Sodium Butyrate
Sodium Butyrate scored 6.0 / 10 (👍 Worth trying) on the BioHarmony scale as a Substance → Exogenous Metabolite.
Sodium butyrate scores 6.0/10. It's a benign short-chain fatty acid your colon already makes, with a small but real human signal for ulcerative colitis, though upper-gut absorption and thin metabolic data keep confidence low.
What is Sodium Butyrate?
Sodium butyrate is the sodium salt of butyric acid, a short-chain fatty acid your gut bacteria already make in large amounts when they ferment fiber. It scores 6.0 out of 10.
That score sits where it does for a specific reason. Butyrate is close to perfectly benign, but the human evidence for taking it as a pill is thin and mixed. The benign safety profile is doing most of the work holding the score up, not a deep trial base.
Butyrate is the main fuel for the cells lining your colon, providing most of their energy. It also acts as an HDAC inhibitor, which shifts gene expression toward anti-inflammatory and barrier-protective programs, and it signals through the FFAR2 and FFAR3 receptors.
Those actions are why its best-studied use is inflammatory bowel conditions, especially ulcerative colitis. The mechanism is solid. The question is whether a swallowed capsule delivers enough butyrate to the right place.
That last point is the crux. Uncoated oral sodium butyrate is mostly absorbed high in the gut, before the colon where it needs to act. Coated forms and tributyrin, an odorless ester, try to fix that, and they partly do.
There's a simpler frame worth keeping in mind. Your colon produces butyrate in grams per day from fiber, far more than a pill delivers to the distal colon. For a lot of people, eating more fiber is the real move, and the supplement is a targeted tool for specific situations.
Terminology
A few terms make the rest of this report easier to follow, since the butyrate literature leans on gut and biochemistry jargon.
- SCFA: Short-chain fatty acid. Butyrate, acetate, and propionate are the main ones your gut bacteria produce.
- Butyrate: The active molecule. Sodium butyrate and tributyrin are two supplement forms that deliver it.
- Tributyrin: An odorless ester that carries three butyrate units. It reaches the colon more intact than the sodium salt.
- HDAC: Histone deacetylase, an enzyme that controls gene expression. Butyrate inhibits it, which drives many of its effects.
- FFAR2 and FFAR3: Gut and immune-cell receptors that butyrate signals through, also called GPR43 and GPR41.
- Treg: Regulatory T cell, an immune cell that calms inflammation. Butyrate promotes them in the gut.
- Calprotectin: A stool marker of gut inflammation, used to track inflammatory bowel disease.
- UC: Ulcerative colitis, an inflammatory bowel disease and butyrate's best-supported target.
- Microencapsulation: A coating designed to protect butyrate from upper-gut absorption so more reaches the colon.
How do you take Sodium Butyrate?
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.
View 3 routes and 2 protocols
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Oral (microencapsulated sodium butyrate) | Coated capsule, 150 to 300 mg | 300 to 600 mg daily | 600 mg to 1 g daily |
| Oral (tributyrin) | Odorless glyceride ester, softgel | 300 mg to 1.2 g daily | Up to a few grams divided |
| Oral (uncoated sodium butyrate) | Plain capsule or powder | 600 mg to 4 g daily | Variable |
Protocols
Ulcerative colitis adjunct Clinical
- Dose
- 300 mg twice daily coated
- Frequency
- Twice daily with meals
- Duration
- 8 to 12 weeks alongside standard therapy
Add-on to mesalamine, not a replacement.
General gut support Mixed
- Dose
- 300 to 600 mg coated or tributyrin equivalent
- Frequency
- Once or twice daily with food
- Duration
- Ongoing, reassess at 8 weeks
Often stacked with L-glutamine and probiotics.
How this score is calculated →
What are the benefits of Sodium Butyrate?
