If you have been woken at two in the morning by a big toe so painful you couldn’t stand a bedsheet on it, you already know what gout is. What most people don’t know is that the attacks are the visible part of a chronic condition that keeps working in the background between flares — and that it is one of the most treatable conditions we manage.
What gout is
Gout is a form of inflammatory arthritis caused by uric acid, a waste product your body makes when it breaks down substances called purines. Normally the kidneys clear it. When the level in the blood — the serum urate — stays too high, uric acid forms needle-shaped crystals inside joints. The immune system attacks the crystals, and that fight is the flare: hot, red, swollen, exquisitely painful, usually in one joint at a time, most often the big toe, but also the ankle, knee, or foot.
Between flares the joint can feel completely normal. That is the trap. The crystals are still there, and they are still accumulating.
Why this matters so much in our islands
Gout is not evenly distributed, and Hawaiʻi sits at the wrong end of the curve. In a University of Hawaiʻi analysis of about 92,000 people in the Multiethnic Cohort followed over nearly two decades, Native Hawaiian participants had more than twice the risk of developing gout in later life compared with White participants; Black and Japanese American participants had the next highest risk (Thompson et al., 2022).
The disease also behaves worse here. A 2024 study of gout patients in Hawaiʻi found that Native Hawaiian patients developed gout younger, were more likely to have visible urate deposits called tophi, used the emergency department more often for flares, and were less likely to be seen by a rheumatologist than White patients (Chang et al., 2024). A 2025 review in Nature Reviews Rheumatology describes the same pattern across Indigenous peoples of the Pacific — some of the highest rates of high urate and gout in the world, driven partly by inherited differences in how the kidneys handle uric acid, and compounded by unequal access to good management (Gérard et al., 2025).
Two honest conclusions follow. If gout runs in your family, this is genetics — not a character flaw or a punishment for how you eat. And an emergency room visit for a flare means the underlying condition is not being treated. That gap is fixable in primary care.
A picture of what this can look like
Consider a man in his forties on Hawaiʻi Island who has had four flares in two years. Each time he takes leftover anti-inflammatory pills, waits out three or four days of missed work, and moves on. He was told to cut out beer and shellfish, did it, and flared anyway — so he has decided nothing works. Nobody has checked his serum urate between attacks or started him on a daily medication to lower it. This is an illustrative composite, not a real patient.
That is the most common gout story we see. The flares get treated; the disease doesn’t.
What treatment actually looks like
The American College of Rheumatology’s gout guideline — still the current U.S. guideline — is unusually clear for a clinical document, and it makes two points that change everything for patients (FitzGerald et al., 2020).
Treat the number, not just the pain. The guideline strongly recommends a treat-to-target strategy: use a daily urate-lowering medication, recheck the blood level, and adjust the dose until the serum urate stays under 6 mg/dL. Fixed-dose “set it and forget it” prescribing works less well. Below that target, existing crystal deposits gradually dissolve and flares become less frequent and eventually stop.
Allopurinol first, started low, titrated up. Allopurinol is strongly recommended as the first-line urate-lowering therapy for everyone who needs it — including people with moderate-to-severe chronic kidney disease, who were once excluded. It is started at a low dose (100 mg a day or less, lower with kidney disease) and increased over weeks to months. The guideline also names the failure mode directly: titration should happen over a reasonable time frame, not over years.
Expect flares at the start, and cover for them. When urate levels drop, crystals begin dissolving and that can trigger flares. The guideline strongly recommends anti-inflammatory prophylaxis — colchicine, an NSAID, or low-dose prednisone — for at least three to six months when urate-lowering therapy is started. Many people who “failed allopurinol” actually stopped it during an early flare that prophylaxis would have prevented.
When to start. Urate-lowering therapy is strongly indicated for people with tophi, joint damage from gout, or frequent flares. It is also worth considering after infrequent flares — or even a first flare — in people with moderate-to-severe kidney disease, a serum urate above 9 mg/dL, or kidney stones. One flare with none of those features usually does not require lifelong medication.
On diet: alcohol, high-purine foods, and sugary drinks can contribute, and cutting back is reasonable. But the guideline’s diet recommendations are conditional and rest on limited evidence, while the medication recommendations are strong. Diet alone rarely controls established gout. If someone tells you gout is a food problem you brought on yourself, they are both wrong and unhelpful.
