Gout is the most common, well understood, and well described form of arthritis.

It is also known as gouty arthritis.

It is most manageable rheumatic disease.

The general prevalence of gout is 1–4% of the general population.

It is caused by the deposition of needle like uric acid crystals in joints or in tissues around joints.

It main symptoms is painful swelling and reddening at the affected joint.

In Hindi Gout is known as गठिया.

Gout in Ayurveda

Vatarakta is a Santarpana Janya Vyadhi with much similarity with Gouty arthritis in modern medical science.

Aggravated Vayu enters in various Shakha and Sandhi triggering the vitiation of Rakta. Rakta in turn blocks Vayu resultant in severe painful condition.

In classical ayurvedic texts several formulations are advised for the managing the Vata Rakta. Formulations like Triphala kwath with Madhu, and Milk prepared from Dashmool are used for Sadhya shoola nivarana. Haritaki choorna with Guduchi Swarasa is used for Janugata Vata Rakta. Amla, Haridra, Musta with Madhu, Kokilaksha are used in the form of decoction.

What are the symptoms of gout?

Intense joint pain

Lingering discomfort

Inflammation and redness

How is gout diagnosed?

Clinically gout is classified into asymptomatic hyperuricemia, acute gouty arthritis, intercritical period, and chronic tophaceous gout.

Occurrence of monosodium urate (MSU) crystals in the synovial fluid is the gold standard diagnosis for gout.

MSU crystals deposition in and around the joints tissue form tophi.

Thus the presence of the MSU crystals in joint fluid aspiration or in tophi aspirate is diagnostic feature for it.

Limited range of motion.


Acute gout

The pathogenesis of gout comprises of an initial triggering of monocytes and mast cells followed by activation of neutrophils.

Mast cells are main player during the induction of the acute gouty attack by release of the histamine and IL-1 which causes increase in the vascular permeability and vasodilatation.

Macrophages engulf uric acid crystals before the beginning of the first attack of the gout.

In the beginning monocytes produces abundant quantities of TNF-alpha, IL-1, IL-6 and IL-8 with activation of endothelial cells and engulf the urate crystals.

Different chemotactic factors released by monocytes and mast cells and the local vasodilatation stimulates chemotaxis of the neutrophil.

Presence of the plenty amount of chemotactic elements (leukotrienes, platelet activating factor and interleukins predominantly IL-8) inside the synovium are accountable for 90% of neutrophils activation and exacerbation of acute inflammatory response.

Based on the pathology of the gout, IL-8 can be probable target for managing the attack of acute gout.

The acute attack of gout is usually self-limited and can be resolves within hours to few days of its beginning.

Termination of the acute gout symptoms takes place because of the removal and phagocytosis of crystals by macrophages, which causes the suppression of the cellular and chemokine mediated further process of the activation.

Chronic gout

Chronic gout manifests by prolonged synovitis, bony erosions, cartilage damage and formation of the tophi.

During the chromic gout, presence of the uric acid crystals in the synovium causes the stimulation of chondrocytes to release substantial amount of inflammatory cytokines, nitric oxide and matrix metalloproteases which causes damage to the cartilage.

During the bone erosions and osteoclastogensis IL-1β and activation of receptor for nuclear factor κB and RANK ligand pathway plays important role.

These cytokines are also responsible for the acute flare at lower concentrations in between attacks.


It can be manage using a combination of allopathic medicine, modifying the dietary pattern, with the herbs of the ayurvedic herbs and their formulation and using several home remedies.

Medication for the gout

Several drugs are approved for the treatment of gout, including colchicine, steroids, non-steroidal anti-inflammatory drugs (ibuprofen, naproxen, indomethacin, and aspirin), cyclooxygenase 2 (COX-2) inhibitors (etoricoxib), and allopurinol. Although these agents are effective, they also cause side effects, such as skin allergies, fever, rash, renal dysfunction, aseptic meningitis, and hepatic dysfunction

Acute gout requires pharmacotherapy (nonsteroidal anti-inflammatory drugs, corticosteroids, or colchicine).

Dietary management for gout 

Ingestion of foods rich in purines are the key element which elevate the level of uric acid precursors. These purine rich foods includes foods from animal and seafood origin.

Purine rich foods from vegetables such as beans, lentils, mushrooms, peas, legumes, and dairy products do not bring any risk on hyperuricemia and gout. Thus they can be comes without worrying.

Foods rich in vitamin C, low fat dairy products, and plant oils (like olive, sunflower and soya) are associated with lower risk for hyperuricemia and gout.

Vitamin C help in managing gout by increasing renal excretion of uric acid.

Thus the use of natural products regulate both the production and the excretion of uric acid/ urate, which may helpful in the treatments of hyperuricemia.

Since diet play important role in the uric acid levels so the modification of dietary habit and lifestyle may decrease the uric acid level.

Here are some important dietary modification which may be helpful in the managing the gout.

  • Integrate the vegetarian sources of proteins and decreasing the intake of the fat foods in the diet.
  • Limit or avoid the intake of the protein rich foods such as meat, crustaceans, and yeast.
  • Consumption of beverages like alcohol, mostly beer and spirits, should be avoided or reduced.
  • Sugar sweetened drinks should be avoided.

Ayurvedic management of Gout

A herbal preparation made by mixing equal proportion of Haldi (Turmeric), Methi (Fenugreek seed) and Ginger powder is very effective in managing gout.

Home remedies for managing gout

  • Drink plenty of fluids
  • Applying ice to affected joints
  • Stress management
  • Avoiding high-purine meats
  • Moderation in alcohol intake
  • Weight management reduce the incidence of gout flares.


What causes gout?

  • Gout is a disorder of purine metabolism which result in to hyperuricemia.
  • Deposition of uric acid crystals in the joint cavity triggers the development of gout.
  • At initial time point, it is characterized by pain and swelling of IMTP (inter metatarsophalangeal joint) followed by other Joints. This leads to trouble in daily life of patients.

Can Gout Be Cured?

  • In allopathic system of the medicine it cannot be cure, rather can be managed with a combination of the medication. However in ayurvedic system of medicine it is a kind of Vata Rakta dosha and can be cured with herbs targeting the Vata dosha.

How is gout treated?

  • Use of the NSAIDs or colchicine quickly relieves to early presentation of gout is an acute joint inflammation.

How to Stop Gout from Getting Worse?

It progress in the four steps as follow;

  • High Uric Acid Levels- asymptomatic hyperuricemia
  • Acute Gout- sudden, unexpected nighttime attack of gout symptoms might occur.
  • Intercritical Gout- Gout flare
  • Chronic Gout- also called “tophaceous gout” because the uric acid deposits can form nodules called “tophi,”

What increases your chances for gout?

  • Factors which increases the level of the uric acid such as purine rich foods from animal and seafood origin.

Take home message

To avoid the occurrence of the Gout try to avoid the purine rich foods and consume more plant based foods.


Scientific evidences

Engel B, Just J, Bleckwenn M, Weckbecker K. Treatment Options for Gout. Dtsch Arztebl Int. 2017;114(13):215-222. doi:10.3238/arztebl.2017.0215

Ragab G, Elshahaly M, Bardin T. Gout: An old disease in new perspective – A review. J Adv Res. 2017;8(5):495-511. doi:10.1016/j.jare.2017.04.008


Disclaimer: This content including advice provides a general information only. It is in no way a substitute for trained medical practitioner opinion. Always consult a specialist or your doctor for more information. We do not claim any obligation for this information.


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