Red Meat Tied to High RA Risk; Fruits and Veggies Protective
The risk for developing rheumatoid arthritis (RA) rose with a high intake of red and processed meat vs fruits and vegetables in a case-control study.
METHODOLOGY:
The risk of developing RA based on dietary habits was explored in a Swedish nested case-control study within a prospective study conducted between January 1991 and September 1996 (n = 28,098).
Diet was assessed at baseline using a 7-day menu book, a 168-item questionnaire, and an interview lasting 45-60 minutes, and each RA patient was matched to four control individuals for analysis.
Compliance with the 2015 Swedish Dietary Guidelines for intake of fiber, fruits and vegetables, fish/shellfish, added sugars, and red or processed meat was scored and categorized as low, moderate, or high.
Data from registries and validated electronic medical records identified RA incidence through December 2016; data on rheumatoid factor and anticyclic citrullinated peptide antibody were also retrieved.
TAKEAWAY:
A total of 305 incident cases of RA were identified (76.1% women; 66.9% seropositive), with a mean age of 56.8 years at baseline and an average 12-year interval until diagnosis.
Consuming < 500 g/wk of red and processed meat (adjusted odds ratio [aOR], 0.60; 95% CI, 0.38-0.97) and ≥ 400 g/d of vegetables and fruits (aOR, 0.64; 95% CI, 0.43-0.94) significantly reduced the odds of developing RA.
Lower odds of developing RA were linked to fruits and vegetables (aOR per SD, 0.70; 95% CI, 0.57-0.87) and fiber (aOR per SD, 0.80; 95% CI, 0.64-0.99) vs higher odds with red and processed meat (aOR per SD, 1.31; 95% CI, 1.07-1.59).
Adhering to intake guidelines for all food types was linked to a lower risk for seropositive RA; higher odds were linked to higher consumption of red and processed meat (aOR, 3.43; 95% CI, 1.69-6.96).
IN PRACTICE:
'[The study] findings suggest a dose-response relationship between red/processed meat intake and the risk of seropositive, but not seronegative, RA. This study helps to improve our understanding of the effects of dietary components in RA development, particularly for red and processed meats, but the exact mechanisms behind our findings need further investigation,' the authors concluded.
SOURCE:
This study was led by Rebecka Bäcklund, Lund University, Malmö, Sweden. It was published online on July 10, 2025, in Annals of the Rheumatic Diseases.
LIMITATIONS:
The diet was assessed only at baseline. Data were retrieved from a study that examined the association between diet and cancer, which may have introduced selection bias. Dietary guidelines, especially regarding meat intake, may have changed over time.
DISCLOSURES:
This study received support from the Swedish Rheumatism Association, the Gustav V 80-year fund, the Greta and Johan Kock foundation, and others. The authors declared having no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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The HR was 1.15, or 15% worse for rhythm control. CIs were 0.99-1.34 so the P value for arm was just outside 0.05 but the upper bound or worse case was a 34% higher rate of death in the rhythm control arm. More patients in the rhythm-control group than in the rate-control group were hospitalized, and there were more adverse drug effects in the rhythm-control group as well. AFFIRM was largely interpreted as showing no differences in the two strategies. But, really, there was a strong trend for worse outcomes in the rhythm-control arm. One of the major changes in knowledge that came from AFFIRM is the importance of maintaining oral anticoagulation (AC). In AFFIRM, patients in the rhythm control arm who were maintaining SR could stop their oral AC. This led to a difference in AC use 85% vs 70% rate vs rhythm control. In fact, AFFIRM largely changed the view that patients with AF with either strategy should remain on oral AC. The Sherman et al substudy in JAMA Internal Medicine found that patients who remained on warfarin were 68% less likely to have stroke. A large proportion of ischemic strokes (113 of 157) occurred in patients in whom anticoagulation had been stopped (on the basis of re-established normal sinus rhythm) and who had a subtherapeutic international normalized ratio. Eric's point about AFFIRM is it led to too many patients with AF being told that there was no reason to try to get into SR, and if you don't try, and you leave patients in AF, it becomes impossible to restore SR after a year or so. The other problems (or criticisms) of AFFIRM were that patients had to be able to tolerate rate-control. So highly symptomatic patients were excluded. AFFIRM should never have been applied to these patients. Many of these symptomatic patients were younger, and it is a serious error to just leave a symptomatic younger person with AF forever in AF. 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Drug side effects and ablation complications do occur. My friends, be careful flying close to the sun with rhythm control. One of the biggest mistakes I see in general cardiology is leaping to cardioversion without a plan. CV of AF is fine, but you have to have a plan for what will happen in a week or month when the patient is back in AF. CV doesn't modify the problem of AF. It just resets the heart. In the end: EP is here to help. Get us involved. Especially when there are symptoms. And doubly especially, when there is heart failure. But don't dismiss AFFIRM. It is important trial that shows that rate control is not a terrible strategy in selected patients. GLP-1 RAs Protective Against Stroke, Neurodegeneration? A GLP-1 study purports to show benefit in cerebrovascular health. It actually shows how observational studies can mislead you. The title of the study is, 'Neurodegeneration and Stroke After Semaglutide and Tirzepatide in Patients With Diabetes and Obesity.' 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That's what you expect when healthier patients get one treatment. Immediately better outcomes. If the GLP-1 was better than other drugs, you'd see gradually increasing benefit. Second reason: the mortality benefit is huge. A 30% reduction in death. In the SELECT trial of semaglutide vs placebo in patients with heart disease and obesity, semaglutide only reduced CV mortality by 15%. In the SUSTAIN-6 trial of semaglutide vs placebo, semaglutide had no sig reduction in death or CV death and required a composite endpoint to drive positive results. My overall take, therefore, is that GLP-1 drugs induce weight loss. They do modify disease in patients with obesity and diabetes and patients with obesity and atherosclerotic disease. But whether they reduce important cerebrovascular outcomes like dementia cannot be answered by these confounded observational studies. I am not sure it's worth doing these studies because the only value is to show readers the signs of bias in non-random, retrospective comparison studies.