How we approach gout at Ohana Care Clinic
We think in terms of lōkahi — balance across the connected parts of health — because gout almost never travels alone. High blood pressure, type 2 diabetes, high cholesterol, and kidney disease cluster with it, and some blood pressure medications raise urate while others lower it. So a gout visit here is also a look at your kidneys, your blood pressure, your blood sugar, and your medication list, all part of our primary care and chronic disease service.
We also ask about mood and sleep, and we mean it. Recurrent, unpredictable pain that takes you out of work and away from family is depressing in the ordinary clinical sense of the word, and people in chronic pain sleep badly, which makes pain worse. Because we have psychiatric and primary care providers in the same practice, that doesn’t have to become a separate referral to a separate island — see behavioral health.
And we treat gout as an ʻohana matter, because it is inherited. If gout has hit your parents and your uncles, your siblings and your adult children should know their own urate levels and blood pressure before their first flare, not after their fifth.
Getting care by telehealth
Gout is a good fit for the way we practice. About 85% of our care is delivered by secure video, and the core work of gout management — reviewing flares, checking labs, adjusting an allopurinol dose, planning flare coverage — is a conversation plus a blood test. New primary care patients are seen in person at our Hilo clinic first; after that, most follow-up can happen by video from Puna, Kaʻū, Hāmākua, or anywhere else in the islands, which matters when a flare means you cannot get a shoe on, let alone drive an hour. Lab draws and joint exams happen locally or in the office. We accept Medicaid (QUEST), Medicare, and most major plans, and interpretation is available at no cost.
When to seek care now
Call us the same day, or go to urgent care or the emergency department, if a joint is hot and swollen along with fever or chills, if the pain is severe and involves a joint you have never had gout in before, or if you cannot bear weight. Those need to be evaluated for infection rather than assumed to be gout.
If pain, sleep loss, or feeling stuck has you struggling emotionally, that is worth saying out loud at your visit. If you are in crisis, call or text 988 (Suicide & Crisis Lifeline). From a non-808 number, Hawaiʻi CARES 988 can be reached at 808-832-3100 or toll-free 800-753-6879. In an emergency, call 911.
Medically reviewed by George Mackel, MSN, APRN, NP-C, PMHNP-BC, CARN-AP
President & Owner, OhanaPsych / Ohana Care Clinic
Date published: July 29, 2026
Last reviewed: July 29, 2026
Citations verified: July 29, 2026
This article is general health education from Ohana Care Clinic. It is not a substitute for a personal evaluation by a qualified clinician who knows your situation, and reading it does not create a provider–patient relationship. Do not start, stop, or change a medication based on this article. In an emergency, call 911.
References
Chang, C., Siu, A., Kimata, C., Sawada, H., Mak, V. P., & Lim, S. Y. (2024). Gout in Native Hawaiian patients in Hawaiʻi: Clinical characteristics and disparities. Arthritis Care & Research, 76(5), 712–719. https://doi.org/10.1002/acr.25289
FitzGerald, J. D., Dalbeth, N., Mikuls, T., Brignardello-Petersen, R., Guyatt, G., Abeles, A. M., Gelber, A. C., Harrold, L. R., Khanna, D., King, C., Levy, G., Libbey, C., Mount, D., Pillinger, M. H., Rosenthal, A., Singh, J. A., Sims, J. E., Smith, B. J., Wenger, N. S., … Neogi, T. (2020). 2020 American College of Rheumatology guideline for the management of gout. Arthritis Care & Research, 72(6), 744–760. https://doi.org/10.1002/acr.24180
Gérard, B., Leask, M., Merriman, T. R., Bardin, T., Oehler, E., Lawrence, A., Viali, S., ʻOfanoa, S., Te Karu, L., Stamp, L. K., Dalbeth, N., & Pascart, T. (2025). Hyperuricaemia and gout in the Pacific. Nature Reviews Rheumatology, 21(4), 197–210. https://doi.org/10.1038/s41584-025-01228-7
Thompson, M. D., Wu, Y. Y., Cooney, R. V., Wilkens, L. R., Haiman, C. A., & Pirkle, C. M. (2022). Modifiable factors and incident gout across ethnicity within a large multiethnic cohort of older adults. The Journal of Rheumatology, 49(5), 504–512. https://doi.org/10.3899/jrheum.210394
