Will you get Scurvy on a Carnivore Diet? Bart Kay Returns!

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Paul Saladino1h 4m · 2019-04-04

Claims Made

122

Claims Supported

80

Support Rate

66%

Support rate

80 of 122 claims supported

80 supported42 partial / not

Claims from this content

90

Well SupportedIt is possible to obtain 60 mg of vitamin C daily by eating animal foods nose-to-tail, with liver being richer in vitamin C than muscle meat.Not SupportedSulforaphane may scavenge iodine and act as a goitrogen, with toxic effects.Well SupportedA vitamin C dose as low as 10 milligrams per day was sufficient to correct scurvy in studies from the 1930s and 40s, with no observed clinical benefit from higher doses.Well SupportedThe body consumes glutathione during acute cold exposure, which causes oxidative stress, and uric acid levels decrease and then increase the next day.Well Supported

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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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Environmental hormesis, such as sun exposure, exercise, cold, and heat, activates Nrf2 without the negative side effects of exogenous foreign molecules.

Not SupportedHigh doses of vitamin C can act as pro-oxidants in individuals with G6PD deficiency, potentially causing hemolysis.

Not SupportedSulforaphane is not considered net beneficial and may be net toxic.

Not SupportedVitamin C intake above 30-70mg per day may not provide benefits for humans and higher doses might be dangerous due to conversion to oxalate.

Well SupportedCold stress can induce oxidative stress in the human body, similar to molecules like sulforaphane.

Not SupportedSulforaphane is a toxin that is directly harmful and not beneficial, despite activating Nrf2 and glutathione production.

Well SupportedIndividuals on a carnivore diet including organ meats and minimally cooked meats do not appear to have issues with oxidative stress markers.

Well SupportedLow vitamin C levels may contribute to increased fat storage because vitamin C is essential for carnitine synthesis.

Well SupportedElevated uric acid levels may be a beneficial response rather than a problem.

Well SupportedGlycine deficiency can impair the synthesis of important proteins like collagen and glutathione.

Well SupportedHumans can obtain sufficient vitamin C from consuming animal products, which likely led to the loss of endogenous vitamin C synthesis.

Well SupportedThe amount of vitamin C required to prevent scurvy is significantly lower than the Recommended Daily Intake (RDI).

Well SupportedIn metabolically healthy individuals, increasing meat and organ consumption does not increase uric acid levels because the body can auto-regulate.

Well SupportedSupplementation with glycine, hydrolyzed collagen, gelatin, bone broth, or tendons can help ensure adequate glycine levels.

Partially SupportedTo support glutathione production, individuals should ensure adequate glycine and methionine intake and consume organ meats and connective tissue.

Partially SupportedUric acid and glutathione may function as antioxidant mechanisms to manage reactive oxygen species generated by cold and heat exposure.

Not SupportedHigh doses of vitamin C can be directly toxic to the gut, potentially causing nausea, diarrhea, bloating, and heartburn.

Partially SupportedAdding a small amount of vitamin C supplement is not harmful if individuals are concerned about their intake, although clinical evidence for its necessity is lacking.

Partially SupportedSome individuals may develop scurvy on a carnivore diet if they consume only cured or non-fresh meats, but not if they eat fresh meat.

Partially SupportedThe Recommended Dietary Allowance for vitamin C is based on preventing scurvy, not on supporting optimal enzyme activity or antioxidant function.

Partially SupportedFructose, insulin resistance, and alcohol contribute to decreased uric acid excretion.

Well SupportedCollagen is primarily composed of glycine, proline, and hydroxyproline.

Partially SupportedCollagen supplementation supports tendon and ligament strength in athletes and provides glycine for glutathione production.

Partially SupportedLipid peroxidation, initiated by hydroxyl radicals, creates harmful lipid peroxides.

Partially SupportedSophorafern may increase levels of acrolein and 4-HNE, which are oxidized omega-6 fatty acids.

Partially SupportedUric acid may function as an antioxidant, scavenging reactive oxygen species (ROS) and potentially fulfilling the role proposed for vitamin C.

Partially SupportedVitamin C deficiency leads to a loss of collagen, causing blood vessels to disintegrate, leading to bleeding and potentially death (scurvy).

Partially SupportedSome individuals on a carnivore diet do not supplement with vitamin C and have not experienced scurvy.

Partially SupportedThe human gene that breaks down uric acid is knocked out, and the body recycles 90% of it.

Not SupportedMega-doses of vitamin C supplements or consuming large quantities of oranges can potentially create problems.

Partially SupportedGout may occur in individuals with both high uric acid levels and low glutathione.

Partially SupportedUric acid levels were reduced by approximately 50% one hour after a whole body cold stimulus and returned to baseline within 24 hours.

Partially SupportedThe lowest effective dose of vitamin C to reverse scurvy symptoms is 10mg per day.

Partially SupportedAdequate vitamin C is required for the hydroxylation and subsequent glycosylation of collagen strands to form the functional triple helix structure.

Partially SupportedOxidation is the transfer of electrons from one molecule to another, where the oxidant gains electrons and the reductant loses electrons.

Partially SupportedSufficient glycine, glutamine, and cysteine are required for adequate glutathione levels.

Partially SupportedAnimals subjected to a diet depleted in amino acids required for glutathione production developed type 1 diabetes and pancreatic cell necrosis after uric acid injection.