Upside contribution: 1.56
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 2.8 | 0.700 | |
| Breadth | 15% | 2.8 | 0.420 | |
| Evidence | 25% | 2.4 | 0.600 | |
| Speed | 10% | 2.0 | 0.200 | |
| Durability | 10% | 2.2 | 0.220 | |
| Bioindividuality | 15% | 2.8 | 0.420 | |
| Total | 2.560 |
Upside Rationale
Butyrate's upside is narrow and mechanism-led. The real human signal lives in the gut, specifically inflammatory bowel conditions, and even there the trials are small and unreplicated.
Its efficacy and evidence scores are held down by the same problem, a bulletproof mechanism attached to a thin, mixed human record. Where it does work, the effect is modest and depends on the dose reaching the colon.
Efficacy (2.8/5.0): Butyrate's clearest human effect is in ulcerative colitis, where a microencapsulated sodium butyrate trial found clinical remission of 31.4 percent versus 6.4 percent on placebo as an add-on to standard therapy.
Against that win, a pediatric inflammatory bowel disease trial was negative, and pooled enema studies were null. Earlier work pairing oral butyrate with mesalazine pointed positive but small. This is a targeted gut adjunct, not a broad intervention.
Breadth of Benefits (2.8/5.0): Butyrate is mostly a gut story, which keeps breadth low. The strongest signals are ulcerative colitis and IBS symptom relief, both inside the digestive tract.
The reach beyond the gut is weak. A 2018 crossover trial found an insulin-sensitivity benefit only in lean people, and the mood claims rest on a trial that could not be verified. Real breadth here is limited to gut-driven conditions.
Evidence Quality (2.4/5.0): This is the weak point. The human oral-butyrate literature is a handful of small trials, some positive, some null, with no coherent replicated body yet. A systematic review of butyrate enemas across eight randomized trials found no clear benefit.
The delivery problem compounds it. A breath-test study confirmed uncoated butyrate is absorbed before the colon, so even positive results may not generalize. The broader mechanistic work, like the butyrate-Warburg interaction, is rich but preclinical. Clinically immature.
Speed of Onset (2.0/5.0): Butyrate is slow, or at least slowly measured. The trials read out at 8 to 12 weeks, and few reported earlier interim timepoints.
There's no evidence it acts acutely. A tributyrin phase I trial established tolerability but not rapid symptom change. Plan on a couple of months before judging whether it helps.
Durability (2.2/5.0): Durability data is essentially absent. Almost no trial tracked what happens after you stop, and the one pediatric study that did showed benefit persisting only briefly past a short washout.
In practice this looks like an on-treatment effect that depends on continued dosing. That's fine for a benign supplement, but it means the benefit is not something you build and keep.
Bioindividuality Upside (2.8/5.0): Response is highly variable and depends on your gut and disease state. The clearest example is metabolic, where butyrate worked in lean people but not in metabolic syndrome.
Disease context matters too, since adult ulcerative colitis responded while pediatric inflammatory bowel disease did not. Your microbiome and baseline determine a lot, and that unpredictability cuts against reliability.
What are the risks & downsides of Sodium Butyrate?
Downside contribution: 0.72 (safety risks weighted extra)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety | 30% | 1.6 | 0.480 | |
| Side effects | 15% | 2.2 | 0.330 | |
| Cost | 5% | 2.0 | 0.100 | |
| Effort | 5% | 1.8 | 0.090 | |
| Opportunity | 5% | 2.2 | 0.110 | |
| Dependency | 15% | 1.0 | 0.150 | |
| Reversibility | 25% | 1.2 | 0.300 | |
| Total | 1.560 | |||
| Harm subtotal × 1.4 | 1.764 | |||
| Opportunity subtotal × 1.0 | 0.300 | |||
| Combined downside | 2.064 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 0.724 |
Downside Rationale
Butyrate's downside is small, and that benign profile is the main reason it clears 6.0 on such thin evidence. It is a compound your body makes in bulk every day, so there is no meaningful toxicity to weigh.
