The Gout: what you need to know and 7 things you can do about it.

  1. Gout is an auto-inflammatory disease caused by a disorder in purine metabolism and the resulted chronic elevation of blood (serum) uric acid (i.e., hyperuricemia)
  2. Men have a higher risk of gout at a lower given blood level of uric acid, and at a lower age than women – generally 10 years earlier.
  3. Women who go through early menopause, or have estrogen deficiency are at higher risk than women who progress through menopause at a normal age, due to oestrogen’s role in increasing uric acid excretion.
  4. Insulin resistance increases risk of gout, as insulin reduces uric acid secretion. The relationship between insulin resistance and gout is more pronounced in women than in men.
  5. There is a bi-directional relationship between high blood pressure and gout: ie if you have high blood pressure, your risk of gout goes up (independent of diuretic medication that is taken), and if you have gout, your risk of developing high blood pressure also increases. High blood pressure can result in damage to kidney and a reduction in uric acid excretion, and the inflammation associated with gout can stiffen and damage arterial walls, and reduces production of nitric oxide – which helps widen arteries.
  6. Genetics play a role in determining risk associated with gout – and people with a particular genetic profile (such as those of European descent with the SNP sequence SLC2A9 as an example) have an increased risk, as do those with ABCG2 rs2231142. However, as with any genetic risk factor, lifestyle determines if these genes are switched on or off, so while this information could be useful (and more people are starting to find out their genetic profile and determine what it means for their health), it is your lifestyle habits predominately regulate overall risk
  7. Triglycerides increase in the bloodstream when people overeat refined carbohydrate foods, and recent research suggests a reduction in serum uric acid occurs when triglycerides decrease.
  8. Alcohol intake is associated with an increased risk of gout – beer more so than wine.
  9. Overall fructose load in the diet is the only type of carbohydrate that is known to increase uric acid levels, potentially because when metabolised, it depletes phosphate and therefore doesn’t help produce ATP (energy) in the body and instead increases uric acid production. Fructose from processed food (and particularly sugary sweetened beverages) can elevate insulin levels and increase risk of insulin resistance. There may be a genetic element to this also, with people who have polymorphisms in SLCA9 and ABCG2 genes responding unfavourably to a load of fructose.
  10. A large cross sectional survey found that people following a vegan diet had the highest serum uric acid concentrations compared to fish eaters, meat eaters and vegetarians, independent of smoking status or alcohol intake.
  11. While seafood is often cautioned against for people who experience gout due to its purine content, a number of studies have failed to find a relationship between seafood intake and serum uric acid levels. Those that have found a relationship may not have adjusted for body mass index (BMI), which can confound the relationship as it did in this study. Indeed, those populations who are at greater risk today (such as Maori and Pacific among New Zealand population) enjoyed a traditional diet of predominantly seafood, vegetation, tubers and gout was non-existent.

What to do?

  1. Look after your gut. Bacteroides caccae and Bacteroides xylanisolvens are increased, and Faecalibacterium prausnitzii and Bifidobacterium pseudocatenulatum depleted in the gut of people who experience gout, suggesting a strong correlation with the presence of gout. F prausnitzii is one of the most abundant bacterium in the gut of a healthy individual, helping produce short chain fatty acids butyrate, which is fuel for our gut bacteria, and the provision of B pseudocatenulatum improves markers of gut wall integrity. So these are pretty important! While this doesn’t necessarily mean that the provision of certain bacteria through probiotics will reduce gout attacks, it does suggest that inflammatory processes of the gut play a role in the presentation of gout and provides further evidence of the importance of a diverse population of bacteria in the gut for overall health.
  2. Supplementing with 1500mg vitamin C reduces serum uric acid and its antioxidant functions may also help kidney function by reducing inflammation.
  3. Like your coffee? You don’t have to go without if you have gout and in fact, 4-5 cups per day have found to decrease serum uric acid that isn’t seen with green or black tea, or total caffeine intake. Decaffeinated coffee has afforded similar benefits, leading investigators to suggest the phenol content (phytochemicals) might increase insulin sensitivity and decrease serum insulin, as discussed above insulin levels have a positive correlation with uric acid due to decreased renal excretion. Furthermore, xanthines, either in caffeine or in coffee itself, could inhibit xanthine oxidase – an enzyme that increases reactive oxygen species (and inflammation).
  4. Magnesium intake is associated with a decreased serum uric acid level in males, and marginal intakes is associated with higher levels of markers in the body indicative of inflammation. Magnesium is low in soil which makes dietary sources of the micronutrient not as high as they once were, therefore supplementing with magnesium of 300-600mg/day (depending on bowel tolerance) is likely a good idea. (To be honest, I’m a big fan of magnesium supplementation for pretty much anyone male or female, given it’s a co-factor in over 300 processes in the body).
  5. Tart cherry extract – not just useful for sleep – is found to reduce the prevalence of gout flare ups in cross sectional studies, potentially due to the presence of polyphenols including anthocyanins, and vitamin C found in the fruit, which have anti-inflammatory and antioxidant affects.
  6. The consumption of low fat dairy products is linked to a lower risk of gout in larger population studies.*
  7. Anecdotally (as in, I didn’t find any study on pubmed to support this), baking soda is used to increase pH level of the blood (¼ teaspoon in water), thus making uric acid in the blood able to be excreted. If you know of any studies around this that I’ve missed, let me know!)

