#fructose
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ltwharfy · 4 months ago
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"I'm just holding out for a decent childhood,and I'm not gonna grow up until I get it."- Ben Katz , "Fructose"
Honestly, that's not a bad philosophy. Wish I had thought of that in my 20's.
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xraevyn · 5 months ago
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Friendly healthy reminder to consume fruit & water 💧🍍🍎🍓🍇💦
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gesundheit-politik · 6 months ago
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!!!!
#mecfs
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kramlabs · 1 year ago
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*perhaps the most important Rhonda Patrick interview and information
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f1inl3ey · 1 year ago
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I’m really starting to regret having that apple juice
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sciencesolutions · 2 years ago
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hetheyhedonist · 1 month ago
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Fructose breath test prep be kicking my mental balls because what do you mean I can't even have lemon water? What do you mean I can't have herbal tea? What do you mean I can't have any fruit?????????????
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transparentgentlemenmarker · 4 months ago
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jose96853 · 6 months ago
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COMMON FOOD ADDITIVE LINKED TO TUMOR GROWTH, STUDY FINDS
Recent research from Washington University has uncovered a concerning link between fructose—a common sweetener in many processed foods—and accelerated tumor growth. The study indicates that diets high in fructose can significantly enhance tumor development, even in the absence of changes in weight, blood sugar, or fasting insulin levels. Fructose, a simple sugar naturally present in fruits, is…
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iheartvelma · 6 months ago
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PBS’ chemistry series Reactions explores what’s really going on with Mexican Coke - as Johnny Harris noted in one of his videos, it tests as if there’s no sucrose in it at all, so is it intentionally mislabeled?
Turns out, acidic environments, like the inside of a soda bottle, break down sucrose (cane sugar) into fructose and glucose.
I like how he uses two testing methods - copper precipitate tests as well as using diabetic glucose testers - and does the deep dive on the papers proving it.
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openintegrative · 7 months ago
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Gout: Symptoms & Natural Treatment
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Gout results from the accumulation of uric acid crystals in the joints, causing severe pain and inflammation.
High uric acid levels are often linked to metabolic issues and excessive fructose consumption.
Fructose, not red meat, is a primary contributor to elevated uric acid and gout development.
Proper management of gout involves reducing sugar intake and optimizing nutrient balance.
Addressing underlying metabolic dysfunctions is essential for long-term gout relief.
Introduction
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Gout is a form of arthritis characterized by sudden and severe pain, swelling, and redness in the joints, most often in the big toe.
It occurs when uric acid crystals accumulate in the joints, causing inflammation and pain.
Gout is closely related to high levels of uric acid in the blood, but several factors influence its development, including diet, metabolic health, and lifestyle.
Causes and Risk Factors
Uric Acid and Gout
Uric acid is a natural waste product formed when the body breaks down purines. Normally, uric acid is dissolved in the blood and eliminated through the kidneys.
However, when uric acid levels become too high, it can crystallize and settle in the joints, leading to gout.
The main drivers of elevated uric acid include metabolic issues, fructose consumption, and impaired kidney function.
The Role of Fructose in Gout
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Fructose, found in sugary drinks and processed foods, is a major contributor to high uric acid levels.
Unlike glucose, fructose metabolism rapidly generates uric acid, particularly in the liver. Excessive fructose consumption has been linked to metabolic disorders such as insulin resistance, non-alcoholic fatty liver disease (NAFLD), and gout.
Reducing fructose intake is key to preventing gout flares and managing uric acid levels.
Common Triggers for Gout Attacks
Gout attacks can be triggered by various factors, including:
High consumption of fructose or sugar-laden foods
Alcohol intake, especially beer
Dehydration
Sudden increases in physical activity or stress
Certain medications that raise uric acid levels, like diuretics
Symptoms and Diagnosis
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Common Symptoms
The most common symptom of gout is intense joint pain, often starting in the big toe, though other joints can be affected. Additional symptoms include:
Swelling and redness in the affected joint
Warmth and tenderness around the joint
Limited joint movement due to pain
Gout attacks, which can occur suddenly and last several days
Diagnosing Gout
Gout is typically diagnosed through physical examinations, blood tests to check uric acid levels, and imaging studies like ultrasounds or X-rays to detect uric acid crystals in the joints.
