Gut Bacteria, Stress and the Clock Your Body Runs On

Gut bacteria help set the daily rhythm of your stress response, which runs highest around waking and lowest at night. In mice, removing gut bacteria left the stress hormone released at the wrong times of day, not in the wrong amount.

The same bad news at 7 a.m. and at 10 p.m. does not land on the same body. Part of what sets that difference lives in your intestine.

Ask what gut bacteria and stress have to do with each other and the usual answer is vague and one-directional: stress upsets your stomach. The more interesting finding runs the other way and involves a clock. Your stress response is not a switch that is on or off; it is a system with a daily shape, highest around waking and lowest at night, and that shape appears to depend partly on microbes in your intestine that rise and fall on their own schedule. The part of that system you can put on a chart is autonomic, which is what heart rate variability testing records.

The finding, and its tier

The work that made this concrete removed gut bacteria from mice and watched the timing of their stress response. Depleting the microbiota disturbed stress-related activity in the hippocampus and amygdala across the day, disrupted the brain’s own pacemaker, and left glucocorticoid, the animal equivalent of cortisol, secreted in the wrong pattern rather than the wrong amount. The stress system was hyper-activated at the sleep and wake transition, and stress-sensitive behavior was impaired at specific times of day and not at others. Microbiota transplants confirmed the effect came from the daily oscillation of the microbes themselves, and pointed to Limosilactobacillus reuteri as a candidate organism.

This is mouse work. No one has removed a person’s gut bacteria to watch their cortisol rhythm, and no one should. Human trials here also tend to isolate a single psychiatric diagnosis and exclude the comorbid, metabolically inflamed patient most likely to be living this, so the human evidence arrives in pieces from different studies. The pieces point the same way.

Human evidence, in the pieces that exist

Start with the microbes. In 1,976 adults from a German population cohort, specific gut organisms showed 24-hour swings in abundance, and 13 of them had lost that rhythm in people with type 2 diabetes. The arrhythmic pattern was confirmed in an independent cohort of 1,363 people and predicted diabetes in 699 people sampled 5 years earlier. A daily rhythm in your intestine is real, measurable, and already known to break in metabolic disease.

Next, what those organisms make. In a controlled crossover study, 9 healthy adults were sampled around the clock after three nights of normal sleep and again after three nights cut to 4.5 hours, with meals and calories held identical. Sleep restriction alone flattened the daily rhythm of microbe-derived compounds in their blood, including butyrate. The diet did not change. The timing did. What short sleep does to blood sugar is the metabolic half of the same story.

Then the stress hormone. In 4,047 British civil servants, a flatter fall in cortisol across the day predicted death over the following years at 1.30 times the rate per standard deviation of flattening, driven mostly by cardiovascular death at 1.87. Morning cortisol alone predicted nothing. A meta-analysis of 179 associations from 80 studies found flatter daily slopes associated with worse health overall, with the largest effect on immune and inflammatory outcomes, 0.288 against 0.147 across all outcomes. The shape of the curve carries the information; a single value does not. Note where the effect was largest: a flattened stress curve travels with inflammation, which is how a broken clock feeds metaflammation. Depression that has lifted can leave a lasting cognitive risk on top of that inflammatory load, discussed in why remitted depression still warrants a cognitive baseline.

Why the shape breaks, and who breaks it

Two biological drivers sit underneath. The first is lost oscillation in the gut community, which in the animal work is what the brain’s pacemaker and stress system appear to read. The second is autonomic tone: in seventy-five community adults, lower vagally mediated heart rate variability went with more depressive symptoms and a different gut microbial profile, and in a randomized trial in 43 patients with depression and 43 controls, three months of a multi-species probiotic improved morning vagal function. One small trial is a mechanism, not a treatment.

The third driver is neither. Your gut is the first brain in this sequence and the organ in your skull is the second, and the first brain takes its cues from when you eat, sleep and see light, all of which are now set by work schedules rather than biology. Shift work, screens after midnight and late dinners are decisions made by an economy, not personal failings. Antibiotics belong in the same category of upstream exposure: in a database study of 202,974 people with depression and matched controls, a single course of penicillin went with 1.23 times the odds of depression, rising to 1.56 with more than 5 courses. A necessary antibiotic is still necessary; what recovery after antibiotics looks like is what is worth knowing. Diet reaches the same inflammatory machinery in the mouth, where it can be seen directly, as explained in how sugar inflames the gums.

What a standard visit measures, and what it misses

A routine visit takes one blood pressure and heart rate while you sit still, usually mid-morning, and calls it your baseline. If stress comes up, it comes up as a word rather than a measurement. A one-time cortisol level is nearly uninterpretable without the time of day beside it, because it is supposed to be high in the morning and low at night. The useful information is the pattern across the day and the balance between the branches of your nervous system, and one reading captures neither. Symptoms that point to the autonomic side are a better reason to measure than a lone cortisol value.

The autonomic side you can chart

Say the limits first. Measura [Cardiometabolic and Autonomic Health Analysis] has no microbiome, stool or breath test, and it does not measure Limosilactobacillus reuteri or any other organism. Cortisol is blood work your physician orders, and the draw time is part of that result. Measura is a testing service: it measures and sends findings to your physician, and it does not treat. What it can put on a chart is the autonomic side of the same stress response:

• Heart rate variability records beat-to-beat variation in your heart rhythm, which reflects the balance between the vagal and sympathetic branches at the time of recording.
• Cardiac autonomic reflex tests record how heart rate and blood pressure answer standardized challenges such as deep breathing and standing.
• Autonomic nervous system testing looks more broadly at how the automatic nervous system is regulating the body in one visit.

None of these diagnoses a stress disorder, and none reads your gut bacteria. Their value is comparison: the same measurement, in the same person, under the same conditions, at the same time of day. What your nervous system shows when stress reaches the stomach covers the digestive side, and what a heart reading shows about the vagus nerve and anxiety covers the limits of reading vagal tone as a mood measure. If your schedule is the driver, night shift health risks you can measure is the practical version.

What to do with this

The lever is timing, and it is unglamorous. Anchor the clock with early light, a consistent wake time including weekends, and a last meal that is not competing with sleep, because each is an input the pacemaker actually reads. Feed the organisms that oscillate with fiber and fermented food rather than a supplement chosen from a label. Protect sleep duration, since three short nights were enough to flatten microbial rhythms in the blood of healthy volunteers.

Then measure rather than guess. Note when symptoms occur, not only that they occur, since a stress response that fails at one hour is a different problem from one that is high all day. Ask your physician whether an autonomic baseline is worth having and when to repeat it, and ask that any cortisol draw be recorded with its time. Mention medication that affects heart rate before testing, because it changes the result, and leave prescription changes to your physician. A stool microbiome report cannot tell you any of this; what a gut microbiome test cannot measure explains why. Unmeasured is unmanaged, and in this system the hour on the clock is part of the measurement.

Frequently asked questions

References

• Tofani, G. S. S., Leigh, S. J., Gheorghe, C. E., Bastiaanssen, T. F. S., Wilmes, L., Sen, P., Clarke, G., & Cryan, J. F. (2025). Gut microbiota regulates stress responsivity via the circadian system. Cell Metabolism, 37(1), 138-153.e5. https://doi.org/10.1016/j.cmet.2024.10.003
• Reitmeier, S., Kiessling, S., Clavel, T., List, M., Almeida, E. L., Ghosh, T. S., Neuhaus, K., Grallert, H., Linseisen, J., Skurk, T., Brandl, B., Breuninger, T. A., Troll, M., Rathmann, W., Linkohr, B., Hauner, H., Laudes, M., Franke, A., Le Roy, C. I., Bell, J. T., Spector, T., Baumbach, J., O’Toole, P. W., Peters, A., & Haller, D. (2020). Arrhythmic Gut Microbiome Signatures Predict Risk of Type 2 Diabetes. Cell Host & Microbe, 28(2), 258-272.e6. https://doi.org/10.1016/j.chom.2020.06.004
• Leone, V. A., Frazier, K., Kaur, M., Chrisler, E. A., Sidebottom, A. M., Tai, E., Tran, V., Li, S., Chang, E. B., Jones, D. P., Van Cauter, E., & Hanlon, E. C. (2026). Short-term sleep restriction in humans alters diurnal circulating metabolite profiles, including those of microbial origin. The Journal of Clinical Investigation, 136(6). https://doi.org/10.1172/JCI189363
• Kumari, M., Shipley, M., Stafford, M., & Kivimaki, M. (2011). Association of diurnal patterns in salivary cortisol with all-cause and cardiovascular mortality: findings from the Whitehall II study. The Journal of Clinical Endocrinology and Metabolism, 96(5), 1478-1485. https://doi.org/10.1210/jc.2010-2137
• Adam, E. K., Quinn, M. E., Tavernier, R., McQuillan, M. T., Dahlke, K. A., & Gilbert, K. E. (2017). Diurnal cortisol slopes and mental and physical health outcomes: A systematic review and meta-analysis. Psychoneuroendocrinology, 83, 25-41. https://doi.org/10.1016/j.psyneuen.2017.05.018
• Ravenda, S., Mancabelli, L., Gambetta, S., Barbetti, M., Turroni, F., Carnevali, L., Ventura, M., & Sgoifo, A. (2025). Heart rate variability, daily cortisol indices and their association with psychometric characteristics and gut microbiota composition in an Italian community sample. Scientific Reports, 15(1), 8584. https://doi.org/10.1038/s41598-025-93137-8
• Morkl, S., Narrath, M., Schlotmann, D., Sallmutter, M. T., Putz, J., Lang, J., Brandstatter, A., Pilz, R., Karl Lackner, H., Goswami, N., Steuber, B., Tatzer, J., Lackner, S., Holasek, S., Painold, A., Jauk, E., Wenninger, J., Horvath, A., Spicher, N., Barth, A., Butler, M. I., & Wagner-Skacel, J. (2025). Multi-species probiotic supplement enhances vagal nerve function – results of a randomized controlled trial in patients with depression and healthy controls. Gut Microbes, 17(1), 2492377. https://doi.org/10.1080/19490976.2025.2492377
• Lurie, I., Yang, Y. X., Haynes, K., Mamtani, R., & Boursi, B. (2015). Antibiotic exposure and the risk for depression, anxiety, or psychosis: a nested case-control study. The Journal of Clinical Psychiatry, 76(11), 1522-1528. https://doi.org/10.4088/JCP.15m09961

