precursors (N-acetyl-cysteine, glycine), mitochondrial peptides (SS-31 / elamipretine, MOTS-c), CoQ10, exercise. Higher = more oxidative damage; lower = better antioxidant defense. KEY CAVEAT: ELISA can over-report due to cross-reactivity; HPLC-MS is more accurate but more expensive. First-morning void recommended. Track trend within same assay/lab; cross-lab comparisons unreliable.