Gout Foods To Avoid
As we’ve discussed in a previous post, moderation in all things is important when you adopt a diet for gout. To recap, the foods highest in purines (a major cause of gout) include organ meats, shellfish, fish roe, and certain oily fish such as anchovies and mackerel. The foods which contain high to medium levels of purines are most meats, poultry, beans and lentils, certain vegetables such as mushrooms, cauliflower and asparagus; and the foods lowest in purines are dairy products, pasta, refined bread and cereals, ice cream and fats.
Alcohol does increase the risk of developing gout, and it may precipitate a sudden and unexpected attack of gout if you’ve experienced a previous attack.
Alcohol has a number of effects on the metabolism of the body: first, it contains high levels of purines; second, it interferes with the removal of uric acid from the body; and third, heavy drinking can produce ketones, which also interfere with the removal of uric acid from the body.
So, as you can imagine, a reduction in alcohol consumption is pretty important: the standard advice is to have three alcohol free days per week, and on the days that you do consume alcohol not to have more than one or two small glasses of wine or a pint of beer. It is true that beer presents a higher risk than wines or spirits: in fact, drinking two glasses of wine a day has not been linked to an increased risk of gout.
In a correctly balanced gout diet, it’s also helpful to consume large quantities of water because this reduces the chance of uric acid crystals forming inside the kidneys. As anyone who has had them can tell you, kidney stones can be extremely painful. The generally recommended quantity of liquid to drink per day is around 1.5 liters: this will include all drinks except alcohol.
There is a limited amount of evidence that coffee has some protective effect against gout. What you should avoid, however, are sweetened soda drinks and fruit juices because the sugar syrup and fructose they contain may well stimulate a gout attack. The best drinks for a diet for gout are pure fruit juice, possibly diluted with water, and semi-skimmed and skimmed milk.
What Causes Gout? (Hint – The Wrong Diet, Among Other Things)
And What Are The Best Remedies For Gout?
One of the most common questions about gout is how much any abnormalities of purine metabolism are responsible for gouty arthritis.
Purine metabolism is essential to the body’s well-being, since it is essential to the production of proteins. Nonetheless, it is the dysfunction of this metabolic pathway which is responsible for the development of hyperuricemia (high uric acid in the blood). High uric acid causes the formation of urate crystals in the joints, and these crystals cause gout pain..
The fact is, gout can be caused by several deficiencies or abnormalities of purine metabolism. There is one type of abnormality which focuses upon decreased excretion of uric acid; there is another type which focuses upon an increased synthesis of uric acid. It is this latter group where enzymatic abnormalities appear to be responsible for the formation of high levels of uric acid and the consequent development of gout. But how much of this purine overload comes from the wrong gout diet?
Well, to recap, gout has a number of causes, the primary one being under-excretion of uric acid by the kidneys. This is not a biochemical issue, but it is, even so, one of the predominant causes of gout in adult males and females. Enzymatic deficiencies are the other cause of high levels of serum urate. You can read more about this here.
More mundane factors which are responsible for the development of gout include consuming excessive quantities of alcohol, an association which has been known for over 100 years. Taking a simplistic view, and assuming that alcohol is indeed closely related to the occurrence of gout, both in anecdotal evidence and scientific studies, the question is – what could possibly be causing this association? Well, the answer, of course, is that you are not consuming the correct gout diet.
Alcohol as a cause of gout
There are, in fact, several reasons why alcohol can contribute to the development of chronic gout and the inflammation and pain of acute gout attacks. To start with, alcohol contains high levels of carbohydrates which can predispose an individual towards obesity; and we know that there is an association between obesity and gout. (Losing weight and reducing consumption of foods to avoid with gout is often offered as a gout treatment strategy).
Furthermore, excessive consumption of alcohol induces higher than normal levels of triglycerides or hypertriglyceridemia, which is associated with hyperuricademia and gout. Both long and short-term consumption of alcohol increases the synthesis of urate through an increase in metabolism of adenine nucleotides. Beer, in particular, contains high levels of purines. So the complexity of the correct gout diet is revealed in the interaction of a number of seemingly unrelated factors.
All in all, a number of studies suggest that alcohol effectively induces an increase in urate synthesis, while simultaneously working to reduce the excretion of urates.