Related reading

• Can Stress Cause Stomach Problems? What Your Nervous System Shows
• Vagus Nerve and Anxiety: What a Heart Reading Shows About Your Gut
• Heart Rate Variability

Does Nicotine Raise Heart Rate? What Measurement Can Show

Yes. Nicotine raises heart rate shortly after intake, and the racing pulse belongs to the molecule rather than the smoke, so local delivery does not contain it. Heart rate variability, autonomic reflex testing and arterial stiffness measurement show how your own pulse and vessels respond.

A cholinergic drug does not stay where you put it. If you have read that nicotine calms a colitis flare or moves a stalled bowel, the numbers worth having first are your own pulse, vessels and blood work.

Does nicotine raise heart rate? In people using electronic nicotine delivery devices, the National Academies of Sciences, Engineering, and Medicine graded the evidence as substantial that heart rate climbs shortly after intake. Asked whether those same devices cause clinical cardiovascular events, the committee wrote that no evidence is available either way, which is a statement of ignorance and not a safety claim. The video above, the last one in The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, is about where a drug is placed, not whether anyone should take it. The question here is narrower: if a cholinergic drug is moving through you for any reason, which of your own numbers move with it, and who is watching them?

Why a gut question becomes a heart question

The nervous system in your gut wall is the first brain, and the organ in your skull is the second one, sitting downstream. That first brain runs substantially on acetylcholine, and nicotine imitates acetylcholine well enough to be heard at two separate addresses. One is on the nerve cells of the bowel wall, where the signal drives contraction. The other is a receptor called alpha-7, on immune cells, where acetylcholine turns down release of TNF, one of the loudest inflammatory alarms the body has. That immune requirement was established in mice bred without alpha-7, in which the vagal quieting of TNF disappears. Mouse work, and it reads as mouse work.

Neither address is reachable except through the bloodstream that also supplies your heart and your arteries. So a racing pulse and a spike in blood pressure belong to the molecule rather than to the smoke, and local delivery is not the same thing as contained delivery. Given rectally, the drug peaked in blood 44 to 50 minutes afterward and rose with the dose, and 11 of 14 recorded adverse events fell in the window from 30 to 105 minutes, most at the highest dose studied.

Does nicotine raise heart rate? The one trial that asked never printed a pulse

Forty-five nonsmokers whose ulcerative colitis was quiet were randomized, double-blind, to a nicotine patch or a placebo patch for twelve weeks, with twenty of them getting the drug. The investigators measured platelet volume and a platelet surface marker, a circulating marker of damage to the vessel lining, plasma fibrinogen, white cell count and serum lipids. Fibrinogen fell. Platelet activation, the vessel-lining marker, the white cell count and the lipids did not budge.

Now notice what is missing. Fibrinogen rises with inflammation anywhere, so in an inflamed bowel a falling fibrinogen may be reporting on the colon rather than on the arteries. Twenty exposed patients over twelve weeks cannot establish cardiovascular safety for anybody. And the report carries no blood pressure and no heart rate, the two numbers a patient actually asks about. Across this literature, what was convenient to assay got assayed, and what the person wanted to know was left out.

What can be measured, and what is done elsewhere

Measura [Cardiometabolic and Autonomic Health Analysis] does not look inside your colon. Endoscopy, stool studies and motility studies are gastroenterology tests done in other settings, and those are the tests that describe bowel disease itself. Measura measures; it does not treat, and it does not diagnose on its own. Findings go to the physician who cares for you.

What can be put on a chart is the rest of the body a drug travels through. Heart rate variability records the beat-to-beat variation in the gap between heartbeats. Autonomic nervous system testing and cardiac autonomic reflex tests record how your heart rate and blood pressure answer standard challenges such as standing up and paced breathing. Arterial stiffness and endothelial function testing looks at the large vessels and at how a vessel lining behaves, which is the thing that old patch trial could only approach through a blood marker. Laboratory panels carry the blood work your physician selects, and what a variability number actually means is worth reading before you have one done.

There is a reason to trust your own response over a drug level. Among twenty healthy volunteers given nicotine by mouth and by vein, the serum concentration did not predict who felt unwell. In a rectal pilot, 4 of 10 patients had side effects while their serum nicotine sat low or undetectable. A level describes the drug. Measurement describes you.

Two drivers in the body, one in the market

The biology has two arms that do not point the same way. Cholinergic signaling in the gut wall moves the bowel and quiets the immune cells embedded in it, so withdrawing a twenty-year cholinergic input from a lining that had adapted to it is a physiological event with a named receptor behind it, not a coincidence of timing. The second arm is the autonomic and vascular response to that same alkaloid arriving everywhere at once, layered on whatever metaflammation, the low-grade inflammation that keeps a metabolism irritated, is already running. The third driver is not biology: nobody owns an off-patent molecule, so nobody funds the trial that would settle it, and the dependence does not leave when the smoke does.

There is nothing to buy and nothing to improvise

The book argues about a route: a small dose held against the lining of the lower colon, not a patch on an arm. When a liquid version of that route was randomized, remission reached 27% on nicotine against 33% on placebo. A suppository, meanwhile, has never been given to a human being for anything. One group built such formulations, measured how they let the drug go in a dish, and stopped there. That is an absence of evidence rather than a negative result, and an absence licenses a study, not a prescription.

Two more things are worth keeping straight. Nobody has ever measured how much nicotine reaches rectal tissue, so the local-dose idea rests on blood drawn a compartment away. And on movement, one claim holds and one does not. High-amplitude propagated contractions did appear in healthy subjects after a large dose, with faster transit: mass peristalsis, the wave that empties a colon. No controlled human trial supports using the drug to restart the fasting housekeeping sweep of the stomach and small bowel.

Judging a compound by its reputation instead of its biochemistry is not caution.

Neither is improvising. Nothing is sold for this purpose, no dose has been established outside a trial protocol, and there is no reason for anyone to take up nicotine in any form. Do not start, stop or change a medication because of something you read; that sits with your prescriber. Rescue is not repair, and the first brain answers to being fed and tended long before it answers to an alkaloid.

What to ask before anything changes

• When symptoms began relative to the day you quit, in months or in years.
• Where your disease sits, since every promising signal here lives in the left colon.
• What has already been tried, and whether anything remains in the standard sequence.
• If nicotine is ever offered in any form, the plan for your heart rate and blood pressure, and how long the trial runs before somebody calls it.

More prompts sit in questions worth asking your doctor. Every study behind these figures, with its limits beside it, is in the companion deep dive, and the clinician version is the screening discussion for practices.

