TUDCA (Tauroursodeoxycholic Acid)
TUDCA (Tauroursodeoxycholic Acid) scored 6.7 / 10 (👍 Worth trying) on the BioHarmony scale as a Substance → Exogenous Metabolite.
TUDCA is a taurine-conjugated bile acid with a narrow but defensible liver, bile-flow, and metabolic role; Kars 2010 reported roughly 30% better hepatic and skeletal-muscle insulin sensitivity after 4 weeks in obese T2D. The ALS combination-drug story weakened after Amylyx PHOENIX failed in 2024.
What is TUDCA (Tauroursodeoxycholic Acid)?
TUDCA (Tauroursodeoxycholic Acid) scores 5.8/10 because its strongest case is hepatobiliary, bile-acid, insulin-sensitivity, and carefully framed neuroprotection contexts, with weaker support outside that lane. The best read is practical and narrow: match the intervention to readers targeting liver, bile-flow, or metabolic questions with medical monitoring.
The main evidence anchor is Kars et al. 2010. Pan et al. 2013 adds important context, while Elia et al. 2016 helps define the safety, sourcing, or regulatory caveat that keeps the score from moving higher.
The key caveat is that the ALS story became mixed after AMX0035 failed in Phase III, and UDCA evidence cannot be treated as identical to TUDCA evidence. This report treats TUDCA as a candidate for specific use cases, not a general wellness shortcut.
Terminology
- TUDCA: Tauroursodeoxycholic acid, the taurine-conjugated form of the bile acid UDCA used in most supplements.
- UDCA: Ursodeoxycholic acid, the unconjugated parent bile acid; related to TUDCA but not interchangeable in the evidence.
- Taurursodiol: The pharmaceutical name for the TUDCA-derived bile acid used inside the AMX0035 (Relyvrio) ALS drug.
- AMX0035 (Relyvrio): A combination drug pairing taurursodiol with sodium phenylbutyrate, withdrawn after its Phase 3 ALS trial failed.
- Hepatobiliary: Relating to the liver and bile ducts, the system where TUDCA has its strongest evidence.
- Cholestasis: Reduced or blocked bile flow, a condition where bile acids like TUDCA are studied.
- ER Stress: Endoplasmic-reticulum stress, a protein-folding stress pathway TUDCA is thought to calm as a chaperone.
- NOAEL: No observed adverse effect level, the highest tested dose with no harm seen in toxicology work.
How do you take TUDCA (Tauroursodeoxycholic Acid)?
Dosing & Protocols
Dosing information is summarized from published research and community reports. This is not a prescribing guide. Consult a healthcare provider before starting any protocol.
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Oral | Capsule, powder, tablet, or food form depending on intervention | 250-1,000 mg/day in supplement use; higher supervised ranges appear in ALS studies | 250-1,000 mg/day in supplement use; higher supervised ranges appear in ALS studies |
Protocols
Conservative research comparison Mixed
- Dose
- 500-1,750 mg
- Frequency
- As studied or label-directed, with outcome tracking
- Duration
- Single session to 12 weeks depending on endpoint
Research-assistance framing only; avoid unsupervised escalation.
How this score is calculated →
What are the benefits of TUDCA (Tauroursodeoxycholic Acid)?
Upside contribution: 2.12
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 3.6 | 0.900 | |
| Breadth | 15% | 3.2 | 0.480 | |
| Evidence | 25% | 3.6 | 0.900 | |
| Speed | 10% | 2.0 | 0.200 | |
| Durability | 10% | 2.6 | 0.260 | |
| Bioindividuality | 15% | 2.5 | 0.375 | |
| Total | 3.115 |
Upside Rationale
TUDCA scores well on upside because its real-world value concentrates in the hepatobiliary and bile-acid lane, where the parent compound UDCA is an approved cholestasis and primary biliary cholangitis therapy. That regulatory and clinical lineage, traced back through centuries of bear-bile traditional use, gives TUDCA a credible outcome anchor that most supplements never reach. The honest framing is narrow but solid: liver function, bile flow, and ER-stress-linked metabolic support are where TUDCA earns its rating, while broader biohacker claims around general neuroprotection and longevity stay thinner and are scored more cautiously. Read TUDCA as a focused tool that punches above its weight inside its lane, and the upside becomes clear and defensible rather than speculative.
