Does Chronic Pain Shorten Your Life? What the Death Data Show

Chronic pain is almost always discussed as a quality-of-life problem. It is also a survival problem, and the people carrying it are rarely told so.

Does chronic pain shorten your life? The most recent federal estimate prices chronic pain in the United States at 722.8 billion dollars a year, counting medical care and lost work. Its authors list what the figure leaves out, including the intangible costs of suffering. No line in that ledger counts a death.

The video for Chapter 1 of The Pained Brain, The Cost of Pain Is Paid in Years, introduces the patient behind that number. The book is by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Dr. KrisJay Fucanan, MD. This page goes into what the video had no room for: what predicts an early death in a person who hurts, and what to measure because of it.

Does chronic pain shorten your life? What the large cohorts found

For a long time the published answer was no. Seven community cohorts pooled before the big registries gave a mortality rate ratio of 1.14, not statistically significant. For most of my career my own specialty treated pain as a local structural failure, and those numbers never pushed back.

Then the half-million-person cohorts arrived. Among British research volunteers, pain all over the body carried 2.43 times the rate of death from any cause and 3.24 times the rate of cardiovascular death, compared with people who had no chronic pain.

Heart disease is where much of that excess lands. Among 475,171 adults followed for a median of 7.0 years, widespread chronic pain carried 1.48 times the risk of a major cardiovascular outcome, and that was after body mass index, C-reactive protein and type 2 diabetes were already in the model. The share of that risk attributable to chronic pain was 8.6 percent, against 7.3 percent for diabetes.

Pain keeps adding even inside diabetes. In 19,899 people with type 2 diabetes followed for a median of 13.9 years, each additional painful site raised the hazard of death 1.04-fold and the hazard of cardiovascular disease 1.10-fold.

Interference, not intensity, predicts who dies

This is the finding I would put on every intake form. In 19,487 American adults over 50 followed for twenty years, pain that limited daily activity carried 1.33 times the hazard of death after heart disease, cancer, lung disease, diabetes and body mass were accounted for. Moderate or severe pain that did not limit activity carried 1.05, which was not significant. For a 67-year-old woman, that model put ten-year mortality at 13.0 percent without limiting pain and 20.3 percent with it.

The count of painful places matters as well. Among 384,367 British adults, the hazard of death climbed with each additional site of musculoskeletal pain, from 1.09 at one site to 1.46 at four. A pain score tells me how loud the alarm is. Whether the pain stops you from living, and in how many places it rings, tells me far more about your years.

Fibromyalgia marks the edge of this pattern. Pooled across seven cohorts and 152,933 people, it showed no demonstrable excess in death from all causes, at 1.11, yet the odds of suicide were 5.39. It shortens life another way, which is why mood screening belongs inside a pain evaluation.

Where the risk lives: insulin, visceral fat and an unfinished fire

When statisticians adjust the link between pain and death for weight, diabetes and heart disease, the link shrinks. In the American cohort the hazard fell from 1.52 to 1.33. Most readers take that as pain being explained away. I read it as an address. The risk shrank because part of it was already sitting inside the metabolic disease.

The first driver is insulin. Among American adults without diabetes, the share with insulin resistance rose from 24.8 percent to 38.4 percent between 1999 and 2018. Blood sugar stays normal while insulin climbs, so the chart reads healthy. We have covered how high insulin makes you hurt, and the nerve-level detail is in the post on the hormone that starves your nerves.

The second driver is visceral fat, the fat packed around the organs. It behaves like a gland that releases inflammatory signals all day. In 5,905 American adults, a visceral-fat score predicted chronic pain better than body mass index or waist circumference past age 65. That is why belly fat is not passive storage.

The third piece inverts what most of us were taught. In 98 people with fresh low back pain, the ones who recovered showed more than 5,500 immune genes changing expression and then settling back down. The ones whose pain became chronic showed none. The recovering response was about 75 percent larger. The problem was never inflammation itself. It is inflammation that never finishes, the state we call metaflammation. The human arm of that work is observational, and the direction is still hard to ignore.

It also explains why a normal C-reactive protein settles nothing. Genetically higher CRP does not cause spinal pain. What raised CRP appears to do is amplify. In one population followed forward, hs-CRP at or above 3 mg/L did not predict new chronic pain on its own. Paired with sleeplessness, it carried 2.47 times the odds of chronic musculoskeletal pain. Sleep is not a comfort measure. It is part of the inflammatory equation, and the sleep and pain loop runs both ways.

