Episode Highlights
The Disease of Kings
Why gout plagued the wealthy in centuries past and was once known as Morbus Dominorum, the disease of lords
Unique to Humans
How our evolutionary loss of uricase set us apart from every other species, predisposing us to high uric acid levels
Modern Triggers
The roles of purine-rich foods, alcohol, and especially fructose in driving uric acid spikes and flares
A Rare Case
The story of a patient with a life-threatening brainstem lesion — caused not by a tumor, but by gout crystals
Genetics & Vulnerability
Why Pacific Islanders, Maori, Han Chinese, and Koreans have higher rates due to urate transporter polymorphisms
Lifestyle Solutions
Simple, evidence-backed steps: avoid beer and sodas, moderate meat and seafood, lose excess weight, hydrate well
Protective Foods
Coffee, vitamin C, cherries, and dairy as natural uric acid–lowering allies
Treatment Landscape
From NSAIDs, colchicine, and corticosteroids for flares to long-term prevention with allopurinol, probenecid, and lifestyle change
Beyond Gout
Why lowering uric acid also protects against kidney disease, hypertension, metabolic syndrome, and kidney stones
Show Notes
In this episode, Dr. Ravi Kumar explores gout — an ancient disease that doesn’t have to exist anymore. You’ll learn:
- What gout is — an inflammatory arthritis caused by uric acid crystal deposition, often starting in the big toe but capable of appearing in tendons, kidneys, and even the brainstem
- Why it’s unique to humans — our evolutionary loss of uricase raised uric acid for survival advantages, but now collides with modern diets to cause disease
- Historical perspective — from Henry VIII to Benjamin Franklin, gout has long been associated with indulgence and power
- Modern contributors — purine-rich meats, beer, and high-fructose corn syrup as key drivers of hyperuricemia and flares
- Genetic risk — why Pacific Islanders, Maori, Han Chinese, and Korean populations carry higher susceptibility
- Natural preventives — coffee, vitamin C, cherries, and dairy as protective factors supported by research
- Treatment hierarchy
- Acute flare management: NSAIDs, colchicine, corticosteroids
- Long-term prevention: lifestyle change, uric acid–lowering medications, and when to test for HLA-B*58:01 before starting allopurinol
- The bigger picture — high uric acid isn’t just about gout: it increases risks of kidney stones, hypertension, and metabolic syndrome
- Empowerment message — gout is largely optional. With diet, lifestyle, and awareness, most people can avoid it entirely
By the end of this episode, you’ll understand why humans get gout, how modern diets amplify the risk, and what you can do to ensure it never controls your life.
Transcript
[01:20 –> 01:30] Welcome to the Doctor. Kumar discovery podcast. My name is Doctor. Ravi Kumar. I’m a board certified neurosurgeon and assistant clinical professor of neurosurgery at UNC.
[01:30 –> 01:59] On today’s podcast, we’re gonna be talking about gout. Gout is an inflammatory arthritis that happens from crystallization of uric acid. It occurs when elevated levels of uric acid in the blood crystallize in the joints, most commonly at the base of the big toe, and cause an inflammatory reaction with severe pain. This is something that has been common throughout modern history and specifically only happens in human beings. There’s no animal, no other creature on this earth that develops gout.
[01:59 –> 02:21] Why? Well, we have certain adaptations, which we’ll talk about later, that cause us to have high levels of uric acid, the same molecule that crystallizes and causes gouty arthritis. And we now live in a world where modern diets make elevated uric acid very common in susceptible individuals. This all leads to gout. In the past, gout has been called the disease of kings.
[02:21 –> 03:04] In the seventeenth and eighteenth centuries, gout became so strongly associated with wealth and political influence that it was named Morbus Dominorum, meaning the disease of lords. Famous people throughout history, including King Henry the eighth, Isaac Newton, and Benjamin Franklin, have been known for their suffering with gout. In fact, Benjamin Franklin famously joked that gout was the price he paid for a lifetime of indulgence. Good food, good drink, and good company. The famous physician Thomas Sindenham also described struggles with gout and he famously said, the pain which gout occasions is so exquisite and so acute that it cannot be exceeded by that of the most excruciating torture which the imagination can conceive.
[03:04 –> 03:21] This is coming from a physician who basically said there was no worse pain in the world than gout. That gives you an idea of how horrible and acute gout flare is. Just a quick disclaimer. I’m a doctor, but I’m not your doctor. This information I share here is for educational purposes only.