Frequently asked questions

References

• National Academies of Sciences, Engineering, and Medicine, Health and Medicine Division, Board on Population Health and Public Health Practice, & Committee on the Review of the Health Effects of Electronic Nicotine Delivery Systems. (2018). Public health consequences of e-cigarettes. National Academies Press (consensus study report), Consensus study report, chapter conclusions. https://pubmed.ncbi.nlm.nih.gov/29894118/
• Wang, H., Yu, M., Ochani, M., Amella, C. A., Tanovic, M., Susarla, S., Li, J. H., Wang, H., Yang, H., Ulloa, L., Al-Abed, Y., Czura, C. J., & Tracey, K. J. (2003). Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature, 421(6921), 384-388. https://doi.org/10.1038/nature01339
• Thomas, G. A., Davies, S. V., Rhodes, J., Russell, M. A., Feyerabend, C., & Säwe, U. (1995a). Is transdermal nicotine associated with cardiovascular risk? Journal of the Royal College of Physicians of London, 29(5), 392-396. https://pubmed.ncbi.nlm.nih.gov/8847680/
• Ingram, J. R., Routledge, P., Rhodes, J., Marshall, R. W., Buss, D. C., Evans, B. K., Feyerabend, C., & Thomas, G. A. O. (2004). Nicotine enemas for treatment of ulcerative colitis: A study of the pharmacokinetics and adverse events associated with three doses of nicotine. Alimentary Pharmacology & Therapeutics, 20(8), 859-65. https://doi.org/10.1111/j.1365-2036.2004.02199.x
• Ingram, J. R., Thomas, G. A. O., Rhodes, J., Green, J. T., Hawkes, N. D., Swift, J. L., Srivastava, E. D., Evans, B. K., Williams, G. T., Newcombe, R. G., Courtney, E., & Pillai, S. (2005). A randomized trial of nicotine enemas for active ulcerative colitis. Clinical Gastroenterology and Hepatology, 3(11), 1107-1114. https://doi.org/10.1016/s1542-3565(05)00849-9
• Sandborn, W. J., Tremaine, W. J., Leighton, J. A., Lawson, G. M., Zins, B. J., Compton, R. F., Mays, D. C., Lipsky, J. J., Batts, K. P., Offord, K. P., Hurt, R. D., & Green, J. (1997). Nicotine tartrate liquid enemas for mildly to moderately active left-sided ulcerative colitis unresponsive to first-line therapy: A pilot study. Alimentary Pharmacology & Therapeutics, 11(4), 663-71. https://doi.org/10.1046/j.1365-2036.1997.00208.x
• Compton, R. F., Sandborn, W. J., Lawson, G. M., Sheets, A. J., Mays, D. C., Zins, B. J., Tremaine, W. J., Lipsky, J. J., Mahoney, D. W., Zinsmeister, A. R., Offord, K. P., Hurt, R. D., Evans, B. K., & Green, J. (1997). A dose-ranging pharmacokinetic study of nicotine tartrate following single-dose delayed-release oral and intravenous administration. Alimentary Pharmacology & Therapeutics, 11(5), 865-74. https://doi.org/10.1046/j.1365-2036.1997.00236.x
• Coulie, B., Camilleri, M., Bharucha, A. E., Sandborn, W. J., & Burton, D. (2001). Colonic motility in chronic ulcerative proctosigmoiditis and the effects of nicotine on colonic motility in patients and healthy subjects. Alimentary Pharmacology & Therapeutics, 15(5), 653-663. https://doi.org/10.1046/j.1365-2036.2001.00959.x
• Dash, A. K., Gong, Z., Miller, D. W., Huai-Yan, H., & Laforet, J. (1999). Development of a rectal nicotine delivery system for the treatment of ulcerative colitis. International Journal of Pharmaceutics, 190(1), 21-34. https://doi.org/10.1016/s0378-5173(99)00221-5
• Pandolfino, J. E., & Kahrilas, P. J. (2000). Smoking and gastro-oesophageal reflux disease. European Journal of Gastroenterology & Hepatology, 12(8), 837-842. https://doi.org/10.1097/00042737-200012080-00002

Related reading

• How to Test for MCAS When Your Allergy Tests Keep Coming Back Negative
• Heart Rate Variability

Narcotic Bowel Syndrome: What Testing Can and Cannot Show

The gut side of narcotic bowel syndrome is measured with transit scintigraphy, intestinal pressure studies and breath tests, done in gastroenterology settings and each with blind spots. The rest of long-term opioid therapy can be measured too: attention on cognitive assessment, and metabolic health on laboratory panels and bioimpedance body composition.

A bowel that slows on long-term pain medication usually gets charted as a nuisance. The first brain, the second brain and the metabolism around them can all be measured, and most of it never is.

Narcotic bowel syndrome is abdominal pain that gets worse even while the pain medication meant to control it holds steady or climbs. It sits at the far end of a much more common problem: a bowel that slows on long-term opioid therapy and gets written off as a nuisance. The Pain Pill That Paralyzes Your Gut, the video chapter of The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, makes the clinical argument. The angle here is what can be measured: which gut tests exist, which ones are done somewhere else, and what else in your body is worth putting on a number.

Why does opioid constipation so often go unreported?

Most people do not bring it up. In a European study of 1,200 people with cancer who were taking opioids, 59.5% met formal criteria for opioid-induced constipation, yet only 61.5% of that group described themselves as constipated. Roughly four in ten had a measurably stalled bowel and said nothing.

Those who do mention it often stay stuck. Among 322 survey respondents on an opioid plus a laxative, 81% remained constipated, and about a third had skipped, reduced or stopped their pain medication just to have a bowel movement. That is a dose change made alone, without the person who wrote the prescription knowing.

The reasons are partly economic. A short appointment rewards whatever takes seconds, and a stool softener takes seconds. The question that uncovers the real burden takes minutes. The cost is also social: a person who skips food before leaving the house soon stops leaving it, and loneliness is one of the drivers of chronic pain, not a side note to it.

How do opioids affect the gut?

The gut is the first brain, with its own nerve networks in the bowel wall, and the skull holds the second. An opioid aimed at pain lands wherever its receptor sits, and in the human gut that receptor lines both nerve networks, the immune cells under the lining, and both halves of the reflex that pushes contents forward.

I was taught that opioids simply shut the bowel off, and I repeated it. Recordings in people showed something stranger. Intravenous morphine drove bursts of contraction in the upper small intestine in nine of ten volunteers, firing out of their normal cycle. Contraction without direction does not move anything along. Three days of codeine in healthy volunteers slowed stomach emptying, with a half-time of 144.0 minutes against 95.5, and colonic filling at six hours fell to 11.0% from 51%.

The body builds tolerance to the pain relief. It does not build tolerance to the bowel effect, which persists. As doses rise to chase a pain that adapts, the gut absorbs each increase in full. The practice position is that a stagnant bowel feeds metaflammation, the low-grade inflammation of a disordered metabolism, and that metaflammation turns up the central pain signal. Each end of that chain has been shown in people; the connection between them has been seen in tissue and animals, and no human trial has tested it.

Motility testing is a different test, done elsewhere

Measura [Cardiometabolic and Autonomic Health Analysis] does not measure gut motility. Transit scintigraphy, which follows a labeled meal through the gut, pressure studies of the intestine and breath tests are gastroenterology tests performed in other settings. Each has blind spots. Transit timing says little about the contractions themselves, and the morphine recordings captured when contractions started, not whether they traveled.

Breath testing is shakier still. In a clinic series of 525 breath tests, post-surgical patients taking more motility-slowing drugs, opioids among them, tested positive less often. The researchers’ reading was that the result may reflect how fast contents move rather than bacteria. A result from that instrument deserves careful interpretation before anyone acts on it.

The second brain: attention and cognitive assessment

What long-term therapy does upstairs is measurable. In a small study of chronic low back pain, people on daily opioids for three months or longer were compared with people who had the same pain and took no opioids. The opioid group performed significantly worse on attention and reported lower confidence in managing their pain. Cognitive assessment puts attention, memory and processing on a documented baseline, so a change can be seen instead of guessed at. More on why a baseline matters is in memory and cognitive screening.

Pain processing shifts as well. About 6% of long-term narcotic users develop narcotic bowel syndrome, which is thought to originate in the central nervous system rather than the bowel. Across 27 randomized surgical trials, higher opioid doses during surgery were followed by slightly worse pain afterward. These are findings to discuss with your prescriber, not instructions to act on.

Blood work, body composition and the terrain trials leave out

In that same back pain study, blood cytokines, the chemical messengers of inflammation, showed only minor differences between opioid users and non-users. Blood sits downstream of the gut lining, so a quiet blood panel does not prove a quiet bowel. It does not make blood work pointless either. Trials routinely exclude people with diabetes, depression or fatty liver, which is the terrain many long-term patients actually live in. Laboratory panels and bioimpedance body composition measure that metabolic side directly, and insulin resistance and metabolic health explains why it shapes pain.

The gut microbiome changes too, though Measura does not test stool. In five opioid users in an addiction-treatment sample, microbial diversity was lower, and two groups of bacteria tied to butyrate and bile handling were depleted. Five people is a signal, not a verdict.

What autonomic testing can and cannot add

The morphine effect on the small intestine was blocked by atropine, which means it runs on the same acetylcholine wiring the vagus nerve uses. That makes the bowel problem autonomic in a strict sense. Autonomic nervous system testing, however, reads how the involuntary nervous system regulates heart rate, blood pressure and sweating. It does not record the bowel, and none of the opioid studies here tie an autonomic result to constipation. It belongs in the picture when you have symptoms such as lightheadedness on standing, described in autonomic symptoms, not as a stand-in for a gut test.

What to bring to your next appointment

• How many bowel movements you have in a week, and how many days you strain.
• When your dose last went up, and whether your bowel changed in the weeks after.
• Any time you took a dose late, lowered it or skipped it to have a bowel movement.
• Whether constipation sits on your problem list or only under side effects.
• Any change in attention, memory or confidence you have noticed.

More prompts are in chronic pain and metabolic health. Every study cited above, with what it does not show, is gathered in The Angry Gut deep dive on the narcotic bowel. Clinicians can read the screening version for practices, and long-term PPI use covers the acid pill that stalls digestion higher up.

