Fatty Liver Fibrosis Score: What Your FIB-4 Number Means

A fatty liver fibrosis score such as FIB-4 turns your age, AST, ALT and platelet count into an estimate of liver scarring. A score under 1.3 makes advanced scarring unlikely, and 2.67 or higher points toward advanced fibrosis.

Four values from a routine blood draw can estimate whether a fatty liver has begun to scar. Most people with fatty liver have never seen the result.

A fatty liver fibrosis score estimates whether the fat in your liver has started to turn into scar. The most widely used one, FIB-4, is built from four values already sitting in most charts, your age, two liver enzymes called AST and ALT, and your platelet count, all drawn with routine blood work. It needs no extra needle, yet most people told they have a fatty liver have never heard their number.

How the score is built from routine blood work

The formula multiplies your age by your AST level, then divides by your platelet count multiplied by the square root of your ALT level. AST climbs relative to ALT as liver injury deepens. Platelets drift down as scarring advances, because a stiffening liver backs blood up into the spleen, and the spleen holds on to platelets. Age sits in the formula because scar takes years to lay down.

That age term has a consequence nobody mentions. The same blood results produce a higher score at seventy than at forty, simply because the multiplier is bigger. At the young end, American liver specialists state that FIB-4 has low accuracy in those under age 35, so a low score in a young adult is thin reassurance. The score opens a question. It does not close one, the same limit that applies to any single result on a report.

What the numbers mean, and where the score misleads

A score under 1.3 is the common line for saying advanced scarring is unlikely. American guidance reads a score of 2.67 or higher as pointing toward advanced fibrosis. Between those lines sits a gray zone where the next step is a scan of liver stiffness, done by a liver or imaging service.

Denmark ran the best test beyond a specialty clinic. Researchers screened 3,378 people with a median age of 57: 1,973 from the general population, 953 at risk of alcohol-related liver disease and 452 at risk of fatty liver disease driven by metabolism. Every participant also had a liver stiffness scan. Signs of scarring turned up in 3.4% of the general population, but in 12% and 14% of the two at-risk groups. Of the people who went on to biopsy, 54 had advanced fibrosis.

Here is where the score earns its reputation and its criticism in the same breath. FIB-4 produced false positives in 35% of participants, against 11% for a specialized blood test called ELF, and its accuracy for advanced fibrosis measured 0.73 on a scale where a perfect test scores one. In a 2025 primary care study that included a validation group of 6,468 people, a newer tool proved superior to the Fibrosis-4 index at spotting significant scarring. FIB-4 survives because every input is already on a routine panel. Its job is to decide who needs a closer look, and it does that job best in the people most likely to have disease: those with diabetes, obesity or heavy drinking. In older adults with memory complaints, the same calculation can uncover hidden cirrhosis, explained in why liver scarring can hide inside a dementia diagnosis.

Why fatty liver is never just a liver problem

In 2023 an international panel threw out the name nonalcoholic fatty liver disease. The replacement, metabolic dysfunction-associated steatotic liver disease or MASLD, requires liver fat plus at least 1 of 5 cardiometabolic risk factors, such as a large waist, high blood sugar, high blood pressure or abnormal blood fats. The name finally says what the condition is: a metabolic disease that happens to show up in the liver.

A 2024 review pooled 129 studies that followed people with and without MASLD over time. Against people without it, those with MASLD carried hazard ratios of 1.43 for cardiovascular events, 1.75 for new high blood pressure, 2.56 for diabetes, 1.38 for chronic kidney disease and 1.54 for all cancers. People with advanced liver disease faced a diabetes hazard ratio of 3.60. Most people with a fatty liver will meet a cardiologist or a kidney doctor long before they meet a liver specialist.

For years I read a normal liver panel as a closed question. It is not, because the panel is drawn from arm blood after the liver has already filtered it, and the damage a fatty liver predicts lands mostly outside the liver. Two biological drivers explain that reach. High insulin, the body’s answer to insulin resistance, orders the liver to turn sugar into fat and keep it. At the same time, visceral fat around the intestines drains straight to the liver through the portal vein, delivering fatty acids and inflammatory signals that sustain metaflammation everywhere, artery walls and kidneys included, which is why measuring arterial stiffness belongs beside any liver score. The third driver is economic. Subsidized sweeteners and industrial seed oils sit in most packaged food, so the liver faces a steady supply with no off switch, and the bill arrives decades later as heart attacks, dialysis and transplant lists. The liver is also one of the organs where excess weight raises cancer risk, part of the metabolic link between obesity and cancer.

When fatty liver ends on a transplant list

The far end of the scarring road is cirrhosis, and for some people a liver transplant. Across 169,385 adult liver transplant listings in the United States national registry, 21,789 (12.9%) were for metabolic steatohepatitis, the inflamed form of MASLD, and the proportion of those listings increased threefold between 2002-11 and 2012-22. Hepatitis C fell away over the same years because antiviral pills cure it. Metabolic liver disease has no single pill, because it is manufactured daily by how the body is fed, how much insulin it runs on and where it stores fat.

That is why the European liver, diabetes and obesity societies, in their joint 2024 guideline, call for checking for scarring in people with cardiometabolic risk factors, particularly in the presence of type 2 diabetes or obesity, starting with a blood score such as FIB-4 and moving to a stiffness scan when needed. The same guideline puts dietary change, exercise and weight loss at the center of management. Food, movement and sleep are treatment here because each one lowers insulin, and lower insulin is the signal that lets the liver release its fat. The sugar side of that equation is traced in what sugar does to inflammation.

What Measura can measure around a fatty liver

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service; it measures, and findings go to your physician. It does not image the liver or measure liver stiffness. Ultrasound and elastography are done elsewhere. The FIB-4 inputs are part of the blood work your physician orders, so ask whether anyone has run the calculation. Measura shows the metabolic terrain the score sits in:

• Laboratory panels that can include fasting insulin and high-sensitivity C-reactive protein, the drivers behind liver fat that a glucose test alone never sees.
• Arterial stiffness and endothelial function, because the most common serious consequence of a fatty liver is in the blood vessels.
• Bioimpedance body composition, which estimates fat and muscle separately and shows whether change is moving in the right direction.

How insulin works behind the scenes is explained in insulin resistance and metabolic health, and the heart side of the picture in finding cardiovascular risk early. Unmeasured is unmanaged, and a score nobody calculates protects no one.

Questions to bring to your physician

• Has my FIB-4 score been calculated from my latest AST, ALT and platelet count, and what was it?
• If it falls in the gray zone, who will arrange a liver stiffness scan?
• Since fatty liver raises heart and kidney risk, what is being done to measure my blood vessels?
• Can my insulin be measured, not just my glucose?

The physician-facing version of this screening question, including why the standard enzymes under-read the problem, is in MASLD in primary care: screening when liver enzymes look normal.

Frequently asked questions

References

• Kjaergaard, M., Lindvig, K. P., Thorhauge, K. H., Andersen, P., Hansen, J. K., Kastrup, N., Jensen, J. M., Hansen, C. D., et al. (2023). Using the ELF test, FIB-4 and NAFLD fibrosis score to screen the population for liver disease. Journal of Hepatology, 79(2), 277-286. https://doi.org/10.1016/j.jhep.2023.04.002
• Lindvig, K. P., Thorhauge, K. H., Hansen, J. K., Kjærgaard, M., Hansen, C. D., Johansen, S., Lyngbeck, E., Israelsen, M., et al. (2025). Development, validation, and prognostic evaluation of LiverPRO for the prediction of significant liver fibrosis in primary care: a prospective cohort study. The Lancet Gastroenterology & Hepatology, 10(1), 55-67. https://doi.org/10.1016/S2468-1253(24)00274-7
• Rinella, M. E., Neuschwander-Tetri, B. A., Siddiqui, M. S., Abdelmalek, M. F., Caldwell, S., Barb, D., Kleiner, D. E., & Loomba, R. (2023). AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology, 77(5), 1797-1835. https://doi.org/10.1097/HEP.0000000000000323
• Rinella, M. E., Lazarus, J. V., Ratziu, V., Francque, S. M., Sanyal, A. J., Kanwal, F., Romero, D., Abdelmalek, M. F., et al. (2023). A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology, 78(6), 1966-1986. https://doi.org/10.1097/HEP.0000000000000520
• Chan, K. E., Ong, E. Y. H., Chung, C. H., Ong, C. E. Y., Koh, B., Tan, D. J. H., Lim, W. H., Yong, J. N., et al. (2024). Longitudinal outcomes associated with metabolic dysfunction-associated steatotic liver disease: a meta-analysis of 129 studies. Clinical Gastroenterology and Hepatology, 22(3), 488-498.e14. https://doi.org/10.1016/j.cgh.2023.09.018
• Singal, A. K., Dunn, W., Wong, R., Kulkarni, A., & Kuo, Y. F. (2025). Differential candidate characteristics associated with increasing ALD and MASH among liver transplant listings in the US. Digestive and Liver Disease, 57(5), 578-584. https://doi.org/10.1016/j.dld.2025.01.191
• European Association for the Study of the Liver, European Association for the Study of Diabetes, & European Association for the Study of Obesity. (2024). EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD): Executive Summary. Diabetologia, 67(11), 2375-2392. https://doi.org/10.1007/s00125-024-06196-3

Related reading

• What Does Echogenic Liver Mean? Reading the Numbers Behind the Scan
• MASLD in Primary Care: Screening When Liver Enzymes Look Normal
• Laboratory Panels

How to Test for MCAS When Your Allergy Tests Keep Coming Back Negative

Testing for MCAS takes a paired tryptase draw: one value during or soon after a reaction and one at baseline. Under the strict consensus criteria, an episode counts when tryptase rises to at least baseline times 1.2, plus 2 ng/mL, and a standard allergy panel cannot show it because mast cell activation often involves no antibody.

A shrinking safe-food list and a clean allergy panel are not a contradiction. They usually mean the wrong test was run, at the wrong moment, for the wrong cell.

Flushing after meals, cramping within minutes, a list of safe foods that gets shorter every season, and an allergy panel that says nothing is wrong. When that pattern leads you to search how to test for MCAS, you have already found the first problem: the standard allergy workup looks for an antibody, and mast cell activation often involves no antibody at all.

In She’s Not Allergic to Her Food. She’s Fermenting It., a video drawn from The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, Dr. Padda follows a woman whose symptoms were twice labeled anxiety. What follows is the measurement side of her story: which tests exist, which ones mislead, and what Measura can and cannot add.

Why an allergy panel comes back clean

Mast cells are the sentinels of the first brain, the gut. They sit where the innate and adaptive arms of the immune system meet, and far more than the allergy antibody IgE can set them off. They also talk with sensory nerves in both directions. In irritable bowel syndrome, 34 of 44 patients, 77%, had more of their gut lining occupied by mast cells than controls did, and the cells lying closest to nerves were the ones that tracked pain.

Their chemicals are not harmless. Histamine, proteases, prostaglandins and cytokines drive both pain and a leakier gut wall at the same time. So cramping, loose stool and a permeable lining can be a single process that gets three separate labels and three separate prescriptions. An antibody test cannot see any of it, and the second brain, in the skull, gets blamed for signals coming from below.

Certain drugs can set off mast cells on their own by binding a receptor named MRGPRX2; no antibody or prior sensitization is involved. Morphine, vancomycin, rocuronium and atracurium are among the agents named. A negative allergy test does not clear a reaction to one of them.

How to test for MCAS: the tryptase rule and its rival

Tryptase is an enzyme mast cells release, and it anchors the strict consensus criteria. Normal serum tryptase runs 0 to 11.4 ng/mL. An episode counts when tryptase rises to at least the baseline times 1.2, plus 2 ng/mL, and all three diagnostic criteria must be met, not just one. From a baseline of 10, the bar sits at 14. The authors concede the formula favors specificity, which means it will miss some people.

