⚕️ Educational information only — not medical advice. Read the full disclaimer

Foods to Avoid With Arthritis

Diet is one of the most modifiable levers in joint health. The most discussed foods that worsen arthritis — added sugar and high-fructose corn syrup, refined carbohydrates, industrial seed oils, gluten, A1 dairy, nightshades, and ultra-processed additives — are thought to feed inflammation through distinct biochemical pathways. Below, each dietary trigger is explained with its proposed mechanism and graded honestly: some links are well established, others are emerging, and several are genuinely contested by mainstream rheumatology. This page is a companion to our anti-inflammatory diet for arthritis — the problem here, the plan there.

Important: This page is general educational information, not medical advice. Arthritis varies by person and type. Always consult a qualified healthcare professional before changing your diet, supplements, exercise, or medication, and never stop a prescribed medication without speaking to the prescribing physician.

Key takeaways

  • Fructose (from sugar and HFCS) is metabolized in a way that can raise uric acid, a well-established trigger for gout flares.
  • Refined carbs drive hyperglycemia and Advanced Glycation End-products (AGEs) that may make cartilage brittle — an emerging link.
  • Trans fats are strongly tied to inflammation; the claim that seed oils are pro-inflammatory in humans is contested — randomized trials have not found that linoleic acid raises inflammatory markers.
  • Gluten (outside celiac disease), A1 dairy, and nightshades have no proven link to arthritis; French rheumatology guidelines for inflammatory arthritis advise against gluten-free (without celiac disease) or dairy-free diets. Any personal sensitivity is best assessed through a supervised elimination trial, not blanket avoidance.
  • Alcohol and purine-rich red/processed meats are firmly linked to gout via uric acid; track your inflammation biomarkers to see what matters for you.

Sugar & High-Fructose Corn Syrup

Full guide: Does sugar cause joint pain? — AGEs, fructose and gout, sugary drinks and RA risk, with verified studies.

The modern Western diet is saturated with refined sucrose and high-fructose corn syrup (HFCS). Biochemical research highlights the role of fructose metabolism in driving uric acid and metabolic dysfunction. Unlike glucose, fructose is metabolized largely in the liver by the enzyme fructokinase (KHK), which bypasses the tightly regulated steps of glycolysis and lacks a negative feedback brake.1

Mechanism: fructose → ATP depletion → uric acid

Fructokinase phosphorylates fructose as fast as it enters the cell, causing a rapid depletion of intracellular ATP and inorganic phosphate. The drop in ATP stimulates AMP deaminase, accelerating purine degradation, which culminates in excess uric acid production by xanthine oxidase plus a surge in mitochondrial oxidative stress.123 Elevated uric acid can crystallize in joints to precipitate gout, and has also been linked to insulin resistance and endothelial dysfunction — a possible feed-forward loop, though its causal role in cardiometabolic disease is not fully settled.13

In a 12-year study of about 46,000 men, two or more sugar-sweetened soft drinks a day was linked to an 85% higher risk of gout, and a meta-analysis of prospective cohorts found a 62% higher gout risk with the highest fructose intakes (rated low certainty because only two cohorts were available).45 The 2020 American College of Rheumatology gout guideline conditionally recommends limiting high-fructose corn syrup alongside alcohol and purine intake.6

Strong The fructose → uric acid → gout pathway is well established. Emerging The broader role of this feed-forward inflammatory loop in rheumatoid arthritis (RA) and osteoarthritis is promising but less settled. You can monitor serum uric acid and hs-CRP on our arthritis biomarkers page.

Refined Carbs & Ultra-Processed Foods

Diets heavy in refined carbohydrates — white flour, white rice, and commercial baked goods — rapidly spike blood glucose, producing chronic hyperglycemia. This state accelerates non-enzymatic glycation, yielding Advanced Glycation End-products (AGEs). Cartilage collagen is barely replaced over a lifetime, so AGEs such as pentosidine accumulate steadily with age.7

Mechanism: hyperglycemia → AGEs/RAGE → brittle cartilage

Accumulating AGEs cross-link collagen and make cartilage stiffer and more brittle; in dogs, raising cartilage AGE levels led to more severe experimental osteoarthritis.8 Chondrocytes also carry the AGE receptor RAGE, whose activation switches on NF-κB inflammatory signaling and the cartilage-degrading enzyme MMP-13.9 In line with this, diabetes is associated with osteoarthritis in meta-analysis (odds ratio about 1.46), although only some studies found the link held after adjusting for body weight.10

Emerging The hyperglycemia–AGE–cartilage link is biologically plausible and supported by laboratory and animal work, but most cartilage AGE build-up reflects age and slow tissue turnover, and no human study has shown that cutting refined carbs lowers cartilage AGEs or slows arthritis. Dietary AGEs are a separate issue: the richest sources are fatty, protein-rich foods cooked with dry heat (grilling, frying, roasting), not starches.11 Ultra-processed foods also tend to bundle refined carbs with added fats and additives.