Frequently asked questions

References

• Davies, A., Fagan, N., Gonzalez-Barboteo, J., Chelazzi, C., Economos, G., Elsner, F., Leach, C., Monsen, R. E., Oldenmenger, W. H., Remi, C., van den Beuken-van Everdingen, M., & Wüstefeld, M. (2024). Inadequate management of opioid-induced constipation in European cancer pain patients: Results of a real-world, multicentre, observational study (“E-StOIC”). Supportive Care in Cancer, 32(10), 701. https://doi.org/10.1007/s00520-024-08898-1
• Bell, T. J., Panchal, S. J., Miaskowski, C., Bolge, S. C., Milanova, T., & Williamson, R. (2009). The prevalence, severity, and impact of opioid-induced bowel dysfunction: Results of a US and European patient survey (PROBE 1). Pain Medicine, 10(1), 35-42. https://doi.org/10.1111/j.1526-4637.2008.00495.x
• Sternini, C., Patierno, S., Selmer, I.-S., & Kirchgessner, A. (2004). The opioid system in the gastrointestinal tract. Neurogastroenterology and Motility, 16(Suppl 2), 3-16. https://doi.org/10.1111/j.1743-3150.2004.00553.x
• Lewis, T. D. (1999). Morphine and gastroduodenal motility. Digestive Diseases and Sciences, 44(11), 2178-2186. https://doi.org/10.1023/a:1026684132254
• Halawi, H., Vijayvargiya, P., Busciglio, I., Oduyebo, I., Khemani, D., Ryks, M., Rhoten, D., Burton, D., Szarka, L. A., Acosta, A., & Camilleri, M. (2018). Effects of naloxegol on whole gut transit in opioid-naïve healthy subjects receiving codeine: A randomized, controlled trial. Neurogastroenterology and Motility, 30(5), e13298. https://doi.org/10.1111/nmo.13298
• Manabe, N., Ihara, E., Yomiya, K., Iseki, M., Torii, A., Miwa, H., & Camilleri, M. (2026). Current strategies and future perspectives in the management of opioid-induced constipation: A review of international and Japanese guidelines. Neurogastroenterology and Motility, 38(5), e70343. https://doi.org/10.1111/nmo.70343
• Drossman, D., & Szigethy, E. (2014). The narcotic bowel syndrome: A recent update. American Journal of Gastroenterology Supplements, 2(1), 22-30. https://doi.org/10.1038/ajgsup.2014.6
• Richards, G. C., Lluka, L. J., Smith, M. T., Haslam, C., Moore, B., O’Callaghan, J., & Strong, J. (2018). Effects of long-term opioid analgesics on cognitive performance and plasma cytokine concentrations in patients with chronic low back pain: A cross-sectional pilot study. Pain Reports, 3(4), e669. https://doi.org/10.1097/PR9.0000000000000669
• Essa, H., Hamdy, S., Green, D., Lal, S., McLaughlin, J., Hoffmann, S., Leitao, E., & Paine, P. (2021). Hydrogen and methane breath test results are negatively associated with IBS and may reflect transit time in post-surgical patients. Neurogastroenterology and Motility, 33(6), e14033. https://doi.org/10.1111/nmo.14033
• Gicquelais, R. E., Bohnert, A. S. B., Thomas, L., & Foxman, B. (2020). Opioid agonist and antagonist use and the gut microbiota: Associations among people in addiction treatment. Scientific Reports, 10(1), 19471. https://doi.org/10.1038/s41598-020-76570-9

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• Long-Term PPI Use: What Your Blood Work and Body Can Show
• Glyphosate in Food: What Can Actually Be Measured in You
• Cognitive Assessment

Night Shift Health Risks You Can Actually Measure

A rotating roster changes insulin, appetite and inflammation long before it changes a diagnosis. Most of that happens in markers nobody draws, on a schedule nobody writes down.

The night shift health risks that make headlines are the dramatic ones, but the changes with the strongest evidence are quieter and faster, and they show up in numbers a routine visit rarely records. Your Gut Has Jet Lag, the video for The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, follows an intensive care nurse whose Crohn’s flares followed her schedule changes. Your situation may be different. The questions are the same: what the schedule is doing to your body, what a standard checkup looks at, and which measurements can show what it misses.

Does night shift work cause cancer or diabetes?

Night work carries a probable-carcinogen grade, yet when researchers pooled cancer counts across more than eight million workers, colorectal and breast cancer barely moved. The grade describes what could happen. The counts describe how often it does.

The consistent signal sits in metabolism. Across 21 pooled studies, the diabetes risk attached to shift work was about 10% higher in relative terms; the excess appeared among women rather than men, and health care workers were the highest-risk occupational group. The fastest change is insulin itself. When nine normal-weight young men were held to roughly four hours of sleep for two nights, their HOMA-IR, an insulin resistance index, climbed close to 40% and fasting insulin rose 34%. Two nights. No weight change is needed for that to register in the blood, and no bathroom scale will ever see it.

Is a rotating shift worse than working permanent nights?

A permanent night schedule and a rotating one are different exposures. Among 399 nurses, rotation carried the heaviest symptom load: 81% of rotating-shift nurses reported abdominal pain, compared with 61% on permanent nights and 54% on days. A fixed night schedule is like moving to another time zone. A rotating roster is a red-eye flight every few days, and your first brain, the gut, pays for each landing.

In a laboratory study, adults pushed out of step with their body clock showed higher tumor necrosis factor and C-reactive protein, while their cortisol went down; plain sleep deprivation pushed cortisol up instead. A short night and a shifted night are separate injuries. Dose matters as well. In a 2025 synthesis of 35 studies, a single bad night did nothing measurable to inflammatory markers, while three or more nights of short sleep raised interleukin-6 and C-reactive protein. That is metaflammation built one run of nights at a time.

The schedule is rarely yours to write. Rosters follow staffing budgets, the people covering nights take the shift that is offered, and the pay differential makes a swing hard to refuse.

What does a routine checkup miss in night shift workers?

A routine checkup records weight, blood pressure and perhaps a fasting glucose. It seldom asks when you slept, and a roster almost never reaches the chart. Glucose can sit in the normal range while insulin climbs to keep it there. Appetite shifts quietly too: in 12 healthy young men, two short nights pushed the wish for dense, high-carbohydrate foods up by 33% to 45%. That craving shows up as weight months later, long after anyone could connect it to the schedule.

Timing also distorts the few numbers that are drawn. A blood test taken after one rough week is a snapshot of that week. Without the schedule written beside it, nobody reading the result can tell a run of nights from an ordinary month.

Night shift health risks that measurements can show

Measura [Cardiometabolic and Autonomic Health Analysis] does not do sleep studies. If a sleep disorder is suspected, that evaluation happens elsewhere. What Measura measures is the terrain a disordered schedule acts on, and the results go to your physician.

• Laboratory panels. Fasting insulin with glucose, lipids and inflammatory markers such as C-reactive protein. Note when your last run of nights ended before the draw.
• Heart rate variability. A recording of beat-to-beat changes in heart rhythm, which reflects how the autonomic nervous system, including the vagus nerve, is balancing activity and rest.
• Autonomic nervous system testing. How heart rate and blood pressure respond to breathing and posture changes, which shows whether that regulation holds under a challenge.
• Indirect calorimetry. Resting metabolic rate measured from the oxygen you use and the carbon dioxide you breathe out, instead of estimated from a formula.

The metabolic rate is where the non-obvious finding lives. A randomized trial coached 80 adults with overweight who habitually slept too little; they gained roughly 1.2 extra hours of sleep nightly, and their daily intake dropped by 270 kcal, while energy expenditure did not change at all. The tired body was not burning less. It was eating more. A measured resting rate helps you and your physician tell an intake problem from an expenditure problem instead of guessing. Heart rate variability has not been the outcome in the shift-work studies above; it is included as a direct measure of autonomic regulation, not as a shift-work diagnosis.

What to bring to your appointment

• Write the schedule beside your symptoms: the clock times you slept, not only the number of hours.
• Note the date your most recent run of nights ended.
• Keep meals on consistent clock times across a rotation, since feeding rhythm carries much of the gut’s timing.
• Hold a fixed sleep window on days off instead of swinging back each time.
• Ask whether insulin, not only glucose, has been checked. Insulin resistance and metabolic health explains why.

If your symptoms include lightheadedness, racing heart or digestive swings, autonomic symptoms describes what those tests look at. The book companion, the deep dive on the sleep-deprived microbiome, carries every study with its limits, and the metabolic side of fat stored around the gut is in how to measure visceral fat.

Frequently asked questions

References

• Dun, A., Zhao, X., Jin, X., Wei, T., Gao, X., Wang, Y., & Hou, H. (2020). Association between night-shift work and cancer risk: Updated systematic review and meta-analysis. Frontiers in Oncology, 10, 1006. https://doi.org/10.3389/fonc.2020.01006
• Gao, Y., Gan, T., Jiang, L., Yu, L., Tang, D., Wang, Y., Li, X., & Ding, G. (2020). Association between shift work and risk of type 2 diabetes mellitus: A systematic review and dose-response meta-analysis of observational studies. Chronobiology International, 37(1), 29-46. https://doi.org/10.1080/07420528.2019.1683570
• Benedict, C., Vogel, H., Jonas, W., Woting, A., Blaut, M., Schürmann, A., & Cedernaes, J. (2016). Gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals. Molecular Metabolism, 5(12), 1175-1186. https://doi.org/10.1016/j.molmet.2016.10.003
• Nojkov, B., Rubenstein, J. H., Chey, W. D., & Hoogerwerf, W. A. (2010). The impact of rotating shift work on the prevalence of irritable bowel syndrome in nurses. The American Journal of Gastroenterology, 105(4), 842-847. https://doi.org/10.1038/ajg.2010.48
• Wright, K. P., Drake, A. L., Frey, D. J., Fleshner, M., Desouza, C. A., Gronfier, C., & Czeisler, C. A. (2015). Influence of sleep deprivation and circadian misalignment on cortisol, inflammatory markers, and cytokine balance. Brain, Behavior, and Immunity, 47, 24-34. https://doi.org/10.1016/j.bbi.2015.01.004
• Ballesio, A., Fiori, V., & Lombardo, C. (2025). Effects of experimental sleep deprivation on peripheral inflammation: An updated meta-analysis of human studies. Journal of Sleep Research, 35(1), e70099. https://doi.org/10.1111/jsr.70099
• Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141(11), 846-50. https://doi.org/10.7326/0003-4819-141-11-200412070-00008
• Tasali, E., Wroblewski, K., Kahn, E., Kilkus, J., & Schoeller, D. A. (2022). Effect of sleep extension on objectively assessed energy intake among adults with overweight in real-life settings: A randomized clinical trial. JAMA Internal Medicine, 182(4), 365-374. https://doi.org/10.1001/jamainternmed.2021.8098

Related reading

• How to Measure Visceral Fat When the Scale Says You’re Fine
• Gut Microbiome Test Results: What They Cannot Measure
• Laboratory Panels

Can Stress Cause Stomach Problems? What Your Nervous System Shows

Yes. Stress slows how fast the stomach empties and makes the colon contract more, even while pulse and blood pressure stay normal.

