I chose this image to reflect how complicated uric acid excretion is in itself. Also, further complicated by alcohol and purines from food and drink. So complicated, in fact, that it is hard to see at this scale.

But you can see the original image with the full report at Gout and Diet: A Comprehensive Review of Mechanisms and Management. Where its caption reads:

Figure 1
Potential mechanisms of diet-induced gout progression in humans. Diets provide abundant raw materials of purine, which is mainly metabolized in the liver, promoting uric acid production. Meanwhile, it can interfere with the intestinal environment, homeostasis, and urate transport to induce high levels of uric acid, leading to hyperuricemia and ultimately to gout. Additionally, gouty inflammation is caused by IL-1β production after the activation of NLRP3 by macrophages that ingest MSU crystals, and a second signal is required in humans by stimulating the activation of TLR signaling pathways that can be induced by diets. Moreover, neutrophil infiltration and diet-induced low-grade inflammatory states will exacerbate gouty inflammation. AMP, adenosine monophosphate. ASC, apoptosis-associated speck-like protein containing a caspase recruitment domain. GMP, guanine monophosphate. IL, interleukin. IMP, inosine monophosphate. LPS, lipopolysaccharide. MSU, monosodium urate. MyD88, myeloid differentiation factor88. NF-κB, nuclear factor kappa B. NLRP3, pyrin domain-containing protein 3. TLR, toll-like receptor. TNF, tumor necrosis factor. XO, xanthine oxidase.

As my caption says, there are no easy answers to alcohol and uric acid excretion questions.

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