Does Obesity Cause Cancer? What Your Metabolic Numbers Add

Yes, for a growing list of cancers: higher BMI is tied to greater risk of 19 cancer types, and the risk travels through what excess fat does to blood sugar, insulin and inflammation.

About four in ten US cancers trace to factors people can change, and excess weight ranks second. The deeper driver is metabolic, and most of it goes unmeasured at a routine visit.

Does obesity cause cancer? For a growing list of cancers the evidence now says it does, and the number on the scale is the least interesting part of the answer: the risk travels through what excess fat does to blood sugar, insulin and inflammation, the metabolic damage a routine checkup rarely measures.

How much cancer is tied to things that can change

American Cancer Society researchers estimated that in 2019, 40.0% of new cancers in US adults aged 30 and older, 713,340 of 1,781,649 cases outside common skin cancers, and 44.0% of cancer deaths, 262,120 of 595,737, were attributable to risk factors that can potentially be changed. Cigarette smoking led, at 19.3% of cases and 28.5% of deaths. Excess body weight came second, at 7.6% of cases and 7.3% of deaths, ahead of alcohol at 5.4% and 4.1%.

Treat that 7.6% as a floor for metabolic harm, not a ceiling. The analysis counted excess body weight. High blood sugar, insulin resistance and metabolic syndrome were not on its list of evaluated risk factors, so a person of ordinary weight whose metabolism is failing added nothing to that share. The headline undercounts exactly the person a scale reassures, and the metabolic part of the story has to be read from other studies.

The list of weight-linked cancers keeps growing

In 2024, two cancer epidemiologists writing in The Lancet Regional Health – Europe asked the question directly: is obesity a cause of all cancer types? A 2026 systematic review in Nature Metabolism, with one of those two on its author team, gave the most complete answer so far. It pooled 226 articles covering 1.5 million cancer diagnoses from prospective studies of 25 cancer types and found higher BMI tied to greater risk of 19 cancers and lower risk of 3. Leukemia, non-Hodgkin lymphoma, bladder cancer and glioma were added compared with earlier consensus reports. Waist circumference behaved much like BMI, and genetic studies were generally consistent with the observational findings. Not every cancer, then, but far more than most people assume. Liver cancer is on that list, and the first warning is often a scarring score most patients never see, explained in what a fibrosis score says about a fatty liver.

Metabolic syndrome carries its own risk

Metabolic syndrome is a cluster of findings: a large waist, high blood pressure, high blood sugar, high triglycerides and low HDL cholesterol. A 2024 meta-analysis of 31 prospective cohort studies linked it to higher risk of five digestive cancers: colorectal (relative risk 1.13), esophageal (1.17), pancreatic (1.25), gallbladder (1.37) and liver (1.46). Stomach cancer was the exception. Among combinations of those findings, obesity with high blood pressure and high blood sugar had the strongest link to colorectal cancer, 1.54 in men and 1.27 in women. Genetic studies within the same paper, a way of separating cause from coincidence, supported waist-to-hip ratio, BMI and HbA1c, the three-month blood sugar average, as causes of colorectal cancer.

This evidence is observational and genetic, not randomized, because nobody can assign people to decades of high insulin and wait for tumors; that is exactly why the mechanism carries weight. Why would metabolism feed a tumor? A 2026 review published alongside the meta-analysis names three routes: sex hormones, hyperinsulinemia and chronic inflammation. Insulin is a growth signal. When cells resist it, the pancreas pushes out more, and every tissue that listens to insulin keeps hearing an instruction to grow. Inflamed fat tissue adds a steady stream of alarm chemicals, the metaflammation that keeps repair switched on long after anything needs repairing. Two biological engines, then, and one fuel line. The third driver sits outside the body. A food supply engineered around acellular carbohydrates and industrial seed oils, much of it grown from subsidized commodity crops, keeps both engines fed meal after meal, and then the same system treats the tumor as bad luck.

Colorectal cancer is arriving younger

Colorectal cancer in adults under 50 has been rising since the 1990s, and a 2025 review in Nature Reviews Endocrinology described it as an emerging disease of metabolic dysregulation, climbing alongside obesity and type 2 diabetes in young people. In a 2026 meta-analysis of eleven cohort studies, overweight or obesity carried 1.59 times the odds of early-onset colorectal cancer, and obesity alone 1.81. Among 357 Australian adults referred for colonoscopy, where waist and weight told part of the story, 41.7% had metabolic syndrome, and in those over 40 with a BMI of 25 or more, the adjusted odds were 2.26 for any polyp and 2.64 for an adenoma, the type of polyp that can turn into cancer.

Weight is not the whole explanation, and that matters for anyone who is not heavy. Australian modeling published in 2026 estimated that obesity in adolescence accounts for a growing but small share of early-onset colorectal cancers, rising from 2% to 6% in men, and judged it unlikely to be the main driver of the rise. Read beside the metabolic syndrome findings, that points past the scale toward blood sugar, insulin and inflammation. If you are young, of ordinary weight and told your risk is low because you are not heavy, that reassurance rests on the wrong number. The same trap catches the normal-BMI South Asian or East Asian adult who is skinny fat, thin outside and metabolically inflamed and insulin resistant inside.

Risk is not fixed at the weight you once were

In a population cohort of 800,024 people whose BMI was measured at pre-military evaluations in late adolescence and again in adulthood, those who went from a normal weight to a high one had 1.31 times the risk of obesity-related cancers, and those who stayed heavy had 1.47 times. People who were heavy as teenagers but reached a normal adult weight showed no clear excess, with a hazard ratio of 1.01. Each 5% of weight gained raised the hazard by 3%, and the same held for cancers diagnosed before 50. The trajectory, not the starting point, carried the risk, and a trajectory is something you can track and still change.

Metabolic health, meanwhile, has become the exception. Fewer than 12.2% of US adults qualified as optimally metabolically healthy in NHANES data from 2009 through 2016, and once stricter criteria arrived after 2021 the share fell below 7%. A normal weight does not settle the question. Unmeasured is unmanaged. For older adults with high blood pressure, a waist measure adjusted for weight has been tested against stroke, as covered in waist index screening for stroke.

What a checkup covers, and what measurement adds

Cancer screening itself, such as colonoscopy and mammography, is ordered by your physician and done elsewhere. A standard checkup records weight and blood pressure and usually checks glucose, A1c and cholesterol. What it tends to leave out is fasting insulin, which climbs for years while glucose still looks normal, and any measure of how much of your weight is fat and how much is muscle.

Measura [Cardiometabolic and Autonomic Health Analysis] measures; it does not screen for cancer, diagnose it or treat it, and results go to your physician.

• Laboratory panels can add fasting insulin, C-peptide and high-sensitivity C-reactive protein to glucose, A1c and lipids, putting insulin resistance and inflammation on paper. The pattern is described in what insulin resistance looks like before diabetes.
• Bioimpedance body composition estimates how much of your weight is fat and how much is muscle, which BMI cannot do. It estimates compartments rather than imaging them, so it cannot map the fat packed around your organs the way a scan can; why that deep fat matters is covered in visceral fat vs subcutaneous fat.

Questions worth bringing to your next visit: Am I due for colorectal cancer screening, given my age and family history? What is my fasting insulin, as a number? Do I meet the definition of metabolic syndrome? More prompts are in questions worth asking your doctor, and the background is in insulin resistance and metabolic health.

Frequently asked questions

References

• Islami, F., Marlow, E. C., Thomson, B., McCullough, M. L., Rumgay, H., Gapstur, S. M., Patel, A. V., Soerjomataram, I., & Jemal, A. (2024). Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States, 2019. CA: A Cancer Journal for Clinicians, 74(5), 405-432. https://doi.org/10.3322/caac.21858
• Gunter, M. J., & Berrington de Gonzalez, A. (2024). Is obesity a cause of all cancer types? The Lancet Regional Health – Europe, 46, 101110. https://doi.org/10.1016/j.lanepe.2024.101110
• Watts, E. L., Gonzalez-Feliciano, A., Gunter, M. J., Chatterjee, N., & Moore, S. C. (2026). Adiposity and cancer: systematic review and meta-analysis. Nature Metabolism, 8(6), 1426-1439. https://doi.org/10.1038/s42255-026-01542-8
• Watts, E. L., Gonzalez-Feliciano, A., Gunter, M. J., Chatterjee, N., & Moore, S. C. (2026). Adiposity and cancer: epidemiology, mechanisms and future perspectives. Nature Metabolism, 8(6), 1266-1281. https://doi.org/10.1038/s42255-026-01529-5
• Zhan, Z. Q., Chen, Y. Z., Huang, Z. M., Luo, Y. H., Zeng, J. J., Wang, Y., Tan, J., Chen, Y. X., & Fang, J. Y. (2024). Metabolic syndrome, its components, and gastrointestinal cancer risk: a meta-analysis of 31 prospective cohorts and Mendelian randomization study. Journal of Gastroenterology and Hepatology, 39(4), 630-641. https://doi.org/10.1111/jgh.16477
• Du, M., Drew, D. A., Goncalves, M. D., Cao, Y., & Chan, A. T. (2025). Early-onset colorectal cancer as an emerging disease of metabolic dysregulation. Nature Reviews Endocrinology, 21(11), 686-702. https://doi.org/10.1038/s41574-025-01159-z
• Wang, H., Wu, C., Zhou, S., Shi, Y., Cheng, L., Cao, H., Zhang, Y., & Gao, S. (2026). Body mass index and early-onset colorectal cancer risk: a systematic review and cohort-based meta-analysis. Scandinavian Journal of Gastroenterology, 61(4), 383-396. https://doi.org/10.1080/00365521.2026.2615397
• Kumar, R., Brown, A., Okano, S., Simms, L., Lord, A., O’Sullivan, T., Hartel, G., & Radford-Smith, G. L. (2024). Overweight and obesity are associated with colorectal neoplasia in an Australian outpatient population. Scientific Reports, 14(1), 23501. https://doi.org/10.1038/s41598-024-74042-y
• Min, J., Jenkins, M. A., & Meyers, A. L. (2026). Early-onset colorectal cancer burden attributable to early-life obesity from 2000 to 2020 with projections to 2040. Cancer Epidemiology, 105, 103219. https://doi.org/10.1016/j.canep.2026.103219
• Bendor, C. D., Bardugo, A., Tsur, A. M., Derazne, E., Shemesh, I. I., Bourvine, L., et al. (2026). Adolescent to adulthood weight trajectories and the risk of obesity-related cancers, overall and early-onset: a population-based cohort study. EClinicalMedicine, 91, 103711. https://doi.org/10.1016/j.eclinm.2025.103711

Related reading

• Visceral Fat vs Subcutaneous Fat: What Testing Can Show
• What Insulin Resistance Looks Like Before Diabetes
• Laboratory Panels

Nutrition Before Surgery: What to Have Measured While You Wait

Nutrition before surgery shapes how you heal: malnourished spine surgery patients had 2.10 times the odds of wound complications and 2.77 times the odds of sepsis. The standard preoperative workup checks your heart and lungs for anesthesia, not the materials you need to heal.

An elective operation comes with a date. The weeks before it are the only stretch when your muscle, nutrients and energy use can be measured, and those numbers shape how you heal.

Nutrition before surgery gets treated as a dietitian’s problem, reserved for frail, underweight patients in hospital beds. That framing is wrong: you close a surgical wound, fight infection and rebuild strength with the protein, muscle and micronutrients you carry through the door, and the standard preoperative workup is built to confirm your heart and lungs can handle anesthesia, not to check whether you brought the materials to heal.

What poor nutrition does to recovery

The clearest numbers come from spine surgery. A 2026 review pooled 37 studies that together included 16,987 malnourished patients. Compared with well-nourished patients, those who were malnourished had 1.79 times the odds of surgical complications, 2.10 times the odds of wound complications, 2.77 times the odds of sepsis and 4.05 times the odds of dying. Their odds of delirium were 3.95 times higher and their odds of a prolonged hospital stay 3.46 times higher. If a spine operation is on your calendar, the broader question of what counts as success is covered in lumbar fusion success rate: what to measure before you decide.

