November 24, 20256 min read

Gout and Dry Fasting with the Scorch Protocol

By Yannick Wolfe

Gout is an extremely common problem nowadays. Every second metabolically unhealthy person over the age of 30 seems to be getting it. It's also an issue for metabolically sick dry fasters who are attempting to fix their insulin sensitivity. (Yes, even with the scorch protocol when done incorrectly). Gout is first and foremost an insulin resistance disorder (cellular inability to use glucose optimally). You'll notice that the basis of most diseases, yes, including cancer, is often insulin resistance-based. And you can't heal the underlying cause by never eating carbs again. You can put a temporary pause with keto/carnivore type diets and feel much better, but all this will do in the long run is make you even more insulin resistant day by day.

Gout is not just about purines or kidney clearance

  • Classic teaching: gout = too much uric acid → poor kidney excretion or overproduction from purines (red meat, shellfish, alcohol).
  • Reality: ~70–90 % of gout patients actually have normal or even high urinary uric acid excretion. The main problem is underexcretion in the kidneys caused by insulin resistance.
💡This is why a keto diet can help so much, because it lowers insulin. In the very beginning you may have quite some trouble with flare ups, as you transition into the ketosis state, because the uric acid will be competing with ketones for excretions, while insulin is still relatively high. But if you stick to it, you will break through the hump and have much smoother sailing. But remember, as I always say, the keto diet is a band-aid that addresses high insulin, but doesn't fix the root cause (insulin resistance/bad glucose metabolism).

How insulin resistance directly causes hyperuricemia

How insulin resistance causes high uric acid (hyperuricemia) Insulin resistance leads to chronically high insulin. High insulin acts on the kidney proximal tubule to increase uric acid reabsorption via URAT1 transporters, while also reducing uric acid excretion. The result is rising blood uric acid levels and eventual gout, even when uric acid production is completely normal. THE ROOT CAUSE Insulin resistance drives uric acid buildup STEP 1 Insulin Resistance cells ignore glucose signal STEP 2 Chronic High Insulin body compensates by pumping more STEP 3 Kidney URAT1 over-activated insulin signals: keep uric acid in RESULT High Uric Acid even on normal diet What insulin does to your kidney Increases URAT1 reabsorption of uric acid Reduces fractional excretion of uric acid Blood uric acid rises even if production is normal Fix insulin sensitivity: uric acid drops 1-3 mg/dL Studies: Ter Maaten 1997, Muscelli 1996, Facchini 1996 Classic teaching vs. reality Classic view: Too many purines (meat, shellfish, alcohol) poor kidney clearance from overproduction Reality: 70-90% of gout patients show normal or high urinary uric acid excretion Underexcretion is driven by insulin, not diet Uric acid is a passenger. Insulin resistance is the driver. Treat the cause, not the symptom.
  • Insulin resistance → chronic hyperinsulinemia.
  • High insulin does two bad things in the kidney:
    1. Increases reabsorption of uric acid in the proximal tubule (via URAT1 and other transporters).
    2. Reduces fractional excretion of uric acid → blood levels rise even if production is normal.
  • Multiple studies (e.g., Ter Maaten 1997, Muscelli 1996, Facchini 1996) show that improving insulin sensitivity with weight loss, metformin, or pioglitazone lowers serum uric acid by 1–3 mg/dL, independent of purine intake.
💡Why does being fat play a big role? Fat cells leak fatty acids and inflammation, both negatively affect glucose metabolism, which means insulin won't work as well either. Look up the Randle Cycle. Your mitochondria may struggle when trying to burn both fats and carbs at the same time.

It's quite clear that the main mechanism of action in Gout is the high insulin that is reabsorbing uric acid instead of clearing it!! Another reason why fixing insulin resistance and becoming insulin sensitive is the key! Fruitarians claim that following their diet for a year or two can completely heal insulin resistance, but they fail to mention that this is often for mild to medium insulin resistance. Once your body falls apart and you're metabolically diseased, going on a fruitarian diet will most likely make things even worse!

Fructose / refined sugar is the worst offender

Why fructose causes gout faster than anything else Fructose is metabolized almost entirely in the liver. This causes rapid ATP depletion, which generates AMP, which feeds directly into the purine degradation pathway and produces uric acid. Simultaneously, fructose drives insulin resistance and raises liver fat, worsening systemic uric acid retention. The result is a double hit: an acute uric acid spike plus chronic hyperuricemia. THE WORST OFFENDER Fructose hits uric acid through two separate pathways SUGAR SOURCES Table sugar (50%) HFCS (~55% fructose) LIVER ONLY Fructose metabolism glucose can't bypass the liver PATH A: Direct uric acid spike Rapid ATP depletion in liver fructose consumes phosphate and energy stores AMP accumulates AMP feeds directly into purine degradation Uric acid spike (acute) within hours of fructose consumption PATH B: Chronic retention Insulin resistance + liver fat fructose drives intrahepatic fat (NAFLD) Systemic insulin resistance worsens hyperinsulinemia rises across all tissues Kidney retains more uric acid (chronic) URAT1 over-activated day after day Double hit: acute spike + chronic retention. No other food does both.
  • Fructose (table sugar = 50 % fructose, HFCS ~55 %) is metabolized almost entirely in the liver → rapid ATP depletion → AMP → uric acid (via purine degradation pathway).
  • Fructose also directly induces insulin resistance and raises intrahepatic triglycerides → worsens systemic insulin resistance → further kidney uric acid retention.
  • Result: sugar → acute uric acid spike + chronic insulin-resistance-driven hyperuricemia. This is why metabolic syndrome and gout are so tightly linked.
💡While anyone who knows about bioenergetics and glucose metabolism knows that fructose is not the enemy (if metabolically healthy), it's still being demonized. Do you see why? If you are metabolically damaged/diseased with insulin resistance, fructose will hurt more than anything because of how quickly it creates uric acid, how quickly it can cause NAFLD, nonalcoholic fatty liver disease, and visceral fat around organs in general. However, on the journey to healing insulin resistance, you will have to bump into varying amounts of fructose, and I hope to see each of you on the other side, as fructose-enjoyers.