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

Partially SupportedEating connective tissues like tendons and ligaments, along with organs, is a practice of hunter-gatherer societies and beneficial for health.

Well SupportedHigh concentrations of injected uric acid can cause toxic effects on the islets of Langerhans, leading to necrosis and type 1 diabetes in animals.

Partially SupportedUric acid may be beneficial unless it is dysregulated.

Not SupportedExcess oral vitamin C can act as a pro-oxidant, particularly in individuals with G6PD deficiency, leading to adverse health outcomes.

Partially SupportedUric acid buildup can cause gout and may relate to overall antioxidant status.

Partially SupportedAlcohol inhibits the kidneys' ability to excrete uric acid.

Partially SupportedFructose consumption can cause insulin resistance and affect leptin signaling.

Not SupportedIndividuals with G6PD deficiency should avoid fava beans.

Partially SupportedUric acid may possess antioxidant effects.

Partially SupportedGout presentation can vary among individuals with the same uric acid levels.

Partially SupportedThe human body tightly regulates uric acid levels through kidney excretion.

Partially SupportedThere is no clinical evidence to support the benefit of taking more vitamin C than what is obtained from food.

Partially SupportedThere are alternative ways to increase glutathione levels without consuming sulforaphane, which can increase dangerous lipid peroxides and acrolein.

Partially SupportedUric acid is an antioxidant and is largely derived from meat consumption.

Partially SupportedAdequate and optimal glutathione status can be achieved without sulforaphane or other oxidatively stressful plant molecules.

Not SupportedLarge doses of vitamin C may lead to vitamin B12 deficiency.

Not SupportedLarge doses of vitamin C may contribute to vitamin B12 deficiency.

Partially SupportedInjected high concentrations of uric acid in rabbits and rats have shown a toxic effect on the islets of Langerhans in the pancreas.

Partially SupportedReactive oxygen species (ROS) are free radicals found in mitochondria, and not all redox reactions involve oxygen.

Partially SupportedFree radicals are produced in mitochondria during cellular respiration, particularly within the electron transport chain.

Partially SupportedThe transfer of electrons is fundamental to human chemistry and biological processes, including those in mitochondria.

Partially SupportedVitamin E, superoxide dismutase, glutathione, and uric acid may be the primary antioxidants in humans, not vitamin C.

Partially SupportedA historical experiment involved a diet excluding vitamin C-containing foods, with some participants receiving 70mg, 10mg, or zero ascorbic acid.

Partially SupportedAscorbic acid in supplements may act as a pro-oxidant, particularly in red blood cells via the G6PD mechanism.

Partially SupportedNo differences in health were found between participants receiving 70 milligrams of vitamin C per day compared to those receiving 10 milligrams per day in the Sheffield study.

Partially SupportedEndogenous antioxidant molecules like vitamin C, vitamin E, and glutathione manage free radicals by donating or gaining electrons.

Partially SupportedA study published in January 2006 investigated the amount of vitamin C humans need to function optimally.

Partially SupportedBiological or physiological markers for vitamin C deficiency in the absence of clinical scurvy signs could not be found in one study.

Partially SupportedHumans lost the enzyme involved in uric acid breakdown, leading to higher levels of urate/uric acid compared to most mammals that can synthesize vitamin C.

Partially SupportedThe body uses its supply of antioxidants to neutralize reactive oxygen species generated during oxidative stress.

Partially SupportedUric acid acts as an antioxidant by donating electrons to neutralize reactive oxygen species.

Not SupportedThe hypothesis that gout is solely a crystallization reaction based on concentration is an oversimplification.

Partially SupportedWhole body cold exposure reduces the redox potential of mitochondria, leading to an inflammatory response and oxidative stress.

Partially SupportedCold stress is a more evolutionarily consistent climatic stress than sulforaphane and lacks dangerous side effects.

Partially SupportedThere may be an interplay between high uric acid and low glutathione, potentially linked to oxidation.

Partially SupportedOxidation involves losing an electron, while reduction involves accepting an electron.

Partially SupportedA high methionine diet can lead to glycine deficiency by causing the body to use glycine to buffer excess methionine.

Partially SupportedHumans require a minuscule amount of vitamin C primarily for effective collagen synthesis.

Partially SupportedHormetic effects occur when a very small dose of a substance induces a positive outcome, but a larger dose causes a toxic effect, following a J-shaped curve.

Partially SupportedScurvy primarily occurs when individuals do not consume fresh meat.

Partially SupportedNeither Paul Saladino nor Bart Kay have taken vitamin C supplements for periods ranging from 14 to 24 weeks.

Partially SupportedVitamin C is a cofactor essential for collagen formation.

Partially SupportedIn redox reactions, an oxidant donates electrons to a reductant, the reductant is oxidized, and the oxidant is reduced, in a coupled process.

Partially SupportedOxidants are named because oxygen is a powerful oxidant, not necessarily because the process involves molecular oxygen.

Partially SupportedEndogenous antioxidants, such as vitamin C and vitamin E, are involved in stopping lipid peroxidation.

Partially SupportedInadequate vitamin C leads to poor collagen formation, affecting wound healing and causing bleeding issues.

Partially SupportedThree ounces of liver contains 30 milligrams of vitamin C.

Partially SupportedOxidation is the loss of electrons and reduction is the gain of electrons.