The real caveats are mild and specific, the sodium load at gram doses, a small blood-pressure signal, the notorious smell, and the opportunity cost of a pill versus simply eating more fiber.
Safety Risk (1.6/5.0): Sodium butyrate is very benign, because it is an endogenous metabolite your colon produces in grams daily. No serious toxicity appeared across the trials reviewed, even in dose-escalation work.
The one thing to watch is that a 2024 trial found oral butyrate slightly raised blood pressure, plausibly from the sodium at gram doses. A separate butyrate enema blood-pressure study probed the vascular effects directly. That is a mild, population-specific caution, not an intrinsic danger of the molecule.
Side Effect Profile (2.2/5.0): The common issues are gastrointestinal, gas, bloating, and loose stool, usually in the first days or after a dose increase, and they tend to settle. The bigger practical problem is the smell.
Uncoated sodium butyrate reeks of rancid butter, and some people burp it. Coating helps, tributyrin fixes it. A T2D proof-of-concept trial reported the usual mild GI profile without serious events.
Financial Cost (2.0/5.0): Cost is moderate. Coated sodium butyrate and tributyrin run roughly 20 to 40 dollars a month. It's not expensive, but it's pricier than the cheapest supplements, and the fiber alternative that raises butyrate naturally is cheaper still.
Time/Effort Burden (1.8/5.0): Effort is low. It's one or two capsules a day with meals. The only friction is the smell of uncoated forms and the memory of taking it consistently, since any benefit builds over weeks rather than doses.
Opportunity Cost (2.2/5.0): This is the most real of the small downsides. A calcium-butyrate metabolic trial and others suggest modest effects, but for a healthy person the pill may crowd out the better-supported move, eating more fiber and resistant starch, which raises colonic butyrate far more.
Dependency/Withdrawal (1.0/5.0): There's no dependency, tolerance, or withdrawal with butyrate. You can start and stop freely with no rebound, which fits a compound your body already produces continuously.
Reversibility (1.2/5.0): Fully reversible. Stopping butyrate returns you to your baseline gut physiology with no lingering changes. Nothing about it makes a permanent alteration.
Is Sodium Butyrate worth it?
Sodium butyrate earns a 6.0 as a benign, mechanistically sound gut-support tool with thin human evidence. Take it as a colon-targeted add-on for ulcerative colitis or IBS, use a coated form or tributyrin so it reaches the colon, and give it two to three months. Don't expect metabolic, mood, or anti-aging benefits, since that evidence is weak or unverified.
For a healthy person, the better first move is usually more fiber and resistant starch, since your colon makes far more butyrate that way than any capsule delivers. The supplement earns its place mainly when your own production is low or a specific gut condition is in play.
✅ Best for: People with ulcerative colitis or IBS who want a benign add-on to standard therapy and will use a colon-targeted form. People coming off a low-fiber or carnivore-style diet while their own butyrate production recovers. Anyone with documented low short-chain fatty acid production or dysbiosis working under a practitioner.
Tributyrin users who want the benefits without the smell or the sodium load also fit here, as do people who simply tolerate fiber poorly and need another route to colonic butyrate.
❌ Avoid if: You are salt-sensitive, hypertensive, or have kidney disease and would use gram-level sodium butyrate doses, where the sodium and the blood-pressure signal matter. Use tributyrin instead, or skip it. You are pregnant or breastfeeding, since controlled human data is absent.
Skip it too if you are a healthy person chasing metabolic, mood, or longevity benefits, because the evidence there is weak or unverified and your money is better spent on more dietary fiber and resistant starch.
What is Sodium Butyrate best for?
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
Gut Health / Microbiome: 5.5/10
Score: 5.5/10Gut health is butyrate's core use, and the signal is real but modest. Two small 2025 ulcerative colitis trials are the best evidence, including a microencapsulated sodium butyrate add-on study (n=98) that found clinical remission of 31.4 percent versus 6.4 percent on placebo. A pediatric IBS trial with calcium butyrate reported 73 percent treatment success versus under 4 percent. The catch is that a pediatric IBD trial was negative, and enema studies pooled null. It works best as a colon-targeted add-on to standard therapy for inflammatory bowel conditions, not a cure or a general gut cure-all.