The practical point is timing. The test is a pair: one value during or soon after a reaction and one at baseline. The paired draw is also the value most often missing from a chart.

A competing framework argues those criteria miss most patients and puts prevalence as high as 17% of the general population, while admitting in its own text that overdiagnosis is a risk. Both camps have a case. Anyone who gives you the diagnosis owes you which rulebook they used.

There is a genetic piece too. Carriers of hereditary alpha-tryptasemia made up 4% of healthy blood donors yet 29% of people with non-clonal mast cell activation, and carriers ran higher baseline tryptase. The strict committee suggests considering genotyping at a tryptase of 8 ng/mL or higher. That trait explains a number; in the cohort studied, it did not predict later anaphylaxis in patients whose illness began another way.

What histamine intolerance testing gets wrong

Many people land on a histamine intolerance label first. When referred patients were given histamine and placebo without knowing which, the diagnosis was excluded in 84.7% of them, and 62.7% reacted to the placebo. Only 4 of 59 had objective symptoms to histamine and not to placebo. The blood enzyme level often sold as a histamine intolerance test could not sort reactors from everyone else.

That does not mean the symptoms are imagined. It means dietary histamine is the wrong target for most people handed a low-histamine list. The histamine that matters appears to be made inside the gut: mice raised without gut microbes and given stool from IBS patients with high urinary histamine developed gut pain and mast cell activation, and when people with IBS ate less fermentable carbohydrate, their pain and the histamine in their urine both dropped.

The incentives explain why this gets missed. A food list costs nothing to hand out, antihistamines refill forever, and the hour needed to find out why the cells are firing is an hour the system does not reward.

Where Measura fits, and where it does not

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service. It measures and sends results to your physician; it does not diagnose or treat. Tryptase, histamine, genotyping, biopsies and other mast cell tests are specialized tests done elsewhere, ordered by your physician or an allergist. Measura does not run them beyond general laboratory panels.

The bridge is the company mast cell problems keep. Orthostatic intolerance, hypermobility, gut overgrowth and polypharmacy travel together with mast cell activation, and in a chart review of low-dose naltrexone in dysautonomia, orthostatic intolerance was the reason for prescribing in 27.78% of patients. If standing makes your heart race or your head swim, that part is measurable:

• Autonomic nervous system testing looks at how blood pressure and heart rate regulation respond to position and stress.
• Cardiac autonomic reflex tests check heart rate responses to breathing and standing maneuvers.
• Heart rate variability gives a baseline reading of vagal tone.

Those results do not confirm or rule out MCAS. They document an autonomic picture your physician can weigh alongside tryptase and history. The overlap with joint hypermobility is covered in EDS and POTS, and the leaky-wall side in how to test for leaky gut.

What low-dose naltrexone is, and is not

Low-dose naltrexone often comes up with this diagnosis, and it is commonly mislabeled. Calling it a mast cell stabilizer gets the pharmacology backward. Naltrexone is inactive at MRGPRX2, the receptor opioids use to fire mast cells. The proposed route is indirect and upstream: a brief opioid blockade followed by a rebound rise in the body’s own endorphin, which may act on lymphocytes including regulatory T cells, plus antagonism of Toll-like receptor 4, the sensor for bacterial fragments, which thins the inflammatory signals that keep gut mast cells primed. The TLR4 link rests on cell and animal work, and the lymphocyte link is the least settled. In a survey of 553 patients, self-rated benefit averaged 5.6 out of 10, against 6.3 for antihistamines. Any medication decision belongs with your physician.

Questions to bring to your appointment

• Which criteria are being used for my diagnosis?
• Was tryptase drawn during a reaction and compared with a baseline value?
• Did the reactions start soon after antibiotics, a stomach bug or an operation?
• Is a drug reaction in my history one that fires mast cells directly?
• Should my dizziness or racing heart on standing be measured?

Once the source is addressed, the long-term upkeep is the subject of how to maintain weight loss and what to measure. Every study above, with its limits, is in the Chapter 31 Deep Dive.

Frequently asked questions

References

• Barbara, G., Stanghellini, V., De Giorgio, R., Cremon, C., Cottrell, G. S., Santini, D., Pasquinelli, G., Morselli-Labate, A. M., Grady, E. F., Bunnett, N. W., Collins, S. M., & Corinaldesi, R. (2004). Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome. Gastroenterology, 126(3), 693-702. https://doi.org/10.1053/j.gastro.2003.11.055
• Stassen, M., Hartmann, A.-K., Delgado, S. J., Dehmel, S., & Braun, A. (2019). Mast cells within cellular networks. The Journal of Allergy and Clinical Immunology, 144(4S), S46-S54. https://doi.org/10.1016/j.jaci.2019.01.031
• Hasler, W. L., Grabauskas, G., Singh, P., & Owyang, C. (2022). Mast cell mediation of visceral sensation and permeability in irritable bowel syndrome. Neurogastroenterology and Motility, 34(7), e14339. https://doi.org/10.1111/nmo.14339
• Valent, P., Akin, C., Nedoszytko, B., Bonadonna, P., Hartmann, K., Niedoszytko, M., Brockow, K., Siebenhaar, F., Triggiani, M., Arock, M., Romantowski, J., Górska, A., Schwartz, L. B., & Metcalfe, D. D. (2020). Diagnosis, classification and management of mast cell activation syndromes (MCAS) in the era of personalized medicine. International Journal of Molecular Sciences, 21(23), 9030. https://doi.org/10.3390/ijms21239030
• Afrin, L. B., Ackerley, M. B., Bluestein, L. S., Brewer, J. H., Brook, J. B., Buchanan, A. D., Cuni, J. R., Davey, W. P., Dempsey, T. T., Dorff, S. R., Dubravec, M. S., Guggenheim, A. G., Hindman, K. J., Hoffman, B., Kaufman, D. L., Kratzer, S. J., Lee, T. M., Marantz, M. S., Maxwell, A. J., … Molderings, G. J. (2020). Diagnosis of mast cell activation syndrome: a global “consensus-2”. Diagnosis (Berlin, Germany), 8(2), 137-152. https://doi.org/10.1515/dx-2020-0005
• González-de-Olano, D., Navarro-Navarro, P., Muñoz-González, J. I., Sánchez-Muñoz, L., Henriques, A., de-Andrés-Martín, A., Peralta-Arjonilla, D., Mayado, A., Jara-Acevedo, M., García-Montero, A. C., Orfao, A., & Álvarez-Twose, I. (2023). Clinical impact of the TPSAB1 genotype in mast cell diseases: a REMA study in a cohort of 959 individuals. Allergy, 79(3), 711-723. https://doi.org/10.1111/all.15911
• Bent, R. K., Kugler, C., Faihs, V., Darsow, U., Biedermann, T., & Brockow, K. (2023). Placebo-controlled histamine challenge disproves suspicion of histamine intolerance. The Journal of Allergy and Clinical Immunology: In Practice, 11(12), 3724-3731.e11. https://doi.org/10.1016/j.jaip.2023.08.030
• De Palma, G., Shimbori, C., Reed, D. E., Yu, Y., Rabbia, V., Lu, J., Jimenez-Vargas, N., Sessenwein, J., Lopez-Lopez, C., Pigrau, M., Jaramillo-Polanco, J., Zhang, Y., Baerg, L., Manzar, A., Pujo, J., Bai, X., Pinto-Sanchez, M. I., Caminero, A., Madsen, K., … Bercik, P. (2022). Histamine production by the gut microbiota induces visceral hyperalgesia through histamine 4 receptor signaling in mice. Science Translational Medicine, 14(655), eabj1895. https://doi.org/10.1126/scitranslmed.abj1895
• Lansu, K., Karpiak, J., Liu, J., Huang, X.-P., McCorvy, J. D., Kroeze, W. K., Che, T., Nagase, H., Carroll, F. I., Jin, J., Shoichet, B. K., & Roth, B. L. (2017). In silico design of novel probes for the atypical opioid receptor MRGPRX2. Nature Chemical Biology, 13(5), 529-536. https://doi.org/10.1038/nchembio.2334
• Zapata, N., Georgiadi, E., Cantrell, C., Rilinger, R. G., Levine, M. A., & Wilson, R. (2025). Low-dose naltrexone for managing pain and autonomic symptoms in patients with dysautonomia. Cureus, 17(6), e86538. https://doi.org/10.7759/cureus.86538

Related reading

• How to Maintain Weight Loss When the Scale Stops Telling the Truth
• Does Nicotine Raise Heart Rate? What Measurement Can Show
• Laboratory Panels

Bile Acid Malabsorption After Gallbladder Surgery: What to Measure

After gallbladder surgery, the measurement to ask for is a bile acid test, arranged by your physician or a gastroenterologist, because bile acid diarrhea is one of the most common causes of urgent, loose stools and one of the least often tested. A positive breath test belongs before any antibiotic for overgrowth.

Loose stools and fat intolerance years after gallbladder surgery often get treated as a bacterial problem. The real cause is frequently bile arriving at the wrong time, and it is rarely measured.

Bile acid malabsorption, called bile acid diarrhea in most of the research, means bile acids are reaching the colon, and the colon answers by flooding the bowel with water. After gallbladder removal it is one of the most common explanations for urgent, loose stools, and one of the least often tested. The video above, The Liver Flush Is Soap, presents Chapter 28 of The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes. It follows a woman of fifty-nine who spent eleven years after her surgery unable to face a fatty meal, and who received four courses of antibiotics for a bacterial overgrowth her breath tests never confirmed.

The gap in her care was a missing measurement. Nobody asked where her bile was going. What follows is what a routine visit tends to check, what it skips, and which numbers are worth having before anyone writes a fifth prescription.

What happens to bile after gallbladder removal?

A gallbladder holds bile between meals and squeezes it out when fat arrives. Once it is removed, bile drips into the gut around the clock, with or without food. Two problems follow. Fat that bile never breaks into droplets is not absorbed, and the vitamins that ride along with fat are lost too, a supply problem that starts before the intestine ever gets a chance. Bile also acts as a guard. In people whose bile duct is completely blocked, bacterial endotoxin from the gut crosses into the blood, and in a small surgical series, giving a bile salt by mouth before the operation kept it out.

That guard matters beyond digestion. The Angry Gut calls the gut the first brain and the skull the second brain, and bacterial debris slipping past a weak defense feeds metaflammation, the steady, low-grade metabolic inflammation underneath insulin resistance and chronic pain. A bowel that misfires all day is not a private nuisance. It belongs to the metabolic picture.

Why is SIBO blamed so often after gallbladder surgery?

Dr. Padda expected the missing organ to be what lets bacteria climb upward, and he would have told this patient exactly that. The surgical data corrected him. In a prospective study of people after abdominal surgery, overgrowth ran 37.6% against 13.3% in healthy controls, but gallbladder removal carried the smallest risk of the operations compared, 17.1%, while stomach surgery reached 96.2%. In a second study of gallbladder disease, the group most likely to test positive was people who still had their gallbladder and their stones, at 40.5%.

So a sluggish gallbladder is worse than an absent one, and bile that sits still is the real fault. The antibiotics kept coming anyway. Part of the reason is the clock: ordering a breath test means preparation instructions and a second appointment, while writing a prescription fits inside the visit already underway. Antibiotics for overgrowth have a legitimate trigger, and that trigger is a positive test. Four courses without one describe a habit, not a diagnosis.

How common is bile acid diarrhea?