Your pulse can look calm while your gut is anything but. The stress response that slows digestion is real, and part of it shows up on autonomic measurements.

Researchers have recorded it with instruments rather than guessing. Can stress cause stomach problems in a person whose tests all come back normal? In healthy volunteers exposed to loud noise, half of a meal cleared the stomach in 105.0 minutes at rest but needed 130.8 minutes under stress, while the stomach still relaxed normally to receive the food.

The video Two Doctors, One Bowel, Nobody in Charge, from The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, starts with a man whose gastroenterologist blamed stress and whose psychiatrist blamed his bowel. Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service; it measures and sends results to your physician. The angle here is measurement: which part of that stress response can be put on a chart, and which part cannot.

Can stress cause stomach problems when your pulse looks calm?

Dr. Padda admits he used the word stress for years as a way to close a visit once a scope looked clean. The physiology made him stop. When healthy people with a pressure catheter in the colon were given a mental stressor, the colon produced more pressure waves. Only a physical stressor raised pulse and blood pressure. The mental one moved the bowel while those two vital signs stayed flat, and the colon kept going after the stressor ended.

That is the non-obvious part. A normal pulse and blood pressure at your appointment say very little about what your gut is doing. In a separate study, the stomach’s electrical rhythm after a meal became less regular under stress, falling from 82.0% to 66.0%. Heart rate variability recorded at the same moment showed the vagal signal dropping and the sympathetic signal rising. The coarse vital signs missed the shift; the finer autonomic measure did not.

How are the gut and the brain connected?

The book calls the gut the first brain and the organ in the skull the second brain. The vagus nerve is the main cable between them, and digestion runs on its rest-and-digest branch. Fear turns that branch down. The stomach loses its beat and the colon overreacts.

The dial works in the other direction too. In 18 healthy volunteers, techniques that raised vagal tone increased stomach contractions, and cardiac vagal tone itself rose measurably compared with a sham session. One session in healthy people is a mechanism, not a treatment trial. It still matters for you, because it shows that the nerve fear quiets can be measured and moved.

Can anxiety cause lasting stomach problems like IBS?

Two town-wide outbreaks tested the question no ethics board would approve. After contaminated water in Walkerton, irritable bowel syndrome among exposed residents fell from 28.3% to 15.4% over eight years, yet their odds stayed 3.12 times those of unexposed neighbors. Anxiety or depression before the outbreak helped predict who stayed ill. After a German outbreak, 16.9% developed new IBS, and anxiety and somatization scores predicted it. How severe the infection had been did not.

Three drivers show up together. Two are biological: a vagal brake that stress releases, and a background of inflammation. In 2,555 Marines, higher C-reactive protein before deployment predicted who later developed PTSD symptoms, and in this model metaflammation is a common source of that fuel. The third is social. Gut care and mental health care sit in separate buildings with separate schedules, and a patient split between them has nobody in charge of the whole picture. Across 648,375 people, PTSD and irritable bowel syndrome traveled together at nearly triple the odds.

What does a standard stomach workup check, and what does it miss?

A typical workup for stomach or bowel symptoms looks for structural and inflammatory disease: a scope, blood markers, sometimes stool studies. Those answer important questions. When they come back clean, the visit often ends with the word stress and no measurement of the nervous system that the motility studies implicate.

Some popular add-on tests do not help. Stool microbiome reports are heavily shaped by diet, body weight and transit time, and in 2,004 children early-life stress barely registered in them. Blood permeability panels fared no better: in veterans, seven such markers neither tracked PTSD severity nor agreed with one another. Measura does not offer stool or permeability testing; those are different tests done elsewhere.

What can autonomic testing show about stress and digestion?

• Heart rate variability measures the beat-to-beat variation in your heart rhythm, a window on the balance between the vagal and sympathetic branches.
• Cardiac autonomic reflex tests record how heart rate and blood pressure respond to simple challenges such as deep breathing and standing up.
• Autonomic nervous system testing looks more broadly at how the automatic nervous system regulates the body.

Be precise about the limit. None of these tests diagnoses irritable bowel syndrome, Crohn’s disease or any bowel disorder, and none measures your gut directly. IBS is diagnosed by your physician from your symptoms and workup. What autonomic testing adds is a recorded picture of the nervous system state that stress research ties to digestion. If you want to know what an HRV result means, read heart rate variability: what the number means, and the symptoms that suggest autonomic trouble are listed under autonomic symptoms.

The treatments with the strongest evidence here are aimed at the nervous system. Across 67 randomized trials and 7,441 patients, cognitive behavioral therapy and gut-directed hypnotherapy beat waiting-list control, and telephone therapy still showed a 61.6-point lower symptom score at 12 months in 558 patients. Decisions about therapy and medication stay with your physician. The stress hormone side of this story is in cortisol and belly fat, the waistline and memory side in a leaky blood-brain barrier, physicians can read the clinical version, and every study is in the Chapter 13 Deep Dive. Timing matters too: gut microbes help set the daily rhythm of the stress response, explained in gut bacteria and stress.

Frequently asked questions

References

• Rao, S. S., Hatfield, R. A., Suls, J. M., & Chamberlain, M. J. (1998). Psychological and physical stress induce differential effects on human colonic motility. The American Journal of Gastroenterology, 93(6), 985-990. https://doi.org/10.1111/j.1572-0241.1998.00293.x
• Yin, J., Levanon, D., & Chen, J. D. Z. (2004). Inhibitory effects of stress on postprandial gastric myoelectrical activity and vagal tone in healthy subjects. Neurogastroenterology and Motility, 16(6), 737-744. https://doi.org/10.1111/j.1365-2982.2004.00544.x
• Lee, H. S., An, Y.-S., Kang, J., Yoo, J. H., & Lee, K. J. (2013). Effect of acute auditory stress on gastric motor responses to a meal in healthy volunteers. Journal of Gastroenterology and Hepatology, 28(11), 1699-1704. https://doi.org/10.1111/jgh.12309
• Frøkjaer, J. B., Bergmann, S., Brock, C., Madzak, A., Farmer, A. D., Ellrich, J., & Drewes, A. M. (2016). Modulation of vagal tone enhances gastroduodenal motility and reduces somatic pain sensitivity. Neurogastroenterology and Motility, 28(4), 592-598. https://doi.org/10.1111/nmo.12760
• Marshall, J. K., Thabane, M., Garg, A. X., Clark, W. F., Moayyedi, P., & Collins, S. M. (2010). Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut, 59(5), 605-611. https://doi.org/10.1136/gut.2009.202234
• Andresen, V., Löwe, B., Broicher, W., Riegel, B., Fraedrich, K., von Wulffen, M., Gappmayer, K., Wegscheider, K., Treszl, A., Rose, M., Layer, P., & Lohse, A. W. (2016). Post-infectious irritable bowel syndrome (PI-IBS) after infection with Shiga-like toxin-producing Escherichia coli (STEC) O104:H4: A cohort study with prospective follow-up. United European Gastroenterology Journal, 4(1), 121-131. https://doi.org/10.1177/2050640615581113
• Ng, Q. X., Soh, A. Y. S., Loke, W., Venkatanarayanan, N., Lim, D. Y., & Yeo, W.-S. (2019). Systematic review with meta-analysis: The association between post-traumatic stress disorder and irritable bowel syndrome. Journal of Gastroenterology and Hepatology, 34(1), 68-73. https://doi.org/10.1111/jgh.14446
• Eraly, S. A., Nievergelt, C. M., Maihofer, A. X., Barkauskas, D. A., Biswas, N., Agorastos, A., O’Connor, D. T., & Baker, D. G. (2014). Assessment of plasma C-reactive protein as a biomarker of posttraumatic stress disorder risk. JAMA Psychiatry, 71(4), 423-431. https://doi.org/10.1001/jamapsychiatry.2013.4374
• Hoisington, A. J., Stamper, C. E., Stearns-Yoder, K. A., Haghighi, F., Lowry, C. A., & Brenner, L. A. (2023). A cross-sectional study of correlations among blood-based biomarkers for intestinal permeability: A pilot study of United States veterans with posttraumatic stress disorder symptoms. Brain, Behavior, & Immunity – Health, 34, 100702. https://doi.org/10.1016/j.bbih.2023.100702
• Thakur, E. R., Khasawneh, M., Moayyedi, P., Black, C. J., & Ford, A. C. (2025). Efficacy of behavioural therapies for irritable bowel syndrome: a systematic review and network meta-analysis. The Lancet Gastroenterology & Hepatology, 10(12), 1075-1088. https://doi.org/10.1016/S2468-1253(25)00238-9

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EDS and POTS: Measuring What a Normal Workup Misses

With EDS and POTS, autonomic testing measures how your nervous system regulates heart rate and blood pressure when you stand, which standard gut and heart workups are not built to do. Cardiac autonomic reflex tests and heart rate variability put that regulation on a number; your physician makes any diagnosis.

