Eric Berg alias The Microbiome Mogul

Eric Berg is not licensed or approved by Florida Board of Chiropractic Medicine to diagnose, treat, or cure Research has found that one of the strongest drivers of gout is insulin resistance. When you have insulin resistance, it becomes more difficult for the kidneys to flush out uric acid..

Research has found that one of the strongest drivers of gout is insulin resistance. When you have insulin resistance, it becomes more difficult for the kidneys to flush out uric acid.

Supports

Multiple mechanistic and clinical studies support a link between insulin resistance/hyperinsulinemia, reduced renal urate excretion, hyperuricemia, and increased gout risk. ^[3] The indexed review on uric acid, gout, and metabolic syndrome notes that euglycemic hyperinsulinemia experimentally decreases urinary excretion of uric acid, sodium, and potassium, consistent with insulin acting on the kidney to retain urate and thereby raise serum uric acid in insulin‑resistant states. Observational work in diabetics shows that insulin resistance is positively associated with fasting serum uric acid concentrations, supporting a relationship between impaired insulin action and higher urate levels. ^[1][2] The study on waist circumference, insulin resistance, and uric acid from CHARLS reports that uric acid influences the relationship between central obesity and insulin resistance, reinforcing that hyperuricemia and insulin resistance are intertwined components of metabolic syndrome. ^[4] Broader academic literature (outside the indexed list) and recent reviews describe that insulin resistance and visceral adiposity upregulate renal urate transporters (such as URAT1 and GLUT9) and decrease fractional excretion of urate, leading to hyperuricemia, and that metabolic syndrome and insulin resistance are strong risk factors for incident gout. Together, these data support the general claim that insulin resistance is an important driver of hyperuricemia and gout and that it can impair the kidney’s ability to clear uric acid.

Contradicts

The specific assertion that insulin resistance is “one of the strongest drivers” of gout is more assertive than the available evidence, which shows a multifactorial etiology for gout (genetic variants in urate transporters, dietary purine and alcohol intake, diuretics, kidney disease, and other metabolic factors) in addition to insulin resistance. ^[3][4] High‑quality data demonstrate that insulin resistance and hyperinsulinemia are associated with hyperuricemia, but they do not establish that insulin resistance is the single or dominant driver compared with other causes. Moreover, mechanistic studies in rare, severe forms of insulin resistance suggest that hyperuricemia can arise via increased uric acid synthesis rather than decreased renal excretion, and that in some extreme receptor‑defect insulin‑resistant states uric acid levels may actually be lower, indicating the relationship is complex and not uniformly explained by reduced renal urate clearance. ^[1][2] Some work also suggests that lowering uric acid (for example, with allopurinol) can improve insulin resistance markers, implying bidirectional or shared pathways rather than a simple unidirectional causal chain. Overall, while insulin resistance clearly contributes to hyperuricemia and gout risk, the evidence does not cleanly support the influencer’s framing that insulin resistance is uniquely one of the strongest drivers or that impaired kidney flushing of uric acid is always the main mechanism.

Mainstream view

Mainstream medical and scientific opinion is that gout is driven primarily by chronic hyperuricemia, which arises from a combination of genetic predisposition (particularly variants in renal and intestinal urate transporters), dietary and lifestyle factors, kidney function, and components of metabolic syndrome including insulin resistance and obesity. ^[3][4] Insulin resistance and the associated hyperinsulinemia are recognized contributors to elevated serum uric acid and gout risk, in part via renal effects on urate handling and in part via shared metabolic pathways, but they are not viewed in isolation as the strongest or only causal driver. ^[2] Current evidence supports that insulin resistance and hyperinsulinemia can reduce renal uric acid excretion and increase serum urate in common cardiometabolic conditions, and guideline‑level discussions treat insulin resistance as an important modifiable risk factor among several others rather than the singular dominant cause. ^[1] Clinically, management of gout focuses on urate‑lowering therapy, dietary modification, and addressing metabolic syndrome (including insulin resistance), reflecting this multifactorial understanding.

In their own wordsWatch sourceArchived copy

“Research has found that one of the strongest drivers of gout is insulin resistance.”

Rule: Fla. Stat. § 460.403(9)(a)

See every doc bro who says they can treat or advise on Diabetes and blood sugar

Eric Berg is not licensed or approved by Florida Board of Chiropractic Medicine to advertise The #1 Best Protocol to Reverse Gout (& Prevent It) as within their scope of practice.

The #1 Best Protocol to Reverse Gout (& Prevent It)

Supports

The strongest support for a gout protocol comes from major guidelines and systematic reviews showing that urate-lowering therapy (ULT) is the core evidence-based strategy for long-term gout control and prevention. ^[6][7][8] The 2020 American College of Rheumatology guideline strongly recommends starting ULT in patients with tophaceous gout, radiographic damage, or frequent flares, using allopurinol as first-line therapy, and titrating to a serum urate target of less than 6 mg/dL. ^[5] A systematic review for the ACP guideline found that ULT lowers serum urate and reduces the risk of acute gout attacks. More recent evidence also supports a treat-to-target approach with serial urate monitoring rather than fixed-dose treatment. The same guideline and related summaries recommend flare prophylaxis with colchicine, NSAIDs, or glucocorticoids when initiating ULT, which is relevant because starting ULT can precipitate short-term flares.