A teaching hospital scanned 1,071 people in a row who had been sent in for chronic diarrhea. Bile acid diarrhea turned up in 42.7% of them, and having had the gallbladder removed ranked among three features that predicted an abnormal result. The more surprising figure: 61.0% of those referred had no known risk factor, and 35.7% of that group had the condition anyway. Severity among positive results was mild in 31.7%, moderate in 34.4% and severe in 33.9%.

That particular scan is not offered in the United States, so the numbers travel but the exact route to a diagnosis does not; a gastroenterologist picks the method available here. For a patient the takeaway is simpler. Chronic loose stools after gallbladder surgery have a name, a test and a treatment, and it is fair to ask whether anyone has looked.

Does a liver flush remove gallstones?

The internet fix for bile trouble is an olive oil and citrus flush, which produces green, stone-shaped lumps in the toilet. In the one case where someone sent them to a laboratory, they held no cholesterol, bilirubin or calcium, the building blocks of a real gallstone, and they melted into oil after ten minutes at 40 degrees. They were soap, made in the gut from the drink itself, and the woman still had her gallstones. Something you can see in a toilet bowl has not been measured.

Do TUDCA or milk thistle improve bile flow?

The same standard applies to bottles. Tauroursodeoxycholic acid, sold as TUDCA, borrows its reputation from a prescription relative, ursodeoxycholic acid, whose pooled trials in its own liver disease shifted blood tests without reducing deaths. The best metabolic trial of TUDCA itself gave obese men and women 1,750 mg daily; after four weeks, liver and muscle insulin sensitivity were up by about 30%, and nothing in the gut or the bile was measured. Milk thistle lowered two liver enzymes in pooled trials, with no effect at a BMI of 30 or above. No product sold to boost bile flow has been shown to raise measured bile flow in a person.

None of that is a reason to start or stop anything on your own. It is a reason to ask, for anything you take, which number is supposed to move and when it will be checked. Every change to a prescription or a supplement belongs in a plan made with your physician.

Bile acid malabsorption: what Measura measures and what it does not

Measura [Cardiometabolic and Autonomic Health Analysis] does not test bile, the gallbladder or gut bacteria. Bile acid tests, gallbladder imaging and breath tests for overgrowth are different tests, arranged elsewhere by your physician or a gastroenterologist. What Measura can add is the metabolic terrain that gallbladder trouble keeps company with. In the study of 265 people with gallbladder disease, the disease was independently linked to fatty liver and metabolic syndrome as well as overgrowth.

• Laboratory panels, chosen with your physician, can show the blood sugar, insulin and lipid patterns of insulin resistance long before a diabetes diagnosis. Insulin resistance and metabolic health explains why those early numbers matter.
• Bioimpedance body composition splits your weight into fat, muscle and water, something a bathroom scale cannot do. See body composition, not BMI.

Every result goes to the physician who ordered it. Measura measures; it does not diagnose bile acid diarrhea or treat it.

Questions to bring to your physician

• Could my symptoms be bile acid diarrhea, and how would we test for it here?
• Did a positive breath test come before every antibiotic course I was given?
• Gallbladder disease keeps company with fatty liver and metabolic syndrome. Have mine been checked?
• For each supplement I take, which number should change, and when do we look again?

Why bile works as a signal is covered in the earlier post on bile, and once drainage works the gut wall still has to close, which is where the next post on healing time picks up. Every study named here, with its limits, is in the Chapter 28 book companion. Unmeasured is unmanaged: the woman in the video ate a restaurant meal at four months, her first since the surgery, once someone measured the right thing.

Frequently asked questions

References

• Lim, S. J., Gracie, D. J., Kane, J. S., Mumtaz, S., Scarsbrook, A. F., Chowdhury, F. U., Ford, A. C., & Black, C. J. (2019). Prevalence of, and predictors of, bile acid diarrhea in outpatients with chronic diarrhea: a follow-up study. Neurogastroenterology and Motility, 31(9), e13666. https://doi.org/10.1111/nmo.13666
• Kim, Y. J., Paik, C. N., Jo, I. H., Kim, D. B., & Lee, J. M. (2021). Serum gastrin predicts hydrogen-producing small intestinal bacterial overgrowth in patients with abdominal surgery: a prospective study. Clinical and Translational Gastroenterology, 12(1), e00291. https://doi.org/10.14309/ctg.0000000000000291
• Kim, D. B., Paik, C. N., Song, D. S., Kim, Y. J., & Lee, J. M. (2018). The characteristics of small intestinal bacterial overgrowth in patients with gallstone diseases. Journal of Gastroenterology and Hepatology, 33(8), 1477-1484. https://doi.org/10.1111/jgh.14113
• Cahill, C. J., Pain, J. A., & Bailey, M. E. (1987). Bile salts, endotoxin and renal function in obstructive jaundice. Surgery, Gynecology & Obstetrics, 165(6), 519-522. https://pubmed.ncbi.nlm.nih.gov/3120329/
• Sies, C. W., & Brooker, J. (2005). Could these be gallstones?. Lancet, 365(9468), 1388. https://doi.org/10.1016/S0140-6736(05)66373-8
• Kars, M., Yang, L., Gregor, M. F., Mohammed, B. S., Pietka, T. A., Finck, B. N., Patterson, B. W., Horton, J. D., Mittendorfer, B., Hotamisligil, G. S., & Klein, S. (2010). Tauroursodeoxycholic acid may improve liver and muscle but not adipose tissue insulin sensitivity in obese men and women. Diabetes, 59(8), 1899-1905. https://doi.org/10.2337/db10-0308
• Rudic, J. S., Poropat, G., Krstic, M. N., Bjelakovic, G., & Gluud, C. (2012). Ursodeoxycholic acid for primary biliary cirrhosis. Cochrane Database of Systematic Reviews, 12(12), CD000551. https://doi.org/10.1002/14651858.CD000551.pub3
• Shahsavari, K., Ardekani, S. S., Ardekani, M. R. S., Esfahani, M. M., Kazemizadeh, H., Jamialahmadi, T., Iranshahi, M., Khanavi, M., & Hasanpour, M. (2025). Are alterations needed in Silybum marianum (Silymarin) administration practices? A novel outlook and meta-analysis on randomized trials targeting liver injury. BMC Complementary Medicine and Therapies, 25(1), 134. https://doi.org/10.1186/s12906-025-04886-y

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How to Test for Mold Toxicity: What a Panel Can Prove

No blood or urine test currently proves mold made you sick: urine mycotoxin panels have no FDA-approved version, no healthy reference distribution and no validated cutoff. What can be established is your exposure history, the building’s damage and the measurable state of your own physiology.

A mold panel feels like an answer because it prints a number. Before you buy one, look at what stands under that number, and at which measurements in your own body can actually move a plan.

People asking how to test for mold toxicity are usually one click from a shopping cart: a urine panel, a marker set, a protocol sold as one package. Hold that click, because any test worth paying for has to clear three bars. It measures something real. It has a distribution of healthy, unexposed people standing under its numbers. And the answer changes what happens next. The chapter video, Mold Illness: Fix the Basement, Skip the Panel, grades the mold claims tier by tier. What follows sorts the measurements by those three bars.

The compounds are real, and that is not the argument

Start where nobody disputes anything. Aflatoxin, a mold toxin that grows on stored crops, is classified as carcinogenic to humans and causes liver cancer. That burden sits mostly in sub-Saharan Africa, Southeast Asia and China, where largely uncontrolled contamination of food meets high rates of hepatitis B. Name the population, because the population is the whole meaning of the number. A Midwestern basement is not that population.

Milder compounds, meanwhile, are in nearly everyone. Fifty pregnant American women were sampled at four separate points, blood and urine both. One grain toxin, deoxynivalenol, turned up in 99% of their urine samples at a median of 23 ng/mL. The carcinogenic aflatoxins were not detected in any sample at all. So a laboratory finding a mycotoxin in you has proved only that you eat food. That is why the interesting question was never presence but amount, and amount is where a panel goes quiet.

Amount can be measured, just not by the panels sold for it. In that same group of women, estimated intake ran over the tolerable daily limit for deoxynivalenol at 28% of the measurements on average and for zearalenone at 2%. Judged against the stricter human biomonitoring guidance value, the deoxynivalenol figure averaged 48%. Every sample with a quantified ochratoxin A level carried a margin of exposure under 10,000, which regulators treat as a flag for possible concern. Food was the route in that study. Not one damp basement was in it.

Why a urine mycotoxin panel cannot come back positive

Mycotoxin and urine panels are not Measura [Cardiometabolic and Autonomic Health Analysis] tests. They are different tests, ordered from outside laboratories, and the reason to know that is not modesty about the menu. No urine mycotoxin assay has FDA approval. Traces sit in everyday groceries, so healthy people excrete them too. The lab regulations governing these panels never ask whether the assay measures the thing it claims to measure.

One federal case report shows what that does to a family. The panel returned ochratoxin at 2.8 parts per billion where the laboratory drew its positive line at 2.0, and trichothecenes at 0.4 where that line sat at 0.2. Each compound carries its own threshold, and each result landed above its own. The panel was positive twice over on its own terms. Investigators then pulled out drywall, carpet and ceiling tiles, and found neither water damage nor significant fungal growth. Without a validated threshold, a number cannot be positive. It can only be higher than a line somebody chose.

What a damp building is proven to do

The building evidence is stronger than the blood work, and it is graded honestly by the people who wrote it. The 2004 American synthesis found sufficient evidence linking damp indoor spaces to some upper respiratory symptoms. A 2024 European guideline sorts the outcomes into tiers: respiratory disease sufficient, atopic eczema limited or suspected, gastrointestinal effects inadequate or insufficient. The gut itself, the first brain, sits in the weakest tier of the best document in the field, and pretending otherwise would make everything else here worth less.

Scale matters too. Sensitization to mold across the general European population runs 3% to 22.5%, and about 5% of people are predicted to develop some allergic airway symptoms from molds over a lifetime, mostly from outdoor rather than indoor species. Outside the chest, the measured signal is old and blunt: across 597 households in 1989, adults in damp, moldy homes described more symptoms, including nausea and vomiting; the count climbed as the damp got worse, and the pattern survived adjustment for smoking, unemployment and overcrowding.

The repair with the cleanest human data

Pooled trials of repairing damp, moldy houses lowered the odds of adult wheezing to 0.64 and of rhinitis to 0.57, on moderate-quality evidence. In children, asthma days did not move against information alone, and no included study measured a gut outcome at all. Even the occupational medicine paper that flatly rejects the diagnosis agrees that mold growth at home, school or work should not be tolerated.

Notice who pays. Drying a foundation properly is expensive and slow, ignoring it costs nothing today, and the person who signs for the work is rarely the person sleeping above it. A panel, by contrast, can be sold to the tenant tonight. Follow the invoice and you can predict which claim gets marketed and which repair gets postponed another winter.

How to test for mold toxicity in the body while the wall dries

A stall in recovery deserves a second explanation, not just a louder version of the first one. Two biological drivers sit under most of these stories. The intestinal barrier is one: mycotoxins degrade its physical, mucus, immune and microbial layers, though that work is built in cells and animals rather than people. The immune system is the other, where asthma, allergic rhinitis, sinusitis and hypersensitivity pneumonitis are well defined while the newer mold illnesses remain largely unproved.

Both of those are more measurable as terrain than as toxin. Laboratory panels can put metabolic and inflammatory markers on a page for your physician, which is how metaflammation and insulin resistance stop being adjectives. Autonomic nervous system testing measures how your nerves regulate heart rate, blood pressure and sweating, which is the machinery behind feeling wiped out and unsteady on standing. Cognitive assessment records where your thinking sits today, and that is a baseline rather than a verdict about mold; American toxicology states there is no documented evidence that inhaled indoor fungi cause a chronic toxic encephalopathy. Measura measures and reports. Your physician decides what any finding means and what to do.