Hypermobility rarely stays in the joints. When the racing heart, the fatigue and the unsettled gut all come back normal on standard tests, the regulation behind them can still be measured.

If you live with hypermobile Ehlers-Danlos syndrome or hypermobility spectrum disorder, you may already know the EDS and POTS pairing from experience: the racing heart and gray-out on standing, the fatigue, the gut that never settles, and a stack of tests that all came back normal. Respondents to one large international survey reported a mean gap of 22.1 years between their first symptoms and a name for them. In Collagen Is the Wall, Not the Paint, the video companion to The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, the case is made for why a collagen body is a whole-body problem. The question here is a measuring one: which parts of that picture can actually be put on a number.

Why does EDS affect more than the joints?

Collagen is not decoration. It is the footing the gut lining stands on, the framework of blood vessels, and the tissue that holds joints together. The gut is the first brain, the organ that decides what gets into the body, and its wall is built on that same collagen scaffold. When collagen is made wrong, the effects show up wherever that scaffold works.

The numbers bear that out. Pooled across studies, people with hypermobility had 4.29 times the odds of chronic gut symptoms compared with controls. The trouble does not stop at the bowel. In the same pooled data, orthostatic intolerance, feeling unwell when upright, affected 35.9%, chronic fatigue 49%, and migraine 38.2%. Postural tachycardia pooled at 21.9%, although the range around that figure ran from 5.2% to 59.1%, wide enough that nobody should quote it as a precise rate. In the survey, 71.4% reported dysautonomia, a patient-reported label rather than a tested one.

The pattern is clear even where the mechanism is not. Autonomic symptoms are common enough in this population that they deserve measurement, not a shrug.

Why do EDS and POTS tests keep coming back normal?

Most gut and heart workups are built to find structural disease that kills: a tumor, a blocked vessel, an inflamed bowel. They are good at that job. They are not built to measure how the nervous system regulates heart rate, blood pressure and sweating when you stand up, and so they return normal in person after person.

Even the gut findings run against expectation. When symptomatic patients had pressure studies of the upper intestine, bowel motility problems were actually less common in the hypermobile group, 13% against 34%. The commonest complaints were heartburn, reflux and trouble swallowing, not a sluggish bowel. A body that moves food normally but still feels awful is one more reason to look beyond the bowel.

The delay has a social cause as well as a biological one. A patient whose scans stay clean gets labeled anxious, and a system paid to find structural disease has little reason to count the rest. Meanwhile the research money for collagen products flowed toward skin and wrinkles, where the customers were, not toward the gut or the nervous system.

What can autonomic testing show in EDS and POTS?

Measura [Cardiometabolic and Autonomic Health Analysis] has no test for collagen or connective tissue, and it does not diagnose Ehlers-Danlos syndrome or POTS. What it can measure is the autonomic side of the story, the regulation that so many hypermobile patients describe but rarely see documented. Results go to your physician, who makes any diagnosis.

• Autonomic nervous system testing looks at how the involuntary nervous system is regulating the body.
• Cardiac autonomic reflex tests record how heart rate and blood pressure respond to standardized maneuvers, including changes in posture.
• Heart rate variability measures the beat-to-beat variation that reflects autonomic balance; what that number means is its own topic.

A measured result changes the conversation. Instead of describing a racing heart that nobody saw, you arrive with a recording of how your system actually behaved.

Balance, muscle and the protein nobody counts

Lightheadedness on standing is not only unpleasant; it is a fall risk. Vestibular and balance testing measures how steady you are, which matters for anyone who grays out when they stand. More on that link is in dizziness, balance and falls.

Muscle is the other half. Bioimpedance body composition separates muscle from fat, something a scale cannot do. That matters because the best evidence for collagen supplements is in joints, not guts, and in a review of randomized trials the muscle results were inconsistent and mostly positive only when collagen was paired with exercise.

Then there is the raw material. The gut lining rebuilds itself continuously from protein you eat. When healthy volunteers were fed only by vein for 14 days, their gut lining thinned from 645 to 512 microns. An inflamed, underfed lining feeds metaflammation, the low-grade inflammation that keeps the whole system irritated. I once thought of repair like a construction site: deliver the lumber and the wall goes up. The research in malnourished children proved me wrong. Feeding is necessary, but a gut under attack does not rebuild on protein alone. Still, nothing rebuilds without it. Add up three ordinary days of protein before assuming you eat enough, and notice whether eating alone, painful teeth or a poor appetite is quietly taking it off the plate.

What to bring to your appointment

• A written list of symptoms on standing: racing heart, gray-out, fainting or near-fainting.
• How long symptoms have gone without a name, and which tests were already normal.
• Your gut symptoms, especially reflux and trouble swallowing.
• Three days of food with protein totaled.
• Every medication, including any started within a year of new bowel symptoms.
• A question: can my autonomic function, balance and muscle be measured, not just described?

Every study behind these figures sits in the companion deep dive for The Angry Gut. The stomach side of nutrient absorption is covered in atrophic gastritis and B12 absorption, and physicians can read the screening version for practices.

Frequently asked questions

References

• Kulin, D., Holtmann, G., Fairlie, T., Staller, K., Nurko, S., Keefer, L., Drossman, D. A., Jones, M. P., Talley, N. J., & Ford, A. C. (2026). Meta-analysis: Chronic gastrointestinal symptoms and comorbidities in hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders. Alimentary Pharmacology & Therapeutics, 64(5), 574–589. https://doi.org/10.1111/apt.70856
• Daylor, V., Griggs, M., Weintraub, A., Byrd, R., Petrucci, T., Huff, M., Byerly, K., Fenner, R., Gensemer, C., Norris, R. A., & Patel, S. (2025). Defining the chronic complexities of hEDS and HSD: A global survey of diagnostic challenges, life-long comorbidities, and unmet needs. Journal of Clinical Medicine, 14(16), 5636. https://doi.org/10.3390/jcm14165636
• Sweerts, K. W. E., Mujagic, Z., Keszthelyi, D., & Conchillo, J. M. (2025). Analysis of antroduodenal motility in patients with hypermobility spectrum disorders/hypermobile Ehlers-Danlos syndrome. Alimentary Pharmacology & Therapeutics, 61(4), 702-705. https://doi.org/10.1111/apt.18471
• Brueckheimer, P. J., Costa Silva, T., Rodrigues, L., Zague, V., & Isaia Filho, C. (2025). The effects of type I collagen hydrolysate supplementation on bones, muscles, and joints: A systematic review. Orthopedic Reviews, 17, 129086. https://doi.org/10.52965/001c.129086
• Buchman, A. L., Moukarzel, A. A., Bhuta, S., Belle, M., Ament, M. E., Eckhert, C. D., Hollander, D., Gornbein, J., Kopple, J. D., & Vijayaroghavan, S. R. (1995). Parenteral nutrition is associated with intestinal morphologic and functional changes in humans. JPEN. Journal of Parenteral and Enteral Nutrition, 19(6), 453–460. https://doi.org/10.1177/0148607195019006453
• Rachmadi, R. A., Ariani, Y., & Alatas, F. S. (2024). Impact of nutritional supplementation on environmental enteric dysfunction (EED) in children living in rural areas: A systematic review. Arquivos de Gastroenterologia, 61, e23159. https://doi.org/10.1590/S0004-2803.24612023-159
• Bassila, C., Bassila, J.-C., & Slim, M. (2026). Efficacy and safety of hydrolyzed collagen supplementation on skin health outcomes: A systematic literature review of randomized controlled trials. European Journal of Clinical Nutrition, 80(9), 867–885. https://doi.org/10.1038/s41430-026-01778-3

Related reading

• Atrophic Gastritis: When Your Stomach Stops Absorbing B12
• Are Seed Oils Bad for You? What Your Numbers Can Actually Show
• Autonomic Nervous System Testing

Vagus Nerve and Anxiety: What a Heart Reading Shows About Your Gut

Heart rate variability records the vagus nerve’s effect on your heartbeat, and in studies of people with gut disorders, low vagal tone tracked inflammation and adrenaline rather than anxiety or mood scores. It is a stand-in for the gut, not a window into it.

The nerve that joins your gut and your brain cannot be sampled like blood. It can be measured where it touches the heart, and that reading is useful once you know its limits.

The vagus nerve, anxiety and calm are usually discussed as a chain in which soothing the nerve soothes the mood. The measurements tell a more specific story: vagal tone tracks inflammation and adrenaline more closely than it tracks mood. The nerve cannot be sampled like blood, but its effect on the heart can be measured, and knowing what that number does and does not mean separates a useful reading from a misleading one.