Industrial Seed Oils & Trans Fats

Industrial seed oils — canola, soybean, corn, and cottonseed — are rich in omega-6 polyunsaturated fatty acids, primarily linoleic acid. Proponents argue that the hyper-abundance of these oils skews the omega-3 to omega-6 ratio, and that excess arachidonic acid is metabolized via the COX and LOX pathways into pro-inflammatory eicosanoids, specifically Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4). The biochemistry is real: arachidonic acid is a precursor of these mediators, which is why many anti-inflammatory drugs target that pathway.12

Contested: Contested The leap from that pathway to "seed oils inflame joints" is not supported by human trials. A systematic review of 15 randomized controlled trials in healthy adults found that adding linoleic acid to the diet did not raise CRP, cytokines, TNF-α or other inflammatory markers,13 and a review of human feeding studies found that cutting linoleic acid by up to 90% or raising it six-fold did not change arachidonic acid levels in blood phospholipids.14 The fair caveat: high omega-6 intakes may blunt some of the anti-inflammatory effects of omega-3s, and the interaction is not fully understood.12 No trial has tested seed-oil avoidance as an arthritis treatment.

What has been tested in rheumatoid arthritis is a diet low in arachidonic acid itself — which comes mainly from meat, eggs and other animal foods, not from seed oils. In a small 8-month study of 68 patients, the low-arachidonic-acid diet reduced tender and swollen joints and enhanced the benefit of fish oil.15 Fish-oil supplements on their own have shown only a small, low-certainty benefit on RA pain and joint counts in meta-analysis of placebo-controlled trials.16

Strong By contrast, industrial trans fats from partially hydrogenated oils are well documented to promote systemic inflammation: in the Nurses' Health Studies, women with the highest intakes had 10–12% higher levels of soluble TNF receptors, and observational and experimental evidence also links trans fats to endothelial dysfunction.1718 Direct arthritis data are limited, but the U.S. FDA no longer recognizes partially hydrogenated oils as safe, so artificial trans fats are now largely gone from the U.S. food supply.19 Avoiding any that remain is among the least controversial dietary steps, and forms part of our anti-inflammatory plan.

Gluten & Wheat

Full guide: Gluten and joint pain — celiac arthritis, gluten sensitivity vs. fructans, and why to test before going gluten-free.

For some patients with rheumatoid and psoriatic arthritis, gluten is described as a trigger. Gluten peptides — specifically gliadin — resist complete digestion. In laboratory studies, gliadin triggers release of zonulin, a protein that loosens the tight junctions of the gut lining and increases intestinal permeability ("leaky gut"). The effect was sustained in intestinal tissue from people with celiac disease but only brief and smaller in tissue from people without it.2021

Mechanism (proposed): gliadin → zonulin/leaky gut → immune cross-reaction

Proponents argue that a more permeable gut lets food and microbial antigens reach the immune system, and that gluten-driven immune activation may cross-react with joint tissue — a form of molecular mimicry (see the gut-joint axis). Reviews by these researchers suggest gluten-free diets may help in some non-celiac autoimmune diseases, while acknowledging that human studies are still needed.22 The closest arthritis trial randomized 66 people with active RA to a vegan, gluten-free diet or a balanced non-vegan diet for a year: 34% vs about 4% met the ACR20 improvement criteria (intention-to-treat), and antibodies to gliadin and milk protein fell in responders. Because the diet removed many foods at once, it cannot show that gluten itself was the culprit.23

Emerging Contested Evidence is strongest in celiac disease, which genuinely requires strict gluten avoidance. For everyone else, the French Society for Rheumatology's 2022 recommendations state that gluten-free diets should not be proposed for inflammatory rheumatic disease in the absence of celiac disease,24 and a Cochrane review judged the effects of elimination and vegan diets in RA uncertain because the trials were small, poorly reported and at moderate to high risk of bias.25 If you suspect a sensitivity, get tested for celiac disease before cutting gluten, then consider a physician-supervised trial.