The take-home?

While a low purine diet is often recommended as a dietary prescription for people with gout, many purine-containing foods (such as seafood and vegetables) do not contribute to hyperuricemia or gout and may in fact be protective. The effects of red meat consumption on serum acid levels are arguably hard to disentangle from other elements of the modern dietary pattern, and are often in conjunction with higher alcohol intake, lower fruit and vegetable consumption and higher fast-food intake – all contributors to inflammation in the body. In addition, the agricultural practices of the cattle industry in countries such as the US where many of the epidemiological studies that associate red meat with poor health (including higher serum uric acid levels) include the use of antibiotics, poor farming practices and animals that are grain and not grass fed, altering the fatty acid profile of the meat to be higher in omega 6, pro-inflammatory fats. Furthermore, processed and fresh meat is often grouped together – thus a steak is viewed the same as a hamburger from a fast-food outlet – the latter often being in the company of a bun, fries, mayonnaise made with industrial seed oils and a sugar sweetened beverage – the adverse effects which many, myself included, argue cannot be adjusted away by a statistician when determining risk.

*I don’t think you need to start consuming low fat dairy if right now you’re enjoying the benefits of full-fat dairy in the context of an awesome diet. I think this could well be indicative of overall lifestyle patterns. I’d be surprised if there were studies showing that risk of gout is increased in a diet that is whole food, minimally processed, an abundance of vegetables that also incorporated full-fat dairy products.

 

Gallstones and your gall bladder 101: what, why, who (and generally speaking) what to do?

Until this week I had no idea how prevalent gall bladder inflammation (cholecystitis) and gallstones were. And in who. A lovely client of mine had experienced cholecystitis for years. She was actually none the wiser as equally suffered from irritable bowel syndrome too so had lumped the symptoms (upper abdominal pain, particularly after a fatty meal) into the same category as ‘digestive issues’ which we had been working on (and she had been having success with) over the last few months. It wasn’t until this week that she called me to say she was diagnosed with gallstones and was going in for emergency surgery to remove it that I thought – hmm, is that unusual? Turns out it’s not.

The gall bladder is required to store the bile that is required for fat digestion. If a person is experiencing inflammation (systemic or local) this can irritate the gallbladder and cause significant abdominal pain after eating which usually subsides in the hours that follow. Gallstones are a result of reduced gallbladder function, where the bile isn’t released as it should be and can become thick and sticky, forming stones that can be the size of pebbles to the size of golf balls. There are three types of stones; black pigment stones (related to cirrhosis – scar tissue build up in the liver – or haemolytic disorders – breakdown of red blood cells); brown pigment stones (related to an infection in the gall bladder) but overwhelmingly in the western world, the prevalence of the third type of stone – a cholesterol rich one – is increasing, accounting for around 70% of gallstones. Pain occurs if one of these get stuck in the bile duct – this may also subside. However if you experience continual pain, or begin to have more frequent attacks, then it is generally recommended that something needs to be done.

I had always associated gallstones with people of an older age bracket, but that was just because I’d never had a reason to look into it at all. In fact, this week I was bombarded by young, fit women who responded to a post I put on my Facebook page related to cholecystitis and gallstones that had all experienced problems and subsequently had their gallbladders removed. Now not all people suffering from cholecystitis have gallstones, and not everybody with gallstones experience pain – indeed some remain asymptomatic for most of the time. However, there is a surprisingly high number of people that experience problems with either condition and in New Zealand it’s estimated that 20% of people aged 30y – 75y will be affected. Now that is a LOT of people who may be having problems with either cholecystitis or gallstones and potentially not even know it. The pain experienced in an attack may be in isolation of other symptoms, or put down to ‘normal digestive issues’.