Then keep the instrument you already own. Keep a dated log instead of a memory: the day symptoms changed, the address you woke up at, and anything that happened to the house beforehand. Pollen does the same away-better, home-worse trick on a seasonal calendar, so dates are what separate the two. Sleep, food and movement have more room to work once an exposure is gone, which is the physiological reason the repair comes before the rebuild. Nothing here is a reason to start, stop or change a medication. The graded studies, with their full numbers and their limits, are in the chapter companion, and the barrier argument has its own measurement story.

Frequently asked questions

References

• International Agency for Research on Cancer. (2012). Aflatoxins. In: Chemical agents and related occupations (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 100F). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 100F, Aflatoxins monograph, Evaluation section. https://www.ncbi.nlm.nih.gov/books/NBK304413/
• Krausová, M., Ayeni, K. I., Gu, Y., Borutzki, Y., O’Bryan, J., Perley, L., Silasi, M., Wisgrill, L., Johnson, C. H., & Warth, B. (2024). Longitudinal biomonitoring of mycotoxin exposure during pregnancy in the Yale Pregnancy Outcome Prediction Study. Environment International, 194, 109081. https://doi.org/10.1016/j.envint.2024.109081
• Kawamoto, M., & Page, E. (2015). Notes from the field: Use of unvalidated urine mycotoxin tests for the clinical diagnosis of illness — United States, 2014. MMWR. Morbidity and Mortality Weekly Report, 64(6), 157-158. https://pubmed.ncbi.nlm.nih.gov/25695323/
• Hurraß, J., Heinzow, B., Walser-Reichenbach, S., Aurbach, U., Becker, S., Bellmann, R., Bergmann, K.-C., Cornely, O. A., Engelhart, S., Fischer, G., Gabrio, T., Herr, C. E. W., Joest, M., Karagiannidis, C., Klimek, L., Köberle, M., Kolk, A., Lichtnecker, H., Lob-Corzilius, T., … Wiesmüller, G. A. (2024). AWMF mold guideline “Medical clinical diagnostics for indoor mold exposure” – Update 2023 AWMF Register No. 161/001. Allergologie Select, 8, 90-198. https://doi.org/10.5414/ALX02444E
• Platt, S. D., Martin, C. J., Hunt, S. M., & Lewis, C. W. (1989). Damp housing, mould growth, and symptomatic health state. BMJ (Clinical Research Ed.), 298(6689), 1673-1678. https://doi.org/10.1136/bmj.298.6689.1673
• Sauni, R., Verbeek, J. H., Uitti, J., Jauhiainen, M., Kreiss, K., & Sigsgaard, T. (2015). Remediating buildings damaged by dampness and mould for preventing or reducing respiratory tract symptoms, infections and asthma. Cochrane Database of Systematic Reviews, 2015(2), CD007897. https://doi.org/10.1002/14651858.CD007897.pub3
• Hardin, B. D., Kelman, B. J., & Saxon, A. (2003). Adverse human health effects associated with molds in the indoor environment. Journal of Occupational and Environmental Medicine, 45(5), 470-478. https://doi.org/10.1097/00043764-200305000-00006
• Leikin, J., Holland, M. G., Kurt, T. L., McKay, C. A., & Stolbach, A. I. (American College of Medical Toxicology). (2025). ACMT position statement: Medical toxicology considerations in the diagnosis and treatment of patients with concerns about mold-related inhalation exposures. https://www.acmt.net/wp-content/uploads/2025/08/PS_250813_ACMT-Position-Statement-Mold-Related-Inhalation-Exposures.pdf
• Gao, Y., Meng, L., Liu, H., Wang, J., & Zheng, N. (2020). The compromised intestinal barrier induced by mycotoxins. Toxins, 12(10), 619. https://doi.org/10.3390/toxins12100619

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Methane Breath Test: What the Gas Shows and What It Cannot

A methane breath test measures a gas your gut microbes make from food and you exhale. Under the North American Consensus, 10 ppm or higher is positive, which points to active methane-making organisms and is strongly tied to constipation, though it is not a full diagnosis on its own.

A stool report lists who lives in your gut. The gas you exhale shows what they are doing today, and that difference decides whether a result can guide anything.

A methane breath test asks your gut a different question than a mail-order stool kit does. The kit counts names. The breath measures work: gas that microbes made from your food, carried through your blood and released at your lungs. For someone who has spent months bloated or straining, with a folder of contradictory reports and no clear answer, that shift from census to activity is the whole point. The video Your Gut Bacteria Breathe Out Through Your Mouth makes the case on camera. One thing needs saying plainly first: breath testing is not a Measura test. It is ordered by your physician and done by a gastroenterology practice or laboratory elsewhere. What Measura can add in the same person comes later.

A list of residents is not a record of their work

My position on gut testing fits in one line: the census is not the activity. When European experts sent one identical stool sample to six commercial microbiome services in 2024, three rated diversity excellent or good, one unfavorable and two average. None disclosed the reference population behind its labels. The panel judged the interpretations premature and of limited clinical utility.

Even a flawless laboratory would hit a deeper wall. In adult men whose stool was sequenced for both DNA and RNA, only 44% of the pathways the community commonly carried were actually switched on. A gene on a list is a capability. It is not evidence that anything is happening. Stool consistency shifts the markers too, so part of a diversity score reflects how fast that sample moved on the day you mailed it.

I used to treat the organism names on those reports as findings and aim treatment at them. They were a head count, and a head count cannot tell you who is causing trouble.

What does a breath test actually measure?

Your own cells produce no hydrogen. Any hydrogen in your breath came from microbes fermenting something. Methane works the same way, with a twist: the organisms that make methane use up four molecules of hydrogen for each one of methane. A heavy methane producer can therefore show a flat hydrogen line. That is why the North American Consensus calls for measuring hydrogen, methane and carbon dioxide at the same sitting, and why a laboratory reading hydrogen alone can call a methane producer normal.

The consensus also fixes the rules, and a result means little without them. For overgrowth, hydrogen has to climb 20 ppm or more above its starting value within 90 minutes. A methane level of 10 ppm or higher is positive. Preparation is specified: antibiotics avoided for four weeks and an 8–12 hour fast. Follow the instructions of the physician who orders your test, including about any medication.

Is methane linked to constipation?

Methane is where the gas earns its place. Across studies, breath methane is tied to constipation at an odds ratio of 3.51, and people whose overgrowth is mainly methane are five times as likely to be constipated as people whose overgrowth is mainly hydrogen. A single fasting methane of 10 ppm or more matched the full two-hour test at 86.4% sensitivity and 100% specificity. It stayed stable for 14 weeks without treatment and dropped within two days of antibiotics.

That behavior matters for anyone who describes the problem as bloating. The word you use sends a workup in one direction; a measured gas can send it in another. A number that holds still when nothing changes and moves when treatment does is what a usable marker looks like.

How far can you trust a methane breath test?

Not blindly. In the pooled research, 35.5% of irritable bowel patients came back positive, against 29.7% of healthy comparison subjects. When positive glucose tests were repeated with a tracer following the sugar, 48% turned out to be the colon fermenting sugar that arrived early. Changing protocols at one center moved positivity from 29.7% to 39.5%. The gastroenterology society guidance says openly that the definition of overgrowth still lacks precision.

That evidence is modest, and it still beats the usual alternative, which is a symptom, a guess and a prescription. A rough reading of the right activity is more useful than a polished report on the wrong question.

What Measura can measure in the same person

Measura [Cardiometabolic and Autonomic Health Analysis] does not run breath tests, stool tests or microbiome panels. Where it fits is the body around the bowel, because gut gas and metabolism turn up in the same patients. In a small study of eleven adults with prediabetes and obesity who were methane positive, the eight whose breath methane cleared after antibiotics also showed changes in LDL, total cholesterol and insulin late in a glucose tolerance test. There was no control group, and extra calorie harvest from food did not change. That is a lead, not a result, and a reason to look at the metabolic side instead of assuming it is fine.

• Laboratory panels can show glucose, insulin and lipids. Society guidance also notes that overgrowth can leave a trace on ordinary blood work: a high folate beside a low vitamin B12. See which laboratory runs the blood work.
• Bioimpedance body composition separates muscle from fat, which a BMI in the obesity range cannot do. More is in insulin resistance and metabolic health.

The social driver is plain once you see it. A stool kit arrives with colored bars and a reason to buy another. A gas measurement sells no refills. Results from both kinds of testing belong with your physician, who decides what they mean.

Questions to bring before your next gut test

• Which gases will the laboratory measure: hydrogen, methane and carbon dioxide?
• Will the test follow the North American Consensus substrate, dose and cutoffs?
• Was overgrowth ruled out before any lactose or fructose breath test?
• Has inflammation been excluded with a calprotectin or C-reactive protein?
• Have my insulin, lipids, folate and B12 been checked?

Every study above is in the Angry Gut companion deep dive on breath and biomarker testing. The appetite side of gut signaling is in what causes sugar cravings, and physicians can read the clinical version on methanogen overgrowth.

Frequently asked questions

References

• Rodriguez, J., Cordaillat-Simmons, M., Badalato, N., Berger, B., Breton, H., de Lahondès, R., Deschasaux-Tanguy, M., Desvignes, C., D’Humières, C., Kampshoff, S., Lavelle, A., Metwaly, A., Quijada, N. M., Seegers, J. F. M. L., Udocor, A., Zwart, H., Maguin, E., Doré, J., & Druart, C. (2024). Microbiome testing in Europe: Navigating analytical, ethical and regulatory challenges. Microbiome, 12(1), 258. https://doi.org/10.1186/s40168-024-01991-x
• Abu-Ali, G. S., Mehta, R. S., Lloyd-Price, J., Mallick, H., Branck, T., Ivey, K. L., Drew, D. A., DuLong, C., Rimm, E., Izard, J., Chan, A. T., & Huttenhower, C. (2018). Metatranscriptome of human faecal microbial communities in a cohort of adult men. Nature Microbiology, 3(3), 356-366. https://doi.org/10.1038/s41564-017-0084-4
• Rezaie, A., Buresi, M., Lembo, A., Lin, H., McCallum, R., Rao, S., Schmulson, M., Valdovinos, M., Zakko, S., & Pimentel, M. (2017). Hydrogen and methane-based breath testing in gastrointestinal disorders: The North American Consensus. The American Journal of Gastroenterology, 112(5), 775-784. https://doi.org/10.1038/ajg.2017.46
• Kunkel, D., Basseri, R. J., Makhani, M. D., Chong, K., Chang, C., & Pimentel, M. (2011). Methane on breath testing is associated with constipation: A systematic review and meta-analysis. Digestive Diseases and Sciences, 56(6), 1612-8. https://doi.org/10.1007/s10620-011-1590-5
• Takakura, W., Pimentel, M., Rao, S., Villanueva-Millan, M. J., Chang, C., Morales, W., Sanchez, M., Torosyan, J., Rashid, M., Hosseini, A., Wang, J., Leite, G., Kowalewski, E., Mathur, R., & Rezaie, A. (2022). A single fasting exhaled methane level correlates with fecal methanogen load, clinical symptoms and accurately detects intestinal methanogen overgrowth. The American Journal of Gastroenterology, 117(3), 470-477. https://doi.org/10.14309/ajg.0000000000001607
• Shah, A., Talley, N. J., Jones, M., Kendall, B. J., Koloski, N., Walker, M. M., Morrison, M., & Holtmann, G. J. (2020). Small intestinal bacterial overgrowth in irritable bowel syndrome: A systematic review and meta-analysis of case-control studies. The American Journal of Gastroenterology, 115(2), 190-201. https://doi.org/10.14309/ajg.0000000000000504
• Lin, E. C., & Massey, B. T. (2016). Scintigraphy demonstrates high rate of false-positive results from glucose breath tests for small bowel bacterial overgrowth. Clinical Gastroenterology and Hepatology, 14(2), 203-8. https://doi.org/10.1016/j.cgh.2015.07.032
• Quigley, E. M. M., Murray, J. A., & Pimentel, M. (2020). AGA Clinical Practice Update on small intestinal bacterial overgrowth: Expert review. Gastroenterology, 159(4), 1526-1532. https://doi.org/10.1053/j.gastro.2020.06.090
• Mathur, R., Chua, K. S., Mamelak, M., Morales, W., Barlow, G. M., Thomas, R., Stefanovski, D., Weitsman, S., Marsh, Z., Bergman, R. N., & Pimentel, M. (2016). Metabolic effects of eradicating breath methane using antibiotics in prediabetic subjects with obesity. Obesity (Silver Spring), 24(3), 576-82. https://doi.org/10.1002/oby.21385

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Glyphosate in Food: What Can Actually Be Measured in You

A urine glyphosate level describes yesterday, not your life, and no reference range exists to hold it against. What can be measured in you is the terrain underneath the worry: blood panels for fuel handling, body composition, resting energy use and small-fiber nerve function.