Older adults having bone and joint operations show the same pattern. Across 11 studies with 201,338 older orthopedic surgery patients, malnutrition picked up by a screening tool went with 1.65 times the risk of complications and 2.17 times the risk of death after surgery. In hip and knee replacement, a low score on the Geriatric Nutritional Risk Index went with 1.59 times the odds of a surgical site infection across 221,810 patients.

Frailty multiplies it. In 1,361 adults aged 65 or older having elective surgery, the people who were both malnourished and frail before the operation had 5.36 times the risk of dying within a year and 4.83 times the odds of major complications, compared with people who were neither.

Malnourished does not have to mean thin

Many people picture malnutrition as someone visibly wasting away. The measurements say otherwise. A 2026 review of knee replacement studies covering more than 93,000 patients found that people with sarcopenia, meaning too little muscle, had more complications, falls, fractures and repeat operations, and regained knee motion and walking speed more slowly, particularly when low muscle came together with obesity. A larger body can hold a small muscle reserve, and a bathroom scale cannot tell the difference. The same gap between weight and nourishment is explained in can you be overweight and malnourished.

Two biological forces drain those stores at once, and they feed each other. Metaflammation, the low-grade inflammation that travels with excess body fat and with chronic pain, keeps pulling on protein. Pain cuts how much you move, so muscle wastes in exactly the months a joint or spine is failing, and a smaller muscle reserve leaves less to draw on when the operation adds its own stress. The third force is the system. Surgical scheduling runs on a date and a clearance form, and the clearance form has no line for muscle, nutrients or energy use. Nobody fills in a box that does not exist. Clinicians screening for this pattern have a separate guide in screening for malnutrition when a patient has obesity.

Why one blood number is not enough

Blood albumin, a protein made by the liver, is the shortcut the system reaches for, because it is already on the panel. It does carry a signal. Across 40 studies with 477,701 patients, low albumin before surgery went with 2.88 times the odds of lung complications and death after general anesthesia, and 4.03 times in orthopedic surgery. Yet the reviewers of the orthopedic studies pointed out that single blood values such as albumin forecast complications with limited precision. A normal albumin does not prove you are well nourished, and a low one does not say what is missing. That is why screening tools combine several measures, and why muscle, nutrients and energy use are worth measuring directly.

Why measuring first changes the plan

Some of this risk responds to the weeks before the date. A 2024 Cochrane review of 16 randomized trials with 2,164 people having digestive surgery found that standard oral nutrition drinks made little difference to complications when well-nourished and malnourished patients were pooled together. In the patients who were already malnourished or losing weight, the same drinks probably reduced infections, with a risk ratio of 0.58. A separate 2024 analysis of 12 trials with 1,201 patients having surgery for digestive cancers found that nutrition supplements taken before surgery lowered infectious complications, with an odds ratio of 0.63, and raised albumin, although hospital stays were no shorter. Both reviews studied digestive surgery, so the metabolically complex patient headed for a joint or spine operation is barely represented. Trials are built that way to get a clean answer; the physiology still applies to you, and your own numbers are how you find out whether it does.

This is the part most patients never hear. The benefit showed up in the people who were actually short. So the first question is not what to eat before surgery. It is whether you are short at all, and on what, and nobody can answer that from your weight. Get the answer while there is still time on the calendar to act on it, and put it in front of the surgeon and physician who will decide what to do with it. Many people facing joint surgery also carry a metabolic driver in those joints, described for physicians in metabolic osteoarthritis screening.

What a routine preoperative visit checks, and what it misses

A typical preoperative evaluation reviews your heart and lungs, your medications and a basic blood panel, and it records your weight. What it usually leaves out is any measurement of muscle, a look at nutrient status beyond that basic panel, and a number for how much energy your body actually burns.

Measura [Cardiometabolic and Autonomic Health Analysis] measures and reports to your physician; it does not operate, prescribe or clear anyone for surgery. Three of its measurements fit the weeks before an elective procedure:

• Bioimpedance body composition estimates muscle, fat and water separately while you stand on a platform for a couple of minutes, so a low muscle reserve shows up even when your weight looks ample. The difference is laid out in body composition, not BMI.
• Laboratory panels can include nutrient markers such as vitamin B12, zinc and red blood cell magnesium, inflammatory markers such as C-reactive protein and ferritin, and blood sugar alongside insulin. Albumin and vitamin D come from the blood work your physician orders.
• Indirect calorimetry measures your resting energy use from the air you breathe in and out, which gives any nutrition plan a real starting number instead of an estimate.

Repeated under the same conditions before the date, these turn a vague instruction to eat well into numbers that can be checked. Unmeasured is unmanaged, and an elective operation is the rare situation where you know exactly how long you have to measure.

Questions to bring to your surgeon or physician

• Has my nutrition been screened, and with which tool?
• Is my muscle mass known, or only my weight?
• Would my albumin, vitamin D or B12 change anything about timing or preparation?
• If my results show a shortfall, is there time to address it before the date, and who will manage that?
• Who will look at my results again before the operation?

More prompts are collected in questions worth asking your doctor.

Frequently asked questions

References

• Ashraf, A., Kaghazchi, A., Jelkin, G., Karnati, J., Lunasco, L., Abid, S., et al. (2026). Malnutrition and adverse outcomes after spine surgery: a systematic review and meta-analysis. The Spine Journal, 26(10), 2045-2074. https://doi.org/10.1016/j.spinee.2026.06.015
• Li, D., Shi, J., Zheng, J., & Hu, Y. (2026). Nutritional screening tools as predictors of surgical outcomes in geriatric orthopedic patients: a meta-analysis. Aging Clinical and Experimental Research, 38(1), 51. https://doi.org/10.1007/s40520-025-03306-y
• Du, M., Liu, T., Liu, Y., Guo, J., Ma, X., Zhai, L., et al. (2026). Preoperative GNRI and surgical site infection risk after total joint arthroplasty: A systematic review and meta-analysis. Biomolecules & Biomedicine, 26(10), 1706-1719. https://doi.org/10.17305/bb.2026.13414
• Dong, L., Hu, B., Wen, F., Shi, S., Liang, Y., Qin, L., et al. (2026). Association between malnutrition and frailty and postoperative mortality in older surgical patients. Clinical Nutrition, 63, 106695. https://doi.org/10.1016/j.clnu.2026.106695
• Za, P., Minelli, M., Esposito, C., Longobardi, V., Vasta, S., Calafiore, G., & Della Rocca, F. (2026). Sarcopenia and Postoperative Outcomes Following Total Knee Arthroplasty: A Systematic Review of Observational Studies. Journal of Clinical Medicine, 15(14). https://doi.org/10.3390/jcm15145523
• Wang, X., Tang, H., Zheng, M., & Xu, F. (2026). Hypoalbuminaemia contributes to postoperative pulmonary complications and mortality: a systematic review and meta-analysis. BMC Anesthesiology, 26(1). https://doi.org/10.1186/s12871-025-03329-y
• Sowerbutts, A. M., Burden, S., Sremanakova, J., French, C., Knight, S. R., & Harrison, E. M. (2024). Preoperative nutrition therapy in people undergoing gastrointestinal surgery. Cochrane Database of Systematic Reviews, 4, CD008879. https://doi.org/10.1002/14651858.CD008879.pub3
• Zou, Q., Yin, Z., Ding, L., Ruan, J., Zhao, G., Wang, X., et al. (2024). Effect of preoperative oral nutritional supplements on clinical outcomes in patients undergoing surgery for gastrointestinal cancer: A systematic review and meta-analysis. Medicine, 103(39), e39844. https://doi.org/10.1097/MD.0000000000039844

Related reading

• Can You Be Overweight and Malnourished? What Your Numbers Show
• Lumbar Fusion Success Rate: What to Measure Before You Decide
• Bioimpedance Body Composition

Ketones as Brain Fuel: The Entrance Insulin Resistance Cannot Close

Ketones fuel the brain without insulin: they enter nerve cells through carriers that depend on neither insulin nor the GLUT4 glucose transporter. When insulin resistance closes part of the glucose supply to the memory circuits, ketones still get in.

The memory circuits partly depend on an insulin-sensitive glucose door. Ketones use a different entrance, and that single difference explains why researchers keep testing them in the insulin-resistant brain.

An insulin-resistant brain is not out of fuel; it is locked out of one fuel while the other sits in the bloodstream unused. Using ketones for brain fuel matters because they walk in through an entrance insulin does not guard, while in the memory circuits the glucose doors partly answer to insulin. That is plumbing, not diet-book language, and the insulin side of it shows up on fasting laboratory panels. When insulin signaling fails, that difference decides whether a nerve cell is starving or simply switching fuels. Measura [Cardiometabolic and Autonomic Health Analysis] does not prescribe diets or supply ketones; it measures the insulin and fuel picture that makes the question relevant to you.

Two fuels, two ways in

Most of the time the brain burns glucose. Transporter proteins carry it across the blood-brain barrier and into cells, and most of that traffic does not need insulin. The exception matters. Nerve cells in the hippocampus, the structure that turns experience into memory, also use an insulin-responsive glucose transporter called GLUT4 when demand spikes, the way a grocery store opens extra checkout lanes at rush hour. If insulin stops working, those extra lanes stay closed exactly when the line is longest.

Ketones, mainly beta-hydroxybutyrate and acetoacetate, are made by the liver from fat when insulin runs low: overnight, during longer fasts or with carbohydrate restriction. They enter nerve cells through a separate family of carriers that depends on neither GLUT4 nor insulin. That independence is the reason researchers began asking whether ketones could keep an insulin-resistant brain running. How normal ketosis differs from the medical emergency of ketoacidosis is explained in ketosis vs ketoacidosis.

What happened when the insulin door was shut

This is mouse work. In a 2024 study, researchers at the University of Rochester and Stony Brook University took thin slices of mouse hippocampus and chemically blocked GLUT4, creating a short-term version of insulin resistance in living tissue. The circuit linking two hippocampal regions, called CA3 and CA1, degraded in several ways at once. Synaptic activity fell. Long-term potentiation, the strengthening of connections that underlies learning, weakened. Signals traveled along nerve fibers less reliably, and groups of cells fell out of step with one another.

Then the researchers added D-beta-hydroxybutyrate, the main ketone the body makes. It did not restore everything, but it rescued conduction along the fibers, the synchronization between cells and long-term potentiation. The non-obvious point is where the rescue landed. Memory depends on timing, on many cells firing together within thousandths of a second, and timing is expensive. When fuel runs short, precision fails long before cells die. A brain with enough energy on paper can still lose the synchrony that learning requires.

A slice of mouse tissue is not a person. Human trials of ketones usually isolate one diagnosis and exclude the metabolically complicated patient, so the mechanism has to carry more of the explanation here than it would in a simpler field. Why the insulin gate deserves a blood test of its own is argued in fasting insulin as an early screen.

Human brains: glucose uptake falls, ketone uptake holds

A research group in Sherbrooke, Quebec, measured both fuels in living brains using PET scans with two tracers, one for glucose and one for the ketone acetoacetate. In 10 people with mild Alzheimer’s disease, average age 76, compared with 29 cognitively normal adults, average age 75, gray matter took up 13% less glucose. Ketone uptake did not differ. In a second comparison of 24 healthy older adults, 20 with mild cognitive impairment and 19 with early Alzheimer’s disease, a glucose shortfall of about 7% had already appeared in one region, the cingulate gyrus, at the mild impairment stage, while ketone metabolism still matched the healthy group.