[03:21 –> 03:53] It’s not meant to diagnose or treat any medical condition. Knowledge is power, and my goal is to empower you with unbiased, non dogmatic information so you can better understand complex health issues and make informed decisions with your own health care provider. And one more note, this podcast is completely separate from my role as assistant professor at UNC. To really understand gout and what can be done about it, we first need to look at how it typically presents. The classical presentation is something called podagra, which is inflammation of the first tarsometatarsal joint at the base of the big toe.
[03:54 –> 04:19] This causes a large swollen red and exquisitely painful foot. It’s warm, tender and inflamed and the pain can be so severe to make even the weight of a bed sheet unbearable. A flare like this usually lasts about seven to ten days before it resolves. But gout doesn’t just happen in the big toe. It can affect the plantar fascia, the Achilles tendon, the knee, the elbow, essentially anywhere in the body where the temperature is slightly cooler than the body’s core.
[04:19 –> 04:39] That cooling lowers the threshold of uric acid for crystallization. When flares keep happening and uric acid levels stay high, chronic toffee can form. These are hardened accumulations of uric acid and inflammatory cells in the subcutaneous tissues. That’s right under the skin. Over time, they can break down nearby joints and cause permanent disability.
[04:39 –> 05:04] Ptofi can even appear in places you might not expect, the spine, the ears, the kidney, leading to kidney stones and chronic kidney disease. In fact, gout and kidney disease often go hand in hand. If someone is having repeated gout flares, it’s likely that their kidney function is also declining. Gout can also have an atypical presentation that catches even the most experienced physician off guard. A perfect example is from when I was fresh out of residency.
[05:04 –> 05:20] I was in my very first practice. I was on call and a woman was admitted to the hospital with essentially quadriplegia. She couldn’t even swallow her own saliva and couldn’t move her arms or legs. She was having trouble breathing and was bound to a wheelchair. Her life was rapidly slipping away from her.
[05:21 –> 05:39] An MRI of her brain showed a growth at the very base of her skull, pressing into the front of her brain stem. That pressure explained her rapidly worsening symptoms. Without intervention, she had no chance of recovery. The lesion would continue to grow, slowly destroying her brain stem. It would either take her life or turn her into a vegetable.
[05:39 –> 05:47] I studied the scan. I had no idea what the lesion was. Was it a tumor? Some kind of inflammatory process? Even the neuroradiologist was stumped.
[05:47 –> 06:15] The only real option was surgery, a very high risk procedure called a far lateral craniotomy. I opened the tissue on the back of her neck and head and drilled away the bottom of her skull. In under 40 times magnification, I created a tiny corridor through the delicate vessels and nerves, the kind that if I damaged, would cause a brainstem stroke and coma. At the front of her brainstem, I found the lesion. I carefully separated it from the base of her skull and removed it entirely.
[06:15 –> 06:31] I sent it to the pathologist to be reviewed. And soon after surgery, she began to move her arms and legs again. She no longer needed her tracheostomy, which helped her breathe, and she started swallowing again. The neurologic recovery was immediate and traumatic. But we still didn’t know what the lesion was.
[06:31 –> 06:46] The pathologist was baffled. They sent it to another center and finally we got the answer. It was gout. A gouty pophus had grown from the base of her skull into her brain stem. I had never seen a case like it and since then I’ve never seen another case like it.
[06:47 –> 07:08] But it’s a powerful reminder that uric acid crystals can form in unexpected places. While the most common presentation is monoarthritis, gout in the big toe, it can also appear in the spine, in the ears, and even at the base of the brain. If the conditions are right, gout is an equal opportunity offender. So how do you know if your uric acid levels are elevated? The best way is with a blood test.
[07:08 –> 07:30] You’re at high risk for uric acid crystallization when your levels are above 6.8 per deciliter. The safer range is below six point zero. I tell people to make sure they’re at least under six point zero milligrams per deciliter of uric acid. Even though that’s not perfect, it’s probably the point where crystallization becomes less likely even under extreme conditions. So how common is gout?
[07:31 –> 07:56] Well, unfortunately, it’s extremely common. Historically, it plagued the wealthy because of their diets. But now, everyone has access to rich food. You can be the poorest person in a first world nation and still eat as well as the richest people did in the past centuries when wealth and prosperity were far more segregated. According to the NHANES study from 2015 and 02/2016, gout affected three point nine percent of adults in The United States.