There is no test that ties a residue on your produce to what lives in your gut. The mechanism has been measured in animals, never in a person, and the rest of your terrain can still be put on a number.

Glyphosate in food is the exposure nobody counts. Intake forms ask how many courses of antibiotics you have taken; not one of them asks what was sprayed on the lettuce you ate most days for a decade. The Antibiotic on Your Salad, the Chapter 22 video for The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, sets out why a weed killer aimed at a bacterial enzyme belongs in a conversation about your gut. The question here is narrower and more practical: what can honestly be put on a number in you, and what cannot.

Why your own cells were the wrong place to look

The compound does one thing. It jams a single enzyme in the shikimate pathway, the assembly line plants and bacteria use to build three amino acids they cannot live without. Your cells never carried that pathway. That fact is the whole safety case, regulators accepted it, and on a human cell it holds. The other half of the sentence is where the testing stopped. Bacteria do carry the pathway. Species by species, the target enzyme comes in a vulnerable version and a resistant one, and when that sorting was done across thousands of organisms, 54% of the core human gut microbiome held the vulnerable version. The authors called their own figure conservative. A second team read gene expression rather than gene presence and reached the opposite conclusion: incomplete pathways, mostly idle, in settled adult guts. Two computational surveys, two answers, and no living community measured in either.

Your gut is the first brain. It decides what enters the body and sets the inflammatory tone the second brain in your skull then has to work inside. A compound that changes which organisms hold which niche is not a poisoning story, it is a staffing story, and vacancies in the first brain are where metaflammation gets its opening. The reason the question stays open is not scientific mystery. Spraying happens at the scale of a subsidized commodity crop, and the safety tests that cleared it were designed before anyone believed the flora in a cecum were worth counting. No budget line, no measurement.

Is there a test for glyphosate in food?

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service with a fixed library, and nothing in it measures pesticide residue, herbicide levels in urine, or which organisms live in your bowel. Those are different tests, run elsewhere, and the honest thing to say about the ones sold directly to patients is that no reference range exists to hold your result against. A urine level describes yesterday, not your life. Levels dropped significantly in people who had gone without food for most of a day, which is precisely how investigators worked out that the exposure rides in on meals. Measura measures. Your physician interprets, diagnoses and decides.

What has been measured, and in whom

Exposure is close to universal. Four out of five Americans aged six and older carried a detectable level, 81.2% to be exact, when a nationally representative set of urine samples was tested; the sample ran to 2,310 specimens. The number of studies that pair that urine sample with a stool sample in the same person is zero. Every finding about gut communities behind the video comes from rodents, insects or a benchtop simulator, and that is the tier of the evidence, stated plainly.

It is still worth knowing what the animals showed. Rats dosed for ninety days at the whole European daily allowance accumulated shikimic acid in the cecum, the biochemical fingerprint of the blocked enzyme, in a living mammal, at a dose a regulator had signed off on. That signal never turned up in serum, which is where safety testing looks. Mice dosed near the American allowance showed altered gut communities and more markers of intestinal inflammation. Nobody has shown harm to a human microbiome, because nobody has looked. A study that could settle it would feed volunteers a known dose for years while excluding anyone with a disturbed gut, a metabolic disease or a long medication list, which excludes almost everyone carrying the symptoms.

What can be measured in you instead

An exposure you cannot measure does not leave you with nothing to measure. The terrain underneath the worry, how you handle fuel, what your body is built of, how much you burn and how your small nerve fibers are working, is measurable today.

• Laboratory panels put the metabolic picture in blood: fuel handling, inflammation and organ function, drawn and reported rather than estimated from a chart.
• Bioimpedance body composition separates muscle from fat, which a bathroom scale cannot do, and body composition is not the same as weight.
• Indirect calorimetry measures the energy you actually burn at rest instead of predicting it from height, weight and age.
• Sudomotor testing reads how the sweat glands driven by your smallest nerve fibers respond, which matters when tingling or burning in the feet travels alongside the bowel symptoms.

Why bother, when the exposure itself stays unmeasured? Because the background almost everyone is standing on is worse than they think. Fewer than 7% of US adults are metabolically healthy on the tighter criteria applied after 2021, down from fewer than 12.2% on NHANES 2009-2016. Fewer than 3% of patients in our own clinic clear that bar, and fewer than 1% of chronic pain patients do, which are practice-reported figures from our own population, not trial outcomes, and individual results vary. A person worried about residue on produce usually has two or three measurable problems that nobody has counted yet.

The window where a stripped gut matters most

Here is the part that rarely gets said. Gene expression measured in a settled adult gut describes an ordinary day in someone who is not sick. It says nothing about a community rebuilding itself after a course of antibiotics, an abdominal operation or a hospital stay, when bacteria have to manufacture their own amino acids rather than scavenge them from a crowded neighborhood. Quiet at rest is not quiet under load. If this exposure ever matters to you, the likeliest moment is the stretch right after your gut has been cleared down to bare ground, not an average Tuesday. That is also the stretch when the rest of the picture, fuel handling and muscle and nerve function, is easiest to move.

What to bring to your appointment

• A dated timeline: when the bloating or loose stools started, and what else changed that season.
• Every antibiotic course, abdominal operation and inpatient stay you can remember.
• Which foods you eat raw, and where that produce comes from.
• Your full medication and supplement list.
• One question worth asking: which of my measurable systems has nobody measured yet? More are listed in questions worth asking your doctor.

Every study behind the argument, with what each one does and does not show, sits in the book companion for The Angry Gut. Physicians asked for a test they cannot order can read the screening version written for practices.

Frequently asked questions

References

• Leino, L., Tall, T., Helander, M., Saloniemi, I., Saikkonen, K., Ruuskanen, S., & Puigbò, P. (2021). Classification of the glyphosate target enzyme (5-enolpyruvylshikimate-3-phosphate synthase) for assessing sensitivity of organisms to the herbicide. Journal of Hazardous Materials, 408, 124556. https://doi.org/10.1016/j.jhazmat.2020.124556
• Mesnage, R., & Antoniou, M. N. (2020). Computational modelling provides insight into the effects of glyphosate on the shikimate pathway in the human gut microbiome. Current Research in Toxicology, 1, 25-33. https://doi.org/10.1016/j.crtox.2020.04.001
• Ospina, M., Schütze, A., Morales-Agudelo, P., Vidal, M., Wong, L.-Y., & Calafat, A. M. (2022). Exposure to glyphosate in the United States: Data from the 2013-2014 National Health and Nutrition Examination Survey. Environment International, 170, 107620. https://doi.org/10.1016/j.envint.2022.107620
• Mesnage, R., Teixeira, M., Mandrioli, D., Falcioni, L., Ducarmon, Q. R., Zwittink, R. D., Mazzacuva, F., Caldwell, A., Halket, J., Amiel, C., Panoff, J.-M., Belpoggi, F., & Antoniou, M. N. (2021). Use of shotgun metagenomics and metabolomics to evaluate the impact of glyphosate or Roundup MON 52276 on the gut microbiota and serum metabolome of Sprague-Dawley rats. Environmental Health Perspectives, 129(1), 17005. https://doi.org/10.1289/EHP6990
• Lehman, P. C., Cady, N., Ghimire, S., Shahi, S. K., Shrode, R. L., Lehmler, H.-J., & Mangalam, A. K. (2023). Low-dose glyphosate exposure alters gut microbiota composition and modulates gut homeostasis. Environmental Toxicology and Pharmacology, 100, 104149. https://doi.org/10.1016/j.etap.2023.104149
• Walsh, L., Hill, C., & Ross, R. P. (2023). Impact of glyphosate (Roundup) on the composition and functionality of the gut microbiome. Gut Microbes, 15(2), 2263935. https://doi.org/10.1080/19490976.2023.2263935

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Long-Term PPI Use: What Your Blood Work and Body Can Show

Long-term PPI use shows up first in blood work: two or more years on the pill carried 1.65 times the odds of vitamin B12 deficiency, rising to 1.95 on higher doses, with minerals pointing the same way. Bioimpedance body composition adds the belly fat behind reflux pressure.

Years on an acid pill can quietly change what your body absorbs, and the rebound when you stop is real. Neither shows up at a routine visit unless someone decides to measure.

Long-term PPI use usually begins as a short course that nobody ends. A proton pump inhibitor such as omeprazole is started for a few weeks, and years later no one has checked what a stomach held near neutral has changed elsewhere. The video The Heartburn Pill You Can’t Quit, from The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, makes the full case about the drug. The angle here is measurement: what the pill can change in your own numbers, what a routine visit leaves unchecked, and which of those changes a test can actually show.

The correction: low acid does not cause reflux

For years I repeated an elegant idea to patients. Reflux happens because the stomach makes too little acid, and without enough acid the valve at the top of the stomach never gets the signal to close. It was tested in people, and it failed. Heartburn patients took omeprazole twice a day for a week while a sensor counted every upward splash, acidic or not. The number of reflux events did not go down. Only their chemistry changed, with the acid portion falling from 45% to 3%.

The real trigger is mechanical. When 84 people in three weight categories were compared, their valves had similar pressure and length, yet the brief relaxations that let acid escape ran 2.1, 3.8 and 7.3 times an hour, climbing with body weight. The pressure difference across the junction rose with it, from 4.5 to 10.0 mm Hg. Reflux is plumbing under pressure, and much of that pressure comes from the belly.

Why the heartburn comes back harder when you stop

Hold stomach acid down for weeks and the hormone gastrin rises. The cells that answer gastrin multiply, so the acid-making machinery is quietly expanded while it sits switched off. Remove the pill and that extra capacity turns on at once. This is rebound acid hypersecretion, and it is not proof that your original problem is still there.

Two randomized trials tested it in healthy volunteers who had never had reflux. After eight weeks on a proton pump inhibitor, 44% developed clinically relevant acid symptoms in the month after stopping, against 15% on placebo. A second trial with a different drug again found 44%, against 9% on placebo. The flare typically begins somewhere between day 5 and day 14 and settles within a few days for most people, although measured oversecretion can persist beyond 8 weeks.

The system around the prescription does the rest. A refill costs a click. Asking whether the drug still has a job takes a visit nobody schedules. Some people genuinely need acid suppression: after a bleeding ulcer, with erosive esophagitis or Barrett’s esophagus, or while taking an anti-inflammatory every day. Whether you are one of them is a decision for the physician who prescribed it, never a reason to stop on your own.

