Introduction
Fibromyalgia is a chronic condition characterized by widespread pain, tenderness, and decreased pain threshold to pressure and other stimuli [
1,
2]. It is often associated with fatigue, unrefreshing sleep, and cognitive symptoms as well as multiple other somatic symptoms including headache, irritable bowel and bladder symptoms, and depression [
3]. Although the cause of fibromyalgia is unclear, extensive research has helped understanding of fibromyalgia and indicates that fibromyalgia is a central amplification disorder of pain perception resulting from neurochemical imbalances in the central nervous system [
4‐
6].
Alcohol consumption has both harmful and beneficial effects on health. On the one hand, drinking large amounts of alcohol for years is hazardous [
7]. On the other hand, epidemiologic and clinical evidence suggests that moderate drinking is associated with a reduced risk of cardiovascular disease [
8] and ischemic stroke [
9]. In US adults, moderate alcohol consumption is considered a lifestyle behavior that supports cardiovascular health, in conjunction with a prudent diet, regular physical activity, a healthy weight, and not smoking [
10]. Furthermore, regular low-to-moderate alcohol consumption has been associated with better quality of life (QOL), mood, and subjective health in studies of young and older adults [
11‐
16] and a protective factor for better health in a general population with and without chronic musculoskeletal pain [
17,
18].
Studies on alcohol consumption in chronic pain have shown conflicting results. Whereas a systematic review showed no positive association or dose response between alcohol consumption and low back pain [
19], individual studies of men with back pain disability showed that those who consumed large amounts of alcohol had less physical disability, despite similar pain [
20], and those who consumed alcohol regularly were less likely to have associated chronic pain [
21]. Epidemiologic studies on alcohol and rheumatoid arthritis have reported interesting results, namely that moderate alcohol consumption may decrease the risk of rheumatoid arthritis development, severity and progression, possibly by reducing levels of some inflammatory markers [
22‐
24].
Although alcohol consumption is a common lifestyle behavior, no studies to date have examined alcohol consumption in the setting of fibromyalgia. The objective of this study was to evaluate the association between alcohol consumption and symptom severity and QOL in patients with fibromyalgia.
Discussion
Our cross-sectional study demonstrates that for patients with fibromyalgia, low and moderate alcohol consumption was associated with lower fibromyalgia symptoms and better QOL compared to no alcohol consumption. Drinkers had higher education, a lower BMI and a lower frequency of unemployment and opioid use than nondrinkers. Among drinkers, moderate alcohol consumption was associated with lower FIQ pain scores than low and heavy drinkers, and a lower number of tender points than low drinkers even after adjusting for confounding covariates. The reasons for these results are unclear.
To our knowledge, no other reports on alcohol consumption, symptom severity, and QOL in patients with fibromyalgia have been published to date, which limits our ability to further validate our findings. However, in the general population, those who had low to moderate alcohol consumption had better QOL scores in physical and mental domains of SF-36 [
12,
14], especially in the physical domains [
11,
16]. Also, in a cross-sectional study [
21] those who consumed alcohol regularly were less likely to have chronic pain, and regular alcohol consumption has been shown to be protective of better health in a general population with and without chronic musculoskeletal pain [
17,
18], as well as being associated with lower risk and severity of rheumatoid arthritis [
23]. Our results were generally similar to these studies in terms of better QOL scores, especially for the physical domains, for the low and moderate drinkers.
It is notable that we did not observe the same association in heavy drinkers. The only significant finding in heavy drinkers as compared to nondrinkers was better scores on the SF-36 physical functioning scale. This finding suggests that there are other unknown factors or comorbid conditions affecting fibromyalgia symptoms and QOL. Clinical and epidemiological studies have suggested an association between excessive alcohol consumption and major depressive episodes [
31]. Although our study was not meant to adequately assess depression, we did not observe significant differences in the FIQ depression nor SF-36 mental component summary scores between the groups. Binge drinking (five or more drinks on one occasion) is reported to be associated with many health problems, including worse QOL and mental distress [
32,
33]. There were five binge drinkers (16%) in our heavy drinker group, who had overall worse scores in the FIQ and SF-36 than non-bingeing heavy drinkers: mean FIQ total 74.5 (SD 17.1) vs 59.8 (14.7), SF-36 physical component summary 29.8 (7.9) vs 30.1(9.3) and SF-36 mental component summary 26.9 (4.5) vs 43.4 (11.7) in the bingeing vs non-bingeing heavy drinkers, respectively. However, the small number of patients limited further statistical analysis. It is possible that the worse scores in the binge-drinkers affected the overall outcome of heavy drinkers.
We speculated about possible mechanisms by which alcohol consumption attenuates fibromyalgia symptoms, thus resulting in improved QOL. We showed that low and moderate alcohol consumption in patients with fibromyalgia was associated with higher social status, as noted in other studies in terms of employment [
34] and education [
34‐
36], and favorable BMI in drinkers, as also noted elsewhere [
35,
37]. The 1999 to 2006 National Health and Nutrition Examination Survey in the United States [
36] determined that the percentage of drinkers increased with higher education level, and current drinkers had a lower BMI than never drinkers or former drinkers. In our study, even after adjusting for social variables and BMI, we still found the same association that those with low or moderate alcohol consumption had fewer fibromyalgia symptoms and higher QOL than nondrinkers. Thus, socioeconomic status alone apparently does not explain the findings.