Supply mattered as much as access. When people with mild to moderate Alzheimer’s disease took 30 g a day of a medium-chain triglyceride supplement for one month, brain ketone consumption doubled without any change in brain glucose use. In adults with mild cognitive impairment randomized to a ketogenic drink or placebo, brain ketone metabolism rose by 230% after 6 months, and several memory, language and processing-speed scores improved from baseline. The deficit in these brains is specific to glucose, and the second entrance stays open. Whether a whole diet does the same in daily life is covered in what to measure before believing keto helps Alzheimer’s.

Brain networks in living adults, and a limit worth knowing

The Stony Brook group had earlier asked whether fuel type changes how brain networks hold together. Using imaging datasets of 292 and 636 adults spanning young adulthood to old age, they found that network stability, the ability of brain regions to stay in sustained communication, declined with age and tracked cognitive sharpness. In younger adults scanned in an ultrahigh-field scanner, networks became less stable after glucose and more stable with ketones, whether ketosis came from a ketogenic diet or from a ketone ester drink.

Newer work tested people closer to the question. In a 2025 randomized crossover trial of 10 adults with metabolic syndrome and 10 matched adults without it, working memory improved after a single ketone ester drink in both groups. The limit is instructive too. In a 12-week pilot in community-dwelling adults aged 65 and older who were healthy and independent, a daily ketone ester did not change exploratory measures of function or quality of life. Extra fuel appears to matter most where fuel is short, which is exactly why knowing whether your insulin system is failing comes first. The tissue evidence for that failing insulin system is traced in what brain tissue shows about insulin resistance in Alzheimer disease.

Why the insulin entrance closes in the first place

Three forces do most of the work, two of them biological. The first is constant insulin: a pancreas that answers every snack keeps insulin elevated, and cells exposed to a signal that never stops learn to ignore it. The second is metaflammation, the low-grade inflammatory output of overfilled visceral fat, which interferes with the same relay proteins insulin needs inside the cell. The third force is social. Food is engineered and sold to be eaten from waking to bedtime, and a day without a real fasting gap is a day the liver never makes ketones at all. The brain was built to alternate fuels; the modern schedule rarely lets it. How that plays out across the whole body is laid out in insulin resistance and metabolic health. Repeated glucose spikes damage more than the brain, starting with the lining inside every blood vessel.

What a standard visit checks, and what can be measured

A routine visit reports fasting glucose and sometimes hemoglobin A1c. Neither says how much insulin it took to hold glucose there, and nothing in a standard workup shows which fuel your body is burning. Measura measures; it does not treat, and results go to your physician.

• Insulin behind the glucose. Laboratory panels can include fasting insulin alongside glucose and hemoglobin A1c. A blood ketone level, if wanted, is blood work your physician orders.
• Which fuel you burn at rest. Indirect calorimetry measures oxygen used and carbon dioxide produced after a fast and reports a respiratory quotient, which indicates whether you are predominantly burning fat or carbohydrate. The practical side is in metabolic rate and energy.
• A memory starting point. Cognitive assessment records attention, memory and executive function so that any later change is measured against you.

If you take medication for diabetes or blood pressure, any change in eating that raises ketones is a conversation with your prescriber before it starts. Unmeasured is unmanaged, and the brain’s second fuel is only an option for someone who knows the first one is failing.

Frequently asked questions

References

• Kula, B., Antal, B., Weistuch, C., Gackière, F., Barre, A., Velado, V., Hubbard, J. M., Kukley, M., Mujica-Parodi, L. R., & Smith, N. A. (2024). D-ꞵ-hydroxybutyrate stabilizes hippocampal CA3-CA1 circuit during acute insulin resistance. PNAS Nexus, 3(5), pgae196. https://doi.org/10.1093/pnasnexus/pgae196
• Castellano, C. A., Nugent, S., Paquet, N., Tremblay, S., Bocti, C., Lacombe, G., et al., & Cunnane, S. C. (2015). Lower brain 18F-fluorodeoxyglucose uptake but normal 11C-acetoacetate metabolism in mild Alzheimer’s disease dementia. Journal of Alzheimer’s Disease, 43(4), 1343-1353. https://doi.org/10.3233/JAD-141074
• Croteau, E., Castellano, C. A., Fortier, M., Bocti, C., Fulop, T., Paquet, N., & Cunnane, S. C. (2018). A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s disease. Experimental Gerontology, 107, 18-26. https://doi.org/10.1016/j.exger.2017.07.004
• Croteau, E., Castellano, C. A., Richard, M. A., Fortier, M., Nugent, S., Lepage, M., et al., & Cunnane, S. C. (2018). Ketogenic Medium Chain Triglycerides Increase Brain Energy Metabolism in Alzheimer’s Disease. Journal of Alzheimer’s Disease, 64(2), 551-561. https://doi.org/10.3233/JAD-180202
• Fortier, M., Castellano, C. A., Croteau, E., Langlois, F., Bocti, C., St-Pierre, V., et al., & Cunnane, S. C. (2019). A ketogenic drink improves brain energy and some measures of cognition in mild cognitive impairment. Alzheimer’s & Dementia, 15(5), 625-634. https://doi.org/10.1016/j.jalz.2018.12.017
• Mujica-Parodi, L. R., Amgalan, A., Sultan, S. F., Antal, B., Sun, X., Skiena, S., et al., & Clarke, K. (2020). Diet modulates brain network stability, a biomarker for brain aging, in young adults. Proceedings of the National Academy of Sciences of the United States of America, 117(11), 6170-6177. https://doi.org/10.1073/pnas.1913042117
• Graybeal, A. J., Aultman, R. S., Brandner, C. F., Vallecillo-Bustos, A., Compton, A. T., Swafford, S. H., Newsome, T. A., & Stavres, J. (2025). Effects of Ketone Ester Supplementation on Cognition and Appetite in Individuals with and Without Metabolic syndrome: A Randomized Trial. Journal of Dietary Supplements, 22(3), 382-400. https://doi.org/10.1080/19390211.2025.2473371
• Stubbs, B. J., Stephens, E. B., Mansfield, T., Senadheera, C., Diaz, S. R., Peralta, S., et al. (2025). Exploratory functional and quality of life outcomes with daily consumption of the ketone ester bis-octanoyl (R)-1,3-butanediol in healthy older adults: a randomized, parallel arm, double-blind, placebo-controlled, pilot study. The Journal of Frailty & Aging. https://pubmed.ncbi.nlm.nih.gov/41313689/

Related reading

• Keto Diet and Alzheimer’s: What to Measure Before You Believe It
• Ketosis vs Ketoacidosis: What the Numbers Actually Mean
• Laboratory Panels

Brain Insulin Resistance in Alzheimer Disease: Why Type 3 Diabetes

Brain insulin resistance in Alzheimer disease means the brain both makes less insulin and stops answering it, a pattern found in donated brain tissue even from people without diabetes. That is why the disease was named type 3 diabetes.

The label came from pathologists holding brain tissue, not from a glucose meter. What they found explains why a normal blood sugar result says little about the brain’s insulin system.

Alzheimer’s disease earned a diabetes name in a pathology lab, not at a glucose meter. Brain insulin resistance in Alzheimer disease was documented in donated brain tissue, including tissue from people whose charts said they never had diabetes, yet routine care still screens the brain’s fuel problem with a blood sugar test. Measura [Cardiometabolic and Autonomic Health Analysis] cannot look inside a living brain, but it can measure the body-wide insulin picture that travels with it on fasting laboratory panels, years before anyone thinks to ask.

Where the name type 3 diabetes came from

In 2005, a team working in Suzanne de la Monte’s laboratory in Providence, Rhode Island, measured the genes that make insulin and its close relatives, the insulin-like growth factors, along with the receptors that receive those signals. Nerve cells normally make some of these hormones themselves. In brains with Alzheimer’s disease, production was sharply reduced, and so were the receptors and the relay proteins that carry the message inward. The researchers described the disease as a hormonal disorder of the brain that resembles diabetes without being identical to it, and they proposed the term type 3 diabetes.

The combination is the point. Diabetes fails in two ways, too little insulin or cells that stop answering it, and the Alzheimer’s brains were doing both at once.

What the tissue showed: a message that will not pass

Low production was only half the story. In 2012, a group led by Konrad Talbot and Steven Arnold studied the hippocampus, the brain’s memory center, from people who had died with Alzheimer’s disease. Its response to insulin signaling was markedly weakened. The breakdown sat at a relay protein called IRS-1, which sits just inside the cell and passes the insulin signal along. In Alzheimer’s tissue, that relay carried chemical tags that switch it off.

Picture a phone call that connects, rings once and goes dead at the switchboard. Insulin arrives, the receptor picks up, and the relay drops the line.

Three details lift this work above a curiosity. The people studied did not have diabetes. The off-switch tags rose step by step from normal brains to brains with mild cognitive impairment to brains with Alzheimer’s disease, whether or not the person carried the APOE4 risk gene. And the tags tracked worse memory during life even after the researchers accounted for plaques and tangles, the classic hallmarks of the disease. The same tags also rose with small clumps of amyloid, which suggests the damage runs both ways: amyloid may jam the relay, and a jammed relay may speed decline. Physicians can see the screening side of this in screening for insulin resistance past the glucose.

Insulin resistance in a brain without diabetes

This is the part a normal blood sugar result cannot address. Newer autopsy work from the Religious Orders Study, older members of Catholic religious orders in the United States who agreed to yearly testing and brain donation, sharpened the picture. Researchers examined the prefrontal cortex of 150 people, 75 with diabetes matched to 75 without, whose thinking had been tested for a mean of 9.4 years before death.

The surprising result: brains with more activity at a downstream insulin switch called AKT belonged to people whose memory and overall thinking had declined faster. A signal stuck in the on position is not a healthy signal. It behaves like a car alarm that never stops, which the neighbors soon learn to ignore. A 2025 follow-up in 116 members of the same study found that a growth-factor binding protein tied to Alzheimer’s disease partly carried that relationship, one more sign that the insulin system and the disease process are tangled together.

The evidence tier, stated once: autopsy tissue shows what was present at death and cannot prove which change came first. It does establish that the brain’s insulin machinery is abnormal in Alzheimer’s disease, and that the abnormality does not wait for a diabetes diagnosis. Research cohorts also favor clean diagnoses. The patient carrying fatty liver, high blood pressure, poor sleep and a thick waist at once, the one with the most insulin in the bloodstream, is the patient these studies were least built to see, so the mechanism has to be applied to that patient rather than waited on. Because the brain can still take up ketones when insulin signaling fails, how ketones reach an insulin-resistant brain is the natural next question.

The same pattern in living people, years earlier

Studies in living people use a stand-in called HOMA-IR, a calculation from fasting glucose and fasting insulin that estimates how hard the body is working to keep glucose normal. In Australian adults whose thinking was normal, higher HOMA-IR went with weaker verbal memory, executive function and overall cognition, and with more tau protein in spinal fluid. What that estimate means for your own body is covered in insulin resistance and metabolic health.

A Finnish study followed the question across two decades. Researchers selected 43 participants by their HOMA-IR at a mean age of 55.1 and tested them again late in life. Over a 5-year stretch ending at a mean age of 74.8, those who had been insulin resistant in midlife lost more episodic memory, the ability to recall events, than those who had been insulin sensitive, and amyloid build-up carried part of that link. For physicians, the broader list of changeable dementia risks is sorted by what a visit can measure in modifiable dementia risk in primary care.

Why the brain’s insulin problem goes unmeasured

For years I told patients with borderline blood sugar that their results were not too bad. The tissue work above is part of why I stopped. Two biological forces run under a reassuring glucose: a body pouring out extra insulin to hold glucose in range, and a brain whose insulin relay is being jammed by that flood and by amyloid. A third force is not biological at all. The food supply delivers acellular carbohydrate from breakfast to bedtime, the standard visit is built around glucose and hemoglobin A1c because those numbers define diabetes, and memory is handled in a different office from metabolism. Nobody is assigned to the space between them, where insulin resistance before diabetes quietly builds.