Contradicts

The claim is too broad and framed as a single best protocol that can reverse gout, but the evidence supports chronic urate control rather than a universal reversal protocol. ^[6] The peer-reviewed material provided does not identify any one superior “#1” protocol; instead it supports individualized treat-to-target care with ULT and flare prophylaxis. Lifestyle and dietary interventions have at best modest or inconsistent effects, and a recent review reported that evidence on dietary supplements and dietary patterns for gout is inconclusive with only modest benefits in selected interventions. ^[8] Evidence also does not show a dramatic immediate benefit from starting ULT during an acute flare; a 2024 systematic review and meta-analysis found no evidence of harm or benefit, and the trials were small with limited applicability to patients with tophaceous gout or renal impairment. ^[7] The index papers supplied by the user are unrelated clinical trials and do not provide support for gout reversal or prevention claims. The wording “reverse gout” is also misleading because established gout is typically managed by lowering urate to prevent flares and dissolve crystal burden over time, not by a single reversible protocol proven in head-to-head trials.

Mainstream view

Mainstream rheumatology guidance is that gout is best managed with long-term urate-lowering therapy using a treat-to-target strategy, usually allopurinol first-line, plus short-term anti-inflammatory prophylaxis when starting treatment. ^[5][6][8] Prevention is evidence-based when serum urate is maintained below target, but no major guideline endorses a single universal #1 protocol that can reverse gout for everyone. Lifestyle measures may help as adjuncts, but they are not a substitute for urate-lowering therapy in patients with established gout.

In their own wordsWatch sourceArchived copy

“Reverse Gout”

Rule: Fla. Stat. § 460.403(9)(a)

Eric Berg is not licensed or approved by Florida Board of Chiropractic Medicine to advertise Consuming celery and increasing your fluid intake may help your body clear uric acid more quickly. as within their scope of practice.

Consuming celery and increasing your fluid intake may help your body clear uric acid more quickly.

Supports

The influencer’s claim has two parts: celery and increased fluid intake. ^[17] For celery, current evidence is limited but suggests potential uric-acid–lowering effects, mostly in preclinical and small human studies. Apium graveolens (celery) contains flavonoids such as luteolin and apigenin, which have been shown in animal models to lower serum uric acid, inhibit xanthine oxidase, and upregulate renal urate transporters, thereby promoting urate excretion and improving hyperuricemic nephropathy; this supports a plausible mechanistic basis but is not definitive clinical proof in humans. ^[10][18][19] For hydration, there is stronger supporting evidence and physiologic rationale: uric acid is predominantly eliminated via the kidneys, and adequate fluid intake increases urine volume and helps maintain uric acid in solution, which facilitates renal excretion and is commonly recommended in nonpharmacologic gout and hyperuricemia management strategies. ^[9][14] Observational data and small clinical studies in patients with gout or hyperuricemia report that higher water intake is associated with lower serum uric acid and fewer hyperuricemic episodes. ^[20] Major clinical practice resources for gout and hyperuricemia routinely include “stay well hydrated” as part of standard advice, reflecting a consensus that increasing fluids can modestly assist uric acid clearance, particularly in patients without heart failure or advanced kidney disease. ^[11][16]

Contradicts

There is no high-quality evidence (large randomized controlled trials, major guidelines) specifically showing that eating celery or drinking celery juice by itself clinically “clears uric acid more quickly” in humans with gout or hyperuricemia, and no major rheumatology guideline currently endorses celery as a recognized urate-lowering therapy. ^{[9][10][14][15][18][20]} Existing data for celery come mainly from animal models and quasi-experimental or small human studies that are not definitive and may be subject to bias and confounding; they demonstrate biochemical and molecular changes but do not establish robust clinical outcome benefits in gout patients. ^[17][19] Some evidence-based commentaries explicitly note that there is no reliable human clinical trial evidence that celery seed or celery reliably lowers uric acid or prevents gout flares, and that its primary effect is mild diuresis rather than targeted modulation of renal urate handling. Similarly, while increased fluid intake is widely advised and physiologically reasonable, it is a supportive measure with modest effect size; hydration alone is not sufficient treatment for established hyperuricemia or recurrent gout, and excessive fluid intake can be unsafe in patients with heart failure or significant kidney disease. ^[16] No high-quality guideline recommends hydration as a stand‑alone therapy in place of established urate‑lowering drugs such as allopurinol or febuxostat.

Mainstream view

The mainstream medical view is that good hydration is a standard, low-risk supportive measure that can modestly help renal elimination of uric acid and is recommended as part of comprehensive management for gout and hyperuricemia, but it is not a primary or definitive therapy. ^[15][17][19] Celery is considered a low‑purine vegetable and generally safe as part of a balanced diet for gout patients, with some preclinical data suggesting possible urate-lowering and nephroprotective effects; however, it is not recognized by major guidelines as an evidence-based treatment for accelerating uric acid clearance, and any benefit is viewed as speculative or modest at best. ^{[9][10][14][18][20]} Standard care for clinically significant hyperuricemia and gout relies on lifestyle measures (reducing high‑purine foods, limiting alcohol, managing weight) plus pharmacologic urate‑lowering therapy when indicated, with hydration encouraged as an adjunct and celery viewed, if at all, as a potentially helpful but unproven dietary component rather than a therapeutic agent. ^[12]

In their own wordsWatch sourceArchived copy

“Consuming celery and increasing your fluid intake may help your body clear uric acid more quickly.”

Rule: Fla. Stat. § 460.403(9)(a)