Gout is the most common form of chronic, progressive, inflammatory arthritis. Its prevalence continues to increase worldwide. This condition seems to baffle several fields of medicine who deal with patients suffering with the relentless disease, including podiatrists, chiropractors, rheumatologists, and general practitioners alike.
The deposits of MSU, monosodium urate, crystals into the synovial fluid and other tissues take place when the serum uric acid concentration exceeds its solubility. As this progresses, these deposits can occur just about anywhere in the body and lead to chronic pain, bone erosions, tophi, and general joint deformities. This condition can become downright debilitating, and rather difficult to treat.
Treatments for acute Gout flares typically involve dietary adjustments, urate lowering drugs, xanthine oxidase inhibitors, and symptom/pain relieving medications. However, for the 2% of these cases that suffer with Refractory Gout (uncontrolled, chronic and recurring attacks), treatment can be quite challenging. This stage of Gout is rather relentless and often resistant to common management therapies and medications.
Once Gout attacks become chronic, they often become tophaceous, where nodular masses of uric acid are deposited in soft tissue areas of the body. While most tophi is believed to be visible, studies have shown only 25% being detected by a physical exam. Imaging known as DECT, dual-energy computed tomography, has painted a very different picture with the detection of large masses of non-visible tophi all throughout the body, including the organs.
Does this mean that virtually ALL gout is already tophaceous by the time the first attacks occurs? The simple answer is ‘yes’. While it may begin small and only microscopically visual, its destructive path can lead to dangerous changes within the body, and eventually show up on the outside of the body, as well.
Gout flares begin with the combination of hyperuricemia and associated chronic inflammation. Uric acid excretion is conducted largely by the kidneys (around 65-75%), with the other 25% or so excreted by the GI tract. Under-excretion of uric acid makes up close to 90% of those that suffer with Hyperuricemia. Only 10% is caused by over-production.
Causes of Hyperuricemia
Under-excreters of urate (~90%)
| Drugs or Dietary Habits- | Clinical Disorders- | |
|---|---|---|
| Diuretics | Diabetic ketoacidosis | Renal insufficiency |
| Low doses of salicylates | Lead nephropathy | Polycystic kidney disease |
| Ethambutol | HTN | Familial juvenile hyperuricemic nephropathy |
| Pyrazinamide | Medullary cystic kidney disease | Dehydration |
| Laxative Abuse (alkalosis) | Lactic acidosis | Starvation |
| Levadopa | Salt restriction | Obesity |
| Methoxyflurane | Hyperparathyroidism | Hypothyroidism |
| Cyclosporine | Diabetes insipidus | Toxemia of pregnancy |
| Tacrolimus | Sarcoidosis | Bartter’s syndrome |
| Chronic beryllium disease | Down syndrome |
Overproducers of urate (~10%)
| Drugs or Dietary Habits- | Clinical Disorders Leading to Purine Overproduction- | |
|---|---|---|
| Ethanol | Myeloproliferative disorders | Lymphoproliferative disorders |
| Diet rich in purines | Polycythemia vera | Malignant diseases |
| Pancreatic Extract | Hemolytic disorders | Psoriasis |
| Fructose | Obesity | Tissue Hypoxia |
| Nictonic acid | Glycogenosis III, V, VII | |
| Warfarin | ||
| Ethylamino-1,3,4thiadiazole | Inherited Enzyme Defects | |
| 4-Amino-5-imidazole carboxamide riboside | HPRT deficiency | |
| Vitamin B12 (patients with pernicious anemia) | Increased PRPP synthetase | |
| Cytotoxic drugs | Glucose-6- phosphatase deficiency (glycogenosis I) |
Source: Becker MA, Jolly M. Clinical gout and the pathogenesis of hyperuricemia. In: Koopman WJ, Moreland, LW, eds. Arthritis & Allied Conditions. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:chap 113.
If you take a careful look at this chart, you will see the large discrepancy between the two contributors to hyperuricemia, 90% stemming from under-excretion, with only 10% sourced from over-producing uric acid. That might make many scratch their head after years of worrying about their diet, purines, and their own ‘personal triggers’, only to find out a mere 10% stems from food choices?
Which indirect offenders involved in your diet and lifestyle could be contributing to the 90% under-excreting category?
The broader picture will show you how fructose, acidic food choices, acidic lifestyle choices, lack of water, lack of exercise, stress, vitamin and mineral deficiencies, alcohol consumption, prescription medications, etc. can all lead to kidney and liver insufficiencies, lactic acidosis, dehydration, and generalized inflammation.
70% of uric acid production stems from unhealthy, dying cells. You can see from this picture that unhealthy cells have trouble both ridding of waste products (extra uric acid) AND absorbing nutrients. Every negative thing we expose our body to on a daily basis contributes to the demise our of healthy cells, and furthers disease.
You may have ‘trigger foods’ that spark an attack. A purine-rich meal may push your ‘already full’ glass over the edge and into an attack. However, be sure to understand things were already brewing and these triggers simply tipped the scale. There is a much larger picture here, and a management approach that will be key to avoiding the damage and doom of advanced stage Gout. Cellular repair and regeneration is the ONLY way to do this!
Cellular repair is possible, and 100% necessary to truly address the problem. It cannot be done without a fully comprehensive repair approach (diet, lifestyle, water, and high-potency, cell repairing herbs and vitamins.)