What a routine visit checks, and what a measurement can show

No test can see insulin signaling inside a living person’s hippocampus. The tissue studies were done after death, and the brain scans used in research are performed at imaging centers, not by Measura. What can be measured is the body-wide terrain the tissue keeps pointing to, plus a starting point for memory.

• Blood work. Laboratory panels can include fasting insulin and fasting glucose, the two inputs to HOMA-IR, the estimate the cohort studies used, alongside hemoglobin A1c.
• A thinking baseline. Cognitive assessment records memory, attention and executive function today, so a later score is compared with your own starting point. More is in memory and cognitive screening.

Measura measures; it does not diagnose Alzheimer’s disease, and results go to your physician. How a normal glucose can hide the insulin side is covered in type 3 diabetes and a normal blood sugar test.

The lesson in the name is timing. The tissue shows the insulin relay failing in people without diabetes, and the living cohorts show midlife insulin resistance predicting memory loss decades later. Muscle is the body’s largest glucose sink, and working muscle can pull glucose in through a route that needs less insulin, which is one physiological reason movement and a lighter carbohydrate load reduce the insulin your pancreas must produce. Those levers belong in a conversation with your physician, and they are easier to use when you know where your numbers start. Unmeasured is unmanaged. Questions worth bringing:

• Has my fasting insulin ever been measured, or only my glucose?
• Do we have a record of my memory and thinking to compare against later?

Frequently asked questions

References

• Steen, E., Terry, B. M., Rivera, E. J., Cannon, J. L., Neely, T. R., Tavares, R., Xu, X. J., Wands, J. R., & de la Monte, S. M. (2005). Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease–is this type 3 diabetes? Journal of Alzheimer’s Disease, 7(1), 63-80. https://doi.org/10.3233/jad-2005-7107
• Talbot, K., Wang, H. Y., Kazi, H., Han, L. Y., Bakshi, K. P., Stucky, A., et al., & Arnold, S. E. (2012). Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of Clinical Investigation, 122(4), 1316-1338. https://doi.org/10.1172/JCI59903
• Tong, H., Capuano, A. W., Carmichael, O. T., Gwizdala, K. L., Bennett, D. A., Ahima, R. S., Arnold, S. E., & Arvanitakis, Z. (2024). Brain Insulin Signaling is Associated with Late-Life Cognitive Decline. Aging and Disease, 15(5), 2205-2215. https://doi.org/10.14336/AD.2023.1117
• Tong, H., Petyuk, V. A., Sendtner, M., Sood, A., Bennett, D. A., Capuano, A. W., & Arvanitakis, Z. (2025). Alzheimer’s disease-related cortical proteins modify the association of brain insulin signaling with cognitive decline. Journal of Alzheimer’s Disease, 104(3), 667-677. https://doi.org/10.1177/13872877251319463
• Laws, S. M., Gaskin, S., Woodfield, A., Srikanth, V., Bruce, D., Fraser, P. E., et al., & Verdile, G. (2017). Insulin resistance is associated with reductions in specific cognitive domains and increases in CSF tau in cognitively normal adults. Scientific Reports, 7(1), 9766. https://doi.org/10.1038/s41598-017-09577-4
• Pietilä, E., Karrasch, M., Helin, S., Snellman, A., Viitanen, M., Jula, A., Rinne, J. O., & Ekblad, L. L. (2026). Midlife insulin resistance and brain beta-amyloid accumulation as predictors of change in late-life cognitive function – A 20-year follow-up study. Neurobiology of Aging, 167, 29-41. https://doi.org/10.1016/j.neurobiolaging.2026.06.004

Related reading

• Type 3 Diabetes: What a Normal Blood Sugar Test Can Miss
• Insulin Resistance and Dementia: Screening Past the Glucose
• Laboratory Panels

Sugar and Gum Inflammation: The Gauge in Your Mouth

Sugar drives gum inflammation: young adults eating the most added sugar had about 1.42 times the rate of gum disease, and cutting refined carbohydrate cut gum bleeding by more than half while plaque stayed the same.

Your gums are the only inflamed tissue you can look at in a mirror. When they bleed, the question worth asking is what else in you is running hot.

Almost every tissue that sugar inflames is hidden. Sugar and gum inflammation is the exception: the gums are the one inflamed surface in your body you can look at in a mirror, and they bleed on contact when something is wrong. That makes them a gauge, and it makes the standard advice about them oddly small. Brush better, floss more, come back in six months. The gauge is reporting on your metabolism, and almost nobody reads it that way, even though the blood markers of insulin resistance and inflammation are a routine draw.

What the mouth evidence actually shows

Start with intake rather than brushing. Among 2437 adults aged 18 to 25 in the third National Health and Nutrition Examination Survey, those in the highest third of added sugar consumption had about 1.42 times the prevalence of periodontal disease compared with the lowest, after adjustment for smoking, poverty, education, body mass index and known diabetes. The association was stronger the more teeth were involved, at about 1.73 times for disease in two or more teeth. In a later analysis of the same survey covering 4473 adults aged 30 to 50, the heaviest sugar-sweetened beverage drinkers carried roughly 2.19 times the odds of periodontitis.

Those are observational, and diet questionnaires are blunt instruments. The experiments that follow are small and short, and none was built around the patient with diabetes, obesity and a long medication list, because trials isolate one variable and that patient is the one they leave out. They push the same way under control. In a randomized pilot, adults who switched for 4 weeks to a diet low in refined carbohydrate and richer in omega-3 fats, vitamins C and D, antioxidants and fiber cut bleeding on probing from 53.57% of sites to 24.17%, while their plaque scores did not change. A second randomized trial of an anti-inflammatory diet reproduced the drop in gum bleeding, again with plaque unchanged.

The strangest result is the most instructive. Ten volunteers lived for 4 weeks in a reconstructed Stone Age settlement with no toothbrushes, no floss and no refined sugar. Plaque rose, as it must, from 0.68 to 1.47 on the index used. Bleeding fell anyway, from 34.8% of sites to 12.6%. Plaque was not what drove the inflammation; what the plaque was being fed was.

Two engines, one visible symptom

The first engine is local and microbial. Fermentable sugar arriving several times a day shifts which organisms thrive in the film on your teeth and below the gumline, and the shifted community is the one that provokes an immune response. Brushing is necessary and not sufficient: you are removing a film whose composition is set by what you eat.

The second engine is systemic, and it has a name: metaflammation. Excess fructose and sucrose produce low-grade inflammation throughout the body and shift both the oral and the intestinal microbial community, so the gums are inflamed by something that is also inflaming tissue you cannot see. Your gut is the first brain in this sequence, taking delivery of the load; the mouth is the window onto it. The third driver is neither microbial nor metabolic. Added sugar is built into most packaged and restaurant food, so the exposure repeats whether or not anyone chose it. That is an engineering decision made upstream of your kitchen, which is why measuring the host rather than the additive is the practical response. Inside the arteries, a thin sugar coating takes the same hit after every spike, described in the lining that high blood sugar strips first.

The number the dental chart cannot give you

In 3616 adults without diabetes in the continuous National Health and Nutrition Examination Survey for 1999 to 2004, insulin resistance rose with the depth of the pockets around the teeth: each additional millimeter of average probing depth went with a 1.04-fold higher insulin resistance score. The association concentrated in people whose white cell count was already high, where the deepest quartile of probing depth carried about 2.60 times the risk of marked insulin resistance. Inflammation was both the middle step and the condition that decided who was affected. Glucose can sit in range through all of it, which is why fasting insulin beside a normal A1C says more.

A small pilot took the question to people in their early twenties. Of 20 patients with no diabetes diagnosis, the high-sugar group had a mean insulin resistance score of 2.52 against 1.60 in the low-sugar group, and their measured area of inflamed gum ran 329.44 square millimeters against 54.02. That is cross-sectional and tiny, a direction rather than a finding.

The longitudinal evidence is what changed recently. A 2026 systematic review of 28 longitudinal studies covering more than 300,000 participants found that people with periodontitis at the start were 18 to 25% more likely to be newly diagnosed with type 2 diabetes during follow-up, with the relationship running both ways. In a Korean national cohort of 43,713 adults followed for up to nine years, severe periodontitis carried about a 1.10-fold higher risk of developing metabolic syndrome, strongest in people in their fifties. Bleeding gums prove nothing metabolic in any one person. Across populations, they run ahead of trouble. Joints that carry no weight tell a similar metabolic story, covered for clinicians in metabolic screening in hand osteoarthritis.

What a routine visit checks, and what it leaves out

Your dentist measures pocket depth, bleeding and bone loss. Your physician records weight and blood pressure and may order a glucose or an A1C. Both are doing their jobs, and the two charts rarely meet. Nothing in that sequence asks the question the evidence raises: is the inflammation in this person’s mouth keeping company with insulin resistance, an inflammatory signal in the blood, and fat in the wrong compartment? Who should be tested lists the patterns that justify asking.

Measuring the body the gums belong to

Say the limit first. Measura [Cardiometabolic and Autonomic Health Analysis] does not examine gums, does not probe pockets and has no saliva or microbial test. A dentist or periodontist does that work, and nothing here replaces it. Measura is a testing service that measures the body those gums belong to and sends findings to your physician.

• Laboratory panels cover fasting insulin reported beside glucose and A1C, and inflammatory markers including high-sensitivity C-reactive protein. Insulin rises years before glucose moves, which is the window the studies above describe.
• Bioimpedance body composition separates fat from muscle, so a normal weight stops standing in for a normal metabolism.

One timing detail: an inflammatory marker drawn the day after a deep cleaning reads high because of the cleaning, so space them. For the sugar side in more depth, does sugar cause inflammation follows fructose through the liver and the fat cell, and gum disease and dementia handles the brain claim and what the evidence supports. Why the pull toward sugar is not a willpower story is covered in what causes sugar cravings.

What to ask for, at two appointments

At the dentist, ask for a full-mouth examination rather than a spot check, and ask for your bleeding percentage, so you have a number to compare later. At your physician, ask for fasting insulin alongside glucose and an inflammatory marker, and say out loud that your gums bleed, because that sentence rarely reaches a medical chart.

Then change the input, not just the brushing. The diet experiments above halved gum bleeding in four weeks with no change in hygiene, which makes your own gums a fast, visible check on whether a dietary change reached your tissues. Results go to your physician, who decides what they mean, and medication changes belong in that conversation. Insulin resistance and metabolic health explains what the blood work looks for. Unmeasured is unmanaged, and this is the rare case where the first gauge is one you can read yourself.