Joint fluid tests can also confirm the presence of uric acid crystals.
Treatment and Management
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Dietary Adjustments
Managing gout involves making key dietary changes to reduce uric acid levels and prevent gout flares. Prioritizing nutrient-dense, low-sugar foods while reducing fructose intake is needed.
Contrary to popular belief, red meat is not a major cause of gout and provides essential nutrients like iron, zinc, and B vitamins.
Instead, eliminating sugary foods and drinks, especially those containing high-fructose corn syrup, is essential for reducing gout risk.
Medication Options
Medications are often prescribed to manage gout, especially during acute flare-ups. These include:
Nonsteroidal anti-inflammatory drugs (NSAIDs): Used to reduce pain and inflammation.
Colchicine: Helps reduce inflammation during a gout attack.
Allopurinol: Lowers uric acid levels by reducing its production in the body.
Probenecid: Increases uric acid excretion through the kidneys.
While medications are effective, long-term management should focus on lifestyle changes that address the underlying causes of high uric acid.
Long-Term Management Strategies
In addition to dietary changes and medications, managing gout involves other lifestyle adjustments:
Stay hydrated to support kidney function and uric acid excretion.
Maintain a healthy weight to reduce the metabolic stress associated with high uric acid levels.
Limit alcohol consumption, as it can interfere with uric acid excretion and trigger gout attacks.
Preventing Gout Flares
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Reducing Fructose Intake
As fructose significantly contributes to elevated uric acid levels, cutting back on sugary drinks and processed foods is vital.
A diet rich in whole, low-carbohydrate foods supports metabolic health and prevents gout flares.
Optimizing Nutrient Intake
Eating a bioavailable nutrient-rich diet ensures the body gets essential nutrients like copper, which plays a key role in managing oxidative stress and iron regulation.
Proper nutrient balance helps the body manage uric acid more effectively.
Beta-hydroxybutyrate (BHB)
Beta-hydroxybutyrate (BHB) is one of the main ketone bodies produced by the liver during fat metabolism.
BHB is produced through a process called ketogenesis, where fats are broken down into ketones in the liver.
This occurs during times of carbohydrate restriction, fasting, or prolonged exercise. The body converts stored fat into ketones, with BHB being the primary ketone that circulates in the bloodstream and provides energy.
Beta-hydroxybutyrate (BHB) has shown promising effects in reducing inflammation related to gout. Research indicates that BHB inhibits the NLRP3 inflammasome, a key driver in gout’s inflammatory response, particularly in neutrophils.
This inhibition reduces the production of IL-1β, a pro-inflammatory cytokine involved in gouty flares.
The anti-inflammatory properties of BHB offer a potential therapeutic avenue for treating gout, providing relief from the intense joint pain and inflammation associated with the condition.
Exercise and Weight Management
Regular physical activity and maintaining a healthy weight help improve insulin sensitivity, reduce inflammation, and lower the risk of metabolic conditions that contribute to gout.
However, sudden intense physical activity may trigger gout attacks, so exercise should be moderate and consistent.
Conclusion
Gout is a painful condition rooted in metabolic imbalances and high uric acid levels. While often misunderstood, the primary contributors to gout are fructose consumption and metabolic dysfunction, not red meat. Managing gout requires a combination of dietary changes, medication when needed, and long-term lifestyle adjustments that target the root causes of elevated uric acid. By focusing on reducing fructose intake and optimizing metabolic health, individuals can effectively manage and prevent gout flare-ups.
FAQs
What causes gout?
Gout is caused by the accumulation of uric acid crystals in the joints, often triggered by metabolic issues, fructose consumption, and impaired kidney function.
Is red meat a cause of gout?
No, red meat is not a primary cause of gout. The real culprit is excessive fructose consumption, which raises uric acid levels.