[07:56 –> 08:15] That’s about nine point two million people at that time. With population growth and assuming the percentage has stayed the same, that number is now closer to thirteen point five million people in The US alone. Globally, about fifty four million people struggle with gout. From 1990 to 02/2019, the prevalence increased by twenty two percent. It’s getting worse, not better.
[08:15 –> 08:45] It’s also more common in men than in women, especially men above the age of 60. And there are clear ethnic differences. Pacific Islanders, Maori, Han Chinese, Korean, Japanese populations tend to have higher rates of gout due to small genetic changes that affect how quickly uric acid is reabsorbed or excreted. We’ll come back to these genetic differences later because they play a big role in why gout hits certain groups harder than others. So now that we know what gout is, the next logical question is, why?
[08:45 –> 08:56] Why is this happening? Why is it that human beings are the only species on the planet that develop gout? Is it something we’re eating or is it something about our biology? The answer is both. Let’s start with biology.
[08:57 –> 09:30] Humans have lost an enzyme called uricase. In our hominid ancestors, as they evolved towards becoming human, they lost this enzyme which normally breaks down uric acid into a lantoin. In animals that still have uricase, uric acid levels stay very low, usually between 0.51 milligram per deciliter. In humans with gout, uric acid levels are often over 6.8 milligrams per deciliter, well above the crystallization threshold. Even when we compare ourselves to our closest primate relatives, chimpanzees, gorillas, and orangutans, who also don’t have uricase enzymes like us, our levels are much higher.
[09:31 –> 09:52] These primates typically have uric acid around two to three milligrams per deciliter. The highest is in chimpanzees and they rarely exceed four milligrams per deciliter, still far below the point where crystals form. So we’re unique in two ways. We’re the only species with uric acid levels this high, and we’re the only species that develops gout. So why did we lose uricase?
[09:52 –> 10:16] What was the evolutionary advantage? Because there had to be a reason. Well, at normal levels, uric acid acts as an antioxidant. If you listen to my podcast on vitamin c, you’ll remember that humans also lost the ability to make vitamin c, a trait most other animals still have. Without the ability to make vitamin c, there were times in our history, like long winters without fresh fruit or vegetables, when our vitamin c intake dropped very low.
[10:16 –> 10:42] Vitamin c is critical for antioxidant protection. In those periods, uric acid could step in and provide antioxidant protection. You can imagine if a primate couldn’t make vitamin c and was also breaking down its uric acid with uricase, they would lose both sources of antioxidant defense when vitamin c intake was low. By losing uricase, we kept uric acid levels higher giving us a backup antioxidant system. There was another likely advantage too.
[10:42 –> 11:04] As humans spread across the globe, sodium availability varied dramatically. Coastal populations had plenty of salt, but inland populations often didn’t. Sodium is essential for life, so conserving it can become critical. Elevated uric acid helped with that. It increased sodium reabsorption in the kidneys through the renin angiotensin system, which meant we held on to salt more effectively.
[11:04 –> 11:34] In other words, high uric acid essentially created a mild controlled form of kidney impairment that helped us conserve sodium when it was scarce. So uric acid helped our ancestors survive. First by protecting against oxidative stress when vitamin c was scarce, and second by helping conserve sodium when salt was hard to come by. The problem is we’re still uric acid sparing organisms, but now we live in a world where our diet drives uric acid production far higher than it ever would have been in the past. Okay.
[11:35 –> 11:59] So if you think about gout as a disease of kings, a disease of the affluent, back in the day, what did the wealthy have that the poor didn’t have? They had meat and they had alcohol, two of the biggest uric acid producing foods you can consume. And why are meat and alcohol uric acid producing? Well, it all comes down to something called purines. Purines are the building blocks of DNA and RNA, which makes up our genetic code.
[11:59 –> 12:23] They’re also the building blocks of ATP, which is our cell’s main energy storage molecule, and they’re part of signaling molecules like NADH, CAMP, and CGMP. Purines are essential to life. Every function from transcribing DNA into RNA to producing energy depends on them. Without purines, you can’t survive. This means any living food you eat, whether it’s plant or animal, contains purines.
[12:23 –> 12:46] It has DNA, it has RNA, it has these signaling molecules, it has ATP, but some foods are richer in purines than others. Why does that matter? Because purines break down directly into uric acid. So if you eat something high in purines, you’ll end up with more uric acid in your blood. If your body already has all the purines it needs, the excess is broken down and your uric acid levels climb.
[12:46 –> 13:09] The foods with the highest purine contents are organ meats, red meat, pork, seafood, and beer. These are the biggest offenders in modern diet because they load the body with the raw material that eventually becomes uric acid. If you think back to Benjamin Franklin, he loved beer. He loved decadent foods and he paid for it with gout that followed him throughout his life. So purine rich foods are one problem.