Frequently asked questions

References

• Shanmugasundaram, S., & Karmakar, S. (2024). Excess dietary sugar and its impact on periodontal inflammation: a narrative review. BDJ Open, 10(1), 78. https://doi.org/10.1038/s41405-024-00265-w
• Lula, E. C., Ribeiro, C. C., Hugo, F. N., Alves, C. M., & Silva, A. A. (2014). Added sugars and periodontal disease in young adults: an analysis of NHANES III data. The American Journal of Clinical Nutrition, 100(4), 1182-1187. https://doi.org/10.3945/ajcn.114.089656
• Alves-Costa, S., Nascimento, G. G., Peres, M. A., Li, H., Costa, S. A., Ribeiro, C. C. C., & Leite, F. R. M. (2024). Sugar-sweetened beverage consumption and periodontitis among adults: A population-based cross-sectional study. Journal of Clinical Periodontology, 51(6), 712-721. https://doi.org/10.1111/jcpe.13961
• Demmer, R. T., Squillaro, A., Papapanou, P. N., Rosenbaum, M., Friedewald, W. T., Jacobs, D. R., & Desvarieux, M. (2012). Periodontal infection, systemic inflammation, and insulin resistance: results from the continuous National Health and Nutrition Examination Survey (NHANES) 1999-2004. Diabetes Care, 35(11), 2235-2242. https://doi.org/10.2337/dc12-0072
• Woelber, J. P., Bremer, K., Vach, K., Konig, D., Hellwig, E., Ratka-Kruger, P., Al-Ahmad, A., & Tennert, C. (2016). An oral health optimized diet can reduce gingival and periodontal inflammation in humans – a randomized controlled pilot study. BMC Oral Health, 17(1), 28. https://doi.org/10.1186/s12903-016-0257-1
• Woelber, J. P., Gartner, M., Breuninger, L., Anderson, A., Konig, D., Hellwig, E., Al-Ahmad, A., Vach, K., Dotsch, A., Ratka-Kruger, P., & Tennert, C. (2019). The influence of an anti-inflammatory diet on gingivitis. A randomized controlled trial. Journal of Clinical Periodontology, 46(4), 481-490. https://doi.org/10.1111/jcpe.13094
• Baumgartner, S., Imfeld, T., Schicht, O., Rath, C., Persson, R. E., & Persson, G. R. (2009). The impact of the stone age diet on gingival conditions in the absence of oral hygiene. Journal of Periodontology, 80(5), 759-768. https://doi.org/10.1902/jop.2009.080376
• Caleb, C. L., Dharuman, S., Sundhar, M. P., Chellapandi, S., & Balaji, U. G. (2025). Evaluation of the association between insulin resistance and the development of periodontitis in individuals with varying levels of dietary sugar intake – A pilot study. Journal of Indian Society of Periodontology, 29(3), 279-283. https://doi.org/10.4103/jisp.jisp_125_24
• Botelho, J., Singh, S., Varenne, B., Rendell, N., Harada, Y., Proenca, L., Machado, V., & Valentim Bitencourt, F. (2026). Oral health and diabetes: a systematic review and meta-analysis. The Lancet Public Health, 11(8), e555-e566. https://doi.org/10.1016/S2468-2667(26)00149-0
• Hwang, S., Kim, H. Y., Kang, S., Kim, J., Song, S., & Park, G. R. (2026). Association of periodontitis with incidence of metabolic syndrome in Korea: A retrospective cohort study. Journal of Periodontology. https://doi.org/10.1002/jper.70169

Related reading

• Does Sugar Cause Inflammation? What Your Numbers Can Show
• Gum Disease and Dementia: What Is Proven and What to Measure
• Laboratory Panels

Can Belly Fat Cause Chronic Pain? What 32,409 MRI Scans Show

Belly fat is tied to chronic pain: in abdominal MRI scans of 32,409 adults, more visceral and subcutaneous fat meant pain in more parts of the body, most strongly in women.

Aching in your back, knees and shoulders at once gets filed under getting older. Large MRI studies point to a different common thread: where your body stores fat.

Can belly fat cause chronic pain? When your back, knees and shoulders all hurt at once, you leave with three explanations, three referrals and the word arthritis. Abdominal MRI scans of 32,409 adults point to one common thread instead: the fat stored deep inside your abdomen rises in step with the number of places that hurt, most of all in women, and a scale cannot see it, though a body composition test gets you closer.

What the MRI study measured

Researchers at the University of Tasmania used the UK Biobank, a long-running British health study, to examine adults who had abdominal MRI scans (50.8% women, average age 55.0). The scans split belly fat into two compartments. Visceral fat sits inside the abdominal wall, packed around the intestines and liver. Subcutaneous fat sits under the skin, the part you can pinch. Participants reported pain in the neck or shoulder, back, hip or knee, or pain all over the body, and many were scanned and questioned again at a second imaging visit.

As each type of fat went up, the count of painful sites went up with it, step by step, in both sexes. Higher levels of adipose tissue were also associated with greater odds of reporting chronic pain in both sexes, not just pain in more places.

Visceral fat, subcutaneous fat and pain in women and men

• Women. Each standard-deviation rise in visceral fat came with 2.04 times the odds of pain in more sites. For subcutaneous fat the figure was 1.60.
• Men. The odds rose 1.34 times for visceral fat and 1.39 times for subcutaneous fat.

The ratio of visceral to subcutaneous fat tracked pain as well, and the authors attribute the larger effect in women to sex differences in fat storage and hormones. Why the two compartments behave differently is covered in the difference between visceral and subcutaneous fat.

In men, the pinchable fat under the skin carried as much pain risk as the deep fat around the organs. The comfortable story that outer fat is the harmless kind collapses the moment you ask about pain.

This is an observational study, and the arrow runs both ways: pain cuts movement, stillness stores fat, fat feeds pain. What the data demolish is the idea that aching in four places is four separate cases of wear and tear.

Why fat in the belly makes the whole body hurt

A knee carries body weight. A neck does not carry more of it when your waist grows, yet the neck hurt more too. Load cannot explain that. Something traveling in the blood can, and the authors conclude that fat stored where it does not belong is involved in how multisite pain develops.

Two biological drivers run the cascade. The first is fat behaving as an organ. Swollen fat tissue around the abdomen releases inflammatory messengers into the circulation, a steady low-grade fire called metaflammation, and inflamed nerve endings fire at lower thresholds, so ordinary pressure and ordinary movement start to register as pain. The second is insulin. Deep abdominal fat and a fat-loaded liver force the pancreas to pour out more insulin to keep blood sugar normal, and that strained metabolism starves small nerves and slows the repair of muscles and tendons after every day of use.

The third driver is economic, and it is the one nobody writes on a prescription pad. Agricultural subsidies make acellular carbohydrates and industrial seed oils the most available calories in the country, most jobs keep people seated all day, and a person who already hurts moves less and sleeps worse. Every one of those loads the abdominal depot. None of it is a willpower failure. It is a food system and a work system doing exactly what they were built to do. Chronic stress feeds the same depot through its own hormonal loop, traced in how cortisol and belly fat feed each other. The timing of the stress response matters as much as its size, which is where gut bacteria and the daily stress rhythm come in.

What your weight and BMI cannot tell you

A second UK Biobank analysis looked at 500,107 adults aged 40 to 69 and compared ways of describing body fat. Body fat percentage measured by bioimpedance, a small electrical signal passed through the body, correlated with body mass index at 0.85 in women and 0.80 in men. Total fat and body mass index mostly tell the same story. Shape told a different one: waist-to-hip ratio was the only measure still tied to a higher risk of death after full adjustment, 1.21 in women and 1.19 in men when the highest and lowest ends of the range were compared.

A third analysis of abdominal MRI from 33,889 UK Biobank participants linked visceral fat, fat infiltrating the muscles along the spine, and chronic back pain in both sexes. Your scale answers how much. Your pain is answering where. The practical ways to measure the second question are laid out in how to measure visceral fat when the scale says you are fine. Clinicians have a waist-to-weight ratio that flags this depot in older patients with high blood pressure, described in the weight-adjusted waist index and stroke.

What happens to pain when the weight comes off

For years I treated the joint that hurt and handed the waistline a pamphlet. The trial evidence has made that division indefensible. In STEP 9, 407 adults with obesity and painful knee osteoarthritis (81.6% women, average body mass index 40.3) were followed for 68 weeks. Everyone received counseling on physical activity and a reduced-calorie diet; two thirds also received a weekly weight-loss injection and the rest a placebo. Weight fell 13.7% with the drug and 3.2% with placebo. On a pain scale of 0 to 100, pain dropped 41.7 points with the drug and 27.5 points with placebo.

Look hard at the placebo group: a modest loss on counseling alone, and their pain still fell. The people who lost the most weight hurt the least. Nothing here is a reason to start or stop any medication; that decision belongs to you and your physician.

No trial has yet tested whether shrinking visceral fat eases pain in several body sites, because trials enroll one diagnosis at a time and screen out the person with metabolic disease, obesity and pain in four places, the exact person the MRI study describes. The mechanism has to carry the decision. Movement, sleep and food are treatment, each with a physiological why: contracting muscle pulls sugar out of the blood without extra insulin, deep sleep lowers the inflammatory tone that sensitizes nerves, and cutting acellular carbohydrates lowers the insulin load that locks fat in the abdominal depot. The fat that drives pain is also tied to cancer risk, laid out in how weight and metabolic dysfunction connect to cancer.

What measurement can show

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service. It measures, it does not treat, and results go to your physician. It does not perform MRI; imaging that separates visceral from subcutaneous fat is done elsewhere. What Measura adds in the same person:

• Bioimpedance body composition estimates fat mass and muscle mass separately. It cannot isolate visceral fat, but repeat tests show whether you are losing muscle while keeping fat.
• Laboratory panels can include fasting insulin and high-sensitivity C-reactive protein, the metabolic and inflammatory output of that fat, which a glucose-only panel never sees.

How pain and metabolism connect in everyday care is covered in chronic pain and metabolic health. Unmeasured is unmanaged, and a pain nobody traces to its terrain gets managed forever.

What to ask at your next visit

• Has anyone measured where my fat sits, or only what I weigh?
• Can my blood work include fasting insulin and an inflammation marker, not just glucose?
• If I lose weight, how will we know whether it came from fat or from muscle?

More questions worth bringing are in questions to ask a pain management doctor about your numbers, and holding on to a loss once it happens is covered in how to maintain weight loss when the scale stops telling the truth.

Frequently asked questions

References

• Kifle, Z. D., Tian, J., Aitken, D., Melton, P. E., Cicuttini, F., Jones, G., & Pan, F. (2026). MRI-derived abdominal adipose tissue is associated with multisite and widespread chronic pain. Regional Anesthesia and Pain Medicine, 51(4), 371-378. https://doi.org/10.1136/rapm-2024-105535
• Wiebe, N., & Tonelli, M. (2025). Associations of body fat and inflammation with non-communicable chronic diseases and mortality: a prospective cohort study of the UK Biobank. BMJ Open, 15(10), e092962. https://doi.org/10.1136/bmjopen-2024-092962
• Niglas, M., Whitcher, B., Amiras, D., Thanaj, M., Basty, N., Bell-Bradford, C., Thomas, E. L., & Bell, J. D. (2026). Detecting scoliosis at scale using automated cobb angle analysis in the UK biobank. European Spine Journal. https://doi.org/10.1007/s00586-026-10239-1
• Bliddal, H., Bays, H., Czernichow, S., Uddén Hemmingsson, J., Hjelmesæth, J., Hoffmann Morville, T., Koroleva, A., Skov Neergaard, J., et al. (2024). Once-weekly semaglutide in persons with obesity and knee osteoarthritis. The New England Journal of Medicine, 391(17), 1573-1583. https://doi.org/10.1056/NEJMoa2403664

Related reading

• How to Measure Visceral Fat When the Scale Says You’re Fine
• Cortisol and Belly Fat: What Chronic Stress Leaves You Can Measure
• Bioimpedance Body Composition

How to Maintain Weight Loss When the Scale Stops Telling the Truth

To maintain weight loss, measure more than weight: repeat body composition to see whether fat or muscle came back, a laboratory panel for insulin and glycemic drift, and resting energy use measured by indirect calorimetry. There is no fixed end point; the workload falls with time, but the checking does not.

Losing the weight is the part everyone plans for. The year after, when support thins out and only the scale is watching, is where most results quietly leak away.

Most people who lose weight get one instruction for afterward: keep weighing yourself. That makes the scale the maintenance instrument, and the scale is the one number that cannot tell you whether you kept the right thing. If you are searching how to maintain weight loss, the better question is what is actually holding underneath the pounds a year later.

The video There Is No Discharge Date, from The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, answers a patient who is finally well and wants to know when he can stop. He cannot stop, but the work gets lighter each year. Measurement is how you confirm it is getting lighter without sliding backward.

Why maintenance fails quietly

Two biological drivers pull a body back toward where it started. The first lives in the gut, the first brain. Its microbial community answers to food on a clock measured in days: volunteers moved onto an animal-based diet with almost no fiber saw their community shift within a day and swing back two days after the diet ended. The deeper arrangement of that community, its enterotype, follows years of eating instead. A vacation moves the quick layer. A decade of habit moves the slow one. The second brain, in your skull, receives reports from both.