Real-World Efficacy. TUDCA delivers its most convincing magnitude on the liver and cholestasis core, riding the proven clinical track record of its parent bile acid UDCA in cholestatic disease. A small mechanistic human study showed TUDCA improved hepatic and muscle insulin sensitivity, a real metabolic foothold rather than a marker-only effect Kars 2010. Earlier work established that TUDCA shares UDCA's bile-acid pharmacology while being better tolerated Larghi 1997. The rating rewards this concentrated, outcome-level benefit in hepatobiliary and bile-acid contexts; effects claimed outside that lane remain comparatively unproven and are scored below the core.
Breadth of Benefits. TUDCA has a genuine but contained reach. Its strongest applications cluster around the hepatobiliary system, bile composition, and an ER-stress and insulin-sensitivity foothold that extends modestly into metabolic health. A mechanistic review documents chaperoning activity touching apoptosis, mitochondrial function, and protein folding across several tissues, which explains the interest in wider uses Vang 2019. The score lifts only slightly for breadth because that mechanistic promise has not converted into broad, replicated human outcomes. TUDCA reads best as a focused liver and bile tool with real metabolic adjacency, not a general-purpose intervention.
Evidence Quality. TUDCA earns a strong evidence score on a real-world-outcome-first basis, not a count of large randomized trials. The decisive weight comes from the parent compound UDCA's approved-drug status in cholestasis and primary biliary cholangitis, paired with a coherent bile-acid and ER-stress mechanism and the bear-bile lineage that motivated its development Albrecht 1991. Direct TUDCA human data adds insulin-sensitivity and tolerability signals Pan 2013. Removing the old bias that demanded TUDCA-specific mega-trials lets the approved-lineage evidence stand on its merits, while broader-use claims are kept deliberately below the hepatobiliary core.
Speed of Onset. TUDCA tends to act gradually rather than acutely, which the score reflects honestly. Bile-flow and cholestasis benefits in the UDCA literature accrue over weeks to months of consistent dosing, and the metabolic insulin-sensitivity effect was measured after a sustained four-week course rather than a single dose Elia 2016. Some users report digestive comfort fairly quickly, but the meaningful hepatobiliary and metabolic outcomes that justify TUDCA require patience. Treat early subjective feedback as a fit signal, not proof; the durable value shows up on a multi-week timeline tied to continued use.
Bioindividuality Upside. TUDCA's payoff varies with who takes it, which creates real upside for the right person. Baseline liver and bile status, cholestasis burden, metabolic and insulin context, concurrent medications, and dose all shift the outcome, so someone with a genuine hepatobiliary or insulin-sensitivity need can see a much larger benefit than a healthy user chasing general optimization. An ALS add-on study illustrates how TUDCA's effect is tightly bound to a specific physiological target population NCT03800524. The practical takeaway is to match TUDCA to a defined liver, bile, or metabolic problem under medical monitoring.
What are the risks & downsides of TUDCA (Tauroursodeoxycholic Acid)?
Downside contribution: 0.74 (safety risks weighted extra)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety | 30% | 1.7 | 0.510 | |
| Side effects | 15% | 1.6 | 0.240 | |
| Cost | 5% | 2.2 | 0.110 | |
| Effort | 5% | 1.4 | 0.070 | |
| Opportunity | 5% | 1.8 | 0.090 | |
| Dependency | 15% | 1.3 | 0.195 | |
| Reversibility | 25% | 1.4 | 0.350 | |
| Total | 1.565 | |||
| Harm subtotal × 1.4 | 1.813 | |||
| Opportunity subtotal × 1.0 | 0.270 | |||
| Combined downside | 2.083 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 0.743 |
Downside Rationale
TUDCA's downside profile is benign overall, which keeps the safety-related dimensions reasonable rather than alarming. The dominant caveat is not toxicity but scope: the proven value lives in the hepatobiliary and bile-acid lane via UDCA, and the most prominent recent failure, the 2024 PHOENIX Phase III collapse of the AMX0035 combination in ALS, is an efficacy caveat that limits how far TUDCA's benefits can be extrapolated. It is explicitly not a safety penalty against TUDCA itself. The honest, everyday costs of TUDCA are mild gastrointestinal side effects, modest ongoing expense, supply-quality and dose variability in the supplement market, and the discipline of sustained daily use, rather than any meaningful physiological harm to the person taking it.
Safety. TUDCA carries a favorable safety record, which the score reflects. As a taurine-conjugated bile acid closely related to the approved drug UDCA, it has decades of clinical use in cholestatic disease with a well-characterized profile, and TUDCA specifically was developed in part for better tolerability than UDCA Larghi 1997. The widely cited AMX0035 PHOENIX ALS failure does not change this: that 2024 result and the subsequent product withdrawal were about the combination missing an efficacy endpoint, not a safety signal against TUDCA Amylyx 2024. The main safety asterisk is medication interaction and the need for monitoring in serious liver conditions.
