Gout and Me
Dispelling the “rich man’s disease” myth
Gout has been referred to as the “rich man’s disease” or even the “disease of kings.” Henry VIII suffered from gout. He was indeed rich and a king, too. I too dealt with gout but am neither (last time I checked anyway). That hasn’t stopped people from cracking the odd Henry VIII joke when I mention my gout.
When you hear the word “gout”, even if you’re not quite sure what it is, it conjures up visions of an excess of rich food and drink. Which fits Henry VIII. His legendary appetite makes him the portly poster boy for gout. Easy to imagine him feasting on roasted meats, game, and pies, washing them down with copious amounts of wine. Bloated and in pain after.
I want to dispel the “rich man’s disease” myth. It may have been true in the past, but has not been the case for a long time. If anything, in the modern age, it is a “poor man’s disease.” Or rather, a poor person’s disease.
I also want to demystify gout and explain it in plain, simple terms and also share my personal experience with the so-called “disease of kings.”
What is gout?
It’s a form of inflammatory arthritis. Needle-like crystals form between joints causing excruciating, throbbing pain which some women have reported as being worse than childbirth. It’s the worst pain I’ve ever experienced.
Gout usually occurs in the big toe joint but can happen in other joints too, and does in later stages. Causing permanent joint damage and deformities if not managed. Called a “flare-up” when mild and an “attack” when severe. An “acute gout attack.”
It’s caused by a build-up of uric acid. That’s a natural waste product from the body, flushed out in urine. “Hyperuricemia” or elevated uric acid in the blood is the precursor condition. It can happen for a range of reasons, from genetics to problems with kidney function preventing them from removing excess uric acid. Other factors such as insulin resistance and diabetes also complicate things. The human body is a complex system of systems.
Uric acid is produced when the body breaks down natural substances called “purines.” That can result from the body breaking down its cells (a normal thing) or from “purine rich” foods. Purines are mostly found in meat and fish, the worst offenders being offal, shellfish, and red meat. Other meat and fish also contain moderate amounts of purines, as do some vegetables such as broccoli and asparagus, although these are less of a concern. Alcohol (and the yeast in beer) is a huge problem and so is sugar, particularly fructose. These increase uric acid production by interfering with its removal.
It’s all about the concentration of uric acid in the blood (so dehydration plays a role too). When concentrated, uric acid molecules stack into crystals (monosodium urate), becoming needles of torment. As poor Henry would have found after eating and drinking all his favourites in large quantities.
Demographics
In Henry’s time the poor couldn’t afford meat or fish in abundance and sugar was virtually unheard of outside of natural sources such as fruit or honey. The poor subsisted mostly on grains, cereals and vegetables, meat being a luxury. Even the “table beer” popular across Medieval Europe at the time typically had an alcohol content of 1% or less. So only the well-to-do could “enjoy” the “privilege” of gout. It was indeed a rich person’s disease.
Fast forward to our modern era and since the mid-twentieth century massively industrialised farming and food production has brought us all cheap and readily available purine rich foods. Heavily processed meat products with offcuts including offal. Parts even the animal would be surprised it had. Especially the products at the lower end of the market made with “mechanically reclaimed meat“ or “pink slime.”
Add to that all the sugary drinks and refined carbohydrates, which quickly turn into sugar in the bloodstream and so are essentially sugar too.
It is now very cheap to elevate your uric acid and blood sugar levels. That’s obvious looking at the epidemics of obesity, heart disease and diabetes, all comorbid with gout, in our “developed” societies.
You no longer have to be rich. You don’t have to be a king. We’ve democratised gout.
Let’s look at some facts.
In the US gout has more than doubled from the 1960s to the 1990s. It affects 9.2 million Americans, almost 4% of the population. In the UK it’s gone from 1.4% of the population in 1999 to 2.49% in 2015. That’s around 1 in 40 people in both countries. It affects men more than women, around four times as much, mostly due to hormonal differences that expedite uric acid removal in premenopausal women (meaning women are at greater risk later in life).
So what’s the makeup of the people with gout or at risk of developing gout? From Rising burden of gout in the UK but continuing suboptimal management: a nationwide population study published in the British Medical Journal (emphasis mine):
The reasons for current geographic variation in gout most likely relate to differences in socioeconomic status, life-style and nutrition and although gout historically was considered a disease of affluence, the converse may now be true. The UK morbidity statistics from general practice (1970–1971) reported that people with non-manual skilled occupations had the highest whereas professional occupations had the lowest standardised consulting ratio for gout.
A study published by Frontiers also looks at the level of education attainment and incidence of gout:
According to the primary IVW method utilized, receive 4.2 years of additional education was associated with a 27.6% lower risk of gout.
Another study looking at ethnic and socioeconomic disparities in the US published on MDPI:
Gout was rare among Black adults in the US until the 1940s and 1950s, similar to Black adults in Africa, especially in rural areas where traditional agricultural and dairy-based diets were common. Subsequently, following worsening in diet quality and quantity, the frequency of metabolic conditions such as obesity, diabetes, and hypertension, as well as gout, rapidly rose overall, although disproportionately among Black Americans.