The second driver is insulin resistance and the low-grade inflammation that rides along with it, metaflammation. Neither shows up on a scale. In mice, a microbiome altered by earlier obesity persisted after successful dieting, sped up regain, and passed that tendency on to mice raised without their own microbes, with the regain traced to lower flavonoid levels and reduced energy expenditure. That is animal work with no human confirmation yet, and it is still the clearest mechanism on record for why a body does not simply stay where the diet left it.

The third driver is economic. Pooled studies set a helpful daily fiber target of 25 to 29 grams, far above what most Americans eat, because the cheap default in the grocery store is refined starch with the husk removed. Maintenance programs are then built as if people will keep showing up on their own.

What the long trials say about keeping it off

The landmark prevention trial gave adults with impaired glucose tolerance a 7% weight-loss target and 150 minutes of weekly activity. New diabetes fell by 58%, against 31% on metformin. Fifteen years later the gap had narrowed: cumulative diabetes reached 55% with lifestyle, 56% on metformin and 62% on placebo. Participants who never developed diabetes, whatever arm they were in, showed 28% fewer complications in the small blood vessels, so the result a person reached mattered more than the group they started in.

In adults who already had type 2 diabetes, intensive support produced 8.6% weight loss at one year, which wore down to 6.0% against 3.5% in the comparison group, and the trial was stopped for futility at 9.6 years. In the national prevention program, 35.5% of enrollees hit the 5% goal, median attendance was 14 sessions, and every extra session attended went with another 0.3% of body weight lost.

Put those side by side and one pattern stands out. Intensity fades, and results fade with it. That is not a judgment about willpower. It is a dosing problem, and a dosing problem can be tracked.

What a routine follow-up checks, and what it misses

A typical maintenance visit records weight, blood pressure and perhaps a glucose marker. Each has value. None of them answers the questions that decide whether the loss is holding in the way that protects you:

• What came back, fat or muscle? The two read the same on a bathroom scale and mean very different things for your metabolism.
• Is the metabolic load drifting? Blood sugar can sit in range while the underlying insulin resistance creeps back.
• Has resting energy use changed? A formula assumes an average body. Yours just changed shape.

Tissue shows what a delivered dose can do. In a 52-week study of people with steatohepatitis confirmed on biopsy, 25% saw the liver inflammation resolve overall, yet among those who lost 10% or more of their weight, 90% had resolution and 45% had scarring regress. Liver biopsy and liver imaging are separate tests done elsewhere, not Measura tests. The lesson is that the amount of change delivered, not the name of the plan, moved the tissue.

How to maintain weight loss over time

Measura [Cardiometabolic and Autonomic Health Analysis] is a testing service. It measures and sends the findings to your physician; it does not diagnose disease or treat it. For someone in the maintenance phase, four measurements line up with the drivers above:

• Bioimpedance body composition estimates fat mass and lean mass separately, so a repeat test shows which one moved. More on that in body composition, not BMI.
• Laboratory panels follow glycemic markers, insulin and lipids from one visit to the next, where drift can appear while weight still looks steady.
• Indirect calorimetry measures your resting energy use from the air you breathe instead of estimating it from height and weight.
• Heart rate variability gives a reading of autonomic tone, the nervous traffic that runs between the first brain and the second.

No single result is the point. The same measurements, repeated, make change visible while it is still small. Timing is covered in how often to repeat cardiometabolic testing.

Adherence is the dose, and it can be seen

For years I ended visits by jotting a line about eating better and moving more, and I counted it as a plan. It was a wish with no instrument attached. What changed my mind was watching numbers follow what people actually did rather than what they were told. In a year-long Mediterranean diet trial in older adults, microbial change scaled with how closely people followed the diet, not with their assigned group, and the favored organisms tracked with less frailty and lower inflammatory markers.

Food tools also do different jobs in the first brain. In a seventeen-week trial in healthy adults, fiber expanded the community’s machinery for breaking down complex carbohydrates without raising diversity, while fermented food raised diversity and lowered 19 of 93 circulating inflammatory proteins. No Measura test reads your microbiome; stool and breath tests are done elsewhere. What a repeat visit can follow is the metabolic picture downstream of it.

Capability counts as well. Among insured patients in primary care, activation, the know-how and confidence to run your own care, lined up with 12 of 13 outcomes in the expected direction. A report you can read for yourself feeds that directly, and understanding your results walks through one.

What to ask at your next visit

• Can my follow-up include body composition, not just weight?
• Can insulin be checked alongside my glucose markers, and repeated on a schedule?
• What is the smallest version of this plan I could still be doing a year from now?
• If adding fiber makes me feel worse, is the order of the plan the problem rather than the fiber?

No discharge date does not mean effort forever at the same level. It means the effort shrinks while the checking continues. The barrier work this maintenance protects is in the gut-wall post, and the people who stay unwell anyway are the subject of how to test for mast cell activation. The Chapter 30 Deep Dive carries each study cited here along with what it cannot show.

Frequently asked questions

References

• Knowler, W. C., Barrett-Connor, E., Fowler, S. E., Hamman, R. F., Lachin, J. M., Walker, E. A., Nathan, D. M., & Diabetes Prevention Program Research Group. (2002). Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med, 346(6), 393-403. https://doi.org/10.1056/NEJMoa012512
• Diabetes Prevention Program Research Group. (2015). Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over 15-year follow-up: the Diabetes Prevention Program Outcomes Study. Lancet Diabetes Endocrinol, 3(11), 866-75. https://doi.org/10.1016/S2213-8587(15)00291-0
• Wing, R. R., Bolin, P., Brancati, F. L., Bray, G. A., Clark, J. M., Coday, M., Crow, R. S., Curtis, J. M., Egan, C. M., Espeland, M. A., Evans, M., Foreyt, J. P., Ghazarian, S., Gregg, E. W., Harrison, B., Hazuda, H. P., Hill, J. O., Horton, E. S., Hubbard, V. S., … Yanovski, S. Z. (2013). Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med, 369(2), 145-54. https://doi.org/10.1056/NEJMoa1212914
• Ely, E. K., Gruss, S. M., Luman, E. T., Gregg, E. W., Ali, M. K., Nhim, K., Rolka, D. B., & Albright, A. L. (2017). A National Effort to Prevent Type 2 Diabetes: Participant-Level Evaluation of CDC’s National Diabetes Prevention Program. Diabetes Care, 40(10), 1331-1341. https://doi.org/10.2337/dc16-2099
• Thaiss, C. A., Itav, S., Rothschild, D., Meijer, M. T., Levy, M., Moresi, C., Dohnalova, L., Braverman, S., Rozin, S., Malitsky, S., Dori-Bachash, M., Kuperman, Y., Biton, I., Gertler, A., Harmelin, A., Shapiro, H., Halpern, Z., Aharoni, A., Segal, E., & Elinav, E. (2016). Persistent microbiome alterations modulate the rate of post-dieting weight regain. Nature, 540(7634), 544-551. https://doi.org/10.1038/nature20796
• Vilar-Gomez, E., Martinez-Perez, Y., Calzadilla-Bertot, L., Torres-Gonzalez, A., Gra-Oramas, B., Gonzalez-Fabian, L., Friedman, S. L., Diago, M., & Romero-Gomez, M. (2015). Weight Loss Through Lifestyle Modification Significantly Reduces Features of Nonalcoholic Steatohepatitis. Gastroenterology, 149(2), 367-78.e5. https://doi.org/10.1053/j.gastro.2015.04.005
• Ghosh, T. S., Rampelli, S., Jeffery, I. B., Santoro, A., Neto, M., Capri, M., Giampieri, E., Jennings, A., Candela, M., Turroni, S., Zoetendal, E. G., Hermes, G. D. A., Elodie, C., Meunier, N., Brugere, C. M., Pujos-Guillot, E., Berendsen, A. M., De Groot, L. C. P. G. M., Feskins, E. J. M., … O’Toole, P. W. (2020). Mediterranean diet intervention alters the gut microbiome in older people reducing frailty and improving health status: the NU-AGE 1-year dietary intervention across five European countries. Gut, 69(7), 1218-1228. https://doi.org/10.1136/gutjnl-2019-319654
• Wastyk, H. C., Fragiadakis, G. K., Perelman, D., Dahan, D., Merrill, B. D., Yu, F. B., Topf, M., Gonzalez, C. G., Van Treuren, W., Han, S., Robinson, J. L., Elias, J. E., Sonnenburg, E. D., Gardner, C. D., & Sonnenburg, J. L. (2021). Gut-microbiota-targeted diets modulate human immune status. Cell, 184(16), 4137-4153.e14. https://doi.org/10.1016/j.cell.2021.06.019
• David, L. A., Maurice, C. F., Carmody, R. N., Gootenberg, D. B., Button, J. E., Wolfe, B. E., Ling, A. V., Devlin, A. S., Varma, Y., Fischbach, M. A., Biddinger, S. B., Dutton, R. J., & Turnbaugh, P. J. (2014). Diet rapidly and reproducibly alters the human gut microbiome. Nature, 505(7484), 559-63. https://doi.org/10.1038/nature12820
• Greene, J., & Hibbard, J. H. (2012). Why does patient activation matter? An examination of the relationships between patient activation and health-related outcomes. J Gen Intern Med, 27(5), 520-6. https://doi.org/10.1007/s11606-011-1931-2

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• How to Test for MCAS When Your Allergy Tests Keep Coming Back Negative
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Probiotics After Antibiotics: What Recovery Actually Looks Like

In the strongest study of probiotics after antibiotics, a multi-strain capsule delayed the return of the gut’s native community compared with recovering unaided, while a transplant of the person’s own banked stool restored it within days. That study measured composition, not symptoms, so track recovery with a dated symptom log and repeated measures of function.

The course worked, the bloating left, and weeks later it came back. What refills a gut after antibiotics can be studied, and the part of you a stool report never sees can be measured.

The question of probiotics after antibiotics tends to arrive the same week a course ends, when a patient wants something to put back. In The Weeds Were Never the Problem, the chapter video from The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, the example is a woman of fifty-five on her third round of treatment for small intestinal bacterial overgrowth. Each course cleared the problem. Each good stretch afterward was shorter than the last. That shrinking stretch is the most honest number in her chart, and it is one she can count herself.

Probiotics after antibiotics: what the strongest study found

The best test of that question followed people through three paths after a drug course: recover without help, take a multi-strain probiotic, or receive back their own stool, banked before the antibiotics. The capsule strains did settle into the gut lining. Yet compared with unaided recovery, the native community and the body’s own gene activity returned in a way the authors called markedly delayed and persistently incomplete. Autologous stool restored both within days.

Read the limits before the headline. That study measured which organisms were present and what the gut tissue was expressing, not symptoms, infections or anything a patient feels. It does not prove a capsule makes a person sicker. It shows that adding a handful of passing strains is not the same as rebuilding a resident community, and that a supplement can slow the rebuild.

Why an emptied gut refills with the wrong crowd

An antibiotic removes more than the overgrowth. It also clears the residents that normally keep newcomers from taking hold, a defense called colonization resistance. The organisms quickest to return tolerate bile and oxygen and often carry resistance genes, while the bacteria that make butyrate, a fuel for the colon lining, grow slowly and strictly without oxygen. They lose a race that starts on an empty field.

A deliberate experiment in healthy young men who took four days of three last-resort antibiotics showed the shape of it. Overall composition drifted back toward baseline within roughly six weeks. At 180 days, though, most of the men were still missing nine species that all of them had carried before treatment, and species holding beta-lactam resistance genes had been favored during the refill. The first brain, rebuilt by whatever arrives fastest, does not simply return to where it was, and the second brain lives downstream of that terrain.

