Boost Immunity With Your Fisrt Line of Defence !

Gout & Excessive Uric Acid Reduce Immunity & Increase Inflammation with a marked link to Reactive Oxygen Species… The dead have left some clues….

by in Boost Immunity 14/10/2020

By Prithu Nath

Although Uric acid is an antioxidant, a major recipient of reactive oxygen species, which is found in excess in people who have not survived covid 19, excess Uric Acid in turn reduces Immunity and Increases Inflammation.   Thus one must maintain Uric Acid to optimum Levels.

During the Viral Season we want our Immune System to be functioning Optimally. But the structures formed when a person has high Uric Acid or is suffering from Gout can lower immunity and increase inflammation as the same are ingested by our Neutrophils and Monocytes. There is a link between inflammation caused by Uric Acid and ROS , Reactive Oxygen Species as this has been found in high levels in people who have not survived Covid-19. Please ferefer to our previous article on ROS here:-

By doing away with Purine Rich Foods and adding Herbs that Heal we have been careful in incorporating this aspect of Immunity Suppression in Sanjivni Amrit Regimen.

Our Herbs too have an answer to this problem as they help in lowering the presence of high Uric acid Levels gently but instantaneously, thereby relieving inflammation and Freeing up our immune system that is essential for warding off the Viral Pathogens.

Natural Ways to Reduce Uric Acid in the Body
  1. Limit purine-rich foods.
  2. Avoid sugar.
  3. Avoid alcohol.
  4. Lose weight.
  5. Balance insulin.
  6. Add fiber.
  7. Reduce stress.
  8. Check medications and supplements.

1. Lemon herbs

Sanjivni Amrit Regimen stresses on comsuming Vitamin C rich lemon herbs which can reduce inflammation in the body by increasing formation of calcium carbonate in the body. Lemon juice can be made using herbs. Lemon juice contains citric acid, an organic substance which can help in dissolving uric acid crystals. It also decreases concentration of uric acid in the body. Vitamin C strengthens the connective tissue and reduces pain in joints. One glass of fresh lemon juice every day can help in dissolving uric acid.

2. High Purine Rich Foods to Avoid

  • bacon.
  • liver.
  • sardines, Seer, Mackrel and anchovies.
  • Alchohol
  • dried peas and beans.
  • oatmeal.
  • Cauliflower
  • Spinach
  • Mushrooms (excepting Shitake)

Gout is one of the most severe and frequent rheumatic diseases. Clinical manifestations of gout arise from uric acid crystal deposition in the musculoskeletal tissue. At high concentrations of uric acid in the body (hyperuricaemia), needle-shaped monosodium urate (MSU) crystals are formed. The structures are ingested by neutrophils and monocytes and thereby trigger robust activation of the inflammasome, an intracellular protein complex mounting an inflammatory response. Inflammasome activation builds interleukin-1, which acts as a proinflammatory mediator and induces vasodilation, recruitment of additional leucocytes and the expression of proinflammatory cytokines and chemokines. This process is associated with the clinical manifestation of an acute gout attack. Such attacks, however, stop rather rapidly and the process of resolution of inflammation in gout is now better defined. Neutrophils having ingested MSU crystals undergo a specific form of cell death called NETosis, which is characterised by the formation of neutrophil extracellular traps (NETs). During this process, DNA is extruded, allowing the dense packaging of MSU crystals as well as the degradation of proinflammatory cytokines, thereby allowing the stopping of the inflammatory process. Reactive oxygen species are essential for forming NETs and for allowing the resolution of inflammation in gout. This process of NETosis is critical for understanding tophaceous gout, since tophi are composed of NETs and densely packed MSU crystals.

Asymptomatic hyperuricaemia affects ~20% of the general population, with variable rates in other countries. Historically, asymptomatic hyperuricaemia was considered a benign laboratory finding with little clinical importance in the absence of gout or kidney stones. Yet, increasing evidence suggests that asymptomatic hyperuricaemia can predict the development of hypertension, obesity, diabetes mellitus and chronic kidney disease and might contribute to disease by stimulating inflammation. Although urate has been classically viewed as an antioxidant with beneficial effects, new data suggest that both crystalline and soluble urate activate various pro-inflammatory pathways.