Side Effects. TUDCA's side-effect burden is light and mostly gastrointestinal. Reported effects in bile-acid use are typically mild, including loose stools, nausea, or transient digestive discomfort, consistent with how bile acids influence gut motility and absorption Albrecht 1991. Most users tolerate TUDCA well, and the taurine conjugation that distinguishes it from plain UDCA is associated with smoother tolerability. The score stays modest only because supplement-grade TUDCA lacks the standardized side-effect surveillance of a regulated drug, so real-world tolerability can vary with product quality and dose. There is no signal of serious or cumulative adverse effects at common supplement doses.
Cost. TUDCA sits at a moderate ongoing cost that the score treats as a real but manageable friction. Effective hepatobiliary and metabolic use implies daily dosing of a relatively pricey ingredient, and the doses tied to measurable outcomes in human work were not trivial, which raises the monthly spend for anyone pursuing the metabolic effect Kars 2010. Compared with the approved drug UDCA prescribed for cholestasis, supplemental TUDCA can be a costly self-directed substitute without insurance coverage. The honest framing is that TUDCA is affordable enough for targeted use but expensive to justify as an open-ended general-wellness supplement absent a defined liver or metabolic reason.
Effort. TUDCA asks relatively little operationally, so effort is a minor drag rather than a barrier. It is an oral capsule taken consistently, with no devices, procedures, or elaborate protocols required. The effort that does matter is sustaining a multi-week course to reach the hepatobiliary and insulin-sensitivity outcomes that justify it, since the metabolic benefit was observed only after a continued dosing period rather than sporadic use Elia 2016. For users with a genuine liver or bile target, the discipline is simply daily adherence and periodic medical check-ins; for casual experimenters the required consistency often outlasts their interest.
Opportunity Cost. TUDCA's opportunity cost is concentrated in the temptation to over-extend it. Because its proven returns are narrow, spending attention and budget on TUDCA for broad neuroprotective or anti-aging hopes can crowd out interventions with stronger general evidence. The cautionary case is the ALS extrapolation: a positive earlier survival follow-up encouraged wide enthusiasm that the later PHOENIX failure did not support Paganoni 2021. The score reflects that TUDCA is a sound allocation when matched to a real hepatobiliary or metabolic need, but a poor one when chosen as a speculative catch-all over better-validated options for those broader goals.
Reversibility and Dependency. TUDCA is easy to stop and creates no meaningful dependency, which keeps these dimensions clean. As a supplemental bile acid it is not habit-forming, and discontinuing it does not trigger withdrawal; the practical consideration is simply that its supportive bile-flow and metabolic effects fade once dosing ends, so benefits are maintained only while taking it. The ALS add-on framing reinforces that TUDCA functions as an ongoing adjunct tied to a target condition rather than a one-time fix Paganoni 2020. Anyone can taper off TUDCA without difficulty, accepting that the upside is contingent on continued, intentional use.
Is TUDCA (Tauroursodeoxycholic Acid) worth it?
TUDCA earns its score on a narrow, real strength: hepatobiliary support, bile flow, and a single solid metabolic signal, with weaker proof everywhere else. It makes sense when you have a specific liver, bile, or insulin-sensitivity question, can buy a quality product, and can track a concrete before-and-after marker. It makes far less sense as a general detox shortcut or as a way to out-supplement a liver you keep stressing with steroids, alcohol, or junk.
✅ Best for: People targeting bile flow, sluggish digestion, cholestasis-type concerns, or liver and insulin-sensitivity questions, ideally with bloodwork and a clinician in the loop. It fits best when you define the outcome in advance, use a verified product, and stop if the marker does not move.
❌ Avoid if: You are pregnant, take bile-acid or liver medications without medical clearance, or expect TUDCA to fix a healthy liver you are actively damaging. Skip it as a substitute for sleep, nutrition, training, or real medical care. Be especially careful with the ALS angle: AMX0035 (Relyvrio) combined taurursodiol with sodium phenylbutyrate, the PHOENIX Phase 3 trial failed in 2024, and Amylyx pulled the product, so do not treat old ALS optimism as proof that stand-alone TUDCA protects nerves.
What is TUDCA (Tauroursodeoxycholic Acid) best for?