A stool report is a roster, not a function test

Stool microbiome panels, breath tests and endoscopy are different tests done elsewhere. Measura [Cardiometabolic and Autonomic Health Analysis] does not sequence stool, measure intestinal gases or scope the bowel. That matters less than it sounds, because a list of names answers a narrower question than most people expect. In one capsule transplant trial in irritable bowel syndrome, the transplant measurably raised fecal diversity, and quality of life at three months still favored placebo. Membership rose. Function did not.

The food data make the same point from the other side. In a trial of healthy adults who had taken no antibiotic, more than doubling fiber intake, from 21.5 to 45.1 grams a day, left diversity unchanged across the group. Eating 6.3 servings of fermented food a day raised it, and 19 of 93 inflammatory serum proteins fell, although that trial missed its own primary outcome. No study has yet tested fermented food for repopulation after an eradication course; that is a gap in trial design, not a verdict on the biology.

Count the interval, not the organisms

After one course cleared the breath test, the test was positive again at three months for 12.6% of patients, and the share climbed to 27.5% by six months and 43.7% by nine. Those three checkpoints are where recurrence was actually measured, so they are the sensible places to look again. Clearance and recovery also split apart: only 67.7% of patients with confirmed clearance reported feeling better.

The predictors were not microbes. Long-term use of a proton pump inhibitor, an acid-reducing drug, raised the odds of recurrence more than threefold, and a history of appendix removal carried close to six times the odds. Whether an acid reducer is still needed is a conversation for the prescribing physician, never a reason to stop one alone. There is an economic tilt as well: a branded antibiotic comes with trials, packaging and a sales force, while a jar of fermented milk has no sponsor, so what goes back in after the drug rarely gets studied or discussed. For years the kill got counted as the win, and the good weeks were nobody’s metric.

What Measura can put a number on while the gut rebuilds

Measura measures the host rather than the microbes. Judged by function, recovery is what your body does across those months, and several parts of that are measurable. Laboratory panels put metabolic and inflammatory markers in front of your physician, the metaflammation picture a gut-focused workup often leaves out. Bioimpedance body composition tracks muscle and fat compartments, which matters when months of symptoms have reshaped how and what someone eats. Heart rate variability describes autonomic tone, the nervous system’s regulation of heart rhythm and recovery.

None of these tells anyone whether overgrowth has returned; that remains a breath test your physician orders elsewhere. What they provide is a record of how you are functioning at the same checkpoints, so a flat breath test and a body that is still struggling are not confused with each other. Findings go to your physician. Keep your own log alongside: how many good weeks the last course bought, written as a number. The studies behind every figure here, with their populations and limits, are in the chapter companion, and the case for measuring before treating comes first.

Frequently asked questions

References

• Suez, J., Zmora, N., Zilberman-Schapira, G., Mor, U., Dori-Bachash, M., Bashiardes, S., Zur, M., Regev-Lehavi, D., Ben-Zeev Brik, R., Federici, S., Horn, M., Cohen, Y., Moor, A. E., Zeevi, D., Korem, T., Kotler, E., Harmelin, A., Itzkovitz, S., Maharshak, N., … Elinav, E. (2018). Post-antibiotic gut mucosal microbiome reconstitution is impaired by probiotics and improved by autologous FMT. Cell, 174(6), 1406-1423.e16. https://doi.org/10.1016/j.cell.2018.08.047
• Caballero-Flores, G., Pickard, J. M., & Núñez, G. (2022). Microbiota-mediated colonization resistance: mechanisms and regulation. Nature Reviews Microbiology, 21(6), 347-360. https://doi.org/10.1038/s41579-022-00833-7
• Palleja, A., Mikkelsen, K. H., Forslund, S. K., Kashani, A., Allin, K. H., Nielsen, T., Hansen, T. H., Liang, S., Feng, Q., Zhang, C., Pyl, P. T., Coelho, L. P., Yang, H., Wang, J., Typas, A., Nielsen, M. F., Nielsen, H. B., Bork, P., Wang, J., … Pedersen, O. (2018). Recovery of gut microbiota of healthy adults following antibiotic exposure. Nature Microbiology, 3(11), 1255-1265. https://doi.org/10.1038/s41564-018-0257-9
• Halkjær, S. I., Christensen, A. H., Lo, B. Z. S., Browne, P. D., Günther, S., Hansen, L. H., & Petersen, A. M. (2018). Faecal microbiota transplantation alters gut microbiota in patients with irritable bowel syndrome: results from a randomised, double-blind placebo-controlled study. Gut, 67(12), 2107-2115. https://doi.org/10.1136/gutjnl-2018-316434
• Wastyk, H. C., Fragiadakis, G. K., Perelman, D., Dahan, D., Merrill, B. D., Yu, F. B., Topf, M., Gonzalez, C. G., Van Treuren, W., Han, S., Robinson, J. L., Elias, J. E., Sonnenburg, E. D., Gardner, C. D., & Sonnenburg, J. L. (2021). Gut-microbiota-targeted diets modulate human immune status. Cell, 184(16), 4137-4153.e14. https://doi.org/10.1016/j.cell.2021.06.019
• Lauritano, E. C., Gabrielli, M., Scarpellini, E., Lupascu, A., Novi, M., Sottili, S., Vitale, G., Cesario, V., Serricchio, M., Cammarota, G., Gasbarrini, G., & Gasbarrini, A. (2008). Small intestinal bacterial overgrowth recurrence after antibiotic therapy. The American Journal of Gastroenterology, 103(8), 2031-5. https://doi.org/10.1111/j.1572-0241.2008.02030.x
• Gatta, L., & Scarpignato, C. (2017). Systematic review with meta-analysis: Rifaximin is effective and safe for the treatment of small intestine bacterial overgrowth. Alimentary Pharmacology & Therapeutics, 45(5), 604-616. https://doi.org/10.1111/apt.13928
• van Nood, E., Vrieze, A., Nieuwdorp, M., Fuentes, S., Zoetendal, E. G., de Vos, W. M., Visser, C. E., Kuijper, E. J., Bartelsman, J. F. W. M., Tijssen, J. G. P., Speelman, P., Dijkgraaf, M. G. W., & Keller, J. J. (2013). Duodenal infusion of donor feces for recurrent Clostridium difficile. The New England Journal of Medicine, 368(5), 407-15. https://doi.org/10.1056/NEJMoa1205037

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What Causes Sugar Cravings? The Numbers a Scale Cannot Show

Sugar cravings come mainly from what you have been eating and the signals your gut sends, not from character: on an ultra-processed menu, adults ate about 508 more calories a day, and eight weeks of a daily high-fat, high-sugar snack rewrote food preferences with no change in weight.

A craving that shows up at four in the afternoon and again after nine is not random. Anything that keeps a timetable has machinery behind it, and part of that machinery can be measured.

Ask most people what causes sugar cravings and the answer comes back as a verdict on character. The research points somewhere less insulting and far more useful. What you have been eating rewrites what you want, the first brain in your gut files a report on every meal with the second brain in your skull, and the metabolic cost can pile up while your weight sits still. That last part is a measuring problem. If the bathroom scale is the only number anyone checks, the changes that matter most never get recorded. The video Your Sugar Craving Has a Schedule traces the gut route; the question here is what could actually be put on paper for you.

What causes sugar cravings that keep a timetable

The pattern described in The Angry Gut is precise. The pull arrives late in the afternoon and again at night. It wants sweet and starchy food and almost never protein. It fades after a couple of weeks of better eating, then returns within days of one bad weekend. A character trait does not switch on and off like that. A system answering to its recent diet does.

A controlled ward study shows how strong the food effect is. Twenty adults were admitted and offered either ultra-processed or unprocessed meals that matched on everything a label lists, then allowed to eat as much as they liked. On the ultra-processed menu they took in roughly 508 more calories every day. Their weight went up 0.9 kg over two weeks and came back down when the menu changed. Nothing about the people changed between those two weeks. Only the food did.

Why can appetite change before your weight does?

A second experiment is the one that should retire the willpower speech for good. Adults of normal weight ate a daily high-fat, high-sugar snack for eight weeks. Afterward they liked low-fat food less and their brains reacted more strongly to food cues, and none of that tracked their body weight or the metabolic markers the team followed. The appetite had been rewritten with nothing to show for it on a scale.

A sweetener trial adds a second warning. Forty-five adults who did not usually drink sweeteners had a series of sweetened drinks. Sucralose on its own left insulin sensitivity alone. Sucralose arriving together with a carbohydrate lowered it. The gut judged what was delivered, not what the taste promised. In a small teenage arm that was halted for safety, HOMA-IR, a blood-based estimate of insulin resistance, jumped past 12.9 from a starting point under 3.5 in two of the three participants. That is too few people to call a result, and it leans the same way as the adult data.

I told patients for years to eat less and try harder, and I thought that was help. I was handing an instruction to an organ that does not take instructions. The snack study changed my mind because preference moved while the scale did not.

What does a routine checkup miss about sugar cravings?

A standard visit usually records weight and blood pressure and may add a glucose check. Those numbers are worth having. They were also not where the changes above showed up. The snack study moved appetite and brain response with weight flat, and the sweetener study moved insulin sensitivity in about ten days, a shift no scale can register.

Food addiction, the label many people with cravings are handed, is scored with a questionnaire. Pooled across 272 studies, about 20% of people meet its criteria, rising to 55% among people already diagnosed with binge eating. There is no blood test behind that score, and researchers still disagree about whether it names a disease at all.

Then there is the driver no lab report prints. Refined carbohydrate is the cheapest calorie on the shelf because farm policy made it cheap, and it is built to win the exact contest those studies measured. The exposure is subsidized, and the patient is billed for a personality defect.

What can testing show about sugar cravings?

Measura [Cardiometabolic and Autonomic Health Analysis] does not test gut bacteria, does not score food addiction and does not treat cravings. It measures, and the results go to your physician. Three measurements fit the questions a scheduled craving raises.

• Laboratory panels can look at glucose and insulin together, so the question becomes how hard your body is working to keep sugar in range, not only whether it is high yet. More on that terrain is in insulin resistance and metabolic health.
• Indirect calorimetry measures the energy you burn at rest from the air you breathe, instead of guessing it from a formula. When a ward study finds hundreds of extra calories eaten on processed food, your own measured burn turns a vague argument into arithmetic. See measured versus estimated metabolic rate.
• Heart rate variability records beat-to-beat variation that reflects autonomic balance. The vagus nerve carries gut signals toward the brainstem, but this measure does not read cravings. It gives a baseline for the nervous system those signals travel through.

Where the gut bacteria fit, and where the proof ends

The bold claim is that gut microbes steer your appetite. In humans, the firmest finding is about one bacterial product. Propionate, a fatty acid bacteria make from fiber, was delivered directly to the colon in healthy men, and their intake at a buffet-style meal fell 9.5% while a reward region of the brain cooled toward pictures of high-calorie food. Feeding bacteria 30 g of inulin a day in 59 overweight adults also quieted reward regions, but the planned eating outcome came out null.

No human study has shown a defined microbial change producing a craving. Among 105 women, food addiction scores lined up with obesity and with four bacterial genera, at one moment in time. That is mechanism and association, stated as such, and it is still the best guide for real patients who arrive with insulin resistance, poor sleep and a medication list that would bar them from any tidy trial. The practical lever does not depend on the bacteria anyway: stop feeding refined carbohydrate every day and the organisms that thrive on it lose their edge, while the insulin resistance and metaflammation that daily habit sustains lose their fuel.

What to bring to your next appointment

• The clock times your cravings arrive and what, exactly, you reach for.
• Whether sweetened drinks usually come alongside starchy food.
• What happened the last time you ate well for two straight weeks.
• A question: can my insulin be measured along with my glucose?
• A second question: has my resting metabolic rate ever been measured, or only estimated?

Every study above, with its population and limits, is in the Angry Gut companion deep dive on cravings. The next measuring question, what a gut test can and cannot tell you, is in the methane breath test explained. How sugar feeds inflammation is covered in does sugar cause inflammation, and physicians can read the screening version for practices.