Faulty glucose oxidation (low mitochondrial function) ties it together

  • Insulin-resistant tissues shift toward incomplete glucose oxidation → more lactate.
  • Lactate competes with uric acid for excretion in the kidney (same organic anion transporters) → further reduces uric acid clearance.
  • Chronic high lactate + high insulin + high fructose-derived uric acid = perfect storm for gout.
💡It becomes clearer and clearer. If you can fix insulin resistance, you will fix gout. You will most likely fix all your other problems, too. The key is to know where to start. Sometimes you're so far gone that switching to carbs is not the answer; you need bridging solutions. You start with preparing for a dry fast, which will help wipe the slate clean and start a cascade of stem cell regeneration. Then you pair it with the T3 therapy and adjacent therapies to strengthen it. Then, based on symptoms, you will either repeat the cycle, continue cycling T3, or move on to additional therapies, all the while your insulin resistance will be improving, and your energy will keep going up. Life starts getting brighter and brighter. If only you knew how amazing life can be. Better than you remember it.

Why meat/red wine/beer are unfairly blamed

  • They do contain purines, but in the presence of insulin resistance, the kidneys can’t clear even normal amounts of uric acid.
  • When insulin sensitivity is restored (keto, fasting, metformin studies), people can often eat steak and drink red wine again without gout attacks.
💡It was never really the meat. The mix of meat and sugar WHILE in a metabolically diseased body causes these problems. And it all happened through a mix of stress, viruses/bacteria, PUFA's, excessive fat, and chemicals in our food.

Dry fasting + T3 as an aggressive reversal strategy

How dry fasting plus T3 therapy reverses gout at the root Dry fasting drives insulin near zero, triggers autophagy, clears inflammatory lactate, and temporarily spikes then crashes uric acid. Adding T3 therapy amplifies every step: T3 increases mitochondrial respiration, improves glucose oxidation, clears lactate faster, directly improves insulin sensitivity, and upregulates renal uric acid excretion in the opposite direction from insulin. Together they address every mechanism behind gout. THE REVERSAL Dry fasting + T3 hit every gout mechanism at once DRY FASTING removes water + food simultaneously T3 THERAPY (LIOTHYRONINE) active thyroid hormone, directly to cells Insulin drops to near zero URAT1 stops over-retaining uric acid kidney excretion normalizes Autophagy + mitochondrial turnover damaged cells cleared, mitochondria renewed improves glucose oxidation capacity Blood lactate + cytokines drop sharply lactate no longer competes with uric acid for kidney excretion (same transporters) Uric acid: temporary spike then crash protein breakdown raises it briefly at first then plummets as insulin hits zero and kidney excretion normalizes Increases mitochondrial respiration cells burn glucose more completely less glucose goes to lactate Raises basal metabolic rate lactate clearance speeds up frees up kidney transporters for uric acid Improves insulin sensitivity in liver and muscle (rodent + human data) addresses the root: insulin resistance itself Upregulates renal uric acid excretion T3 modulates URAT1 in the opposite direction from insulin: excretes, not retains thyroid hormone directly supports clearance + Combined effect: insulin reset + mitochondrial rebuild + kidney excretion restored Not a purine restriction. A metabolic correction.
  • Dry fasting
    • Massive drop in insulin (near zero).
    • Strong autophagy and mitochondrial turnover.
    • Profound lowering of blood lactate and inflammatory cytokines.
    • Uric acid often rises temporarily (protein breakdown), then crashes hard when insulin plummets and kidney excretion normalizes.
  • Adding T3 (liothyronine, active thyroid hormone) Therapy
    • T3 powerfully increases mitochondrial respiration and glucose oxidation capacity.
    • Raises basal metabolic rate → improves lactate clearance.
    • Directly improves insulin sensitivity in liver and muscle (multiple rodent and some human studies).
    • Increases renal uric acid excretion (thyroid hormone upregulates URAT1 in the opposite direction from insulin).
💡Both these methods are fairly simple, but need to be adapted to your situation. You can read more about them and more scenario-specific concepts in The Scorch Protocol or book a call with me.

Bottom-line take-home points

  • Modern gout is primarily a disease of insulin resistance and fructose-driven uric acid production, not just purines.
  • Sugar (especially fructose) is far worse than meat for most people with gout.
  • Improving insulin sensitivity (via low-carb, keto, fasting, metformin, GLP-1 agonists, etc.) is the most evidence-based way to lower uric acid without drugs.
  • Dry fasting + T3 is an extreme approach that makes physiological sense (massive insulin reset + mitochondrial/thyroid upregulation).

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