Anti-Inflammatory: 5.0/10
Score: 5.0/10Butyrate's anti-inflammatory action is well grounded in mechanism, since it inhibits HDACs and promotes regulatory T cells in the gut. In the active ulcerative colitis trial (n=36), oral sodium butyrate lowered ESR and improved the partial Mayo score versus placebo. Fecal calprotectin and CRP also fell in the oral-plus-standard-therapy data. The boundary is that almost all of this is local gut inflammation in disease populations, not a demonstrated systemic anti-inflammatory effect in healthy people. For gut-driven inflammation it is a reasonable adjunct, and the effect tracks with reaching the colon.
| Use Case | Score | Summary |
|---|---|---|
| ○ Metabolic Health Primary | 3.8 | The metabolic picture is weak where it matters. A 2018 crossover trial found oral butyrate improved insulin sensitivity only in lean subjects, with no effect in the metabolic syndrome group most likely to seek it. Later proof-of-concept work is underpowered. Do not expect metabolic benefit from a butyrate pill on its own. |
| ○ Immune Function Primary | 4.0 | The regulatory-T-cell and gut-barrier mechanisms are strong on paper, but human outcome data for immune support outside inflammatory bowel disease is thin. Mechanistically promising, clinically unproven for general immunity. |
| ○ Blood Sugar / Glycemic Control Primary | 3.6 | Glycemic effects are inconsistent and mostly appear in combination protocols or in already-healthy people, not in isolation for people with poor glucose control. Treat any blood-sugar benefit as unproven for the typical buyer. |
| ○ Pediatric Use | 3.5 | Some pediatric IBS and IBD trial data exists, mixed, and only in clinical contexts. |
| ○ Liver / Detoxification | 3.2 | A small calcium-butyrate trial in metabolic-associated fatty liver showed some benefit, but it is underpowered and not replicated. |
| ○ Energy / Fatigue | 3.0 | Some people report steadier energy as gut inflammation settles, but no direct fatigue trials support this. Indirect at best. |
| ○ Geriatric / Aging Population | 3.0 | Gut and inflammatory uses are relevant to older adults, but the sodium load matters more with kidney or blood-pressure issues. |
Frequently Asked Questions
Does oral sodium butyrate actually reach the colon?
Uncoated oral sodium butyrate is mostly absorbed in the stomach and upper small intestine before it reaches the colon, where its main actions happen. A breath-test study showed coating delays release by hours. That is why microencapsulated forms and tributyrin, an odorless ester that survives further down the gut, are the versions with the better rationale. If you take a plain, uncoated capsule, a lot of the dose likely never gets where it needs to go.
What is sodium butyrate good for?
Sodium butyrate's best evidence is for inflammatory bowel conditions, especially ulcerative colitis as an add-on to standard therapy. A 2025 trial found higher remission with coated butyrate, and IBS symptom trials are cautiously positive. Beyond the gut, the evidence thins fast. Metabolic and mood claims are weak or unverified. Think of it as a targeted gut-support tool for specific conditions, not a broad wellness supplement.
Is sodium butyrate safe?
Sodium butyrate is very benign, since it is a compound your colon already makes in grams every day from fiber. No serious toxicity showed up across the trials reviewed. The two real caveats are the sodium load at gram-level doses, which matters if you are salt-sensitive or have kidney disease, and a 2024 trial where oral butyrate slightly raised blood pressure. Tributyrin sidesteps the sodium issue entirely.
Why does sodium butyrate smell so bad?
