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Uric Acid: Part 3 of a 3-Part Series

Low Levels of Uric Acid and Diseases Associated with it

Blood uric acid levels are considered low (hypouricemia) at 2mg/dl or less (R).

It is not considered to be a medical condition, but a useful medical sign.

Uric Acid is Lower in Multiple Sclerosis, Parkinson’s Disease, and Motor Neuron Disease

Lower blood values have been associated with several nervous system disorders such as:

  • Multiple sclerosis (MS) (R)
  • Alzheimer’s disease (AD) (R)
  • Huntington’s disease (HD) (R)
  • Parkinson’s disease (PD) (R)

It has been proposed that higher blood uric acid levels may be neuroprotective. In a large population-based cohort study, a negative relationship was observed between gout and Parkinson’s disease in patients aged 65 and above. A similar trend has been shown between uric levels and Huntington’s disease, suggesting that uric acid may play a role in preventing neurodegeneration (R,R2).

Uric Acid is Reduced in Optic Neuritis

Uric acid levels are lower in patients with optic neuritis, an inflammatory demyelinating disease of the optic nerve that is often the first symptom of Multiple Sclerosis (R).

Wilson’s Disease Can Lead to Low Uric Acid Levels

Wilson’s disease is a disease in which copper accumulates in tissues of vital organs like the brain and liver. It can lead to decreased blood uric acid levels because of associated kidney problems (i.e., Fanconi syndrome) that increase urinary uric acid excretion (R).

What Causes Low Uric Acid Levels?

Medication/Treatments

Hypouricemia can be found in 1% of hospitalized patients. In most cases, the cause is related to drugs like salicylates, allopurinol, x-ray contrast agents and glyceryl guaiacholate (R).

In addition, drugs like losartan  (an angiotensin II receptor antagonist drug), fenofibrate (drug of the fibrate class, mainly used to reduce cholesterol levels) and some non-steroidal anti-inflammatory drugs (NSAIDs) reduce the serum uric acid (SUA) levels (R).

Also, forced diuresis (increased in urination) used mainly in the treatment of renal colic (abdominal pain from kidney stones) in suicide-attempt patients may result in hypouricemia (R).

Genetics

The human urate transporter 1 (URAT 1) and human glucose transporter-like protein 9 (GLUT 9) are two kidney urate transporters.

A genetic mutation in these two transporters is responsible for idiopathic hypouricemia (R).

The gene SLC2A9 encodes a protein that helps transport uric acid in the kidney. Variants of this gene are known to have significant associations with blood uric acid (R).

Cancer

Several malignant diseases including Hodgkin’s disease, sarcoma, glioblastoma and a variety of carcinomas have been associated with hypouricemia (R).

Diet

By following a low purine diet, uric acid levels can be lowered by only 15% at most (R).

Mineral intake/deficiency

In a case study of molybdenum deficiency, blood hypouricemia was present (R).

Inadequate dietary Zinc intake can lead to lower uric acid levels. This effect is more common in women taking oral contraceptives (R).

Patients with high copper/Fe levels experience hypouricemia (R).

Magnesium intake is correlated with less likelihood of high uric acid levels in males. This might be to magnesium’s laxative effect, which may play a potential role in increasing the excretion of uric acid (R).

Hormones

Estrogen suppresses the production of the protein that eliminates urate in the kidney (proximal tubule epithelial cell organic anion transporter), while androgens stimulate it. This explains the lower serum urate levels in postmenopausal women as opposed to men (R).

Treatment with Agents that Increase Uric Acid Levels

1) Inosine

Inosine, a uric acid precursor, is the most effective way to increase uric acid levels (R, R2).

2) Zinc

Zinc normalizes uric acid levels if you are deficient (R).

3) Animal Products

Animal products increase levels in general (R).

4) Alcohol Consumption

Alcoholic drinks increase uric acid levels (R).

5)  Sodium

A high sodium diet can lead to an increase in blood uric acid levels over time (R).

6) Intense Exercise

Uric acid levels rise after strenuous exercise, potentially a result of purine nucleotide degradation during conditions of high energy usage (R).

Technical:

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Source: (R)

Uric acid antioxidant activities:

  • Uric acid acts as a strong antioxidant and scavenges reactive oxygen species and chelates transition metals (R,R2).
  • Uric acid prevents peroxynitrite-induced protein nitrosation, fat and protein peroxidation, and the inactivation of tetrahydrobiopterin BH4, a cofactor necessary for NOS (RR2, R3).
  • Uric acid protects low-density lipoprotein from Cu2+-mediated oxidation but increases the oxidation of already oxidized low-density lipoprotein (R).

Uric acid pro-oxidant and inflammatory activities:

  • By increasing arginase activity, uric acid diverts l-arginine from nitric oxide (NO) generation to urea production. Uric acid also directly reacts with nitric oxide (NO) to produce nitrosated uric acid, and the nitroso group can then be transferred to glutathione (GSH) for transport to another accepting molecule (R).
  • In the presence of oxygen, uric acid reacts with nitric oxide (NO) to produce 6-aminouracil (R).
  • Uric acid uptake in fat cells activates NADPH oxidase and stimulates the production of reactive oxygen species, which can initiate an inflammatory reaction (R).
  • Uric acid can activate the NF-κB and MAPK pathway in vascular smooth muscle cells and increase the production of cyclooxygenase and monocyte chemoattractant protein-1 (MCP-1) (R).

Uric Acid: Part 3 of a 3-Part Series

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