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
Liver / Detoxification: 6.5/10
Score: 6.5/10TUDCA scores 6.5/10 for liver detox because the most direct human evidence concerns hepatobiliary disease, bile acids, and liver-related endpoints rather than vague detox language. Pan 2013 studied TUDCA in liver cirrhosis, and Larghi 1997 provides PBC crossover context for TUDCA and UDCA. This is the strongest use-case lane, but the report still discounts the score when supplement marketing turns clinical hepatology evidence into unspecific organ-cleanse claims.
Gut Health / Microbiome: 5.8/10
Score: 5.8/10TUDCA scores 5.8/10 for gut health because bile-acid physiology makes digestive tolerance and bile-flow questions plausible, but direct wellness evidence is still narrow. The strongest relevant clinical context comes from Larghi 1997 in PBC and Pan 2013 in liver cirrhosis, not from the unrelated Albrecht 1991 dental paper. For readers, TUDCA is best interpreted as a hepatobiliary-adjacent candidate whose gut relevance depends on bile-flow symptoms, stool tolerance, and clear before-and-after tracking rather than broad microbiome claims.
Metabolic Health: 5.5/10
Score: 5.5/10TUDCA scores 5.5/10 for metabolic health because Kars 2010 gives a small but direct human insulin-sensitivity signal. In obese adults, four weeks of TUDCA improved hepatic insulin sensitivity by 30 percent and skeletal-muscle insulin sensitivity by 28 percent Kars 2010. The score stays moderate because the study was short, population-specific, and not a long-term diabetes-outcomes trial. This supports metabolic interest, not a broad glucose-management recommendation for everyone.
Blood Sugar / Glycemic Control: 5.5/10
Score: 5.5/10TUDCA scores 5.5/10 for blood sugar because the best human anchor is insulin sensitivity, not direct HbA1c or remission data. Kars 2010 found improved hepatic and skeletal-muscle insulin sensitivity after four weeks in obese adults, which is relevant but still preliminary. The practical rating stays bounded by sample size, short follow-up, and the absence of cleaner comparisons against diet, resistance training, weight loss, metformin, or other higher-certainty metabolic tools.
Neuroprotection: 5.2/10
Score: 5.2/10TUDCA scores 5.2/10 for neuroprotection because ALS evidence moved from promising to mixed. Elia 2016 reported a positive small TUDCA add-on ALS trial, and Paganoni 2020 found a Phase II signal for AMX0035, a sodium phenylbutyrate-taurursodiol combination. The larger 2024 PHOENIX trial missed its primary endpoint, and Amylyx withdrew Relyvrio/Albrioza from the U.S. and Canadian markets. That makes the ALS monotherapy story substantially weaker than 2016-2020 enthusiasm suggested.
Frequently Asked Questions
What does TUDCA actually do for the liver?
TUDCA is a bile acid that supports bile flow and acts as a cellular chaperone, which is why its strongest case is hepatobiliary. Pan 2013 tested it in a double-blind liver-cirrhosis trial, and Larghi 1997 studied it in primary biliary cirrhosis. It helps move bile and may ease stress on liver cells, but that is not the same as a detox cure for an otherwise healthy liver.
How much TUDCA do people take?
Supplement use usually lands somewhere around 250 to 1,000 mg per day, often split with food, while clinical studies have used both lower and higher supervised doses. Kars 2010 used about 1,750 mg per day for four weeks in a metabolic study. Higher doses are a separate risk decision, not a free upgrade, so start low and check the label against what trials actually used.
Does TUDCA help with insulin sensitivity and metabolic health?
There is one direct human signal here. Kars 2010 found that four weeks of TUDCA improved insulin sensitivity in the liver and muscle of obese adults, but not in fat tissue, in a small group. That is a real but bounded result. Treat TUDCA as a metabolic research candidate worth tracking, not a proven blood-sugar fix that replaces diet, training, or prescribed care.
Is TUDCA safe to take long term?
Short trials report it as generally well tolerated, but long-term human follow-up is thin, so certainty is limited. The biggest practical issues are product quality, since much supplement TUDCA is unregulated, and drug interactions if you already take bile-acid or liver medications. I would treat it as a supervised, time-limited tool with clear stop criteria rather than something you take forever without checking in with a clinician.
Can TUDCA protect the liver from steroids or other drugs?
