Nutrients Free Full-Text Alcohol Consumption in Rheumatoid Arthritis: A Path through the Immune System

Nutrients Free Full-Text Alcohol Consumption in Rheumatoid Arthritis: A Path through the Immune System

19 martie 2020
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In addition, a direct treatment of human neuronal cell lines with alcohol exhibited increased reactive oxygen species (ROS) and increased expression of HDAC2 [44]. On the other hand, a direct supplementation of mouse feed with acetate inhibited HDAC2 alcohol withdrawal and detox expression and activity while also increasing histone acetylation [45]. It is possible that in vitro direct treatment of cell lines with alcohol does not match accumulation of alcohol’s metabolites as efficiently as in vivo supplementation.

  1. Structural changes can be reliably determined radiographically [82], whereas the clinical relevance of a meta-analysis may be enhanced if focused on clinically diagnosed disease.
  2. However, when adjusted for gender, alcohol was no longer related to disease activity.
  3. Research shows that moderate drinking might have some benefits for people with RA.
  4. Of note, nutrition in general has been shown to have strong effects on autoimmunity; in a study of alcohol-use and SLE, there was a significant correlation of wine but not beer consumption as a protective factor [31,35].
  5. Dendritic cells (DC) are one of the professional APCs that also play a key role in self-tolerance and have been found in the synovium of RA patients, contributing to proinflammatory process [12].
  6. Nitric oxide (NO) is another compound produced by macrophages, neutrophils, and natural killer (NK) cells, and adds to RA progression [12].

Individual studies categorize drinking habits differently and different regions have varying standards for what they consider to be high-risk drinking. In the UK, men who consume more than 14 standard drinks and women who consume more than 10 per week are considered to be at risk37. We did not differentiate between the different international standards for drinking risk within our analysis as the breadth of literature to do so was unavailable. The mean age also varied between cohorts, which could have an influence on alcohol consumption. However, in linear regression models, gender, smoking status, and antibody status had no relationship with alcohol consumption in RA. The study could also be susceptible to the ecological fallacy, each study may have its own unique relationship that may be diluted when making pooled comparisons.

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All the included studies (Table 1) were observational in design; 16 were cross-sectional [24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39], 10 were cohort [40,41,42,43,44,45,46,47,48,49] and 3 were case–control studies [14, 50, 51]. There were no RCTs or prospective interventional studies yielded from our search. Eleven studies had cohorts with East Asian ethnicity, 9 studies had European cohorts and the remaining 9 had North American cohorts. The mean age of participants across all study designs were over 60 years, with an overall average of 64.4 (38.0–75.6) years. The average mean BMI was found to be 26.4 (23.1–30.3), the mean percentage of females included in the studies was 62.4 (0–79.9)% and an average mean of 15.5 (7.1–63.8)% were smokers. Although our primary analysis revealed a statistically significant negative association between alcohol use and OA, subgroup analyses revealed that this is likely to be an unreliable conclusion.

Furthermore, ex vivo acute ethanol treatment of human peripheral monocytes resulted in decreased p65 phosphorylation and consequently inhibited NF-κB DNA binding [63]. Interestingly, chronic ethanol exposure of human peripheral blood mononuclear cells (PBMC) and mouse macrophage cell lines (J774) induced reactive oxygen species and NLRP3 inflammasome hyperactivation [64]. The authors also came to a conclusion that the metabolites of alcohol, namely, acetaldehyde is the cause of NLRP3 hyperactivation and increased IL-1β secretion [64]. Similar findings on alcohol’s effect on NLRP3 hyperactivation was found in human myeloid leukemia cells (U937) induced with monosodium urate (MSU) crystals [65].

Furthermore, acetaldehyde-treated hepatic cell line exhibited reduced MHC-I presentation of HBV virus, shown to be due to suppression of antigen processing and formation of peptide loading complex in response to IFN [83]. As such, in a clinical study, Mikuls and colleagues demonstrated that RA patients harbor higher concentrations of anti-malonylaldehyde-acetaldehyde (MAA) antibodies in joints [84]. In the same year, another group was able to show that RA patients exhibit increased anti-malondialdehyde modification (MDA) IgG levels correlating with serum TNF-α, IL-6, and CRP [85]. Although measuring direct effects of alcohol in vivo can be challenging, one of the ways it is delineated from the effects of other metabolites of alcohol is by decreasing the time between alcohol administration and quantification of parameters.

Table 1

The more—and longer—people drink, the more they risk developing health problems, such as diabetes, liver disease and even brain shrinkage. Excessive drinking can also lead to high blood pressure, cardiomyopathy and arrhythmia, according to the American Heart Association. Light and moderate drinking increases risk of esophageal and breast cancer, according to the National Cancer Institute.