And while it’s often said that certain types of alcoholic drink are more likely to induce an attack of gout than others, there is no known explanation as to why this should be so, or indeed if it is true at all.
The first line of treatment for gout therefore should undoubtedly be directed at suitable gout dietary and lifestyle changes, with drug treatment given to men and women who remain hyperuricemia despite these lifestyle modifications.
What makes the investigation of the causes of gout more challenging is that hyperuricemia often occurs in association with other metabolic disorders. And if gout is present, then treatment of gouty arthritis may require, nay depend on, the physician determining the cause of that hyperuricemia. The doctor should also offer some kind of treatment which will reduce serum uric acid levels to less than 360 µmol per liter while simultaneously diminishing the number and size of uric acid crystals deposits in the body. Treatment options for gout.
Summary of the causes of gout
So what we know is that gout tends develop when hyperuricemia occurs, and is associated with levels of serum urate (uric acid) higher than 390 µmol per liter. It is often accompanied by obesity, diabetes, and insulin resistance – all of which tend to increase the risk of cardiovascular problems. We also know that gout affects between 1% and 2% of the population; which represents around 20% of people with hyperuricemia.
The term “gout” actually refers to the outcome of excessive levels of uric acid in the body: the deposition of crystals of monosodium urate in the synovial space of the joints (and perhaps urate nephropathy and possibly tophi formation). A gout diet helps to avoid this by reducing uric acid in the blood serum.
If a hereditary disorder is eliminated, then we also know that the main factors responsible for the development of gout include foods rich in purines, obesity, and alcohol consumption. The chance of an individual developing gout increases markedly when serum urate levels rise above 480 µmol per liter.
Possibly because of the Western lifestyle, gouty arthritis is the most common form of arthritis in the population, and its incidence increases rapidly with age. It is about 50% more common than rheumatoid arthritis. Gout medications explained.
One of the factors responsible for the increase in gout in recent years is the use of drugs that inhibit uric acid excretion such as thiazide. Men have a much greater risk of developing gout than women do; this appears to be because of the uricosuric action of estrogen.
As we have observed already, uric acid, or urate, production is the end result of purine metabolism. A notable step in this process is the metabolism of xanthine and hypoxanthine by the enzyme xanthine oxidase. The resulting urate is excreted by the kidneys. Read more here. This is a mechanism susceptible to many different influences, including low-dose aspirin treatment, which reduces the excretion of urate.
The saturation point of uric acid is 400 µmol per liter at 37°C and pH 7.4; once it’s concentration goes beyond this, monosodium urate crystals begin to precipitate out in those parts of the body where the ambient temperature tends to be lower — such as the foot (or occasionally the fingers). Urate crystals promote an inflammatory response in the body, activating the NALP3 inflammasone and promoting the release of pro-inflammatory cytokines, including interleukins 1, 18 and 8.
A gout attack is usually the result of an unexpected and rapid rise in serum urate levels. This can be the product of excessive alcohol consumption or eating a meal high in purines. It appears to be the inflammation of an immune response caused by the release of uric acid from the edge of crystal deposits which triggers an attack of gout. For the sufferer, the usual appearance of gout is an acute episode of monoarticular arthritis at themetatarsophalangeal joint of the big toe: such attacks tend to be self-limiting but are extremely painful, usually start at night, and last for between seven and 10 days.
It is the presence of urate crystals in the joints and connective tissue, and possibly also inside the kidneys, that is responsible for the chronic nature of this problem. Around 90% of men and women who experience an attack of gout will have repeat episodes in five years. The finger joints may be affected, and oligoarticular or polyarticular arthritis may be seen. There are many other conditions which resemble gout, including pseudogout (chondrocalcinosis) where the deposition is calcium pyrophosphate dihydrate crystals, and a condition where calcium oxalate is deposited within the joints.
Foods to avoid with gout
Usually, a diagnosis of gout can be made when the large toe displays characteristic signs of gout, and the serum urate level is increased. It’s also possible for crystals to be extracted from the joint and examined under a polarizing microscope.
Diagnosis is not difficult, but establishing the causes of gout may be more challenging. As we have observed, there is a genetic predisposition to gout. There is also an association between metabolic syndrome and gout. The guidelines for risk assessment recommend measuring fasting blood sugar, and possibly levels of HbA1c, as well as levels of fasting blood lipids/cholesterol, and checking thyroid parameters.