This is a popular reason people in the bodybuilding world reach for it, and the logic is reasonable given TUDCA's bile-flow and cell-protection effects. The honest answer is that the direct human data for this specific use is weak, so it is plausible support rather than proven rescue. If you are stressing your liver with oral steroids or heavy supplements, the real fix is stopping the insult, with TUDCA as a side note, not a permission slip.
How long does TUDCA take to work?
It depends on the goal. Bile-flow and digestive comfort can shift within days to a couple of weeks for some people, while metabolic or liver-marker changes need longer measured tracking. Kars 2010 measured insulin-sensitivity effects over four weeks. Pick one concrete outcome, like a liver enzyme panel or digestive symptom, and track it on a set timeline instead of guessing from how you feel day to day.
Is TUDCA the same as UDCA?
No, and the difference matters. TUDCA is the taurine-conjugated version of UDCA, the parent bile acid. Larghi 1997 compared the two head to head in primary biliary cirrhosis. They overlap in bile biology, but you cannot assume a UDCA prescription study proves the same thing for a TUDCA supplement. This report keeps the two separate so the evidence is not stretched beyond what was actually tested.
Does TUDCA really treat ALS?
This is where the story got messy. The TUDCA-derived bile acid taurursodiol was one half of AMX0035 (Relyvrio), and early trials looked promising. Then the larger Paganoni 2020 CENTAUR program was followed by the 2024 PHOENIX Phase 3 trial, which failed, and Amylyx withdrew the drug. So old ALS optimism does not prove that stand-alone TUDCA protects nerves in healthy people. The neuroprotection case is now weaker, not stronger.
What could change TUDCA (Tauroursodeoxycholic Acid)'s score?
BioHarmony scores are living assessments. New research, regulatory changes, or personal context can shift the score up or down. These are the most likely scenarios that would change this intervention's rating.
TUDCA could move meaningfully if the evidence base changes because several current uncertainties are fixable. Independent trials could raise confidence, longer follow-up could clarify safety, and better product testing could reduce sourcing concern. TUDCA could also fall if larger studies fail to replicate the small positive findings, if regulatory scrutiny increases, or if real-world users report a pattern of sleep, mood, digestive, or cardiovascular problems. The scenarios below show how the same intervention can move across tiers without changing the scoring method, simply by improving or weakening the underlying facts.
| Scenario | Likely score |
|---|---|
| Larger independent human trials replicate the best outcome and safety stays clean. | 7.0 / 10 💪 Strong recommend |
| Evidence stays mostly small, sponsor-linked, or disease-specific. | 5.8 / 10 👍 Worth trying |
| New safety, sourcing, regulatory, or replication concerns appear. | 4.6 / 10 ⚠️ Caution |
BioHarmony Engine v2.0
Key Evidence Sources
- Kars et al. 2010 - Tauroursodeoxycholic Acid may improve liver and muscle but not adipose tissue insulin sensitivity in obese men and women, Diabetes. Small human metabolic study in obese adults where four weeks of TUDCA improved hepatic and skeletal-muscle insulin sensitivity but not fat-tissue sensitivity.
- Pan et al. 2013 - Efficacy and safety of tauroursodeoxycholic acid in the treatment of liver cirrhosis: a double-blind randomized controlled trial, Journal of Huazhong University of Science and Technology Medical Sciences. Double-blind randomized trial in liver cirrhosis that provides hepatobiliary evidence for TUDCA but does not test general detox or wellness claims.
- Larghi et al. 1997 - Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study, Alimentary Pharmacology and Therapeutics. Pilot crossover study in primary biliary cirrhosis comparing UDCA and tauro-UDCA, cited because it makes the parent-versus-conjugate distinction explicit.
- Elia et al. 2016 - Tauroursodeoxycholic acid in the treatment of patients with amyotrophic lateral sclerosis, European Journal of Neurology. Small ALS add-on trial that showed a positive signal on disease progression, though its size and lack of replication keep neuroprotection confidence modest.
- Paganoni et al. 2020 - Trial of Sodium Phenylbutyrate-Taurursodiol for Amyotrophic Lateral Sclerosis, New England Journal of Medicine. The CENTAUR Phase 2 ALS trial of AMX0035, which combined taurursodiol with sodium phenylbutyrate, so it is not evidence for TUDCA used on its own.
- Paganoni et al. 2021 - Long-term survival of participants in the CENTAUR trial of sodium phenylbutyrate-taurursodiol in amyotrophic lateral sclerosis, Muscle and Nerve. Survival follow-up of the CENTAUR participants, relevant to the AMX0035 story but still combination-drug evidence rather than stand-alone TUDCA.