[13:09 –> 13:29] The second is alcohol. Alcohol metabolism produces a molecule called NADH. High levels of NADH cause pyruvate to be converted into lactic acid. Lactic acid is a waste product that, like uric acid, needs to be excreted by the kidneys. The problem is lactic acid and uric acid compete for the same transporters in the kidney.
[13:29 –> 13:51] If your blood is loaded with lactic acid from alcohol metabolism, the kidneys may prioritize getting rid of the lactic acid leaving more uric acid behind in your bloodstream. That’s why alcohol even without purines can raise uric acid levels. When it comes to alcoholic drinks, beer is by far the worst. It’s high in purines, and it contains alcohol. Liquor has also been shown to trigger gout flares.
[13:51 –> 14:12] Wine is different. It’s generally considered neutral. It doesn’t seem to make gout better, but it also has less tendency to make it worse. That said, if someone is highly susceptible to gout, even wine can trigger a flare just because of the alcohol. So to sum it up, purine rich foods like organ meats, red meat, seafood, and beer give your body more raw material to make uric acid.
[14:12 –> 14:25] Alcohol slows down your body’s ability to get rid of uric acid. The next one I wanna talk about, and this is really fascinating, is fructose. Fructose is naturally available in nature. Alcohol is naturally available as well. Rich foods have always been available.
[14:26 –> 14:52] Those three things have always been present in some form in the human diet throughout history. But what’s new is the industrial processing of fructose into high fructose corn syrup and other fructose rich syrups. You can now consume a massive bolus of fructose in one soda can, something that has never existed in evolutionary history. That single shift has caused a massive increase in uric acid levels in human beings. So what does fructose actually do?
[14:52 –> 15:12] Well, fructose is a sugar just like glucose, but the way our body handles it is very different. Glucose, when it’s metabolized for energy, has to pass through a gatekeeper enzyme called phosphofructokinase. This enzyme monitors our energy levels. If we have plenty of ATP, our body’s main energy storage molecule, phosphofructokinase slows things down. It says, hey.
[15:12 –> 15:23] We got enough energy. Let’s store the rest of this glucose. It’s a tightly regulated system. Fructose, on the other hand, bypasses phosphofructokinase entirely. There’s no checkpoint.
[15:23 –> 15:44] It goes straight into rapid unregulated metabolism. Here’s what happens. Fructose is quickly converted into fructose one phosphate. Every time that conversion happens, it uses up one molecule of ATP. When you’re metabolizing a big load of fructose, say from a soda sweetened with high fructose corn syrup, you burn through ATP very quickly.
[15:44 –> 16:05] When ATP is depleted, it’s broken down into AMP. It’s like the drained battery version of ATP. AMP is then funneled directly into the pathway that produces uric acid. That’s why within thirty to sixty minutes of drinking a soda, your uric acid levels spike. And for someone susceptible to gout, that spike alone can trigger a flare.
[16:05 –> 16:25] This isn’t just theory. The rise in gout closely mirrors the rise in fructose consumption. Between 1977 and 1997, soft drink consumption in The US increased by 61% with high fructose corn syrup being the main sweetener. Over that same time, the incidence of gout doubled. That’s not a coincidence.
[16:25 –> 16:52] That’s a direct result of a massive dietary shift towards fructose levels that the human body had never encountered before in its entire evolutionary history. So now we see the picture. Modern diet and lifestyle changes rich in purines, high in alcohol, and loaded with fructose have driven uric acid levels higher than ever leading to the high prevalence of gout that we see today. But there are still other factors we need to consider. We know that humans are naturally high uric acid species.
[16:52 –> 17:15] We’re built that way. Evolutionarily for the reasons that we already talked about, antioxidant protection and sodium retention. But even within our species, certain groups have naturally higher uric acid levels than others. One example is the Maori and the other is South Pacific Islanders. They carry a polymorphism, a small change in the gene called GLUT nine, which is one of the main uric acid transporters in the kidney.
[17:15 –> 17:34] This change reduces uric acid excretion in the urine so blood levels run higher. In these groups of people, the prevalence of gout is about ten to fifteen percent. So when I see phenomenon like this, I always ask, why would they have this? And you have to think about their history. These were long distance ocean voyagers.