The social driver: schooling, work and the year you were born

Two biological drivers are not the whole story. At age 52, 40 percent of Americans born in 1965 without a bachelor’s degree reported pain, against 32 percent of those born in 1955. Pain rose 0.6 percentage points per birth year for people without a degree and 0.2 for those with one, and body mass explained only about a quarter of that rise. Pain is being handed out by education and economics, not only by joints.

That distribution feeds the biology. Losing work means losing income, movement and company, and each pushes insulin the wrong way. In British adults over 60 who began without diabetes, pain at four to seven sites raised the hazard of new type 2 diabetes to 1.198, and body weight carried nearly half of that effect.

What to measure, and what to do with the answer

If limiting pain, the number of painful sites, insulin and visceral fat carry the risk, then a pain evaluation that images only the joint is incomplete. In our practice, the first workup includes a fasting insulin, markers of inflammation, vitamin D and the lipid pattern alongside the examination. Fewer than 1 percent of the chronic pain patients who come to us are metabolically healthy, a practice-reported figure from our own patients, not a trial outcome, and individual results vary.

Opioids sit inside this same picture. Dose carries risk: among 9,940 patients on long-term opioids for chronic non-cancer pain, 100 or more milligrams a day carried 8.87 times the overdose hazard of the lowest doses. So does a forced taper, which is covered in the questions below. The way through is to shrink what the dose is covering for. Under that plan, within ninety days 21 percent of our patients no longer take opioid pain medication, by one year 34 percent, and in our established population under 1 percent stay above 90 morphine milligram equivalents. Those are practice-reported figures from our own patient population, not trial outcomes, and individual results vary. Any dose change belongs with your physician, which is why we call medication a bridge, not a destination.

Here is what returns to you. Ask for your fasting insulin, not only your glucose. Ask that the number of places you hurt, and whether pain stops you doing things, be written in your chart. Guard your sleep as seriously as a prescription. Every study behind these figures, what each one shows and what it cannot show, is in the Technical Supplement to Chapter 1, written to be handed to your doctor. The next step is learning what pain actually is: a signal with a source, not a diagnosis.

Frequently asked questions

Can chronic pain shorten your life expectancy?

In large cohorts, yes. British volunteers with widespread pain died at more than twice the rate of people without chronic pain, and the excess held at 1.47 times after weight, activity, smoking, alcohol and diet were adjusted. The risk concentrates in pain that limits daily life and pain at several sites. It is not a verdict on any one person, and much of it runs through metabolic disease that can be measured. Untreated pain is not a neutral holding position.

Why does chronic pain raise the risk of heart disease?

Pain and heart disease share a terrain: insulin resistance, visceral fat and inflammation that never resolves. Among 475,171 adults, widespread chronic pain carried 1.48 times the risk of major cardiovascular events even with diabetes and C-reactive protein in the model. Pain also drives inactivity and broken sleep, which push the same terrain further in the wrong direction. Here is why we treat insulin before we treat the joint.

Can my blood sugar be normal if I have insulin resistance?

Yes. When cells stop responding to insulin, the pancreas makes more, and glucose can stay normal for years. Among American adults without diabetes, high fasting insulin rose from 28.2 percent to 41.4 percent between 1999 and 2018. A normal A1c does not rule it out, so ask your physician for the fasting insulin number itself. Insulin resistance arrives years before diabetes, and a glucose test misses it.

Is it risky to taper pain medication quickly?

A rapid or forced taper carries its own risk. Even 12 to 24 months after a taper began, overdose or withdrawal events and mental health crises were still elevated, at 1.57 and 1.52 times the rate seen on a stable dose. The safer route lowers what the dose is covering for first, and any change is worked through with your physician. Why an abrupt taper is also harm.

Does a normal CRP mean I have no inflammation?

No. Genetically higher C-reactive protein does not cause spinal pain, and in 5,905 American adults CRP explained only 7.4 percent of the link between visceral fat and chronic pain. The trouble in chronic pain is inflammation that never finishes, which one marker cannot show. CRP means more read beside your sleep than read alone. How a sensitized nervous system lowers its own pain threshold.