How can I prevent gout flare-ups?
Prevent gout flare-ups by reducing sugar and fructose intake, staying hydrated, maintaining a healthy weight, and following a nutrient-dense diet.
What is the role of fructose in gout?
Fructose is metabolized into uric acid, which contributes to gout development. Limiting sugary drinks and processed foods helps manage uric acid levels.
Can gout be cured?
While there is no cure for gout, it can be effectively managed through lifestyle changes, proper diet, and medications that reduce uric acid levels
Research
Ayoub-Charette S, Liu Q, Khan TA, Au-Yeung F, Blanco Mejia S, de Souza RJ, Wolever TM, Leiter LA, Kendall C, Sievenpiper JL. Important food sources of fructose-containing sugars and incident gout: a systematic review and meta-analysis of prospective cohort studies. BMJ Open. 2019 May 5;9(5):e024171. doi: 10.1136/bmjopen-2018-024171. PMID: 31061018; PMCID: PMC6502023.
Bai, L., Zhou, J.-B., Zhou, T., Newson, R.B. and Cardoso, M.A., 2021. Incident gout and weight change patterns: a retrospective cohort study of US adults. Arthritis Research & Therapy, [online] 23(1). https://doi.org/10.1186/s13075-021-02461-7.
Basaranoglu, M., Basaranoglu, G., & Bugianesi, E. (2015). Carbohydrate intake and nonalcoholic fatty liver disease: Fructose as a weapon of mass destruction. Hepatobiliary Surgery and Nutrition, 4(2), 109-116. https://doi.org/10.3978/j.issn.2304-3881.2014.11.05
Cristina, M. (2023). Insulin and the kidneys: A contemporary view on the molecular basis. Frontiers in Nephrology, 3, 1133352. https://doi.org/10.3389/fneph.2023.1133352
Ghio, A.J., Ford, E.S., Kennedy, T.P. and Hoidal, J.R., 2005. The association between serum ferritin and uric acid in humans. Free Radical Research, [online] 39(3), pp.337–342. https://doi.org/10.1080/10715760400026088.
Goldberg, E. L., Asher, J. L., Molony, R. D., Shaw, A. C., Zeiss, C. J., Wang, C., Morozova-Roche, L. A., Herzog, R. I., Iwasaki, A., & Dixit, V. D. (2017). β-hydroxybutyrate deactivates neutrophil NLRP3 inflammasome to relieve gout flares. Cell Reports, 18(9), 2077. https://doi.org/10.1016/j.celrep.2017.02.004
Jamnik, J., Rehman, S., Blanco Mejia, S., de Souza, R.J., Khan, T.A., Leiter, L.A., Wolever, T.M.S., Kendall, C.W.C., Jenkins, D.J.A. and Sievenpiper, J.L., 2016. Fructose intake and risk of gout and hyperuricemia: a systematic review and meta-analysis of prospective cohort studies. BMJ Open, [online] 6(10), p.e013191. https://doi.org/10.1136/bmjopen-2016-013191.
Lanaspa, M.A., Sanchez-Lozada, L.G., Cicerchi, C., Li, N., Roncal-Jimenez, C.A., Ishimoto, T., Le, M., Garcia, G.E., Thomas, J.B., Rivard, C.J., Andres-Hernando, A., Hunter, B., Schreiner, G., Rodriguez-Iturbe, B., Sautin, Y.Y. and Johnson, R.J., 2012. Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Development of Fatty Liver. PLoS ONE, [online] 7(10), p.e47948. https://doi.org/10.1371/journal.pone.0047948.
Lanaspa, M.A., Tapia, E., Soto, V., Sautin, Y. and Sánchez-Lozada, L.G., 2011. Uric Acid and Fructose: Potential Biological Mechanisms. Seminars in Nephrology, [online] 31(5), pp.426–432. https://doi.org/10.1016/j.semnephrol.2011.08.006.
Maiuolo, J., Oppedisano, F., Gratteri, S., Muscoli, C. and Mollace, V., 2016. Regulation of uric acid metabolism and excretion. International Journal of Cardiology, [online] 213, pp.8–14. https://doi.org/10.1016/j.ijcard.2015.08.109.