[17:34 –> 18:00] They likely faced dehydration, low vitamin c intake, and limited food variety on those trips. Higher uric acid may have helped them survive, providing antioxidant protection and helping the body conserve sodium and water. Those without this trait may not have survived the journey. Another group with naturally higher gout risk is the Han Chinese and Koreans. In these groups, gout rates range from six to nine percent, roughly double the average American rate.
[18:00 –> 18:18] They also have polymorphisms that reduce uric acid excretion. It’s estimated that twenty five to thirty percent of people in these populations carry these genetic variants. Of course, it’s not just these groups. Every person handles uric acid a little different. Just like faces and body shapes vary, so does uric acid metabolism.
[18:19 –> 18:38] Some people naturally have lower levels while others will run higher. And in the context of our modern diet and lifestyle, those with naturally higher levels are at greater risk for developing gout. I hope you’re enjoying this episode so far. If you’d do me a quick favor, please like and subscribe on whatever platform you’re listening on. And if you can, leave a written review.
[18:38 –> 18:50] It really helps the algorithms share and spread the show to more people. The more ears we reach, the more impact this clear unbiased information can have. That’s the whole goal. So thank you. I truly appreciate it.
[18:50 –> 19:12] Okay. So what do we know so far? We know gout is an inflammatory arthritis that happens in humans because of our naturally higher uric acid levels. We also know there are genetic factors in certain ethnic groups and just differences between individuals that make some people more likely to have higher uric acid levels and develop gout. So with that knowledge, what can we do about it?
[19:12 –> 19:26] The first thing in any disease process is to change your lifestyle. This is almost zero risk and often produces better results than any drug you could ever take. Think about it like this. If the sink is overflowing, don’t just mop the floor. Pull the plug.
[19:27 –> 19:51] Modifying diet and lifestyle is pulling the plug so the water can drain. You might still have to mop and that’s fine. But if you don’t treat the root cause, taking medication alone is just mopping endlessly while the sink keeps overflowing. So here’s what we can do with diet and lifestyle. Step one, if you’re susceptible to gout, moderate your intake of organ meats and avoid frequent servings of red meat, pork, and high purine seafoods like anchovies.
[19:51 –> 20:06] That doesn’t mean you need to cut these foods out forever. They can be healthy and have significant benefits. But eating them every day if you’re prone to gout is asking for trouble. The goal is balance. Eat in moderation so you can stay gout free and still enjoy nutrient rich foods.
[20:06 –> 20:25] Other meats like chicken are moderate in purine content. Salmon tends to be on the lower end, but you have to be careful with fish. Some like anchovies, sardines, mackerel, herring have very high purine levels. Anchovies are a great example. They’re rich in omega three fatty acids, low on the food chain, and often sustainably sourced.
[20:25 –> 20:47] But if you’re prone to gout, they shouldn’t be a daily staple. In moderation though, most of these foods are fine. Step two, the next thing that carries a massive purine load is beer. If you struggle with gout, whether you’ve had one flare or several, beer really shouldn’t be on your menu anymore. It’s loaded with purines from yeast fermentation of the malted barley, and then it adds alcohol on top of that.
[20:47 –> 21:16] So you get a double hit, a big surge in uric acid from the purines and reduced uric acid excretion from the alcohol. For someone who’s already genetically susceptible, like people of South Pacific or Korean descent, this combination makes things even worse. The body is already less efficient at excreting uric acid, and beer stacks the deck against you. Other alcohols like liquor also reduce uric acid excretion. If you struggle with gout, liquor should only be used in very tight moderation.
[21:16 –> 21:35] Now what about wine? Wine is different. Even though it contains alcohol, it doesn’t seem to raise gout risk in the same way. There may be protective effects from the antioxidants like polyphenols and anthocyanins, which could dampen the inflammatory response to uric acid. We don’t fully understand why, but overall, wine seems to be neutral.
[21:35 –> 22:00] That said, if you have frequent gout flares, avoiding alcohol altogether or at least keeping it to a bare minimum is the safest move. But if your gout is only occasional, the two biggest things you can do are cut back on high purine foods and avoid beer. Okay. Step three, cut out all sources of high fructose corn syrup. So if you drink soda or eat processed foods with high fructose corn syrup or even fructose syrup, you should get rid of it.
[22:00 –> 22:25] It shouldn’t be in your diet anymore because that will lead to massive spikes in uric acid throughout the day. And just one spike can cause a gout flare. So this is something you should be well aware of and just try not to have it in your diet. The last step is weight loss and improving your overall metabolic health. Reducing excess weight, exercising regularly, and staying well hydrated all improve your body’s ability to handle uric acid.
