Caffeine and chronic back pain

61

Caffeine and Chronic Back Pain John M. McPartland,

DO, Julie A. Mitchell,

BS

ABSTRACT. McPartland JM, Mitchell JA. Caffeine and chronic back pain. Arch Phys Med Rehabil 1997;78:61-3. Objective: Tobacco use and other behavioral factors are associated with chronic back pain. Anecdotes suggest excesscaffeine use may also be associated with chronic back pain. We compared caffeine consumption by chronic back pain patients with caffeine consumption by controls. Design: Retrospective case-control study. Setting: A multispecialty outpatient facility. Patients: Sixty new, consecutive patients with chronic back pain compared to 60 new, consecutive patients without chronic back pain. Intervention: Patients were prospectively asked to complete an intake questionnaire. Main Outcome Measure: Daily caffeine consumption was estimated by analyzing the intake questionnaire. Differences between groups were analyzed by both normal and nonparametric statistics. Results: Consumption of caffeine by patients with chronic back pain averaged 392.4mgiday. Controls consumed 149.8mg/ day, a significant difference (p = .OOOl).Men consumed 86% more caffeine per day than women (p = .02). Age and caffeine consumption showed little correlation (Y = .126). Conclusions: Patients with chronic back pain consume over twice as much caffeine as patients without chronic back pain. Confounding variables and possible mechanisms associating caffeine with chronic back pain are discussed. 0 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

E

PIDEMIOLOGICAL STUDIES have found distinct nonanatomic risk factors associated with chronic back pain. Frymoyer’ cites occupational risk factors (repetitive lifting, exposure to vibrations), adverse psychological profiles (higherthan-average rates of depression, anxiety), and other behavioral and dietary risks (tobacco smoking, alcoholism, obesity, and a sedentary life-style). Inadequate attention has been given to caffeine consumption as a risk factor.’ Anecdotal information suggests caffeine may provoke musculoskeletal pain, including “restless legs syndrome,“3 “ burning feet,“4 and trigeminal neuralgia.’ Travel1 and Simon? claim excess caffeine (more than 3 cups a day) causes a persistent contracture of skeletal muscle fibers (‘ ‘caffeine rigors”) and aggravates trigger points in muscles. Lutz7 From the Department of Physical Medicine and Rehabilitation, Alternative Medicine Research Institute and Teacher’s Academy (Dr. McPartland), and the Physical Therapy Department, Porter Hospital (Ms. Mitchell), Middlebury, VT. Submitted for publication April 22, 1996. Accepted June 12, 1996. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to John McPartland, DO, Department of Physical Medicine and Rehabilitation, AMRITA, 53 Washington Street, Middlebury, VT 05753. 0 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/97/7801-3990$3.00/O

lists 14 additional muscular manifestations of caffeinism, including back pain, temporomandibular joint syndrome, and fibromyositis. We evaluated a population of patients with chronic back pain to determine if these patients did indeed consume more caffeine than patients without chronic back pain. SUBJECTS AND METWODS Patients at a multispecialty outpatient facility were prospectively asked to complete an intake questionnaire. As part of this “health history,” patients recorded caffeine intake with regard to source (coffee, tea, cocoa, soft drink, and caffeinated medicines such as Anacin, Excedrin, Fiorinol, Midol, NoDoz, etc), and quantity (number of cups or pills per day). Charts of all patients with chronic back pain diagnosed during a 3-year period were retrospectively reviewed; 60 contained a caffeine history that was properly completed. An equal number of patients without chronic pain during this time period were randomly sampled as controls. Controls had acute problems (injuries, infections, etc) or chronic conditions (pulmonary, psycho-neurological, rheumatological, etc). Chronic pain patients and control patients were similar in age, sex, and race (table 1). Patients younger than 18 years old were excluded. Chronic back pain was diagnosed as nonneoplastic pain of greater than 3 months’ duration with only “soft” objective physical findings. Soft findings included myofascial tender/trigger points, nondermatomal sensory abnormalities, gait disturbances, and paraspinal somatic dysfunctions8 Patients with abnormal roentgenograms or electromyographic tests and symptoms of nerve compression or degenerative joint disease were excluded from the diagnosis of chronic back pain. To calculate total caffeine intake, we used standard values reported by Barone and Roberts’: coffee = 85mg caffeine per 5-0~ cup, tea = 40mg per 5-0~ cup, soft drinks = 15mg per 6oz glass, cocoa = 4mg per 5-0~ cup. Values for medications were based on The Physicians’ Desk Reference and/or package information (examples: Anacin = 32mg, Excedrin = 32mg, Fiorinol = 75mg, Midol = 60mg, NoDoz = 200mg). Some patients (8.3%) recorded their consumption as “excessive” or “too much,’ ’ rather than a numerical value. We estimated these descriptors as five cups, consistent with other reports.’ Statistical analysis was performed using SYSTAT 5.2.1.” Means and standard deviations of caffeine consumption in chronic pain patients and control patients were computed, producing a nonpooled t value. These computations, however, assume caffeine consumption follows a normal distribution. To test this assumption, skewness and kurtosis of the two sample distributions were computed. Based on these results, we reanalyzed caffeine consumption using the nonparametric (nonnormal) Mann-Whitney U statistic of rank sums. RESULTS Mean consumption of caffeine by patients with chronic back pain equaled 392.4mglday. Patients without chronic back pain consumed less than half this amount, 149.8mg/day. These differences are significantly different by the student t test (table 2). Caffeine consumption by both groups, however, did not exhibit a normal distribution. Bell curves of both