The formation of gallstones and cholecystitis is (like most things) possibly due to an interaction between both genetic and environmental factors. Genetically, a mutation in a protein that may be responsible for the delivery of phospholipids and bile from the liver will increase the risk, as will having a genetic predisposition – the latter increasing your risk four-fold. In addition – and this is what sparked my attention from the Facebook posts – the presence of an autoimmune disorder (Crohns disease, celiac disease) or even a sensitivity to gluten increases risk. The first possible reason for this could be from increased inflammation due to the nutrient malabsorption, or a defect in the gallbladder ability to empty – both resulting in a reduction in gallbladder function. Alternatively, it could be that the gallbladder disease is the result of the same immune system attacks that occur with an autoimmune condition. Regardless of the mechanism, there is a very real relationship here.

Other factors that increase the risk of gallstones are taking an oral contraceptive pill, being pregnant, or having had multiple pregnancies. The increased oestrogen levels affect gallbladder motility (delaying bile release from the gallbladder) and increase cholesterol saturation of bile (cholesterol is the backbone of our sex hormones). A high carbohydrate intake in pregnant women (particularly fructose) is also associated with increased incidence, and there is a link between pregnancy, pancreatitis and gallstone risk. Weight loss, weight cycling or fasting can also increase risk of gallstones as fat is being rapidly broken down and there is increased secretion of cholesterol into bile. With these factors in mind, it is no wonder women are at greater risk (two-thirds of those in the US with gallbladder disease are women). Equally a diet that is higher in processed refined food and calories increases the risk with higher circulating insulin and triglycerides as a consequence of the standard western diet. People who are overweight or obese, or have risk factors associated with the metabolic syndrome are at an increased risk – now this may well be due to the previous point, however this has also been found independent of diet; those with a fat deposition around the middle are more likely to experience problems. Indeed this type of fat patterning is related to reduced function of the liver (and non-alcoholic fatty liver disease) which may result in fat build up and cirrhosis also related to gallbladder function.

A question that arose on my Facebook page was whether athletes were at greater risk compared to the general population.I had a good look around the literature and only came across a couple of studies that related a high training load to problems with the gallbladder. As athletes we place ourselves under a lot of training stress – chronically this leads to increased inflammation. Haemolysis can also occur in susceptible athletes who heavily exert themselves which again impacts on inflammatory pathways. This inflammation is in the absence of gallstones but may well lead to gallstone formation as it reduces gallbladder function. If you combine this with an intolerance to certain food (as a number of endurance athletes also experience), then there are certainly links between the two despite an absence of academic literature out there. Changes to liver enzymes after an extreme endurance event may place an athlete at risk, and interestingly, this case study illustrated how inflammation due to higher intensity training led to a thickening of the gallbladder tissue and an increased tension in the absence of stones or bile buildup (‘sludge’). The removal of the gallbladder stopped this tension and the athlete was pain-free. In this instance, surgery was potentially the only route as it wasn’t related to stones. But if you do suffer from gallbladder problems with or without gallstones and don’t want to go down the surgical route, what are your other options?

For those with problematic gallstones, a first approach may be sound wave therapy to break down stones so they can move down the intestine and be excreted without the risk of getting stuck. Similarly, ingesting a naturally occurring bile (in the form of ursodeoxycholic acid) may also gradually break down the stones. However many people continue to suffer symptoms associated with gallstone attacks after these treatments. Though not in the academic/medical literature, I’ve read a lot of people do an olive oil/lemon juice protocol which (it appears) involves fasting/apple juice/anywhere from 1 cup to 3 cups olive oil and lemon juice/sleeping then warm water. I’ve actually just lumped a lot of different components of these protocols to give you an idea of what you can find if you can go searching… not to recommend you try it (it’s not my place to do that!)

For those with problems related to inflammation of the gallbladder, or with gallstones that are symptomatic, an anti-inflammatory diet is the way to go – removal of grains, dairy, legumes, refined processed food and a focus on fruits, vegetables and animal protein. These foods are rich sources of antioxidants and are not going to cause stress on the digestive system, thereby they are your best line of defense. For some, following an auto-immune protocol that also removes eggs, nightshade vegetables, nuts and seeds initially may be required, with further supplementation to help heal the gut. If you have neither of the above and are currently losing weight, research suggests that following a higher fat diet for weight loss is protective against developing gallstones when compared to a lower fat diet. Further, there is limited research that vitamin C supplementation can prevent gallstones by promoting the conversion of cholesterol to bile salts in the gall bladder.

And what if you have the surgery to remove your gallbladder? Is it low fat foods from here on in? This seems to vary a LOT from person to person. Some people can continue to include good amounts of healthy fat in their diet with no noticeable digestive issues. While some notice a vast improvement with the addition of digestive enzymes, others don’t notice any change. It’s best not to drink fluid around meals so you don’t dilute your stomach acid and obviously try to eat as ‘clean’ as possible –following a paleo approach will ensure nutrient intake is optimal.