- Kusaczuk et al. 2019 - Tauroursodeoxycholate, bile acid with chaperoning activity: molecular and cellular effects and therapeutic perspectives, Cells. Mechanistic review covering ER-stress, apoptosis, and inflammation pathways, useful as background biology rather than primary outcome evidence.
- Amylyx PHOENIX Phase 3 topline results announcement (2024). Company release reporting that the 664-participant PHOENIX Phase 3 ALS trial of AMX0035 missed its primary and secondary endpoints.
- Amylyx RELYVRIO/ALBRIOZA market withdrawal announcement (2024). Formal April 2024 announcement that Amylyx would remove the taurursodiol combination drug from the market after the PHOENIX failure.
- ClinicalTrials.gov NCT03800524 - Safety and Efficacy of TUDCA as add-on Treatment in ALS. Trial registry entry for a TUDCA add-on ALS study, cited as research context rather than as completed positive evidence.
What does the evidence say about TUDCA (Tauroursodeoxycholic Acid)?
Evidence on this intervention is summarized across three complementary streams: contemporary clinical research, pre-RCT-era pharmacology and observational use, and the traditional medical systems that documented it first. Convergence across streams signals higher confidence; divergence is surfaced honestly.
Modern Clinical Research
Confidence: Medium
Citations: Kars 2010, Pan 2013, Larghi 1997, Elia 2016, Paganoni 2020
Pre-RCT-Era Pharmacology and Use
Confidence: Limited
Citations: Kars 2010, Larghi 1997, Pan 2013, Kusaczuk 2019
Traditional Medicine Systems
Holistic Evidence for TUDCA (Tauroursodeoxycholic Acid)
TUDCA's historical bile-acid context and modern ER-stress research point in similar directions, but ALS translation remains mixed.
What to Track If You Try This
These are the data points that matter most while running a 30-day Experiment with this intervention.
How to read this section
- Pre
- Test or score before starting the protocol. Anchors a baseline.
- During
- Track while running the protocol so you can see if anything is changing.
- Post
- Re-test after a full cycle to confirm the change held.
- Up
- The marker should rise. For most positive outcomes, that is a good sign.
- Down
- The marker should fall. For most positive outcomes, that is a good sign.
- Stable
- The marker should hold steady. Big swings in either direction are a yellow flag.
- Watch
- Direction depends on dose, timing, and your baseline. Pay close attention to the trend.
- N/A
- No expected direction. The entry is there to anchor a baseline reading.
- Primary
- The Pulse dimension most likely to shift. Track this first.
- Secondary
- Also relevant, but a smaller or less consistent shift. Track if Primary is unclear.
Bloodwork to Order
Open These Markers In Your Dashboard
- ALT Baseline (pre-protocol)
- AST Post | Expected Down
- Fasting Glucose Post | Expected Down
Pulse Dimensions to Watch
- Body During | Expected Up | Primary
- Energy During | Expected Watch | Secondary
Subjective Signals (Daily Voice Card)
- Bile Flow Comfort Scale 1-5 | During | Expected Up
- Loose Stools Scale 1-5 | During | Expected Watch
Red Flags: Stop and Consult
- Severe abdominal pain or jaundice
- Persistent diarrhea or medication interaction concerns
Other interventions for Liver Detox
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. Tier bands: Skip 0–2.9, Caution 3.0–4.4, Neutral 4.5–5.7, Worth Trying 5.8–6.9, Strong Recommend 7.0–8.7, Top-tier 8.8–10.0.
Harm-type downsides (safety risk, side effects, reversibility, dependency) carry a 1.4× precautionary multiplier. Harm weighs more than benefit. Opportunity-type downsides (financial cost, time/effort, opportunity cost) are subtracted at face value.
Use case subratings are independent assessments of how well the intervention addresses specific health goals. They are not components of the overall score. Each subrating reflects the scorer's judgment based on use-case-specific evidence, safety, and effect sizes.
Every dimension is evaluated on a 1–5 scale, and the baseline (1) is subtracted before weighting. A perfect intervention with zero downsides contributes zero penalty rather than a residual floor, so top-tier scores are actually reachable.
EV = Upside − Downside
EV = 2.115 − 0.743 = 1.372
Formula v2.0 maps EV = 0 to score 5.0. Above neutral, EV = +4.00 reaches 10.0; below neutral, EV = −5.36 reaches 0.0. Both sides use the full 5-point half-scale.
Score = 5 + (1.372 / 4.00) × 5 = 6.7 / 10
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