Stomach acid is measured elsewhere

Measura [Cardiometabolic and Autonomic Health Analysis] does not test stomach acid. Gastric pH monitoring, impedance studies, acid output measurement and endoscopy are gastroenterology tests done in other settings, and so is testing for H. pylori. Those tests decide whether reflux is real and whether a stomach truly under-produces acid.

Truly low acid exists, but it is uncommon. Among 248 volunteers aged 65 and over, 84% had acidic stomach contents at rest, and only about 11% consistently made too little. The two main causes are autoimmune gastritis, which destroys the cells that secrete acid, and long-standing H. pylori infection that thins the lining. Symptoms cannot pick those people out, which is why the answer comes from a test your physician orders. The stomach-lining side is covered in atrophic gastritis and B12 absorption. What Measura can measure is the body the acid was protecting.

Does long-term PPI use lower B12 and minerals?

Acid is the step that loosens vitamin B12 from the food protein carrying it. In one large analysis, two or more years on a proton pump inhibitor carried an odds ratio of 1.65 for B12 deficiency, against 1.25 for the weaker H2 blocker class, and the figure climbed to 1.95 in people taking more than 1.5 pills a day. A risk that grows with the dose is hard to dismiss as coincidence.

Minerals point the same way with less certainty. In kidney transplant recipients, low magnesium carried an odds ratio of 2.16, and in renal transplant recipients iron deficiency ran at 1.57, rising to 2.30 on a high dose. Those are narrow, medically complex groups, and their numbers are not your personal odds.

Laboratory panels are how that part of the picture becomes a number instead of a guess. Which markers a panel includes is your physician’s call, and years on an acid suppressor is exactly the history that makes B12 and minerals worth raising. A single result has limits, explained in what a test result can and cannot tell you.

How does a PPI change protein digestion, and why does belly fat matter?

Pepsin, the stomach enzyme that starts breaking down protein, works only in acid. With the pH raised, protein leaves the stomach largely intact and arrives at a small intestine that expected it already opened. The gut is the first brain, and it runs on what it can take apart, not on what sits on the plate.

The other half is fat around the middle. Of the lifestyle measures tested against reflux in a systematic review, only weight loss and raising the head of the bed held up, and both work on pressure. Abdominal fat is also active tissue that feeds metaflammation, the low-grade inflammation that keeps a metabolism irritated, and it has an upstream cause in a food supply that subsidizes acellular carbohydrates. Bioimpedance body composition separates fat mass from lean mass, so weight loss can be tracked as fat lost rather than muscle lost. Why that matters more than weight is explained in body composition, not BMI.

Do PPIs cause dementia, fractures or kidney disease?

Long-term PPI use side effects make frightening headlines. In a three-year trial of 17,598 people assigned at random to pantoprazole or a dummy pill, pneumonia, fractures, kidney disease and dementia were all tracked. Only enteric infection differed, at 1.4% against 1.0%. A dementia hazard ratio of 1.44 from observational data did not reproduce, and reviewers grade most of the fracture evidence as very low to low certainty.

Measura does not scan bones. If you are older and worry about falling, the more useful measurement is of steadiness itself. Vestibular and balance testing records how well you hold your balance, a fall-risk finding worth having for its own sake rather than as a fear borrowed from a pill. More is in dizziness, balance and falls.

What to bring to your next appointment

• The date the prescription started and the reason written down that day.
• Every attempt to stop: which day the symptoms returned and how long they lasted.
• Whether reflux was ever confirmed with a test, rather than inferred from a response to the pill.
• Whether H. pylori, B12 and minerals have been checked, and whether body composition should be measured.

More prompts are in questions worth asking your doctor. The studies behind these figures are in the companion deep dive for The Angry Gut. Physicians can read the screening version for practices, and a pain prescription that stalls the gut even more completely comes next.

Frequently asked questions

References

• Vela, M. F., Camacho-Lobato, L., Srinivasan, R., Tutuian, R., Katz, P. O., & Castell, D. O. (2001). Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: effect of omeprazole. Gastroenterology, 120(7), 1599-606. https://doi.org/10.1053/gast.2001.24840
• Wu, J. C. Y., Mui, L. M., Cheung, C. M. Y., Chan, Y., & Sung, J. J. Y. (2006). Obesity is associated with increased transient lower esophageal sphincter relaxation. Gastroenterology, 132(3), 883-9. https://doi.org/10.1053/j.gastro.2006.12.032
• Reimer, C., Søndergaard, B., Hilsted, L., & Bytzer, P. (2009). Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology, 137(1), 80-87, 87.e1. https://doi.org/10.1053/j.gastro.2009.03.058
• Namikawa, K., & Björnsson, E. S. (2024). Rebound acid hypersecretion after withdrawal of long-term proton pump inhibitor (PPI) treatment: Are PPIs addictive?. International Journal of Molecular Sciences, 25(10), 5459. https://doi.org/10.3390/ijms25105459
• Hurwitz, A., Brady, D. A., Schaal, S. E., Samloff, I. M., Dedon, J., & Ruhl, C. E. (1997). Gastric acidity in older adults. JAMA, 278(8), 659-62. https://pubmed.ncbi.nlm.nih.gov/9272898/
• Lam, J. R., Schneider, J. L., Zhao, W., & Corley, D. A. (2013). Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA, 310(22), 2435-42. https://doi.org/10.1001/jama.2013.280490
• Mohammadi, K., Yaribash, S., Razi, B., & Dashti-Khavidaki, S. (2021). Comparing safety of proton-pump inhibitors versus H2-receptor antagonists in kidney transplant recipients: A systematic review and meta-analysis. Journal of clinical pharmacy and therapeutics, 47(5), 567-574. https://doi.org/10.1111/jcpt.13589
• Kaltenbach, T., Crockett, S., & Gerson, L. B. (2006). Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach. Archives of Internal Medicine, 166(9), 965-971. https://doi.org/10.1001/archinte.166.9.965
• Moayyedi, P., Eikelboom, J. W., Bosch, J., Connolly, S. J., Dyal, L., Shestakovska, O., Leong, D., Anand, S. S., Stork, S., Branch, K. R. H., Bhatt, D. L., Verhamme, P. B., O’Donnell, M., Maggioni, A. P., Lonn, E. M., Piegas, L. S., Ertl, G., Keltai, M., Bruns, N. C., … Yusuf, S. (2019). Safety of Proton Pump Inhibitors Based on a Large, Multi-Year, Randomized Trial of Patients Receiving Rivaroxaban or Aspirin. Gastroenterology, 157(3), 682-691.e2. https://doi.org/10.1053/j.gastro.2019.05.056

Related reading

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• Narcotic Bowel Syndrome: What Testing Can and Cannot Show
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Gut Microbiome Test Results: What They Cannot Measure

A gut microbiome test can be accurate and still answer the wrong question. The organisms highlighted on a report live quietly in people who feel well, and none of it describes what your own body is doing.

A gut microbiome test can be entirely accurate and still answer a question that cannot help you. The printout is persuasive: a logo, two lines under yellow highlighter, a protocol waiting at the end. What the panel did was take attendance in one sample. It named who was present. It said nothing about what any of them were doing, and nothing whatever about what your own body is doing while they live there. The video The Wrong Enemy on Your Stool Report carries that argument from The Angry Gut, by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes. What follows is the measuring half of it.

What does a gut microbiome test actually measure?

The gut is the first brain, and it rearranges its population from one meal to the next. Vagal traffic moves it, and so does whatever arrives in the nutrient stream, which means a species list is a photograph taken on one morning. Work leaves a different kind of evidence: the metabolites a community makes, the immune response it provokes, the gases that come off fermentation. An international consensus panel with sixty-nine authors on it went through the versions of these panels sold straight to the public and could not find evidence that they help a patient in practice. Sixty-nine specialists rarely converge on anything. They converged on that.

The two lines most people carry anyway

Start with the yeast, since it sells the most protocols. Among 317 stool samples from a healthy Human Microbiome Project cohort, Candida albicans appeared in 80.8 percent and baker’s yeast in 96.8 percent. A positive yeast line describes the species, not the person holding the report. Much of the fungal signal traces back to the mouth and the plate, and brushing your teeth more often lowers it.

I should be honest about my own part in this. For years I read a highlighted fungal line as a finding and wrote the antifungal, because that is what I had been taught the line meant. What changed my practice was a randomized, double-blind test of nystatin in the exact symptom cluster patients still bring me: whole-body symptom scores improved 25 percent on the active regimens and 23 percent on placebo alone. The drug cleared the problem it is genuinely indicated for and nothing else. That is what a real indication looks like from the inside.

The protozoan is stranger. Of 296 healthy Malian children tested by PCR, 147 carried Blastocystis, and those children had richer and more diverse bacterial communities than the children without it. An Italian series holds the honest limit: researchers there found it in 22.3 percent of people whose immune systems were weakened and 6.8 percent of people whose were not. Immune status is the variable that decides whether the organism matters, and that judgment belongs to your physician, not to a highlighter.

Stool and microbiome panels are not Measura tests

This needs saying plainly. Measura [Cardiometabolic and Autonomic Health Analysis] does not run stool panels, microbiome sequencing or breath tests. Those are different tests, ordered somewhere else. Measura measures the host — the metabolic, vascular, autonomic and body-composition picture of the person carrying the flora. It measures; it does not diagnose disease on its own and it does not treat. Results go to your own physician to read alongside your history.

What can be measured in you

• Laboratory panels put numbers on the metabolic and inflammatory terrain — metaflammation, the low-grade inflammation that keeps a whole system irritable.
• Bioimpedance body composition separates muscle from fat, which a bathroom scale cannot do at any price.
• Indirect calorimetry measures resting metabolic rate rather than estimating it from an equation built on somebody else’s body.
• Heart rate variability and autonomic nervous system testing describe how the involuntary nervous system is regulating you, which is the same vagal wiring the first brain answers to.
• Sudomotor testing checks how the sweat glands of your hands and feet respond, a window on the small nerve fibers there, which matters when burning or numb feet showed up alongside the gut symptoms.

Why bother, when the organisms themselves are not the target? Because the terrain is measurable and the census is not the disease. Bacteria that make butyrate drive the colon’s lining cells to consume oxygen, which keeps that surface airless; thin those producers out and oxygen leaks in, and the families that expand are precisely the ones equipped to breathe it. That chain was mapped in mice, so hold it as mechanism rather than proof. The human end of it comes from 7,211 Finnish adults followed as long as 15 years, where a diversity score was not significantly associated with dying, while the load of Enterobacteriaceae came with a hazard ratio of 1.14, and the top quarter of that load ran a 34 percent greater risk of death than the bottom quarter. Composition mattered. The headline number on a consumer report did not.

Then the driver nobody prints beside the result. A test that finds something in most healthy people will sell a protocol to most of the people who buy one. The laboratory sells the detection, an online clinic sells the eviction, and your flora settles the difference. Nobody needs to be a villain for an incentive to work that way. And the eviction is measurable too: in 66 healthy adults given a single ordinary antibiotic, fecal diversity stayed reduced for as long as 4 months after clindamycin and 12 months after ciprofloxacin, with the butyrate producers taking the worst of it.

What to take to your appointment

• Every antibiotic and antimicrobial course you can reconstruct, counted as courses rather than years, and what each one was given for.
• Your usual stool consistency across two weeks. It moves a diversity score more than most reports admit.
• Your whole medication list. Acid-suppressing drugs, diabetes drugs and antipsychotics all weaken the resident community’s grip on newcomers, and none of them arrives labeled as a gut drug.
• A question about the plan: if this organism is treated and cleared, which symptom should change, and by when?
• A question about measurement: can my metabolic, autonomic and body-composition numbers be measured instead of described?