Dairy: A1 vs A2 Casein

Casein is frequently named by some patients and integrative practitioners as a trigger of joint pain and stiffness. The proposed mechanism centers on genetic variants of beta-casein. Ordinary cow's milk usually contains a mix of A1 and A2 beta-casein; the A1 type (histidine at position 67) can be cleaved during digestion to release beta-casomorphin-7 (BCM-7), an opioid peptide.26

Mechanism: A1 casein → BCM-7 opioid peptide → gut symptoms

In rodents, A1 casein slows intestinal transit through an opioid mechanism and raises gut inflammatory markers relative to A2.26 In small double-blind crossover trials in people who report trouble with milk, A1 milk produced more digestive discomfort, slower transit and higher markers such as fecal calprotectin than A2-only milk (proline at position 67, which resists BCM-7 release).272829 Results are not entirely consistent — in one 2024 trial, A2 milk caused more bloating and loose stools but less pain and urgency.29

The independent picture is more modest. A GRADE-rated systematic review of 15 randomized trials found moderate certainty that A1 casein causes more digestive symptoms than A2, but low to very low certainty for any other health effect.30 (One earlier systematic review was written by authors with consultancy ties to an A2 milk company.26) For joints specifically: a meta-analysis of cohort studies found no association between dairy intake and rheumatoid arthritis risk;31 a meta-analysis of 11 randomized trials found dairy did not raise CRP, TNF-α or IL-6 in adults (pooled results suggested slight reductions, which disappeared in crossover trials);32 and in a large cohort of men, the highest dairy intake was linked to a 44% lower risk of gout.33

Contested Human evidence for A1 vs A2 concerns digestive comfort in people with self-reported milk intolerance, not arthritis outcomes; no trial has tested A1 avoidance in arthritis, and French rheumatology guidelines advise that dairy elimination should not be proposed for inflammatory rheumatic disease.24 If milk upsets your gut, trying A2 milk or lower-lactose dairy is a reasonable personal experiment; cutting dairy entirely is not a joint treatment, and for gout dairy appears helpful.

Nightshades

Full guide: Nightshades and arthritis — where the claim came from, what the evidence shows, and how to run a fair elimination test.

The Solanaceae family — tomatoes, bell peppers, eggplants, and white potatoes — contains glycoalkaloids, mainly α-solanine and α-chaconine in potatoes.34 The role of nightshades in arthritis is one of the more controversial topics in clinical nutrition: there is no good human evidence that they cause or worsen arthritis in most people, and controlled reviews of elimination diets in RA have found their effects uncertain.25

Proposed harm (sensitive subset)

Potato glycoalkaloids increased gut permeability in cultured cells and worsened colitis in mice genetically prone to bowel inflammation — but not in normal mice.3536 A 2023 gastroenterology review added the hypothesis that they may activate gut mast cells, while describing the human literature as limited.37 Whether any of this reaches the joints in people is unproven.

Possible benefit

In a small 6-week trial in healthy men, pigmented (purple and yellow) potatoes lowered a marker of DNA damage compared with white potatoes, with borderline-significant trends toward lower IL-6 and CRP,38 and in a mouse model of osteoarthritis α-solanine reduced chondrocyte pyroptosis by suppressing NF-κB signaling.39

Testing a personal sensitivity: Contested Some integrative practitioners recommend a strict 30-to-60-day elimination followed by structured reintroduction; our full guide suggests 3–4 weeks as a practical middle ground. This is a personal experiment, not an evidence-based protocol: the only randomized trial of a nightshade elimination diet in rheumatoid arthritis has published a protocol but no results yet.40 Permanent blanket avoidance of nutritious vegetables is not recommended.