In the video Two Doctors, One Nerve, Dr. Gurpreet Singh Padda, MD, MBA, MHP, who wrote The Angry Gut with Ami Michelle Grimes, describes a thirty-four-year-old woman whose bowel trouble came first and whose panic followed a month later. One specialist manages her gut and another manages her anxiety. Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service, and what follows is the measurement side of her situation.

What does the vagus nerve connect?

The book calls the gut the first brain and the brain in the skull the second brain. The vagus nerve is the cable between them. Below the diaphragm it is made mostly of thin, slow sensory fibers, so the bulk of what it carries is information flowing up from the abdomen rather than commands flowing down.

No clinic test reads that abdominal traffic directly. Every practical measurement of vagal activity is taken somewhere else, usually at the heart, and then interpreted. The wiring itself is laid out in the first post in this series. That limit is the first thing to understand before anyone puts a number in front of you.

What does heart rate variability measure?

Your heart rate rises a little as you breathe in and eases as you breathe out. The size of that rhythm is set largely by the vagus nerve, and it is captured as heart rate variability. The two standard vagal measures are RMSSD, the root mean square of successive differences between beats, and high-frequency power. A lower value means less vagal influence on the heart at the time of the recording. The Measura heart rate variability test records this from the heartbeat.

Two limits keep that reading honest. The balance ratio many consumer apps display went from 1.1 to 8.4 when researchers took away most of the nerve input to the heart, so it is not a nerve measurement at all. And heart rate variability reflects cardiac vagal tone; a review of inflammatory bowel disease studies noted it may not reflect vagal tone in the abdomen. It is a stand-in for the gut, not a window into it. For more on the number itself, read heart rate variability: what the number means.

Is low vagal tone linked to anxiety or to the gut?

Healthy controls averaged 39.99 ms on the vagal index across 24-hour recordings in a study of 253 people. Those with functional dyspepsia, a painful stomach with a normal scope, averaged 16.87 ms. Poor sleep, not mood, was the stronger predictor of a low reading in that group. A separate study of people with Crohn’s disease and irritable bowel syndrome found lower vagal tone tracking higher tumor necrosis factor, an inflammatory messenger, in Crohn’s (r = -0.48) and higher epinephrine in irritable bowel syndrome (r = -0.39). Vagal tone showed no link to mood scores in any group.

Put those findings together and her two diagnoses start to look like one picture with three drivers. Inflammatory signals from an irritated lining travel up the nerve and feed metaflammation. Sympathetic overdrive, the adrenaline side of the system, stays switched on while vagal tone sits low. And a care system that sends the bowel to one office and the panic to another never measures the connection between them. Her anxiety is unlikely to settle while her gut keeps sounding the alarm.

What can a vagus nerve test measure, and what can it not?

A Measura autonomic assessment looks at the heart side of the nerve with more than one number:

• Cardiac autonomic reflex tests record how heart rate and blood pressure respond to simple, standardized challenges, adding a structured response to a resting reading.
• Autonomic nervous system testing looks at the wider balance of the automatic nervous system in one visit.
• Laboratory panels describe the metabolic terrain, including markers related to blood sugar and fats, that sits under the inflammation.

Some tests belong elsewhere. Stool tests, capsule studies and scopes are gastrointestinal tests ordered through your physician, not Measura tests. Stool also has a timing problem: in healthy volunteers sampled inside the small intestine, roughly 95% of the bile acids arriving at its far end were taken back up before stool formed. Ear clips and nerve stimulators are treatments, not tests, and Measura offers neither. No Measura result, and no other test, reads what the vagus is carrying up from your gut in real time.

Does breathing training strengthen the vagus nerve?

Dr. Padda was taught that the vagus calms inflammation by signaling the spleen, and he repeated it for years. A 2026 study that used four separate anatomical methods in male mice found the vagal motor fibers do not supply the spleen to any significant degree. The reflex exists, but it runs through sympathetic nerves. That correction matters to readers, because wellness marketing still sells the old route.

The same caution applies to what changes the reading. In randomized trials of people with heart disease, breathing biofeedback lowered blood pressure by about 3.08 mmHg but did not change high-frequency power, the vagal index it is named after. Breathing still earns a place: diaphragm training helped resolve reflux-related cough in 94% of patients against 77%. It simply is not proof of a stronger nerve. That is why a trend inside one person, measured the same way each time, beats a single number or a before-and-after taken minutes apart.

Taking this to your physician

• Describe the order your symptoms began in, including any change in sleep.
• Ask whether an autonomic baseline would help, and how it would be repeated.
• Bring wearable readings as a trend, not a verdict.
• List every medication, since drugs that act on heart rate can change the result.
• Keep both your gut specialist and your mental health clinician informed.

The studies behind these numbers, graded one by one, are in the Deep Dive companion. What happens on the day is covered in what to expect at your appointment. The gut’s inputs start with the medicine cabinet, in what nine bottles hide from your numbers, and continue with what crosses a damaged gut wall.

Frequently asked questions

References

• Shaffer, F., & Ginsberg, J. P. (2017). An overview of heart rate variability metrics and norms. Frontiers in Public Health, 5, 258. https://doi.org/10.3389/fpubh.2017.00258
• Billman, G. E. (2013). The LF/HF ratio does not accurately measure cardiac sympatho-vagal balance. Frontiers in Physiology, 4, 26. https://doi.org/10.3389/fphys.2013.00026
• Kim, K.-N., Yao, Y., & Ju, S.-Y. (2020). Heart rate variability and inflammatory bowel disease in humans: a systematic review and meta-analysis. Medicine, 99(48), e23430. https://doi.org/10.1097/MD.0000000000023430
• Du, L., Yang, J., Jiang, L., Zeng, G., Shu, Y., & Bi, B. (2026). Postprandial attenuation of gastric slow waves in anxiety-depression, with and without functional dyspepsia: associations with heart rate variability and sleep quality. Frontiers in Medicine, 13, 1890716. https://doi.org/10.3389/fmed.2026.1890716
• Pellissier, S., Dantzer, C., Mondillon, L., Trocme, C., Gauchez, A.-S., Ducros, V., Mathieu, N., Toussaint, B., Fournier, A., Canini, F., & Bonaz, B. (2014). Relationship between vagal tone, cortisol, TNF-alpha, epinephrine and negative affects in Crohn’s disease and irritable bowel syndrome. PLoS One, 9(9), e105328. https://doi.org/10.1371/journal.pone.0105328
• Khan, A., Tinajero, A., Moresco, J. J., Yang, J., & Gautron, L. (2026). Anatomical reappraisal of the relationship between vagal preganglionic motor neurons and the spleen in the male mouse. Autonomic Neuroscience: Basic & Clinical, 264, 103394. https://doi.org/10.1016/j.autneu.2026.103394
• Kaneko, K., Aikawa, G., Sakuramoto, H., Ota, Y., Oyama, Y., Tomooka, M., Naya, K., Fukunaga, T., Sugishima, K., & Yamada, T. (2026). Effects of heart rate variability biofeedback on cardiac autonomic function in patients with cardiovascular disease: a systematic review and meta-analysis. Applied Psychophysiology and Biofeedback. https://doi.org/10.1007/s10484-025-09765-3
• Niu, S., Zhang, T., Li, W., Wen, S., Dong, L., Wang, S., Shi, W., Shi, C., Shen, Y., Huang, Q., Tan, Y., Xu, X., & Yu, L. (2024). Positive effect of deep diaphragmatic breathing training on gastroesophageal reflux-induced chronic cough: a clinical randomized controlled study. Respiratory Research, 25(1), 169. https://doi.org/10.1186/s12931-024-02783-5
• Shalon, D., Culver, R. N., Grembi, J. A., Folz, J., Treit, P. V., Shi, H., Rosenberger, F. A., Dethlefsen, L., Meng, X., Yaffe, E., Aranda-Díaz, A., Geyer, P. E., Mueller-Reif, J. B., Spencer, S., Patterson, A. D., Triadafilopoulos, G., Holmes, S. P., Mann, M., Fiehn, O., … Huang, K. C. (2023). Profiling the human intestinal environment under physiological conditions. Nature, 617(7961), 581–591. https://doi.org/10.1038/s41586-023-05989-7

Related reading

• Polypharmacy in the Elderly: What Nine Bottles Hide From Your Numbers
• How to Test for Leaky Gut, and Why Zonulin Is the Wrong Test
• Heart Rate Variability

Is There a Vagus Nerve Test? What Can Actually Be Measured

There is no single vagus nerve test that reads the nerve where it meets your gut. What can be measured is the vagus where it meets the heart, through heart rate variability and cardiac autonomic reflex tests, alongside blood work and body composition.

The nerve linking your gut to your head is built mostly to carry reports upward. No scan reads those reports directly, but the same nerve leaves a measurable trace in the rhythm of your heartbeat.

Anyone searching for a vagus nerve test is usually hoping for one reading that says whether the line between gut and head is working. No such reading exists. What does exist are measurements of the vagus where it meets the heart, plus laboratory and body-composition work describing the metabolic ground that nerve reports on. Knowing which result answers which question keeps a normal number from being mistaken for a clean bill of health.

Dr. Padda’s video You Have the Stomach of a Hyena flips the usual anatomy chart. The gut is the first brain, the organ inside the skull is the second brain, and the cable between them is built mostly to send news upward. Measura [Cardiometabolic and Autonomic Health Analysis] asks the follow-up question a patient would ask: if the gut does that much talking, which part of the conversation can be measured in a living person?