Taking all this together it paints a picture similar to that for gout’s comorbidities: obesity, heart disease and diabetes. Even taking possible ethnicity related genetic predisposition into account, socioeconomic status plays an outsize role in determining who is susceptible to gout.
That picture is: poorer people are at higher risk.
Poor nutritional education. Poor food choices. Reduced access to healthcare in many countries.
Priced out of more expensive organic foods. Trying to get the most “caloric bang for their buck” to feed themselves and their families.
What about present day “rich” people? They would have healthier eating habits, access to higher quality food, be better informed, and have better healthcare. Even those with a predisposition or tendency to overindulge would have better ways of managing gout.
Gout is a “poor person’s disease.” Has been for a while. Not disproportionately a disease of the poor by a huge margin, but it is most definitely not a “rich man’s disease” anymore.
We’ve refined and industrialised food to a point where we can induce a gout attack in someone at risk through a single bad meal choice and a few drinks. I should know, that’s how it started for me.
Gout and me
I grew up poor and wasn’t active. I didn’t know about nutrition. Growing up with a single mother (from 8) who was obese and now has diabetes. I ate junk. Frozen meals, snacks, fast food from my teens up until my thirties. Although I didn’t drink heavily it was normalised in British culture to go out and down six pints without eating. There is no family history of gout that I am aware of.
I had my first gout attack in my early thirties and thought I had stubbed my toe. It was so painful I could barely sleep. After a few more episodes, once or twice a year, I saw my doctor. I had gout. For a long time I didn’t take it that seriously, until recently while travelling and not keeping track of what I was eating or drinking, I had a severe attack. Since then it’s become more frequent.
Is this a legacy of poor diet choices or a genetic predisposition? I don’t know. Maybe some of both. I do know I can stop it from getting worse. I’ve since gone mostly vegetarian and stopped drinking. I’m taking it month by month. I’m fortunate to have the knowledge and means to manage my gout. Many don’t.
Gout can be managed with medication. Prevention is key and medications such as allopurinol and febuxostat lower uric acid, so they help stop concentrations rising to a point where uric acid can crystallise. These medications are usually taken for life. I’m trying to see if I can manage my gout with diet changes alone. Mixed results so far, but it’s early days. Uric acid crystals (monosodium urate) take months or years to dissolve completely. I am at least not making it worse.
Having to be so strict with my diet is taking another toll, that of having to deny myself many of the things I used to enjoy. Right now I’m “close to the edge”, one burger and a couple of beers could trigger an attack. It very much feels like a silent assassin lurking around corners, spying on me, waiting for me to slip up. Ready to ambush me. Not to kill, but to maim. Leaving me hobbling around in agony. So I have to be very careful.
Once that happens, some medications can reduce the severity of the pain. Steroid and non-steroid-based anti-inflammatories — prednisolone, colchicine, naproxen, or ibuprofen. Some or all of these should be on hand for gout sufferers. These only help reduce pain and swelling but aren’t a cure. The risk of permanent joint damage after repeated attacks remains, as well as the risk of developing “tophi” hard lumps of crystal which stay under the skin. That can lead to deformities.
The only real way to “cure” gout is by getting uric acid levels under control.
The healthy range for men is 3.5–7.2 mg/dL or 208–428 µmol/L and 2.6–6.0 mg/dL or 155–357 µmol/L for women.
Mine was 7.08 mg/dL or 420 µmol/L six months ago and is now 6.39 mg/dL or 380 µmol/L, as of my last blood test. This doesn’t account for urate crystals which would have already formed.
That’s my journey with gout and it’s an ongoing one. I’m focusing on the positives of all this making me adopt a healthier diet and habits. Outside of travelling those were already quite good.
I certainly don’t fit the image of Henry and his feasting. For the last decade, I’ve been increasingly active. I run 3–4 times a week as well as regularly strength training. As a result, I’m fairly lean and muscular. As are many others who suffer from gout. You don’t have to be overweight and be eating foie gras, lobster and filet mignon regularly to get gout. You’re more likely to get it eating cheap burgers, sausages and kebabs with beers. A “rich diet” indeed.
It’s not a “rich man’s disease” or the “disease of kings.” They’re able to deal with it better than most. It’s everyone’s disease and more of a burden on the poor. It can be managed with sensible diet and lifestyle choices early on and with medication later. For those who have access. For those who don’t, it can become chronic and debilitating, seriously affecting and limiting quality of life.
Alongside cardiovascular and other serious conditions, gout is a lens on the food we eat, how it’s produced, the level of nutritional education and access to healthcare that people have, and a whole host of other insights into society and what that tells us about the societies we live and their values and inequities.
If someone you know cracks a Henry VIII joke or comments about a rich diet or overindulgence then tell them to read this.
May you never experience a gout attack.
Thank you for reading.