Artificial Sweeteners & Food Additives

Marketed as metabolically inert, non-nutritive sweeteners may still affect the gut microbiome. In cell-culture experiments, saccharin, sucralose and aspartame increased biofilm formation by model gut bacteria (E. coli and Enterococcus faecalis) and their ability to adhere to, invade and kill intestinal epithelial cells.41 In a randomized trial of 120 healthy adults, two weeks of saccharin, sucralose, aspartame or stevia at below acceptable-daily-intake doses altered the gut microbiome, and saccharin and sucralose impaired glucose responses.42 Integrative practitioners link such changes to the leaky-gut pathway behind systemic inflammation, but no study has connected sweeteners to arthritis outcomes, and reviewers note there is still no consensus on how to measure their microbiome effects.43

Additives of concern

  • MSG: animal studies using high doses have reported increased pain sensitivity, but a comprehensive review found little supporting evidence for this (or for "MSG hypersensitivity") at the amounts people actually eat.44 Contested
  • Carrageenan: a seaweed thickener that researchers routinely use to induce inflammation in animal models when testing anti-inflammatory drugs. Whether food-grade carrageenan inflames the human gut is debated; a 2021 review linked it to inflammatory bowel disease and advised limiting exposure, while noting the lack of definitive safety data.45
  • Emulsifiers: in mice, carboxymethylcellulose and polysorbate-80 let gut bacteria encroach on the intestinal lining, causing low-grade inflammation and metabolic syndrome in normal mice and promoting colitis in susceptible ones.46 In a controlled-feeding trial in healthy people, carboxymethylcellulose reduced microbiome diversity and short-chain fatty acids and modestly increased abdominal discomfort.47
  • Artificial dyes & other additives: ubiquitous in ultra-processed foods and under study for effects on gut health and intestinal inflammation.48

Emerging Contested Much of this evidence is from cell and animal models plus short human studies of gut markers; there are no human arthritis outcome data. Ordinary dietary amounts of MSG, for instance, appear generally well tolerated.44

Alcohol, Red Meat & Caffeine Excess

Alcohol is firmly linked to gout. In a 12-year study of men, risk rose with intake — about 2.5-fold at 50 g a day or more — with beer carrying the highest risk, spirits a smaller one and moderate wine none;49 among people who already have gout, more than one to two drinks of any type in the previous 24 hours was associated with a higher risk of a flare, rising with the amount.50 Chronic heavy drinking also alters the gut microbiome and increases intestinal permeability.51 Strong (for gout). For rheumatoid arthritis the picture differs: low-to-moderate drinking has been associated with a lower risk of developing RA in cohort studies,52 though that observational finding is no reason to start drinking, and anyone taking arthritis medication should ask their prescriber about alcohol.

Red and processed meats and some seafood are high in purines, the direct substrate for uric acid: men with the highest meat intake had a 41% higher gout risk,33 and the ACR guideline conditionally recommends limiting purine intake for people with gout.6 Strong for the purine–gout link. The broader claim that red meat drives systemic inflammation is weaker: two meta-analyses of randomized trials found red meat did not raise CRP compared with other diets.5354 Contested for the broader inflammatory contribution, although limiting processed meat is reasonable for general health.

Caffeine excess from coffee and energy drinks raises cortisol in people who are not used to it, but the response is largely blunted — though not eliminated — in daily caffeine users.55 Caffeine has only a very small effect on calcium absorption, and a review found no evidence of harm to bone in people who meet recommended calcium intakes.56 For gout, coffee points the other way: in a large cohort of men, four or more cups a day was associated with a 40–59% lower risk of developing gout.57 Contested Very high intakes may disturb sleep or raise anxiety, but caffeine is not an established arthritis trigger.

Master table: foods that worsen arthritis

A consolidated view of each trigger, its proposed mechanism, the arthritis type most implicated, and the honest evidence grade.

Worst foods for arthritis inflammation — mechanism & evidence
Food / beverage Proposed mechanism Linked arthritis type Evidence
Sugar & HFCS Fructokinase → ATP depletion → uric acid; feed-forward inflammation Gout; metabolic / RA Strong (gout) Emerging (RA)
Refined carbs & ultra-processed foods Hyperglycemia → AGEs/RAGE → brittle cartilage, cytokines Osteoarthritis; RA Emerging
Industrial seed oils Proposed: excess omega-6 / linoleic acid → arachidonic acid → PGE2, LTB4 (not borne out in human trials) General inflammatory Contested
Trans fats Endothelial dysfunction, oxidative stress General inflammatory Strong
Gluten / wheat (gliadin) Zonulin → leaky gut → proposed molecular mimicry Celiac disease; proposed in RA/psoriatic subsets Emerging Contested
A1 dairy (casein) A1 casein → BCM-7 opioid peptide → gut symptoms Digestive symptoms in milk-intolerant people; no arthritis link shown (dairy linked to lower gout risk) Contested
Nightshades (Solanaceae) Glycoalkaloids → gut permeability in susceptible mice; mast-cell hypothesis (also possible benefit) RA; PsA (individualized) Contested
Artificial sweeteners (aspartame, sucralose) Microbiome dysbiosis, biofilm, epithelial invasion Gut-linked / systemic Emerging Contested
Additives (MSG, carrageenan, emulsifiers, dyes) Gut barrier and microbiome changes (mostly animal data); MSG pain claims weak Gut-linked Emerging Contested
Alcohol Uric acid elevation; gut permeability Gout (moderate intake linked to lower RA risk) Strong
Red & processed meats Purines → uric acid; broader inflammation not seen in RCTs Gout; general inflammatory Strong (gout) Contested (inflammation)
Caffeine excess Cortisol rise (blunted in habitual users); very small calcium effect Not established (coffee linked to lower gout risk) Contested
From avoid-list to action plan: Knowing what to remove is only half the picture. See the positive counterpart — our anti-inflammatory diet for arthritis — and learn how to track changes with inflammation biomarkers like hs-CRP and uric acid.

