Will You Get the ‘Rich Man’s Disease’?

Recently by Mark Sisson: A Beer Drinker's Primal Story

Every so often, a health malady arises that seems to clash with Primal living. And when a doctor brings it up, or a family member with intimate knowledge of the illness expresses concern, it can be intimidating and troubling. We’ve all heard how we’ll suffer heart attacks, diabetes, ketoacidosis, lowered marathon performance, kidney disease, and osteoporosis from “eating all that meat,” but that’s not what I’m covering today. No, today the subject is gout, which occurs when excess uric acid crystallizes and accumulates in the extremities. The jagged shards embed themselves in the joints, tendons, and other tissues, causing excruciating pain, inflammation, and swelling, particularly in the big toe. Suffice it to say, it is extremely unpleasant. Sounds great, right?

Let’s move on to the question that prompted today’s post:

Hi Mark,

What’s your take on gout? It apparently runs in my family, and while I haven’t gotten an attack yet, I’ve heard that a “rich diet” is the cause, which as I understand refers to meat and animal fat. Does this mean I shouldn’t eat Primal? What does the science actually say?



In previous centuries, gout was described as a “rich man’s disease” or “the disease of kings.” Ambrose Bierce called it “A physician’s name for the rheumatism of a rich patient.” Basically, it primarily affected the upper class, the royalty, the aristocracy — those who could afford “rich” foods like meat, sugar, and port. In the mid-19th century, uric acid was identified as the causative agent in gout. Where does uric acid come from? Purines.

Purines are in pretty much every cell — plant and animal alike — because they provide some of the chemical structure of both DNA and RNA. When cells are broken down and recycled (like in digestion — yum, love those delicious cells!), their purines get metabolized right along with everything else. Uric acid is a major product of purine metabolism, and this is a good thing; uric acid acts as an antioxidant in our blood, protecting blood vessels from damage. But if for some reason an excessive amount of uric acid (hyperuricemia) is produced, enough to crystallize and lodge in joints and other tissues, you might get gout.

And so the standard tale goes like so:

Since we get uric acid from breaking down purines, the natural solution is to reduce one’s intake of purine-containing foods — right? That seems sensible. Reduce purines, which turn into uric acid, and you reduce hyperuricemia, which causes gout. Boom. Problem solved.

The problem for a Primal eater given this advice, however, is that the richest sources of purines also happen to be some of our most treasured foods: organ meats like sweetbreads, kidneys, liver, and brain; seafood like sardines, anchovies, herring, mackerel, scallops, and mussels; and wild game meat. Even beef and pork are moderate sources of purines. In short, everything we talk about eating on MDA is apparently contraindicated for gout prevention. How do we reconcile without destroying our brains with cognitive dissonance?

Easy. We look for the real problem. What’s more logical? That purines, which appear in all foods and particularly in some of the most nutrient-dense foods (like organs and seafood), are the problem? Or that hyperuricemia, an excess of uric acid, is the problem?

Let’s table the purine talk for awhile, given the importance of purine-rich foods in the ancestral human diet, to look at some other causes of high uric acid. What else causes uric acid to rise?

Dietary Fructose

When the liver is loaded with fructose, whether by excessive intake or a lack of liver-glycogen-burning activity, purine metabolism is disturbed and uric acid spikes. One study (PDF) found that 0.5 g/kg body weight was enough to increase uric acid levels by this mechanism.

Fructose also decreases urinary excretion of uric acid, so it’s a double whammy: fructose both increases uric acid and decreases its excretion.

Read the rest of the article

Listen to Lew’s recent podcast with Mark Sisson