Uric acid is a small, organic, heterocyclic compound found in lower and higher organisms. It is a catabolite of purines (adenine and guanine) derived from RNA and DNA. In most species, uric acid can be processed to highly soluble allantoin, even to ammonia []. Gout as a condition emerged in humans and other primates after the evolutionary loss of uricase, the uric acid catabolic enzyme (mostly confined to the liver) that converts uric acid to allantoic acid. In addition, the kidney filters uric acid but then reclaims most of the filtered load through reuptake []. Such a continuous effort to block the removal of metabolic “waste” may root in several advantages associated with high uric acid.

Uric acid is a strong peroxynitrite scavenger and antioxidant. One clinical observation that may speak to uric acid’s antioxidative effect is the near absence of multiple sclerosis (MS) in gout patients []. It is believed that the peroxynitrite is responsible for myelin degradation in MS, and peroxynitrite production can be blocked by higher uric acid levels. Conversely, there is a strong association of low serum uric acid levels with increased incidence of MS. In both human patients and a murine MS model (experimental autoimmune encephalomyelitis), high serum uric acid levels can reverse the disease progress. It also has been suggested that modest uric acid levels are protective in ischemic stroke []. Despite these potential advantages, it is questionable whether avoidance of MS and other late-life pathological conditions could have created enough evolutionary pressure to promote the loss of uricase, as these diseases do not prevent the carriers from entering the gene pool. One alternative theory suggests that the retention of uric acid can offset hyponatremic states to maintain a sufficiently high blood pressure, and that this was advantageous during past eras in which dietary salt availability was limited []. Another theory, first proposed in the 1950s, suggests that uric acid is structural homolog of caffeine (which in turn is a structural homolog of adenosine), and that high uric acid levels promoted mental alertness for primates and contributed to the development of human intelligence []. This hypothesis has been increasingly supported by experimental observations, although its role in evolution remains to be confirmed.

Monosodium Urate Precipitation and Crystal Formation

In all likelihood, uric acid’s inflammatory effects depend on its precipitation into MSU crystals, and the formation of MSU crystals is an obligatory step in the development of gout. However, the biology of MSU crystal formation is not fully understood. Typically, a serum uric acid level higher than 120 µg/mL (6.8 mg/dL) is defined as hyperuricemia. However, crystallization at this concentration is very difficult to reproduce in vitro in standard buffers []. Also, gout tends to have a rapid onset, whereas the crystallization process in vitro is quite slow. These observations suggest that mechanisms may exist to promote crystal formation in vitro. It is noted that uric acid levels inside a cell can be very high []. However, there have been no reports of intracellular MSU crystal formation. One possible defining factor is the availability of sodium, which is substantially higher in serum than in cytosol.

Hyperuricemia is associated with excessive food intake, particularly certain dietary items such as red meat and alcohol. In addition, large-scale cell death often induces robust MSU precipitation. Consequently, treatment with anticancer therapies (eg, chemotherapy and radiation therapy) is a situation in which uric acid levels need to be actively managed to avoid gouty attack []. Nonetheless, high serum uric acid levels do not uniformly lead to gout, as only about 10% of hyperuricemic patients experience gouty episodes []. However, gout can occasionally occur in individuals with normal uric acid levels []. Clearly, additional factors must be involved in MSU precipitation. MSU crystals rarely appear in central organs or deep cavities but are usually found in extremities, a phenomenon that has been attributed mainly to the subtle decrease in temperature in the distal joints. During the past several decades, mathematical models have been proposed to delineate the rate of crystallization in relation to environmental factors such as the temperature, pH, salt, vibration, and even the materials of the container in which experiments are conducted [].