Frequently asked questions

What foods may worsen arthritis?

The strongest evidence concerns gout: alcohol (especially beer), sugary drinks and fructose, and purine-rich meat and seafood raise gout risk. Artificial trans fats are firmly linked to systemic inflammation. Refined carbohydrates and ultra-processed additives are emerging concerns, while claims about seed oils, gluten (outside celiac disease), A1 dairy, and nightshades are contested and not supported by controlled human trials. This is educational information, not dietary advice.

Are nightshades bad for arthritis?

The role of nightshades is contested. Some sensitive individuals report flares, while other research notes anti-inflammatory compounds. A supervised elimination trial is sometimes used to assess personal sensitivity. Talk to a qualified professional before major diet changes.

Does sugar increase joint inflammation?

Some research suggests excess sugar and fructose may promote uric acid production and advanced glycation end-products linked to inflammation. Individual responses vary, and this page does not provide medical advice.

References

  1. Khitan Z, Kim DH. Fructose: a key factor in the development of metabolic syndrome and hypertension. J Nutr Metab. 2013;2013:682673. PubMed 23762544
  2. Lubawy M, Formanowicz D. High-Fructose Diet-Induced Hyperuricemia Accompanying Metabolic Syndrome-Mechanisms and Dietary Therapy Proposals. Int J Environ Res Public Health. 2023;20(4). PubMed 36834291
  3. Caliceti C, Calabria D, Roda A, et al. Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review. Nutrients. 2017;9(4). PubMed 28420204
  4. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336(7639):309-12. PubMed 18244959
  5. Jamnik J, Rehman S, Blanco Mejia S, et al. Fructose intake and risk of gout and hyperuricemia: a systematic review and meta-analysis of prospective cohort studies. BMJ Open. 2016;6(10):e013191. PubMed 27697882
  6. FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res (Hoboken). 2020;72(6):744-760. PubMed 32391934
  7. Verzijl N, DeGroot J, Thorpe SR, et al. Effect of collagen turnover on the accumulation of advanced glycation end products. J Biol Chem. 2000;275(50):39027-31. PubMed 10976109
  8. DeGroot J, Verzijl N, Wenting-van Wijk MJ, et al. Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis. Arthritis Rheum. 2004;50(4):1207-15. PubMed 15077303
  9. Loeser RF, Yammani RR, Carlson CS, et al. Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis. Arthritis Rheum. 2005;52(8):2376-85. PubMed 16052547
  10. Louati K, Vidal C, Berenbaum F, et al. Association between diabetes mellitus and osteoarthritis: systematic literature review and meta-analysis. RMD Open. 2015;1(1):e000077. PubMed 26535137
  11. Uribarri J, Woodruff S, Goodman S, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010;110(6):911-16.e12. PubMed 20497781
  12. Innes JK, Calder PC. Omega-6 fatty acids and inflammation. Prostaglandins Leukot Essent Fatty Acids. 2018;132:41-48. PubMed 29610056
  13. Johnson GH, Fritsche K. Effect of dietary linoleic acid on markers of inflammation in healthy persons: a systematic review of randomized controlled trials. J Acad Nutr Diet. 2012;112(7):1029-41, 1041.e1-15. PubMed 22889633
  14. Rett BS, Whelan J. Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review. Nutr Metab (Lond). 2011;8:36. PubMed 21663641
  15. Adam O, Beringer C, Kless T, et al. Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Rheumatol Int. 2003;23(1):27-36. PubMed 12548439
  16. Gkiouras K, Grammatikopoulou MG, Myrogiannis I, et al. Efficacy of n-3 fatty acid supplementation on rheumatoid arthritis' disease activity indicators: a systematic review and meta-analysis of randomized placebo-controlled trials. Crit Rev Food Sci Nutr. 2024;64(1):16-30. PubMed 35900212