Butyric acid is the compound behind the smell of rancid butter and parmesan, and humans detect it at very low concentrations, so uncoated sodium butyrate reeks. Coating reduces the smell but does not fully remove it, and some people still burp it. Tributyrin, the ester form, is odorless and is the usual fix for anyone who finds the sodium salt intolerable. The smell is a compliance problem, not a safety one.
Should I take butyrate or just eat more fiber?
Your colon produces butyrate in grams per day when gut bacteria ferment fiber and resistant starch, far more than a capsule delivers to the distal colon. For a healthy person, eating more fiber and resistant starch is the cheaper, better-supported first move. A supplement makes more sense for someone coming off a low-fiber diet, someone whose own production is low, or as a targeted add-on in a diagnosed gut condition.
How much sodium butyrate should I take?
Most modern trials use 300 to 600 mg of coated sodium butyrate daily, often split into two doses with meals. Older metabolic studies used gram-level doses, but more is not clearly better and adds sodium. For ulcerative colitis as an add-on, 300 mg twice daily of a coated form is a common protocol. Tributyrin doses run similar, and it is the better-tolerated option for daily use.
Tributyrin versus sodium butyrate, which is better?
Tributyrin has two practical advantages, it is odorless and it reaches the colon more intact than the sodium salt, which is largely absorbed higher up. It also avoids the sodium load. Sodium butyrate is cheaper and fine on a well-coated product for budget-conscious users. For daily use, chronic gut conditions, or anyone who can't stand the smell, tributyrin is usually the better pick. A phase I trial pushed tributyrin to gram-level doses without serious toxicity.
How long does sodium butyrate take to work?
Butyrate is not fast-acting. The trials measured outcomes at 8 to 12 weeks, and few reported earlier interim timepoints, so give it a couple of months before judging. Durability data after stopping is essentially absent, so any benefit likely depends on continued use. If a coated or tributyrin form has done nothing for gut symptoms after 8 to 12 weeks, it probably is not your tool.
What could change Sodium Butyrate'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.
The most likely mover is a larger, replicated oral-butyrate trial in ulcerative colitis or IBS using a clearly colon-targeted form. A clean positive would lift Efficacy and Evidence together and could push this into the low sevens. A well-powered null would pull it back toward neutral.
The delivery question is the other lever. Better human pharmacokinetic data showing a specific form reliably reaches the colon would raise confidence, while confirmation that little survives the upper gut would lower the ceiling for oral dosing.
| Scenario | Dimension shifts | New Score |
|---|---|---|
| Large replicated UC or IBS trial confirms benefit | Efficacy 2.8 to 3.6, Evidence 2.4 to 3.4 | 6.8 / 10 👍 Worth trying |
| Pharmacokinetics confirm a form reliably reaches the colon | Evidence 2.4 to 3.0, confidence to Moderate | 6.4 / 10 👍 Worth trying |
| Well-powered oral butyrate trial returns null | Efficacy 2.8 to 2.2, Evidence 2.4 to 2.0 | 5.5 / 10 ⚖️ Neutral |
| Metabolic benefit replicates in metabolic syndrome, not just lean | Breadth 2.8 to 3.4 | 6.3 / 10 👍 Worth trying |
| Blood-pressure signal confirmed and clinically meaningful | Safety 1.6 to 2.2 | 5.8 / 10 👍 Worth trying |
| Head-to-head shows fiber clearly beats supplemental butyrate | Opportunity 2.2 to 2.8 | 5.8 / 10 👍 Worth trying |
Key Evidence Sources
- Karlowicz et al. 2025, microencapsulated sodium butyrate add-on in ulcerative colitis. Microencapsulated sodium butyrate add-on ulcerative colitis, clinical remission 31.4 percent versus 6.4 percent, n=98
- Firoozi et al. 2025, sodium butyrate in active ulcerative colitis, ESR and Mayo score. Sodium butyrate active ulcerative colitis, lowered ESR and improved partial Mayo score, n=36