Inflammatory Pathways

MSU crystals can be recognized by innate phagocytes, including dendritic cells (DCs), macrophages, and neutrophils. It has been shown that antigen-presenting cells (APCs) can sense uric acid as one of the proinflammatory endogenous signals released by damaged cells/tissues. These damage-associated molecular patterns can trigger a systemic inflammatory response similar to pathogen-associated molecular patterns []. The list of inflammatory pathways reportedly used by MSU crystals is long. There is no indication that a dominant mechanism will emerge soon. Nonetheless, there have been two major research focuses in the area of crystal responses. One is classical immunology oriented, focusing on processes such as antibody opsonization and complement fixation. The other (more current) area of investigation has focused on the role of immune pattern recognition of MSU structure. This includes responses by Toll-like receptors (TLRs) and leucine-rich repeat motifs (LRRs), which are nucleotide-binding sensor domains on NLRPs, including NLRPs that activate inflammasomes (multimolecular complexes that serve as platforms for interleukin [IL]-1 activation). One of the earliest hypotheses—that crystal recognition occurs mainly through membrane lipid binding—has also recently been undergoing re-examination.

Inflammatory Phagocytosis

Early studies suggest that MSU crystals isolated from sites of gouty inflammation are covered with immunoglobulins, mainly IgG []. Whether this antibody coating is the same phenomenon or a continuation of the antibody-mediated MSU precipitation discussed above is not known. The configurations of these antibodies with respect to the crystal surface have been worked out both in humans (IgG, by electron microscope (EM)) and mice (IgM, by monoclonal antibody fragmentation analysis). Fab portions are used to bind the crystal, while the Fc portion is pointed away []. MSU crystals that have been engulfed by macrophages are often antibody coated as well, suggesting a role for Fc receptor–mediated uptake. In phagocytes, MSU coated with IgG promotes the production of super-oxide anion []. Some data suggest that phagocytic responses to crystals may also be FcR dependent but Fc or IgG independent. In two interesting papers, Naccache et al. [, ] reported that CD16 (FcγRIII) on neutrophils can bind directly to the MSU surface, triggering intracellular tyrosine phosphorylation that is dependent on CD11b. They also reported that the same recognition mechanism can be triggered by a structurally different crystal, calcium pyrophosphate dehydrate. These observations introduce a phagocytic receptor (CD16) into the mix, one that is often linked to strong inflammation. How CD16 might recognize at least two different crystals without the benefit of antibody coating of their surfaces remains to be determined.


Proposed pathways of monosodium urate (MSU)-mediated cellular activation. Uric acid released from injured cells forms MSU crystals upon binding by uric acid–binding antibodies. The crystals convert the complement components via both the classical and the alternative pathways to produce C3a and C5a, as well as membrane attack complexes (MACs). Upon engaging the plasma membrane, MSU interacts with protein receptors Toll-like receptor (TLR)2/4 and CD14, and likely triggers the MyD88/TRIF pathway that leads to nuclear factor-κB (NF-κB) activation. This chain of events may control the activation of antigen-presenting cells (APCs), as well as other proinflammatory cytokine production, with the exception of interleukin (IL)-1β and IL-18. MSU crystals may also bind to cholesterol and trigger lipid sorting, which leads to Syk recruitment by immunoreceptor tyrosine-based activation motif (ITAM)-containing receptors (eg, CD16 and CD32) enriched in the lipid rafts. Syk then turns on phosphatidylinositol 3-kinase (PI3K)-mediated inflammatory phagocytosis. The interaction by MSU with CD16 may be independent of the lipid sorting process. The phagocytosed MSU crystals cause phagolysosomal membrane damage, and cathepsin B released from these vesicles triggers NOD-like receptor protein (NLRP)3 inflammasome activation via a yet-unidentified pathway. This pathway controls the IL-1β production and may be responsible for the systemic inflammation. Question marks indicate suspected links. ROS—reactive oxygen species

The enhanced inflammation to sterile irritants other than cell death (e.g., silica crystals) in the uric acid–depleted mice reported in this paper (5) may offer a glimpse into a protective role for this metabolite in other conditions. One can imagine that sufficient uric acid to induce endogenous inflammatory responses only occurs with large-scale cell death and must be associated with uric acid precipitation; in other words, a general antioxidant is converted into a strong inflammatory stimulant only upon its phase transition (6). Although the work of Kono et al. did not address this specific issue (5), recent data have suggested that serum antibodies against uric acid may facilitate its crystallization (17).