A nerve built to report, and not a single wire

Popular articles claim 80 or 90 percent of vagal fibers carry sensation upward. Nobody has confirmed that ratio by counting fibers in a human vagus, and one rat study often cited for it actually found a larger motor share than textbooks assumed. The construction, though, has been measured. Below the diaphragm, where the nerve serves the gut, human tissue is 94 percent unmyelinated fiber, the thin and slow cable typical of reporting. Up at the neck, the same person’s vagus is 54 percent myelinated.

Two further details change how any result should be read. First, the nerve keeps rebraiding itself along its length, so fibers bound for one organ stay grouped for only a short stretch. Second, vagal does not simply mean calming. In human neck specimens, the right vagus carried on average twice as many sympathetic-type fibers as the left. A reading taken at the heart samples a crowded, mixed cable. It is not a private line to your bowel.

Why can’t a vagus nerve test reach the gut?

The gut end of the system is fast and hidden. In mice, specialized lining cells synapse onto nerve fibers and hand a signal to vagal neurons within 60 to 800 milliseconds, and colon cells that sense a bacterial protein raise vagal firing within seconds. No clinical device listens to that traffic in a person. The human gut wall holds about 168 million neurons of its own, and much of their work never passes through the head at all.

The other signature in the video, stomach acid, also sits outside Measura’s scope. Gastric pH is read with a swallowed capsule or probe. Among 66 healthy people who carried a radio capsule through the gut for as long as two days, stomach pH never left the 1.0 to 2.5 band. That is a different test, performed elsewhere. So are stool, breath and microbiome studies, and Measura does not offer any of them.

What can a vagus nerve test actually measure?

What can be measured is the autonomic nervous system as a whole, and the metabolic body the first brain is wired into.

• Heart rate variability captures the beat-to-beat variation in your heart rate at rest, a window on how the autonomic nervous system, vagal input to the heart included, is setting the pace.
• Cardiac autonomic reflex tests record how heart rate and blood pressure respond to standardized changes such as paced breathing or standing up.
• Autonomic nervous system testing combines several such measurements into a broader picture of regulation.
• Laboratory panels report metabolic and inflammatory markers from a blood draw, with the specific markers chosen alongside your physician.
• Bioimpedance body composition estimates how much of your weight is fat, muscle and water.

Keep the limit in view. None of these reads the abdominal vagus or the nerve network inside the gut wall. An abnormal autonomic result says regulation is strained somewhere; a normal one does not clear the gut. Measura records the numbers, and your own physician weighs them against your history. For how that reading works, see understanding your results.

The ground the first brain reports on

If the head mostly reads the gut, then what the gut has to report matters. The intestinal lining renews itself roughly every 4 to 5 days, rebuilt from recent meals. For most households those meals come from whatever the food system can grow, ship and shelve most cheaply, which largely means grain and things made from grain. Upstream sits a sterilizing gate: put a test organism into a stomach that makes acid and, below pH 4.0, 99.9 percent of it is dead inside thirty minutes.

Across The Angry Gut, the long-run consequence of a mistreated interface is low-grade metabolic inflammation, which Dr. Padda calls metaflammation. That terrain is exactly what blood markers and body composition are designed to describe, which is why they sit beside autonomic testing rather than behind it.

Dr. Padda came to this view late. He spent years as a strict vegetarian, teaching nutrition guidelines he now takes apart, and he describes the turn as something his digestion recognized before his reasoning did. The lesson for a patient is not a diet. It is that the equipment has expectations, and evidence of how it is coping has to be gathered rather than assumed.

What does a routine visit miss about autonomic function?

A standard visit takes a resting pulse and blood pressure, lists your medications and asks about symptoms. Digestive complaints go to one specialist, while palpitations, lightheadedness or poor sleep go to another, and nobody is assigned to ask whether they describe one regulatory system under strain. Acid-suppressing drugs change what reaches the gut, yet they are rarely reviewed with that in mind. Unmeasured is unmanaged, and a pulse taken once while seated is not a measurement of autonomic function.

What should you ask your doctor about vagus nerve testing?

• Has my autonomic function ever been tested, or only my resting pulse?
• If I take an acid-suppressing drug, what is it treating, and does that reason still apply?
• Should my pattern of food tolerance, what sits easily and what brings on bloating, be written into my history?
• Would a metabolic panel and body composition add anything to what my chart already shows?

If you are unsure whether testing fits your situation, start with who should be tested. The studies behind each figure, with their limits, are collected in the Chapter 0 Deep Dive for The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes. The next step in the series is whether inflammation can drive anxiety.

Frequently asked questions

References

• Stakenborg, N., Gomez-Pinilla, P. J., Verlinden, T. J. M., Wolthuis, A. M., D’Hoore, A., Farré, R., Herijgers, P., Matteoli, G., & Boeckxstaens, G. E. (2020). Comparison between the cervical and abdominal vagus nerves in mice, pigs, and humans. Neurogastroenterology and Motility, 32(9), e13889. https://doi.org/10.1111/nmo.13889
• Verlinden, T. J. M., Rijkers, K., Hoogland, G., & Herrler, A. (2016). Morphology of the human cervical vagus nerve: implications for vagus nerve stimulation treatment. Acta Neurologica Scandinavica, 133(3), 173-182. https://doi.org/10.1111/ane.12462
• Kaelberer, M. M., Buchanan, K. L., Klein, M. E., Barth, B. B., Montoya, M. M., Shen, X., & Bohórquez, D. V. (2018). A gut-brain neural circuit for nutrient sensory transduction. Science, 361(6408), eaat5236. https://doi.org/10.1126/science.aat5236
• Evans, D. F., Pye, G., Bramley, R., Clark, A. G., Dyson, T. J., & Hardcastle, J. D. (1988). Measurement of gastrointestinal pH profiles in normal ambulant human subjects. Gut, 29(8), 1035–1041. https://doi.org/10.1136/gut.29.8.1035
• Giannella, R. A., Broitman, S. A., & Zamcheck, N. (1972). Gastric acid barrier to ingested microorganisms in man: studies in vivo and in vitro. Gut, 13(4), 251–256. https://doi.org/10.1136/gut.13.4.251
• Michel, K., Kuch, B., Dengler, S., Demir, I. E., Zeller, F., & Schemann, M. (2022). How big is the little brain in the gut? Neuronal numbers in the enteric nervous system of mice, Guinea pig, and human. Neurogastroenterology and Motility, 34(12), e14440. https://doi.org/10.1111/nmo.14440
• Yang, S., Liu, H., & Liu, Y. (2025). Advances in intestinal epithelium and gut microbiota interaction. Frontiers in Microbiology, 16, 1499202. https://doi.org/10.3389/fmicb.2025.1499202
• Prechtl, J. C., & Powley, T. L. (1990). The fiber composition of the abdominal vagus of the rat. Anatomy and Embryology, 181(2), 101–115. https://doi.org/10.1007/BF00198950

Related reading

• Can Inflammation Cause Anxiety? What Blood Work and Testing Show
• Heart Rate Variability

Heart rate variability: what the number means

Heart rate variability is the constant small variation in the interval between heartbeats as the autonomic nervous system adjusts to breathing, posture and blood pressure. More variation usually means a more responsive system.

There is no single good value, your watch and a clinical device will disagree, and the only comparison worth making is against yourself under the same conditions.

What does heart rate variability measure?

A healthy heart does not beat like a metronome. The interval between beats varies constantly, by small amounts, as the two branches of the autonomic nervous system adjust to breathing, posture and blood pressure. That variation is a sign of a responsive system, and it is quantified in two ways: in the time domain, from the statistics of the interval series, and in the frequency domain, from the rhythms present within it.

Counterintuitively, a heart beating with very little variation is usually the less healthy one. Loss of variability reflects loss of the flexibility that lets the system respond.

What is a good heart rate variability?

There is no single good number, for five reasons.

• It falls with age, substantially and normally.
• It varies enormously between individuals for reasons that have nothing to do with disease.
• It moves with everything you did yesterday — sleep, alcohol, caffeine, a hard training session, an argument, the start of a cold.
• It moves with medication — beta-blockers, anticholinergics, antidepressants and antiarrhythmics all change it, in different directions.
• It depends on how it was measured — posture, breathing rate, recording length, time of day and the algorithm used.

A population reference range for such a measurement is close to useless for an individual. What is not useless is your own value, taken the same way, twice.

Why does my watch show a different HRV?

Different sensor, different sampling, different artifact rejection, different algorithm, and usually a different recording window — often overnight rather than a controlled resting period. Two methods can both be internally consistent and not comparable to each other. Compare within a method, never across.

How is heart rate variability measured?

From an interval series derived from the pulse or the electrocardiogram, at rest under controlled conditions, and then during standardized challenges — deep timed breathing, standing, and a controlled exhale against resistance. The challenges are where most of the clinical information is, because they ask a specific branch of the system to respond and measure whether it does. Cardiac autonomic reflex tests.

What does a low HRV mean?

Repeat it under controlled conditions before concluding anything. If it is genuinely and repeatedly low, the useful next questions are about medication, sleep, glycemic control, deconditioning and any of the conditions that cause autonomic neuropathy. It is a signal to investigate, not a diagnosis.

Autonomic symptoms and the full test description.

Frequently asked questions

Related reading

• Heart rate variability
• Autonomic nervous system testing
• What a result can and cannot tell you