None of this is a reason to start, stop or change a prescription on your own. Take the report and the questions to the physician who knows your history. Unmeasured is unmanaged, and the alternative to measuring is another highlighted line, another eviction, and a thinner room to live in each time.

Every study named above, with its full numbers and the things it cannot show, sits in the companion deep dive for The Angry Gut. For the plain version of what this service does and does not do, read what Measura actually measures, and the metabolic backdrop is in insulin resistance and metabolic health. The meal-timing side of the same story is visceral and subcutaneous fat and the endpoint that counts, and the version written for clinicians is when a stool finding should change care.

Frequently asked questions

References

• Nash, A. K., Auchtung, T. A., Wong, M. C., Smith, D. P., Gesell, J. R., Ross, M. C., Stewart, C. J., Metcalf, G. A., Muzny, D. M., Gibbs, R. A., Ajami, N. J., & Petrosino, J. F. (2017). The gut mycobiome of the Human Microbiome Project healthy cohort. Microbiome, 5(1), 153. https://doi.org/10.1186/s40168-017-0373-4
• Auchtung, T. A., Fofanova, T. Y., Stewart, C. J., Nash, A. K., Wong, M. C., Gesell, J. R., Auchtung, J. M., Ajami, N. J., & Petrosino, J. F. (2018). Investigating colonization of the healthy adult gastrointestinal tract by fungi. mSphere, 3(2), e00092-18. https://doi.org/10.1128/mSphere.00092-18
• Dismukes, W. E., Wade, J. S., Lee, J. Y., Dockery, B. K., & Hain, J. D. (1990). A randomized, double-blind trial of nystatin therapy for the candidiasis hypersensitivity syndrome. The New England Journal of Medicine, 323(25), 1717-1723. https://doi.org/10.1056/NEJM199012203232501
• Kodio, A., Coulibaly, D., Koné, A. K., Konaté, S., Doumbo, S., Guindo, A., Bittar, F., Gouriet, F., Raoult, D., Thera, M. A., & Ranque, S. (2019). Blastocystis colonization is associated with increased diversity and altered gut bacterial communities in healthy Malian children. Microorganisms, 7(12), 649. https://doi.org/10.3390/microorganisms7120649
• Gabrielli, S., Furzi, F., Fontanelli Sulekova, L., Taliani, G., & Mattiucci, S. (2020). Occurrence of Blastocystis subtypes in patients from Italy revealed association of ST3 with a healthy gut microbiota. Parasite Epidemiology and Control, 9, e00134. https://doi.org/10.1016/j.parepi.2020.e00134
• Salosensaari, A., Laitinen, V., Havulinna, A. S., Meric, G., Cheng, S., Perola, M., Valsta, L., Alfthan, G., Inouye, M., Watrous, J. D., Long, T., Salido, R. A., Sanders, K., Brennan, C., Humphrey, G. C., Sanders, J. G., Jain, M., Jousilahti, P., Salomaa, V., … Niiranen, T. (2021). Taxonomic signatures of cause-specific mortality risk in human gut microbiome. Nature Communications, 12(1), 2671. https://doi.org/10.1038/s41467-021-22962-y
• Zaura, E., Brandt, B. W., Teixeira de Mattos, M. J., Buijs, M. J., Caspers, M. P. M., Rashid, M.-U., Weintraub, A., Nord, C. E., Savell, A., Hu, Y., Coates, A. R., Hubank, M., Spratt, D. A., Wilson, M., Keijser, B. J. F., & Crielaard, W. (2015). Same exposure but two radically different responses to antibiotics: Resilience of the salivary microbiome versus long-term microbial shifts in feces. mBio, 6(6), e01693-15. https://doi.org/10.1128/mBio.01693-15
• Porcari, S., Mullish, B. H., Asnicar, F., Ng, S. C., Zhao, L., Hansen, R., O’Toole, P. W., Raes, J., Hold, G., Putignani, L., Hvas, C. L., Zeller, G., Koren, O., Tun, H., Valles-Colomer, M., Collado, M. C., Fischer, M., Allegretti, J., Iqbal, T., … Ianiro, G. (2025). International consensus statement on microbiome testing in clinical practice. The Lancet Gastroenterology & Hepatology, 10(2), 154-167. https://doi.org/10.1016/S2468-1253(24)00311-X

Related reading

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Butyrate Deficiency Symptoms and What a Stool Test Really Shows

Butyrate deficiency has no symptom list of its own: loose stools, bloating, urgency and fatigue belong to twenty conditions. A low stool butyrate mostly samples the 5% of short-chain fatty acids your colon did not absorb.

A stool panel flags butyrate low and the bottle is in the cart before anyone asks what the number sampled. It sampled the remainder after your colon ate.

Butyrate deficiency symptoms is a phrase built on a test result rather than on a disease. Low butyrate gets flagged on mail-order stool panels, and the panels are sold as though the number described the state of your colon. What it mostly describes is the small share your colon did not absorb.

The video Full of Calories, Starving One Cell Deep follows a man of fifty-eight who tracked three thousand calories a day and still had a bowel lining running short of fuel. It belongs to The Angry Gut, by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes. Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service, and stool or short-chain fatty acid panels are not in its library, so the useful question becomes what can be measured in the same person.

What is butyrate, and what makes it?

Butyrate is a short-chain fatty acid, and it is the fuel the lining of the large bowel prefers to burn. Your own cells cannot build it. Bacteria ferment the fiber you cannot digest and hand it over, or the fuel never exists at all. Each day a human colon ferments somewhere between 400 and 600 mmol of these acids, roughly 60:20:20 across acetate, propionate and butyrate.

Demand never pauses. Pooled across 85 studies and 265 people, the cells lining the human gut are replaced about every 3.48 days, so the delivery has to keep arriving. In the language of the book, the gut is the first brain and the organ in your skull is the second brain, and the first brain is the one that meets every meal before anything else does.

What are the symptoms of butyrate deficiency?

Loose stools, bloating, urgency and fatigue belong to twenty conditions, which is why no symptom marks a starved lining. The man in the video had four years of loose stools, a colonoscopy read as normal, and biopsies described as mild nonspecific changes. None of that is a diagnosis. It is a supply problem, and a supply problem announces itself vaguely or not at all.

What does a low butyrate stool test mean?

Here is the rule worth carrying past any panel. Of the short-chain fatty acids made in the colon, 95% are absorbed by the cells that line it, and the 5% that leaves in stool is what a laboratory samples. When those acids are labeled and delivered straight to a human colon, the share turning up in the bloodstream is 2% for butyrate, against 9% for propionate and 36% for acetate. Butyrate is consumed on site.

So a fecal concentration is residue, not production. A low value can equally mean a colon that absorbed well. Dr. Padda repeated the familiar line that butyrate supplies 70% of the colon cell’s energy for years before he opened the 1980 experiment behind it: suspensions of human colon cells from 14 operative specimens, where butyrate accounted for 73% of oxygen consumption in the ascending colon and 75% in the descending, falling to 59% and 72% once ordinary glucose was in the dish as well. He had the unit wrong. It is a share of oxygen used in a dish, never a share of the energy inside a living person, and nobody has measured that inside one.

Can daily medications like omeprazole change gut bacteria?

Two drugs in that man’s morning routine mattered more than anything on his plate. He had taken omeprazole daily since 2015. Across 1,815 people, 211 of them on a proton pump inhibitor, the drug came with lower bacterial diversity and shifts in 20% of bacterial groups, an effect the investigators judged more prominent at population level than antibiotics. Add an acid blocker to a daily anti-inflammatory and the small bowel pays: injury appeared in 44.4% of volunteers against 16.7% without it.

Nobody prescribed that pairing as a plan. It assembled itself out of single reasonable refills, because a renewal takes a minute and a real review takes an appointment that never gets scheduled. Meanwhile the food system subsidizes the calories that feed you and sells capsules for the bacteria those same calories starved. That is the third driver in this story, and it is not biological.

What Measura can measure in the same person

None of the following watches your bacteria work. What they do is describe the metabolic ground your gut is sitting in, which is the part that connects to metaflammation, the low-grade inflammation running underneath insulin resistance and chronic pain.

• Indirect calorimetry measures resting energy use from the air you breathe rather than estimating it from height and weight.
• Bioimpedance body composition separates fat from muscle and water, which a bathroom scale cannot do at any price point.
• Laboratory panels put current numbers behind blood sugar, lipids and inflammatory markers.

Stool testing, breath testing and colonoscopy are different studies, ordered and performed elsewhere. Measura measures; the findings go to the physician who treats you, and the decisions stay there. When every result so far has read normal, the point of measuring is not reassurance. It is putting a current number on the things nobody has actually measured yet.

What to ask before buying another panel

• Ask any panel what it sampled. If the answer is stool, you are reading the remainder after absorption.
• Ask why a daily acid blocker is still on your list, when the reason was last examined, and whether an anti-inflammatory is going down beside it. That is a conversation for your prescriber, never a change you make alone.
• Count the separate plant foods on your last three days rather than the milligrams on a bottle. Higher fiber intake carried a 15-30% decrease in all-cause and cardiovascular mortality, with the benefit greatest between 25 g and 29 g a day.
• Expect gas as fiber rises. Pooled constipation trials, 16 of them with 1,251 adults, found response in 66% given fiber and 41% given control; psyllium and pectin above 10 g a day did that work, and flatulence worsened more than stool consistency improved. Early bloating is expected physiology.

Every study behind the argument, with the numbers it does and does not support, is in the book’s Deep Dive companion. The story continues with the additives that land on the layer this fuel protects, in what no test can tell you about emulsifiers.

Frequently asked questions

References

• den Besten, G., van Eunen, K., Groen, A. K., Venema, K., Reijngoud, D.-J., & Bakker, B. M. (2013). The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of Lipid Research, 54(9), 2325-2340. https://doi.org/10.1194/jlr.R036012
• Boets, E., Gomand, S. V., Deroover, L., Preston, T., Vermeulen, K., De Preter, V., Hamer, H. M., Van den Mooter, G., De Vuyst, L., Courtin, C. M., Annaert, P., Delcour, J. A., & Verbeke, K. A. (2017). Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study. The Journal of physiology, 595(2), 541-555. https://doi.org/10.1113/JP272613
• Roediger, W. E. (1980a). Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut, 21(9), 793-798. https://doi.org/10.1136/gut.21.9.793
• Darwich, A. S., Aslam, U., Ashcroft, D. M., & Rostami-Hodjegan, A. (2014). Meta-analysis of the turnover of intestinal epithelia in preclinical animal species and humans. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 42(12), 2016-2022. https://doi.org/10.1124/dmd.114.058404
• Imhann, F., Bonder, M. J., Vich Vila, A., Fu, J., Mujagic, Z., Vork, L., Tigchelaar, E. F., Jankipersadsing, S. A., Cenit, M. C., Harmsen, H. J., Dijkstra, G., Franke, L., Xavier, R. J., Jonkers, D., Wijmenga, C., Weersma, R. K., & Zhernakova, A. (2016). Proton pump inhibitors affect the gut microbiome. Gut, 65(5), 740-8. https://doi.org/10.1136/gutjnl-2015-310376
• Washio, E., Esaki, M., Maehata, Y., Miyazaki, M., Kobayashi, H., Ishikawa, H., Kitazono, T., & Matsumoto, T. (2016). Proton pump inhibitors increase incidence of nonsteroidal anti-inflammatory drug-induced small bowel injury: A randomized, placebo-controlled trial. Clinical gastroenterology and hepatology, 14(6), 809-815.e1. https://doi.org/10.1016/j.cgh.2015.10.022
• Reynolds, A., Mann, J., Cummings, J., Winter, N., Mete, E., & Te Morenga, L. (2019). Carbohydrate quality and human health: a series of systematic reviews and meta-analyses. Lancet (London, England), 393(10170), 434-445. https://doi.org/10.1016/S0140-6736(18)31809-9
• van der Schoot, A., Drysdale, C., Whelan, K., & Dimidi, E. (2022). The effect of fiber supplementation on chronic constipation in adults: An updated systematic review and meta-analysis of randomized controlled trials. The American journal of clinical nutrition, 116(4), 953-969. https://doi.org/10.1093/ajcn/nqac184
• de Groot, P. F., Nikolic, T., Imangaliyev, S., Bekkering, S., Duinkerken, G., Keij, F. M., Herrema, H., Winkelmeijer, M., Kroon, J., Levin, E., Hutten, B., Kemper, E. M., Simsek, S., Levels, J. H. M., van Hoorn, F. A., Bindraban, R., Berkvens, A., Dallinga-Thie, G. M., Davids, M., … Nieuwdorp, M. (2020). Oral butyrate does not affect innate immunity and islet autoimmunity in individuals with longstanding type 1 diabetes: a randomised controlled trial. Diabetologia, 63(3), 597-610. https://doi.org/10.1007/s00125-019-05073-8
• Jamka, M., Kokot, M., Kaczmarek, N., Bermagambetova, S., Nowak, J. K., & Walkowiak, J. (2021). The effect of sodium butyrate enemas compared with placebo on disease activity, endoscopic scores, and histological and inflammatory parameters in inflammatory bowel diseases: A systematic review of randomised controlled trials. Complementary medicine research, 28(4), 344-356. https://doi.org/10.1159/000512952