- Pietrzak et al. 2022, sodium butyrate in newly diagnosed pediatric IBD, negative. Sodium butyrate newly diagnosed pediatric inflammatory bowel disease, no benefit, n=72
- Jamka et al. 2021, sodium butyrate enemas in IBD, systematic review. Sodium butyrate enemas inflammatory bowel disease systematic review, largely null, 8 RCTs, n=227
- Bouter et al. 2018, oral butyrate insulin sensitivity in lean versus metabolic syndrome. Oral butyrate improved insulin sensitivity in lean subjects only, no effect in metabolic syndrome, n=19
- Verhaar et al. 2024, oral sodium butyrate and blood pressure. Oral sodium butyrate slightly raised blood pressure versus placebo
- Hogue et al. 2025, butyrate enema and blood pressure in Black hypertensive adults. Acute butyrate enema blood pressure study in Black hypertensive adults
- Edelman et al. 2003, tributyrin phase I dose escalation. Tributyrin phase I dose escalation to gram-level doses, limited by pill burden not toxicity. Tributyrin is a related compound that delivers butyrate
- Vernia et al. 2000, oral butyrate plus mesalazine in ulcerative colitis pilot. Oral butyrate plus mesalazine ulcerative colitis pilot, early adjunct evidence
- Gasiorowska et al. 2022, microencapsulated sodium butyrate in IBS, study protocol. Microencapsulated sodium butyrate irritable bowel syndrome study protocol, n=120
- Testa et al. 2026, oral sodium butyrate weight and glucose in overweight and type 2 diabetes. Oral sodium butyrate weight and glucose overweight and type 2 diabetes proof of concept, n=46
- Cristofori et al. 2025, calcium butyrate in pediatric IBS randomized trial. Calcium butyrate pediatric irritable bowel syndrome randomized trial, 73 percent success versus under 4 percent. Calcium butyrate is a related compound that delivers butyrate
- Fogacci et al. 2024, calcium butyrate in liver steatosis and metabolic syndrome. Calcium butyrate liver steatosis and metabolic syndrome randomized trial, n=50. Calcium butyrate is a related compound that delivers butyrate
- Chulenbayeva et al. 2025, short-chain fatty acids in IBD, systematic review. Short-chain fatty acids in inflammatory bowel disease systematic review, observational fecal butyrate depletion. Butyrate is the parent compound
- Vanhoutvin et al. 2009, butyrate colonic delivery and absorption breath test. Butyrate colonic delivery coated versus uncoated absorption breath test, coating delays release
- Donohoe et al. 2012, Warburg effect and butyrate-mediated histone acetylation. Warburg effect and butyrate-mediated histone acetylation, dual effect in normal versus cancer colon cells. Butyrate is the parent compound
What does the evidence say about Sodium Butyrate?
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: Limited
Citations: Karlowicz 2025, Bouter 2018, Jamka 2021
Holistic Evidence for Sodium Butyrate
The mechanism, the endogenous role of butyrate as the colon's main fuel, and the small ulcerative colitis trials point the same direction for gut-targeted use. They diverge from the broader metabolic, mood, and anti-aging marketing, where the human evidence is weak, null, or unverifiable.
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
- Fecal Calprotectin Pre | Expected Down
- CRP During | Expected Down
- Blood Pressure During | Expected Watch
- HbA1c During | Expected Watch
Pulse Dimensions to Watch
- Body During | Expected Up | Primary
- Energy During | Expected Up | Secondary
Subjective Signals (Daily Voice Card)
- Bloating and gas after meals Scale 1-5 | Pre | Expected Down
- Stool regularity Scale 1-5 | During | Expected Up
Red Flags: Stop and Consult
- Rising blood pressure, especially if you are salt-sensitive or have kidney disease and are using gram-level doses.
- Worsening rather than improving gut symptoms after several weeks, which suggests it is not reaching the colon or not the right tool.
Other interventions for Gut Health
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 = 1.560 − 0.724 = 0.836
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 + (0.836 / 4.00) × 5 = 6.0 / 10