[22:25 –> 22:47] These are simple lifestyle changes, but they make a big difference, and they fit perfectly with a healthy diet and lifestyle. I talk a lot about metabolic health in my cardiovascular disease series, and I strongly recommend you go back and listen to that. Improving your metabolic health makes every aspect of your life better, and it also lowers your risk of gout. Okay. So those are the main steps I would follow to modify your diet and lifestyle.
[22:47 –> 23:03] But what about other things you can do? Are there things outside the realm of medication that can lower your gout risk? Actually, there are. One of the most surprising ones is coffee. I’ll admit, I’m a big coffee drinker, so I naturally like seeing studies that say coffee is good for you.
[23:03 –> 23:23] I read the ones that say it’s not too just to keep my mind balanced, but overall, the evidence is pretty solid. Coffee lowers risk of gout. In fact, the more coffee people drink, the lower their risk of gout. One study showed that drinking more than six cups a day reduced gout risk by fifty nine percent. Even decaf seemed to help, though not as much.
[23:23 –> 23:39] Drinking more than four cups of decaf a day was linked to about a twenty seven percent reduction in risk. Why would coffee help? Likely through several mechanisms. Coffee contains polyphenols that inhibit xanthine oxidase. This is the enzyme that converts xanthine into uric acid.
[23:39 –> 24:13] It also contains a compound called theophylline, which competes with uric acid for resorption in the kidney, so more uric acid ends up getting excreted in the urine. And on top of that, coffee’s polyphenols like chlorogenic acid have anti inflammatory and antioxidant effects that reduce systemic inflammation. Another therapy that has shown real benefit in gout is vitamin c. If you remember back to the vitamin c episode we did, and if you haven’t listened to that, I’d encourage you to go listen to it, I talked about why vitamin c is an essential part of living a healthy life, whether you have gout or not. And just getting it from food alone is often not enough.
[24:13 –> 24:35] So how specifically does vitamin c help with gout? Well, studies show that men taking more than fifteen hundred milligrams of vitamin c per day had a forty five percent lower risk of developing gout compared to men who didn’t take supplemental vitamin c. Why does this happen? Well, it comes down to how vitamin c and uric acid interact in the kidneys. Both use the same transporters for reabsorption.
[24:35 –> 25:05] When vitamin c is low, the body pulls more uric acid back in to help with antioxidant protection, and blood levels of uric acid rise. But when you saturate those transporters with vitamin c, meaning your tissues are full and your blood levels are high, uric acid doesn’t get reabsorbed as much. Instead more of it gets excreted in the urine. The evidence backs this up. A double blind placebo controlled trial showed that as little as five hundred milligrams of vitamin C daily for two months lowered uric acid by about half a milligram per deciliter.
[25:05 –> 25:36] Another study showed that a single dose of four grams of vitamin c doubled the excretion of uric acid. And in yet another study, taking eight grams of vitamin c for three to seven days dropped uric acid by two to three milligrams per deciliter. So vitamin c isn’t just good for your overall health, it’s a powerful tool for lowering uric acid levels and reducing gout risk. If you’re gonna supplement, I recommend taking fifteen hundred milligrams of vitamin c per day. The best approach is to split it into smaller doses throughout the day.
[25:36 –> 26:05] For example, take five hundred milligrams three times daily and you’ll get the maximal absorption of the vitamin c. Another potentially powerful way to lower your risk of gout is with cherries, especially tart cherries. The research has been a little mixed, but when you look at the studies that show positive results, the effect is impressive. One study found that eating cherries reduced the risk of gout by thirty five percent. And when cherries were combined with allopurinol, which is one of the first line drugs for gout, the reduction in risk was about seventy five percent.
[26:05 –> 26:29] Another study used what’s called a crossover design. They recruited overweight and obese patients who are at higher risk for gout and gave them either tart cherry juice or a placebo for four weeks. Then they had a washout period and switched the groups. So everyone tried both treatments just at different times. What they found was that tart cherry juice lowered uric acid levels in the blood by almost twenty percent.
[26:29 –> 27:06] That suggests that tart cherries can help reduce hyperuricemia or elevated uric acid levels in the blood, which is the driving force behind gout. So while the evidence isn’t perfectly consistent across every study, cherries, especially tart cherries, look like a safe natural option that can significantly lower your gout risk. Another food that may help lower your risk of gout is milk. The research shows pretty consistently that dairy intake is linked with lower uric acid levels and fewer gout flares. In fact, one clinical trial using milk enriched with certain proteins showed a meaningful drop in flare frequency within just three months.