Related reading

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What Does Low Vitamin D Mean? Reading the Number on Your Report

Low vitamin D means your stored form, 25-hydroxyvitamin D, reads below the cutoff your lab uses, and guidelines set that cutoff anywhere from 10 to 40 ng/mL. The test counts the stockpile, not the working hormone, and assay calibration, cholesterol, body fat and gut absorption all move the number.

A low normal vitamin D result gets filed far more often than it gets explained. The number depends on the assay, the crowd behind the range, and how well your gut absorbs.

What does low vitamin D mean when the report says low normal and nobody calls? In most offices it means a number was filed. It does not tell you whether the number is accurate, which population built the range printed beside it, or why your body is sitting there in the first place.

The video above, Vitamin D Is a Hormone, Not a Vitamin, is Chapter 10 of The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes. Dr. Padda says plainly that for years he called results like that low normal and moved on. The measurement questions are the ones to keep: what the test counts, what bends it, and what else deserves a number in the same person.

What does low vitamin D mean? The test counts the stockpile

Nearly every lab reports 25-hydroxyvitamin D. Sunlight on skin turns cholesterol into the starting molecule, the liver converts that into this storage form, and the kidney converts it again into the working hormone, 1,25-dihydroxyvitamin D. Immune cells and the gut lining finish some of that conversion locally.

The two forms are not close in strength. Across human target genes in laboratory work, the storage form needed an average of 322 nM to reach half of its effect, while the working hormone needed 0.48 nM. Your report reads the size of the woodpile. It cannot tell you how warm the room is.

The system also has a thermostat. When calcium drops, parathyroid hormone speeds activation. When phosphate climbs, fibroblast growth factor 23 slows activation and turns on an enzyme that breaks the hormone down. That feedback is why a bigger dose does not buy a proportionally bigger signal, and why the report and the tissue agree less often than most people expect.

Why can the same blood give a different vitamin D number?

Before anyone interprets a result, two things can move it. One is calibration. After survey assays were restandardized, the American count of people under 50 nmol/L jumped from 22% to 31%, and a German survey moved the opposite way. Nothing changed in anyone’s blood. Only the ruler changed.

The other is cholesterol, and it aims the error at the wrong people. Checked against mass spectrometry, the reference method, the common immunoassay read about 4.0 nmol/L low in people with lower non-HDL cholesterol and 10.2 nmol/L low in people above the cutoff. So the person with insulin resistance and high blood fats is handed a falsely low vitamin D, while the metabolically healthy person is handed reassurance. That error once manufactured an apparent link between high cholesterol and low vitamin D that lived only on the immunoassay.

What is a normal vitamin D level?

A reference range is a description of a crowd. Over 40 guidelines around the world set targets anywhere from 10 to 40 ng/mL. Worldwide, 15.7% of people fall below 30 nmol/L, 47.9% below 50 and 76.6% below 75. Whether a result gets called deficient depends on which committee drew the line.

The crowd itself is skewed. People evolved making this hormone outdoors, then moved into offices, cars and night shifts, and the ranges were drawn from that indoor population. The intake tables came mostly from light-skinned volunteers. For dark-skinned people living at high latitude, holding 97.5% of them above 50 nmol/L through winter took about 2,672 IU a day, far beyond those tables. Extra body fat also stores the molecule away from the bloodstream, which is why bioimpedance body composition belongs in the same file as the blood work. A scale cannot separate fat from muscle, as body composition, not BMI explains.

Can gut problems cause low vitamin D?

Some people run low because their gut cannot let the molecule in. The book calls the gut the first brain, with the skull holding the second, and a first brain that is inflamed or shortened by surgery absorbs less of anything fat-soluble. Bowel patients with active disease carried 1.85 times the odds of being deficient; those who had had surgery, 1.61; those on biologic drugs, 1.78. Genetic work in the Copenhagen and UK Biobank cohorts found that low vitamin D did not cause the bowel disease. The shortfall follows the damage, and a bowel that keeps malabsorbing renews it every morning.

Three drivers stack in that person. Malabsorption shrinks the supply. The high cholesterol that travels with metaflammation bends the assay low. And a care system built around single-organ visits treats a low normal flag as nobody’s job. That is how a real deficit sits unmeasured for years, in a gut that, as bowel inflammation reaching the spine shows, can affect far more than digestion.

Can too much vitamin D be harmful?

The opposite mistake is chasing the number upward, and the harm there is measured in falls. Older women given one 500,000 IU dose a year fell more often, a rate ratio of 1.15, and broke more bones, 1.26, with most of the excess landing in the three months after each dose. Those women had not started out deficient.

Daily dosing has a ceiling as well. In a trial of older adults who were already low and already prone to falling, groups taking 1000 IU or more a day had a hazard ratio of 1.87 for serious falls compared with 200 IU, and 2.48 for falls bad enough to need a hospital. Three years on 10,000 IU daily thinned forearm bone compared with 400 IU. A governed system adapts to excess instead of banking it as benefit.

Fall risk can be measured before it becomes a fracture. Vestibular and balance testing measures how well your balance systems keep you upright, which gives your physician a baseline to weigh against any dosing decision. If unsteadiness is already part of your week, dizziness, balance and falls describes what that testing involves.

What to measure, and what to ask

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service. It measures; it does not treat, diagnose on its own or set a dose, and results go to your physician. For this picture, three measurements fit together: laboratory panels for the metabolic blood work, body composition for the fat and muscle compartments, and balance testing for fall risk. Who handles the blood samples is covered in which laboratory runs the blood work.

Then bring these questions to your physician. Which method did the lab use, immunoassay or mass spectrometry? Could my cholesterol be pulling the result down? Which guideline set the range on my report? If there is a reason I run low, is the plan to correct the shortfall and stop rather than keep climbing? Do not start, stop or change a supplement or medication on your own. Unmeasured is unmanaged, and every study named here, with its limits, is in the Chapter 10 Deep Dive.

Frequently asked questions

References

• Hanel, A., Veldhuizen, C., & Carlberg, C. (2022). Gene-regulatory potential of 25-hydroxyvitamin D3 and D2. Frontiers in Nutrition, 9, 910601. https://doi.org/10.3389/fnut.2022.910601
• Binkley, N., Dawson-Hughes, B., Durazo-Arvizu, R., Thamm, M., Tian, L., Merkel, J. M., Jones, J. C., Carter, G. D., & Sempos, C. T. (2017). Vitamin D measurement standardization: The way out of the chaos. The Journal of Steroid Biochemistry and Molecular Biology, 173, 117–121. https://doi.org/10.1016/j.jsbmb.2016.12.002
• Weiler, H. A., Bielecki, A., Fu, W., Demonty, I., & Brooks, S. P. J. (2024). Cholesterol interference in the assessment of vitamin D status: A Canadian Health Measures Survey biobank project. The Journal of Nutrition, 154(5), 1676–1685. https://doi.org/10.1016/j.tjnut.2024.04.003
• Cashman, K. D., Kiely, M. E., Andersen, R., Grønborg, I. M., Tetens, I., Tripkovic, L., Lanham-New, S. A., Lamberg-Allardt, C., Adebayo, F. A., Gallagher, J. C., Smith, L. M., Sacheck, J. M., Huang, Q., Ng, K., Yuan, C., Giovannucci, E. L., Rajakumar, K., Patel, S., Vanstone, C. A., … Weiler, H. A. (2022). Individual participant data (IPD)-level meta-analysis of randomised controlled trials to estimate the vitamin D dietary requirements in dark-skinned individuals resident at high latitude. European Journal of Nutrition, 61(2), 1015–1034. https://doi.org/10.1007/s00394-021-02699-6
• Shi, S., Feng, J., Zhou, L., Li, Y., & Shi, H. (2021). Risk factors for vitamin D deficiency in inflammatory bowel disease: A systematic review and meta-analysis. The Turkish Journal of Gastroenterology, 32(6), 508–518. https://doi.org/10.5152/tjg.2021.20614
• Lund-Nielsen, J., Vedel-Krogh, S., Kobylecki, C. J., Brynskov, J., Afzal, S., & Nordestgaard, B. G. (2018). Vitamin D and inflammatory bowel disease: Mendelian randomization analyses in the Copenhagen studies and UK Biobank. The Journal of Clinical Endocrinology and Metabolism, 103(9), 3267–3277. https://doi.org/10.1210/jc.2018-00250
• Sanders, K. M., Stuart, A. L., Williamson, E. J., Simpson, J. A., Kotowicz, M. A., Young, D., & Nicholson, G. C. (2010). Annual high-dose oral vitamin D and falls and fractures in older women: A randomized controlled trial. JAMA, 303(18), 1815–1822. https://doi.org/10.1001/jama.2010.594
• Appel, L. J., Michos, E. D., Mitchell, C. M., Blackford, A. L., Sternberg, A. L., Miller, E. R., Juraschek, S. P., Schrack, J. A., Szanton, S. L., Charleston, J., Minotti, M., Baksh, S. N., Christenson, R. H., Shade, D. M., Shiferaw, W. F., Walston, J. D., Guralnik, J. M., Cai, T., & Tonascia, J. (2021). The effects of four doses of vitamin D supplements on falls in older adults: A response-adaptive, randomized clinical trial. Annals of Internal Medicine, 174(2), 145–156. https://doi.org/10.7326/M20-3812
• Burt, L. A., Billington, E. O., Rose, M. S., Raymond, D. A., Hanley, D. A., & Boyd, S. K. (2019). Effect of high-dose vitamin D supplementation on volumetric bone density and bone strength: A randomized clinical trial. JAMA, 322(8), 736–745. https://doi.org/10.1001/jama.2019.11889
• Sosa-Henriquez, M., Torregrosa-Suau, O., Gomez de Tejada-Romero, M. J., & Groba-Marco, M. V. (2025). Rethinking vitamin D deficiency: Controversies and practical guidance for clinical management. Nutrients, 17(22), 3573. https://doi.org/10.3390/nu17223573

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