Frequently asked questions

References

• Hall, K. D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K. Y., Chung, S. T., Costa, E., Courville, A., Darcey, V., Fletcher, L. A., Forde, C. G., Gharib, A. M., Guo, J., Howard, R., Joseph, P. V., McGehee, S., Ouwerkerk, R., Raisinger, K., … Zhou, M. (2019). Ultra-processed diets cause excess calorie intake and weight gain: an inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism, 30(1), 67-77.e3. https://doi.org/10.1016/j.cmet.2019.05.008
• Edwin Thanarajah, S., DiFeliceantonio, A. G., Albus, K., Kuzmanovic, B., Rigoux, L., Iglesias, S., Hanßen, R., Schlamann, M., Cornely, O. A., Brüning, J. C., Tittgemeyer, M., & Small, D. M. (2023). Habitual daily intake of a sweet and fatty snack modulates reward processing in humans. Cell Metabolism, 35(4), 571-584.e6. https://doi.org/10.1016/j.cmet.2023.02.015
• Dalenberg, J. R., Patel, B. P., Denis, R., Veldhuizen, M. G., Nakamura, Y., Vinke, P. C., Luquet, S., & Small, D. M. (2020). Short-term consumption of sucralose with, but not without, carbohydrate impairs neural and metabolic sensitivity to sugar in humans. Cell Metabolism, 31(3), 493-502.e7. https://doi.org/10.1016/j.cmet.2020.01.014
• Praxedes, D. R. S., Silva-Júnior, A. E., Macena, M. L., Oliveira, A. D., Cardoso, K. S., Nunes, L. O., Monteiro, M. B., Melo, I. S. V., Gearhardt, A. N., & Bueno, N. B. (2022). Prevalence of food addiction determined by the Yale Food Addiction Scale and associated factors: a systematic review with meta-analysis. European Eating Disorders Review, 30(2), 85-95. https://doi.org/10.1002/erv.2878
• Byrne, C. S., Chambers, E. S., Alhabeeb, H., Chhina, N., Morrison, D. J., Preston, T., Tedford, C., Fitzpatrick, J., Irani, C., Busza, A., Garcia-Perez, I., Fountana, S., Holmes, E., Goldstone, A. P., & Frost, G. S. (2016). Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods. The American Journal of Clinical Nutrition, 104(1), 5-14. https://doi.org/10.3945/ajcn.115.126706
• Medawar, E., Beyer, F., Thieleking, R., Haange, S.-B., Rolle-Kampczyk, U., Reinicke, M., Chakaroun, R., von Bergen, M., Stumvoll, M., Villringer, A., & Witte, A. V. (2024). Prebiotic diet changes neural correlates of food decision-making in overweight adults: a randomised controlled within-subject cross-over trial. Gut, 73(2), 298-310. https://doi.org/10.1136/gutjnl-2023-330365
• Dong, T. S., Mayer, E. A., Osadchiy, V., Chang, C., Katzka, W., Lagishetty, V., Gonzalez, K., Kalani, A., Stains, J., Jacobs, J. P., Longo, V. D., & Gupta, A. (2020). A distinct brain-gut-microbiome profile exists for females with obesity and food addiction. Obesity, 28(8), 1477-1486. https://doi.org/10.1002/oby.22870
• Fletcher, P. C., & Kenny, P. J. (2018). Food addiction: a valid concept?. Neuropsychopharmacology, 43(13), 2506-2513. https://doi.org/10.1038/s41386-018-0203-9

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What Does Bile Do? It Gives Your Liver Its Orders

Bile emulsifies fat, but its main job is signaling: it tells your liver when to stop and your gut hormones when to fire. Remove the reservoir and the timing changes, which is measurable in some ways and not others.

What does bile do? Almost every answer you have been handed is about grease: bile breaks up fat so you can absorb it. That is true and it is the small half of the job. Bile also carries instructions, and the organ it instructs is your liver. Bile Is a Hormone, Not Soap, the Chapter 23 video for The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, works through the biology. The measuring question is the one worth bringing to an appointment: which parts of this can be put on a number, and which cannot.

What does bile do? It sends instructions, not just detergent

Put a primary bile acid onto human ileal tissue, the last stretch of small intestine, at a dose an ordinary meal produces, and the gene for a hormone called FGF19 switches on 350-fold. In a living person that signal runs on a clock: it climbs after eating, peaks 90 to 120 minutes behind the meal-driven rise in bile acids, and tells the liver to ease off. Fast, and the rhythm disappears.

Notice the direction of the conversation. The gut measures what arrived and tells the organ upstream how much to send next. Your gut is the first brain here, and the liver is taking orders from it, not the other way around. Nothing about that arrangement fits the schoolroom picture of bile as a fluid pushed downhill to dissolve a fried egg.

Why this reaches your blood sugar and your appetite

The same molecule hits a second receptor on the hormone cells of the bowel. When a bile salt was placed against those cells in ten people with obesity and type 2 diabetes, blood glucose fell by up to 3.8 mmol/l and the food eaten at the next unrestricted meal fell by up to 47%. Two days of an oral bile acid in healthy women raised brown fat activity and whole-body energy expenditure.

The cleanest proof that this is signaling rather than digestion is a binding resin that stays in the lumen. Nothing about it enters the bloodstream, so it never reaches the pancreas. Pooled across 17 trials, in a combined 2,950 patients, it still pulled down HbA1c, the average blood sugar reading, by half a percentage point, 0.55% to be precise. A substance your body cannot take up, acting on a receptor in your intestine, moved your blood sugar.

There is a behavioral layer under all of this, and it was prescribed. For decades anyone with a touchy gallbladder was told to keep fat low and keep the organ quiet. Fat arriving in the duodenum is the signal that empties a gallbladder, so a quiet one is a full one, and bile that sits still concentrates. The advice produced the stasis that the surgery later collected.

What changes after gallbladder removal?

The gallbladder is not a bag. Its lining carries the message for that same hormone at roughly 250-fold the level of the nearby small intestine. Remove it and bile acid production rises at least two-fold while the daily rhythm of the hormone flattens out.

The symptom that follows is a timing problem rather than a hormone shortage, and that distinction has been tested directly: when investigators looked for a link between the hormone content of the removed gallbladder and anyone’s bowel habit, they did not find one. What changes is delivery. A gallbladder saves bile between meals and releases it as a bolus when fat arrives; without one, bile trickles all day into a bowel built to receive it in pulses, more of it passes downstream, and the colon reads bile acids as an order to secrete water. That is the loose, urgent stool after a fatty meal.

Then the number that should embarrass the system. Among 9,439 people who had the operation, 202, or 2.1%, were ever investigated for diarrhea afterward. Of those who were tested, 62.8% had bile acid diarrhea, which is named, testable and treatable. Those figures come from an audit of patients a clinician already suspected, so they describe how rarely the question gets asked rather than how common the condition is.

The bile tests are real, and they are not Measura tests

Measura [Cardiometabolic and Autonomic Health Analysis] is built around blood work, body composition and resting metabolism, plus vascular, autonomic, small-fiber, balance and cognitive measurement. Bile acid testing is not in that library, and neither is gallbladder imaging, the nuclear scan that reports an ejection fraction, or breath testing. Those belong to your physician and a gastroenterologist, and the retention scan used in Europe is not licensed in the United States, which is why an American conversation often ends up being about a supervised trial of a binder with a defined endpoint instead. Any of that is a prescribing decision for your own doctor, not something to start or stop on your own.

What can be measured in the same person

What Measura can do is measure the terrain that grew the stone in the first place and the consequences you are living with now. Bile acids sit inside energy regulation, so the metabolic picture is not a side issue here.

• Laboratory panels document fuel handling, inflammation and liver and kidney status in blood, which is where the stone-growing terrain shows up.
• Bioimpedance body composition separates muscle from fat, so months of restricted eating and avoided meals can be seen rather than guessed at. Body composition, not BMI explains why that distinction matters.
• Indirect calorimetry measures what you burn at rest instead of estimating it, which matters when weight has drifted since the operation.

None of those results is a diagnosis. They go to your physician, alongside the bowel history, so the decisions get made with numbers in the room.

What to ask for at your next visit

• When the stool change began: before the operation, weeks after it, or months after it.
• Whether your original pain was the classic biliary pattern or an atypical one.
• If an ejection fraction was measured, what it was and which infusion protocol produced it.
• Whether testing for bile acid diarrhea is available where you live, and if not, what a supervised trial with a stop date would look like.
• Whether your metabolic picture has ever been measured, not just your gallbladder. Insulin resistance and metabolic health covers that ground.

Every study behind these numbers, with its limits stated, is in the book companion for The Angry Gut. The version written for physicians is the screening view of post-surgical complications.

Frequently asked questions

References

• Zhang, J. H., Nolan, J. D., Kennie, S. L., Johnston, I. M., Dew, T., Dixon, P. H., Williamson, C., & Walters, J. R. F. (2013). Potent stimulation of fibroblast growth factor 19 expression in the human ileum by bile acids. American Journal of Physiology. Gastrointestinal and Liver Physiology, 304(10), G940-G948. https://doi.org/10.1152/ajpgi.00398.2012
• Lundåsen, T., Gälman, C., Angelin, B., & Rudling, M. (2006). Circulating intestinal fibroblast growth factor 19 has a pronounced diurnal variation and modulates hepatic bile acid synthesis in man. Journal of Internal Medicine, 260(6), 530-536. https://doi.org/10.1111/j.1365-2796.2006.01731.x
• Adrian, T. E., Gariballa, S., Parekh, K. A., Thomas, S. A., Saadi, H., Al Kaabi, J., Nagelkerke, N., Gedulin, B., & Young, A. A. (2012). Rectal taurocholate increases L cell and insulin secretion, and decreases blood glucose and food intake in obese type 2 diabetic volunteers. Diabetologia, 55(9), 2343-2347. https://doi.org/10.1007/s00125-012-2593-2
• Hansen, M., Sonne, D. P., Mikkelsen, K. H., Gluud, L. L., Vilsbøll, T., & Knop, F. K. (2017). Bile acid sequestrants for glycemic control in patients with type 2 diabetes: A systematic review with meta-analysis of randomized controlled trials. Journal of Diabetes and Its Complications, 31(5), 918-927. https://doi.org/10.1016/j.jdiacomp.2017.01.011
• Barrera, F., Azócar, L., Molina, H., Schalper, K. A., Ocares, M., Liberona, J., Villarroel, L., Pimentel, F., Pérez-Ayuso, R. M., Nervi, F., Groen, A. K., & Miquel, J. F. (2015). Effect of cholecystectomy on bile acid synthesis and circulating levels of fibroblast growth factor 19. Annals of Hepatology, 14(5), 710-721. https://pubmed.ncbi.nlm.nih.gov/26256900/
• Farrugia, A., Attard, J. A., Hanmer, S., Bullock, S., McKay, S., Al-Azzawi, M., Ali, R., Bond-Smith, G., Colleypriest, B., Dyer, S., Masterman, B., Okocha, M., Osborne, A., Patel, R., Sallam, M., Selveraj, E., Shalaby, S., Sun, W., Todd, F., … Arasaradnam, R. P. (2021). Rates of bile acid diarrhoea after cholecystectomy: A multicentre audit. World Journal of Surgery, 45(8), 2447-2453. https://doi.org/10.1007/s00268-021-06147-8
• Wedlake, L., A’Hern, R., Russell, D., Thomas, K., Walters, J. R. F., & Andreyev, H. J. N. (2009). Systematic review: The prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome. Alimentary Pharmacology & Therapeutics, 30(7), 707-717. https://doi.org/10.1111/j.1365-2036.2009.04081.x

Related reading

• Glyphosate in Food: What Can Actually Be Measured in You
• What Causes Sugar Cravings? The Numbers a Scale Cannot Show
• Laboratory Panels