Mainous, A.G., Knoll, M.E., Everett, C.J., Matheson, E.M., Hulihan, M.M. and Grant, A.M., 2011. Uric Acid as a Potential Cue to Screen for Iron Overload. The Journal of the American Board of Family Medicine, [online] 24(4), pp.415–421. https://doi.org/10.3122/jabfm.2011.04.110015.
Muscelli, E., 1996. Effect of insulin on renal sodium and uric acid handling in essential hypertension. American Journal of Hypertension, [online] 9(8), pp.746–752. https://doi.org/10.1016/0895-7061(96)00098-2.
Nakagawa, T., Lanaspa, M. A., & Johnson, R. J. (2019). The effects of fruit consumption in patients with hyperuricaemia or gout. Rheumatology, 58(7), 1133-1141. https://doi.org/10.1093/rheumatology/kez128
Pina, A.F., Borges, D.O., Meneses, M.J., Branco, P., Birne, R., Vilasi, A. and Macedo, M.P., 2020. Insulin: Trigger and Target of Renal Functions. Frontiers in Cell and Developmental Biology, [online] 8. https://doi.org/10.3389/fcell.2020.00519.
Rasool, M., Malik, A., Jabbar, U., Begum, I., Qazi, M.H., Asif, M., Naseer, M.I., Ansari, S.A., Jarullah, J., Haque, A. and Jamal, M.S., 2016. Effect of iron overload on renal functions and oxidative stress in beta thalassemia patients. Saudi Medical Journal, [online] 37(11), pp.1239–1242. https://doi.org/10.15537/smj.2016.11.16242.
Rho, Y.H., Zhu, Y. and Choi, H.K., 2011. The Epidemiology of Uric Acid and Fructose. Seminars in Nephrology, [online] 31(5), pp.410–419. https://doi.org/10.1016/j.semnephrol.2011.08.004.
Singh, J.A., Reddy, S.G. and Kundukulam, J., 2011. Risk factors for gout and prevention: a systematic review of the literature. Current Opinion in Rheumatology, [online] 23(2), pp.192–202. https://doi.org/10.1097/bor.0b013e3283438e13.
Skøtt, P., Hother-Nielsen, O., Bruun, N.E., Giese, J., Nielsen, M.D., Beck-Nielsen, H. and Parving, H.-H., 1989. Effects of insulin on kidney function and sodium excretion in healthy subjects. Diabetologia, [online] 32(9). https://doi.org/10.1007/bf00274259.
Wang, Y., Yang, Z., Wu, J., Xie, D., Yang, T., Li, H. and Xiong, Y., 2020. Associations of serum iron and ferritin with hyperuricemia and serum uric acid. Clinical Rheumatology, [online] 39(12), pp.3777–3785. https://doi.org/10.1007/s10067-020-05164-7.
Yamanaka H. [Alcohol ingestion and hyperuricemia]. Nihon Rinsho. 1996 Dec;54(12):3369-73. Japanese. PMID: 8976122.
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funsimplethings · 1 year ago
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f1inl3ey · 1 year ago
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The hospitals saying I’m fructose intolerant too wtf is my life 😭😭
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bogleech · 1 year ago
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Wouldn't it be entirely possible, even likely, that with all the silly weaknesses vampires and stuff were supposed to have, they'd also turn out to be weak to any number of things that have only been invented more recently? Like who's to say vampires aren't also repelled by the smell of play-doh or driven insane by MIDI music? We've invented so much shit in just the last century there'd be NO predicting this. For all we know they burn to ash if they look at Luigi.
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kramlabs · 1 year ago
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wedmax · 1 year ago
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«The First Curse»
"As if banished from the Garden, I am forbidden of His fruit."
Shout out to my fructose intolerant friends out there, of which there are a few. I hope to raise awareness a bit about it.
Can you read all the symbols depicted in here?
@ wed.max Maxime Clusqeau
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