[27:06 –> 27:32] The benefit seems to come from several mechanisms. Milk proteins like casein and whey promote uric acid excretion in the kidneys. Erotic acid, a natural component of milk, also increases uric acid clearance. And beyond that, certain peptides and minerals in dairy appear to have anti inflammatory effects, dampening the immune response that drives gout flares. Some studies have emphasized low fat dairy, but the protective effect doesn’t seem to come from the lack of fat content.
[27:32 –> 27:51] It’s really about the proteins and the erotic acid in the milk. So those are things you can do to try to prevent a gout flare. But what happens if you actually have a gout attack? That’s a different scenario. Let’s say you’ve made the lifestyle changes, but then one night you had a few beers, couple cans of sardines, and now you wake up with gout.
[27:51 –> 28:10] What do you do? The first step is to reduce the inflammatory response. Here’s why. Uric acid crystals stimulate something in our immune cells, these cells called macrophages, that triggers what’s known as an inflammasome. When this gets activated, it releases interleukin one beta, a cytokine that calls in neutrophils and other immune cells.
[28:10 –> 28:29] That sets off a full blown war inside the joint. The body is trying to destroy the uric acid crystals, but it actually can’t. Instead, you’re left with pain, redness, swelling, and fever, the classic gout flare. So the goal is to calm that reaction as quickly as possible. That’s where medications come in.
[28:29 –> 28:51] NSAIDs like ibuprofen or naproxen are first line options. Low dose colchicine is another because it blocks neutrophils from migrating into the joint. Glucocorticoids like prednisone are also an option because they suppress inflammation. Normally, I prefer to let the immune system do its job, but in this situation, the reaction is pathologic. You want to tamp it down before permanent damage is done to the joint.
[28:51 –> 29:16] If this is your first gout flare, your doctor may want to confirm it by aspirating fluid from the joint and looking for uric acid crystals under the microscope. That’s especially true if the presentation is atypical. But if the swelling is in the first metatarsal joint at the base of the big toe, classic pedagra, then the diagnosis is usually clear. So you’ve had your first gout flare and brought it under control. Should you immediately start on uric acid lowering medications?
[29:16 –> 29:34] Not necessarily. The first focus should be diet and lifestyle. But if you continue to get these flares despite those changes, then your doctor will likely start you on a medication. The first line drug is allopurinol. It works by inhibiting xanthine oxidase, the enzyme that converts xanthine into uric acid.
[29:34 –> 30:02] It’s effective, but there’s an important risk to know about allopurinol and it’s called allopurinol hypersensitivity syndrome. This is a rare but serious reaction with a mortality rate of twenty to twenty five percent. It’s strongly linked to a genetic marker called HLA B fifty eight zero one. People of Han Chinese, Korean, Thai, and African American descent should be tested for this marker before starting allopurinol. If it’s positive, you should avoid the drug at all cost.
[30:02 –> 30:31] But if you’ve already been on allopurinol for more than eight weeks without a reaction but were never tested, you’re likely in the clear. This syndrome usually happens early after starting allopurinol. There’s another xanthine oxidase inhibitor called febuxostat, but studies have shown it carries an increased risk of cardiovascular and all cause mortality. That’s a risk that doesn’t need to be taken, so I generally don’t recommend it. If allopurinol isn’t an option, the next class of drugs are uracocurics.
[30:31 –> 30:59] These are drugs that increase uric acid excretion in the urine. The most commonly used is probenecid which blocks a transporter in the kidney called URAT one. Interestingly, some blood pressure medications also have uricosuric effects. Losartan, an angiotensin receptor blocker, not only lowers blood pressure but also increases uric acid excretion. If you have gout and high blood pressure, you should be on losartan as it will optimize for both of these diseases.
[30:59 –> 31:12] Okay, let’s talk about another scenario. What if you’ve never had gout before? Should you still be concerned about your uric acid levels? The answer is yes. Most people with elevated uric acid never actually develop gout.
[31:12 –> 31:37] But even without gout attacks, high uric acid still has harmful effects on the body. For one, it raises blood pressure. It does this by impairing nitric oxide signaling in your blood vessels, which normally helps relax and expand with each heartbeat. Elevated uric acid also activates the renin angiotensin system in the kidneys, which contributes to both chronic kidney disease and to higher blood pressure. Uric acid also promotes kidney stones.
