Controversial Thoughts: Meat and Organs cause GOUT, right?

PS

Paul Saladino23m · 2020-10-06

Claims Made

40

Claims Supported

36

Support Rate

90%

Support rate

36 of 40 claims supported

36 supported4 partial / not

Claims from this content

31

Well SupportedPolyunsaturated fats may interfere with normal metabolism, potentially leading to pathological insulin resistance at the adipocyte level.Well SupportedAncestral diets, such as those of the Hadza, prioritized meat and organs, and they did not waste any part.Well SupportedMetabolic dysfunction is the primary cause of gout and uric acid issues in individuals who are metabolically healthy.Well SupportedIn metabolically healthy individuals, increasing meat and organ consumption does not increase uric acid levels because the body can auto-regulate.Partially Supported

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A. Volkovreader

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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.

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N. Park

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Would love a "what would change this verdict" RSS feed. Sign me up if it exists.

Organ meats are uniquely nutritious and should be included in the diet.

Partially SupportedGout arises from metabolic dysfunction combined with uric acid production, not solely from consuming purines or uric acid.

Partially SupportedAn abnormal neutrophil-to-lymphocyte ratio (NLR) is associated with gout and allows excess uric acid to become problematic.

Partially SupportedMeat and organs are nutrient-rich sources of nutrition.

Partially SupportedExcessive linoleic acid intake and its oxidative products may activate the innate immune system, leading to a disordered immune response to uric acid and potentially contributing to gout.

Partially SupportedGout is primarily caused by a decreased ability to excrete uric acid, rather than simply by excess purines in the diet.

Partially SupportedMetabolic dysfunction is a third variable connecting various health issues.

Partially SupportedInsulin resistance, not carbohydrate intake itself, is the primary driver of gout.

Partially SupportedMetabolic dysfunction, particularly insulin resistance, is strongly associated with hyperuricemia and gout.

Partially SupportedFasting can increase serum uric acid levels as a waste product of catabolism.

Well SupportedKetosis increases uric acid levels because beta-hydroxybutyrate competes with uric acid for excretion in the kidneys.

Partially SupportedIntermittent fasting can temporarily raise uric acid, blood pressure, and waist circumference, but may decrease hs-CRP.

Partially SupportedFructose intake, particularly from high fructose corn syrup, can lead to triglyceride accumulation due to its distinct metabolic pathway lacking a rate-limiting step.

Partially SupportedElevated uric acid levels do not necessarily mean a person will develop gout.

Not SupportedThe assumption that more uric acid directly equals gout or more LDL directly equals atherosclerosis is flawed.

Partially SupportedGout is caused by the precipitation of uric acid crystals in joints.

Partially SupportedFasting, such as during Ramadan, can lead to a linear increase in serum uric acid levels.

Partially SupportedKetones may deactivate the NLRP3 inflammasome and relieve gout flares.

Partially SupportedUric acid levels below 3.9 mg/dL are considered normal, even with a high intake of meat and organs.

Partially SupportedAlcohol intake worsens gout by increasing uric acid retention and negatively impacting insulin sensitivity and metabolic health.

Partially SupportedAllopurinol inhibits xanthine oxidase to reduce uric acid formation, a common treatment for gout in Western medicine.

Partially SupportedModerate amounts of fructose within evolutionary ranges are not believed to cause major issues or gout in metabolically healthy individuals.

Partially SupportedUric acid is derived from purines in the diet, specifically from the deamination of adenine and guanine.

Limited ResearchInsulin resistance may drive high uric acid levels, or high uric acid may drive insulin resistance, but metabolic dysfunction typically precedes high uric acid.

Limited ResearchFructose may not directly worsen gout in the absence of underlying metabolic dysfunction.

Partially SupportedKetones can interfere with the kidney's excretion of uric acid, potentially leading to temporary increases.

Partially SupportedMaintaining metabolic health is crucial to avoid gout.