Sources

1. Macfarlane, G. J., Beasley, M., & Jones, G. T. (2023). Chronic pain and premature mortality in men and women, using data from UK Biobank. The Journal of Clinical Investigation, 133(5), e166949. https://doi.org/10.1172/JCI166949
2. Ruan, H., Yang, Y., & Grol-Prokopczyk, H. (2026). Which is More Predictive of Mortality-Pain Severity or Pain Interference? Evidence from 20-Year Longitudinal Data. The Journal of Pain, 40, 106192. https://doi.org/10.1016/j.jpain.2026.106192
3. Chen, L., Ferreira, M. L., Nassar, N., Preen, D. B., Hopper, J. L., Li, S., Bui, M., Beckenkamp, P. R., Shi, B., Arden, N. K., & Ferreira, P. H. (2021). Association of chronic musculoskeletal pain with mortality among UK adults: A population-based cohort study with mediation analysis. EClinicalMedicine, 42, 101202. https://doi.org/10.1016/j.eclinm.2021.101202
4. Vaegter, H. B., Støten, M., Silseth, S. L., Erlangsen, A., Handberg, G., Sondergaard, S., & Stenager, E. (2019). Cause-specific mortality of patients with severe chronic pain referred to a multidisciplinary pain clinic: a cohort register-linkage study. Scandinavian Journal of Pain, 19(1), 93–99. https://doi.org/10.1515/sjpain-2018-0094
5. Wu, C., Ke, Y., & Nianogo, R. A. (2025). Trends in Hyperinsulinemia and Insulin Resistance Among Nondiabetic US Adults, NHANES, 1999-2018. Journal of Clinical Medicine, 14(9), Article 3215. https://doi.org/10.3390/jcm14093215
6. Zhu, J., Wang, Y., Yu, G., Li, L., He, J., Liao, H., & Wu, X. (2025). Association between metabolic score for visceral fat and chronic pain: a cross-sectional analysis of NHANES 1999-2004. Frontiers in Nutrition, 12, Article 1545774. https://doi.org/10.3389/fnut.2025.1545774
7. Parisien, M., Lima, L. V., Dagostino, C., El-Hachem, N., Drury, G. L., Grant, A. V., Huising, J., Verma, V., Meloto, C. B., Silva, J. R., Dutra, G. G. S., Markova, T., Dang, H., Tessier, P. A., Slade, G. D., Nackley, A. G., Ghasemlou, N., Mogil, J. S., Allegri, M., & Diatchenko, L. (2022). Acute inflammatory response via neutrophil activation protects against the development of chronic pain. Science translational medicine, 14(644), eabj9954. https://doi.org/10.1126/scitranslmed.abj9954
8. Liang, J., He, X., Ouyang, Y., Song, X., Li, M., Qi, T., Chen, J., Zhang, X., Guo, X., Jia, T., Wu, S., Kou, C., & Bai, W. (2026). Association between chronic pain and type 2 diabetes in older adults: A prospective study in the UK Biobank. The Journal of Pain, 43, 106272. https://doi.org/10.1016/j.jpain.2026.106272
9. Dunn, K. M., Saunders, K. W., Rutter, C. M., Banta-Green, C. J., Merrill, J. O., Sullivan, M. D., Weisner, C. M., Silverberg, M. J., Campbell, C. I., Psaty, B. M., & Von Korff, M. (2010). Opioid prescriptions for chronic pain and overdose: a cohort study. Annals of Internal Medicine, 152(2), 85–92. https://doi.org/10.7326/0003-4819-152-2-201001190-00006
10. Agnoli, A., Xing, G., Tancredi, D. J., Magnan, E., Jerant, A., & Fenton, J. J. (2021). Association of Dose Tapering With Overdose or Mental Health Crisis Among Patients Prescribed Long-term Opioids. JAMA, 326(5), 411–419. https://doi.org/10.1001/jama.2021.11013

Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP, board certified in anesthesiology, pain medicine, interventional pain management, addiction medicine and obesity medicine. Adapted from Chapter 1 of The Pained Brain by Dr. Padda and Dr. KrisJay Fucanan, MD. Last reviewed September 2026.

Dr. Gurpreet Singh Padda, MD, MBA, MHP