  17. Mozaffarian D, Pischon T, Hankinson SE, et al. Dietary intake of trans fatty acids and systemic inflammation in women. Am J Clin Nutr. 2004;79(4):606-12. PubMed 15051604
  18. Mozaffarian D. Trans fatty acids - effects on systemic inflammation and endothelial function. Atheroscler Suppl. 2006;7(2):29-32. PubMed 16713393
  19. Trans Fat — U.S. Food and Drug Administration (FDA). fda.gov/food/food-additives-petitions/trans-fat
  20. Drago S, El Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006;41(4):408-19. PubMed 16635908
  21. Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011;91(1):151-75. PubMed 21248165
  22. Lerner A, Shoenfeld Y, Matthias T. Adverse effects of gluten ingestion and advantages of gluten withdrawal in nonceliac autoimmune disease. Nutr Rev. 2017;75(12):1046-1058. PubMed 29202198
  23. Hafström I, Ringertz B, Spångberg A, et al. A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford). 2001;40(10):1175-9. PubMed 11600749
  24. Daien C, Czernichow S, Letarouilly JG, et al. Dietary recommendations of the French Society for Rheumatology for patients with chronic inflammatory rheumatic diseases. Joint Bone Spine. 2022;89(2):105319. PubMed 34902577
  25. Hagen KB, Byfuglien MG, Falzon L, et al. Dietary interventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009;2009(1):CD006400. PubMed 19160281
  26. Brooke-Taylor S, Dwyer K, Woodford K, et al. Systematic Review of the Gastrointestinal Effects of A1 Compared with A2 β-Casein. Adv Nutr. 2017;8(5):739-748. PubMed 28916574
  27. Jianqin S, Leiming X, Lu X, et al. Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows' milk. Nutr J. 2016;15:35. PubMed 27039383
  28. Ho S, Woodford K, Kukuljan S, et al. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study. Eur J Clin Nutr. 2014;68(9):994-1000. PubMed 24986816
  29. Choi Y, Kim N, Song CH, et al. The Effect of A2 Milk on Gastrointestinal Symptoms in Comparison to A1/A2 Milk: A Single-center, Randomized, Double-blind, Cross-over Study. J Cancer Prev. 2024;29(2):45-53. PubMed 38957588
  30. Küllenberg de Gaudry D, Lohner S, Schmucker C, et al. Milk A1 β-casein and health-related outcomes in humans: a systematic review. Nutr Rev. 2019;77(5):278-306. PubMed 30722004
  31. Asoudeh F, Jayedi A, Kavian Z, et al. A systematic review and meta-analysis of observational studies on the association between animal protein sources and risk of rheumatoid arthritis. Clin Nutr. 2021;40(7):4644-4652. PubMed 34237693
  32. Moosavian SP, Rahimlou M, Saneei P, et al. Effects of dairy products consumption on inflammatory biomarkers among adults: A systematic review and meta-analysis of randomized controlled trials. Nutr Metab Cardiovasc Dis. 2020;30(6):872-888. PubMed 32409275
  33. Choi HK, Atkinson K, Karlson EW, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350(11):1093-103. PubMed 15014182
  34. Friedman M. Potato glycoalkaloids and metabolites: roles in the plant and in the diet. J Agric Food Chem. 2006;54(23):8655-81. PubMed 17090106
  35. Patel B, Schutte R, Sporns P, et al. Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease. Inflamm Bowel Dis. 2002;8(5):340-6. PubMed 12479649
  36. Iablokov V, Sydora BC, Foshaug R, et al. Naturally occurring glycoalkaloids in potatoes aggravate intestinal inflammation in two mouse models of inflammatory bowel disease. Dig Dis Sci. 2010;55(11):3078-85. PubMed 20198430
  37. Kuang R, Levinthal DJ, Ghaffari AA, et al. Nightshade Vegetables: A Dietary Trigger for Worsening Inflammatory Bowel Disease and Irritable Bowel Syndrome? Dig Dis Sci. 2023;68(7):2853-2860. PubMed 37202602