Alcohol may also have a positive association with physical activity [17], which may promote joint overuse, and therefore, increase risk of OA [18]. While there may be an underlying biological effect, with some studies in mouse reporting that alcohol consumption can lead to OA changes [19], the true effect of alcohol in human OA remains speculative. 15 of the best sobriety podcasts to listen to in recovery Overall, there is an association with alcohol consumption and better disease activity scores in patients with RA. The pooled proportion of those with RA who drink alcohol in these cohorts is 56%. When comparing demographic data to alcohol consumption there is no significant correlation between alcohol use and smoking nor gender.

Arthritis is a disease of joints, characterized most commonly by joint swelling, stiffness, and pain. Nonsteroidal anti-inflammatory drugs (NSAID) are drugs that are frequently used to ease inflammation, pain, and stiffness. These drugs prevent an enzyme called cyclooxygenase from making a hormone-like chemical called prostaglandins, one of the body’s biggest contributors of inflammation. The effects of alcohol vary depending on the type of arthritis, medication, and lifestyle.

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Alcohol is one the highest consumed, abused, and addictive substances worldwide. Consequences of alcohol abuse are increased risks for diseases of the cardiovascular system, liver, and nervous system, as well as reduced immune system function. Paradoxically, alcohol has also been a consistent protective factor against the development of autoimmune diseases such as type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis (RA).

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With this in mind, many studies have been undertaken to address a possible link between autoimmune diseases such as RA and alcohol use. Our meta-analysis shows that previous reports of a protective effect of alcohol consumption on risk of osteoarthritis are likely to be inaccurate. The suggested protective alcohol rehab: when andwhy you need rehab for alcohol addiction effect is likely to have been observed due to lack of confounder adjustment. Alcohol use is a public health issue and with mounting global disease burden attributable to alcohol misuse [54] it is increasingly important that recommendations for safe consumption are supported by robust research.

November 2023: Updated COVID-19 Booster Advice for Rheumatology Patients

Several studies suggest that light to moderate alcohol consumption may have a negative association with specific outcomes of cardiovascular [2] and cerebrovascular disease [3]. The evidence for the beneficial effects of alcohol remains controversial. More recent large-scale international studies report that risk of all-cause mortality rises with alcohol consumption [4], and also that there were no risk thresholds beyond which a reduction in consumption would cease to confer risk reduction [5]. The Korea National Health and Nutrition Examination Survey (KNHANES) is a national surveillance system conducted by the Korea Centers for Disease Control and Prevention since 1998 to assess the health and nutritional status of the Korean population. We used data from KNHANES 2012, which not only includes health interview and nutrition surveys, but also health examination information. In the KNHANES 2012, data of 8058 participants were initially collected (Fig. 1).

Researchers need to conduct further studies to explain, understand, and confirm the link between drinking alcohol and the risks of developing RA — and why this may impact females more than males. When a person drinks too much, the alcohol can damage the gut and liver, leading to body-wide inflammation. Scientists closely link alcohol-related medical conditions with chronic inflammation.

Methotrexate, leflunomide and some other disease-modifying antirheumatic drugs (DMARDs) and biologics can elevate liver enzymes and, in some cases, lead to fibrosis and other liver damage. Alcohol use increases that risk, so your doctor may advise limiting your intake to an occasional glass of champagne to celebrate New Year’s or a wedding. Research on alcohol consumption in people taking methotrexate finds over consumption can lead to drug-induced liver injury (hepatotoxicity).

This article examines the research behind how drinking alcohol can affect RA and the interactions between RA drugs and alcohol, and other safety considerations. Drinking alcohol in moderation is typically safe for people with rheumatoid arthritis (RA). In summary, acetaldehyde modifications of self-proteins are able to induce autoimmunity and dysregulate the tight junction in intestinal epithelium, contributing to increased inflammation.

In addition, circulating TFH-like cells have been reported in the blood and synovium of RA patients [110,111,112]. It is plausible that reduced B cell activation, differentiation, GC formation, antibody class switch, and titers are the result of a reduction in IL-21+ TFH cell function as IL-21 has been shown to be a major effector during GC reactions [113]. One major indicator of disease severity is existence of pathogenic antibodies [12,114,115]. It has been shown that serum ACPA and RF antibodies can be detected up to 20 years before the onset of RA and are used in diagnosis of RA [115,116]. Alcohol consumption has been reported to increase antibody titers in patients with alcoholic liver disease (ALD) in comparison to alcoholic patients without ALD [72].

This study provides clinical evidence to understand the effects of alcohol on the pathogenesis of knee OA. The mechanism of the negative relationship between knee OA and alcoholic beverage intake must be further clarified. Among current smokers only, the age adjusted relative risk for women who drank more than four glasses of alcohol a week was 0.77 (0.41 to 1.47), while among never smokers it was 0.38 (0.15 to 0.97). There’s some research to support that people with rheumatoid arthritis (RA) might benefit from a few alcoholic drinks a week, and that that level of alcohol consumption might also reduce the risk of developing RA. At the same time, it is possible that drinking could increase inflammation and make RA symptoms worse.

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