Studies suggest that fibromyalgia is a central amplification disorder of pain perception due to neurochemical imbalances in the central nervous system [
4,
6]. We believe that a more likely mechanism, in view of our finding that alcohol consumption attenuates fibromyalgia symptoms, might be centrally mediated via γ-Aminobutyric Acid (GABA) system. Previous studies have demonstrated that ethanol enhances GABA release in the central nervous system [
38,
39], and it is interesting that a recent study showed that GABA levels in the brain are decreased in patients with fibromyalgia [
5]. Gamma-hydroxybutyrate is a metabolite of GABA and was found to be effective at reducing fibromyalgia symptoms but did not receive Food and Drug Administration approval for the management of fibromyalgia because of concerns about abuse [
40,
41]. Thus, increase in GABA production may represent a mechanism by which alcohol consumption decreases fibromyalgia symptoms.
It is uncertain whether the effect of alcohol on fibromyalgia symptoms and QOL might be mediated by its psychological benefits as a stress reliever or a factor associated with social integration [
12,
42]. Several studies showed that small doses of alcohol were associated with improved mood and decreased depression and tension [
42,
43]. Also, its favorable effects on cardiovascular health might influence QOL, particularly for the elderly [
12]. Alcohol can suppress the synthesis of proinflammatory cytokines and chemokines such as tumor necrosis factor and interleukin-6,
in vivo or
in vitro (or both) [
44,
45], and it may also have a role as an anti-inflammatory factor. However, the association of cytokines with fibromyalgia is controversial [
46], with several studies supporting a positive association [
47,
48], and another study showing no association [
49]. Alcohol may provide short-term analgesic effect as demonstrated in a study by James
et al. [
50], in which alcohol significantly increased the pain threshold and decreased the perception of pain after an infusion of alcohol for 1 hour. In our study, moderate but not heavy drinkers, had significantly lower FIQ pain than all other groups, and it is unlikely that the short-term analgesic effect of alcohol explains the finding.
Alcohol use in our patients was 42%, with most of them being low-drinkers. The rate of alcohol use among our patients with fibromyalgia was lower than the 53% rate for women in the general population [
10]. Our study was based on data from 2001 to 2004. A recent Gallup report showed that rates of alcohol consumption overall have stayed stable in spite of some yearly fluctuations (Gallup report 2012) [
51]. Therefore, we believe our findings are still relevant. We observed significant group differences in opioid use with the lowest use in the moderate drinkers and the highest use in the nondrinkers, suggesting that the nondrinkers may have more severe symptoms than the other groups. We cannot rule out the possibility that the findings were biased by individuals who did not drink alcohol because of more severe symptoms of fibromyalgia. The 3% rate of heavy-drinkers (equivalent to more than one drink per day) in our study was also lower than the 7% rate for US women [
10]. We do not know why the drinking rate was lower in our patient group but speculate that it might be related to 1) decreased social functioning due to chronic pain and therefore, fewer occasions to drink alcohol socially; 2) self-perceived chronic health concerns and lower QOL, leading to different drinking habits; 3) concerns of alcohol interacting with medications such as sedatives or narcotics, and 4) possible under-reporting of drinking.
We urge caution when generalizing the findings of this study because of the relatively small number of moderate and heavy drinkers in the study. Furthermore, we do not recommend that patients with fibromyalgia start or increase drinking for their symptoms. One study showed that alcohol abuse was one of the most frequent psychiatric problems in patients with chronic pain, and a significant portion of chronic pain patients had a history of alcohol abuse before the onset of their pain [
52]. Therefore, our findings should be interpreted carefully.
This study has several limitations. First, the amount of alcohol consumption in this study was self-reported and thus may be biased because of possible under-reporting. However, simple self-administered questionnaires previously have provided useful estimates of alcohol intake [
53,
54]. Our patient population included four patients who were younger than 21 years (drinking reports: none (three patients), low (one patient)), which is the legal drinking age in the US. Our results were the same when we excluded them. Therefore, we kept them in the study. Second, we had small sample sizes for those with moderate and heavy alcohol consumption, and this limited the power to detect associations in the groups. Third, the cross-sectional design of the current study allowed us to say only that low-to-moderate alcohol consumption appeared to be associated with lower fibromyalgia symptoms and improved QOL. However, the reasons for, and the clinical importance of this association cannot be determined in this study, and the associations may be due to unmeasured confounding variables. Fourth, we did not use a validated specific questionnaire for depression, and our study was not meant to adequately assess depression. Therefore, we were not able to do further analysis on comorbid psychiatric diagnoses. Fifth, we did not differentiate former drinkers from abstainers. Previous studies have shown conflicting findings, ranging from worse QOL in former drinkers than abstainers [
13,
14], no difference in subjective health [
55,
56], and better QOL in former drinkers than abstainers [
57]. However, this diversity in results might be due to variations in study design [
8]. We also did not consider the beverage type consumed (for example, beer versus wine versus spirits) because the health effects of alcohol primarily have been attributed to ethanol content rather than to other components of each beverage type [
58‐
60].
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
CHK conceived and designed the study, collected, analyzed and interpreted the data and drafted the manuscript. THO participated in the design of the study, analyzed and interpreted the data, and critically edited and revised the manuscript. AV, CAL and JMT participated in the design of the study and analysis and interpretation of the data and critically reviewed and edited the article. DJC and TDS participated in the analysis and interpretation of the data and critically evaluated the manuscript. All authors read and approved the manuscript for publication.