[31:37 –> 32:01] It increases the risk of uric acid stones but it also raises the risk of calcium oxalate stones. If you’ve ever had kidney stones before, lowering uric acid can cut your risk of forming another one by about fifty percent. Then there are metabolic risk. Higher uric acid levels are linked to nonalcoholic fatty liver disease where fat accumulates inside the liver. From an evolutionary perspective, this may have been useful.
[32:01 –> 32:28] For someone going on long sea voyages or through periods of food scarcity, storing extra liver fat meant having an energy source that could be drawn on at any time. But today, it just drives metabolic dysfunction and poor health. So what levels should you aim for? Well, ideally, serum uric acid levels should be six milligrams per deciliter or lower. That’s the threshold where uric acid can begin to crystallize in the tissues, and it can happen as low as six milligrams per deciliter.
[32:28 –> 32:56] For reference, our primate cousins like chimpanzees and gorillas who also lack uricase tend to run around three milligrams per deciliter. That may be closer to the natural physiological level humans once had before modern diet and lifestyle drove our levels higher. The bottom line is this, lower is better. With a healthy diet and lifestyle, most people can keep their uric acid levels below six without much difficulty. If you have a genetic predisposition, you may need to be more vigilant.
[32:57 –> 33:15] But the goal is the same. Keep uric acid down, and you protect not just against gout, but against a whole range of health problems. The thing with gout is that it’s a modifiable disease. In most cases, you can prevent it with diet and lifestyle. So let’s review actionable insights from this podcast episode.
[33:15 –> 33:32] First, cut back on high purine foods. That means beef, pork, certain seafoods like anchovies, and especially beer. Beer deserves its own category here. It’s a double whammy. Extremely high in purines from yeast fermentation plus the alcohol that blocks uric acid excretion.
[33:33 –> 33:55] If you struggle with gout, beer just shouldn’t be on your menu. I don’t often recommend strict abstention, but this is one of those rare exceptions. Trading your mobility and quality of life for a multi drink just isn’t worth it. The next big factor is fructose, especially high fructose corn syrup. Our bodies were never meant to handle huge boluses of fructose like what you get in a soda.
[33:56 –> 34:16] A single can can spike your uric acid within thirty to sixty minutes, enough to trigger a flare. So if you suffer from gout, sodas and other high fructose foods really have no place in your diet. Again, think about the trade off. Is ten days a pain worth a can of soda? So once we’ve cut out the biggest offenders, we have some other positive things you can do.
[34:16 –> 34:39] Coffee helps. The more you drink, the more uric acid you excrete, with six cups a day cutting gout risk by nearly sixty percent. Vitamin c works the same way, about fifteen hundred milligrams a day reduces risk by forty five percent. I would split that into three doses of five hundred milligrams three times a day for better absorption. And tart cherry juice, while the evidence is mixed, can be powerful when it works.
[34:39 –> 35:02] Some studies show a thirty five percent reduction in flares and up to seventy five percent when combined with allopurinol. Dairy is another tool. If you don’t have a sensitivity to it, including milk in your diet can make a real difference. People who drank the most milk had about forty four percent lower risk of gout compared to those who drank the least. And if you’re lactose intolerant, lactose free milk should do the same exact thing.
[35:03 –> 35:26] If you do have a flare, the first step is stopping the inflammation. NSAIDs, colchicine, or corticosteroids all work. If the flares keep coming back, that’s when uric acid lowering medications like allopurinol come in. But remember, if you’re Han Chinese, Korean, Thai, or African American in descent, you should be tested for the HLA b fifty eight zero one gene before starting allopurinol. So I hope this was useful.
[35:26 –> 35:58] Whether you have gout or not or just higher uric acid levels, the key point is that this is a completely modifiable disease. Even the highest risk patients can often choose whether they develop gout or not simply by changing their diet and lifestyle. Avoid the triggers, support your metabolism, and take advantage of foods and nutrients that help you excrete uric acid. When you do that, the probability of gout fades down to essentially zero, right back down to the levels of our primate cousins who never get gout. And if you know someone who could benefit from this episode, please pass it along.
[35:58 –> 36:25] Information is power, and the more we know, the more we can help ourselves and the people we love. In our next episode, we’ll continue the tribulation series with the story of Edward Jenner and the development of the first vaccine. It’s a story of both discovery and ethical violation. It’s both fascinating and infuriating all at once, and it connects directly to the vaccination debates we face today. So until next time, stay curious, stay skeptical, and stay healthy.
[36:25 –> 36:27] Cheers.