  38. Kaspar KL, Park JS, Brown CR, et al. Pigmented potato consumption alters oxidative stress and inflammatory damage in men. J Nutr. 2011;141(1):108-11. PubMed 21106930
  39. Zhou J, Wu J, Fu F, et al. α-Solanine attenuates chondrocyte pyroptosis to improve osteoarthritis via suppressing NF-κB pathway. J Cell Mol Med. 2024;28(4):e18132. PubMed 38345195
  40. Golmohammadi A, Hosseinikia M, Sadeghi MK, et al. The evaluation of nightshade elimination diet (NED) on inflammatory and rheumatologic markers of rheumatoid arthritis patients: study protocol for a randomized controlled trial. Trials. 2024;25(1):531. PubMed 39127701
  41. Shil A, Chichger H. Artificial Sweeteners Negatively Regulate Pathogenic Characteristics of Two Model Gut Bacteria, E. coli and E. faecalis. Int J Mol Sci. 2021;22(10). PubMed 34063332
  42. Suez J, Cohen Y, Valdés-Mas R, et al. Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance. Cell. 2022;185(18):3307-3328.e19. PubMed 35987213
  43. Conz A, Salmona M, Diomede L. Effect of Non-Nutritive Sweeteners on the Gut Microbiota. Nutrients. 2023;15(8). PubMed 37111090
  44. Zanfirescu A, Ungurianu A, Tsatsakis AM, et al. A review of the alleged health hazards of monosodium glutamate. Compr Rev Food Sci Food Saf. 2019;18(4):1111-1134. PubMed 31920467
  45. Borsani B, De Santis R, Perico V, et al. The Role of Carrageenan in Inflammatory Bowel Diseases and Allergic Reactions: Where Do We Stand? Nutrients. 2021;13(10). PubMed 34684400
  46. Chassaing B, Koren O, Goodrich JK, et al. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature. 2015;519(7541):92-6. PubMed 25731162
  47. Chassaing B, Compher C, Bonhomme B, et al. Randomized Controlled-Feeding Study of Dietary Emulsifier Carboxymethylcellulose Reveals Detrimental Impacts on the Gut Microbiota and Metabolome. Gastroenterology. 2022;162(3):743-756. PubMed 34774538
  48. Seto T, Grondin JA, Khan WI. Food Additives: Emerging Detrimental Roles on Gut Health. FASEB J. 2025;39(13):e70810. PubMed 40622070
  49. Choi HK, Atkinson K, Karlson EW, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363(9417):1277-81. PubMed 15094272
  50. Neogi T, Chen C, Niu J, et al. Alcohol quantity and type on risk of recurrent gout attacks: an internet-based case-crossover study. Am J Med. 2014;127(4):311-8. PubMed 24440541
  51. Bishehsari F, Magno E, Swanson G, et al. Alcohol and Gut-Derived Inflammation. Alcohol Res. 2017;38(2):163-171. PubMed 28988571
  52. Jin Z, Xiang C, Cai Q, et al. Alcohol consumption as a preventive factor for developing rheumatoid arthritis: a dose-response meta-analysis of prospective studies. Ann Rheum Dis. 2014;73(11):1962-7. PubMed 23897767
  53. O'Connor LE, Kim JE, Clark CM, et al. Effects of Total Red Meat Intake on Glycemic Control and Inflammatory Biomarkers: A Meta-Analysis of Randomized Controlled Trials. Adv Nutr. 2021;12(1):115-127. PubMed 32910818
  54. Sun L, Yuan JL, Chen QC, et al. Red meat consumption and risk for dyslipidaemia and inflammation: A systematic review and meta-analysis. Front Cardiovasc Med. 2022;9:996467. PubMed 36247460
  55. Lovallo WR, Whitsett TL, al'Absi M, et al. Caffeine stimulation of cortisol secretion across the waking hours in relation to caffeine intake levels. Psychosom Med. 2005;67(5):734-9. PubMed 16204431
  56. Heaney RP. Effects of caffeine on bone and the calcium economy. Food Chem Toxicol. 2002;40(9):1263-70. PubMed 12204390
  57. Choi HK, Willett W, Curhan G. Coffee consumption and risk of incident gout in men: a prospective study. Arthritis Rheum. 2007;56(6):2049-55. PubMed 17530645