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CAFFEINE

Table

Sample

Chronic Control

pain patients patients

AND

1: Characteristics

n

Male/Female Ratio

60 60

36124 37123

CHRONIC

of Chronic

Sample

Chronic Control

pain patients patients

*Mean values are significantly ‘Rank sums are significantly

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and Control

Patients Mean Age (Standard Deviation)

43.9yr 39.5yr

by Chronic

Pain Patients

and Control

392.4mg 149.8mg

0 to 2550mg 0 to 905mg

1997

p = .OOOl). U = 2555, p = .OOOl).

Age Range

29 to 80yr 18 to 81yr

Patients

Ranse of Dailv Caffeine -Consumption

(473.63mg) (191.31mg)

(10.94yr) (14.91yr)

increase caffeine consumption to enhance daytime alertness). Ochs et alI3 suggest that patients use caffeine to boost their activity level despite continual pain, using it as an “indirect analgesic.’ ’ There are many plausible mechanisms through which caffeine could exacerbate chronic musculoskeletal pain. Cardiovascularly, caffeine is a vasoconstrictor and promotes atherosclerotic artery disease.’ Impaired blood supply is an etiologic factor in low-back pain; this may be how smoking exacerbates low back pain.14 Patients with chronic back pain have narrower, more occluded arteries in the lumbosacral region than people without chronic pain. I5 Neuromuscularly, caffeine increases skeletal muscle twitch response by augmenting Ca2+ release from the sarcoplasmic reticulum. It causes slow-twitch muscles (eg, postural low back muscles) to fatigue more quickly.r6 Caffeine stimulates the release of catecholamines such as epinephrine.‘,i7 Catecholamines sensitize muscle nociceptors, increasing the perception of pain.18 Increasing plasma epinephrine levels exacerbates the already hyperactive dopaminergic state in patients with chronic pain; it also inhibits sleep, further stimulating the paleospinothalamic tract.” Caffeine induces urinary loss of calcium, diminishing mineral content of bone and possibly increasing the rate of vertebral microfractures. A similar effect is caused by nicotine.” The psychological impact of caffeine is another factor. Chronic pain patients are often angry, anxious, tense, and depressed, as measured by a variety of psychologic tests.’ Caffeine increases anxiety.3,2’ Coffee drinkers may have heightened stress responses to everyday situations.” The consumption of caffeine among people with psychiatric disabilities is roughly double that of the general population and influences the subjective experience of their disability.13 Caffeine’s central nervous system arousal may exacerbate pain by heightening patients’ awareness of it. It heightens patient’s perception of hypoglycemia.17 Central nervous system arousal is posited as one of the causes of restless legs syndrome.’ Last, caffeine antagonizes opioids, and possibly endogenous endorphins, sharpening the sensation of pain.23 Finding that patients with chronic back pain consume a lot of caffeine has several implications. Caffeine is not the sole reason for drinking coffee. Like tobacco, people claim an attraction to coffee for its smell and taste. Nevertheless, coffee plants today are selected and cultivated for their drug content, not their taste-the source of most American coffee is no longer aromatic Coffea arabica, but flavor-poor Coffea robusta, which contains twice as much caffeine.” We conclude that coffee is a drug, and routinely question all patients

Mean Dailv Caffeine ConsumDtion* E&ndard Deviation)

different (t = 3.679, different (Mann-Whitney

January

of Caffeine

Pain Patients

McPartland

51/5/3/l 52/5/2/l

DISCUSSION Average adult daily caffeine consumption in the United States is estimated at 200 mg.9 We assumed our control sample would approximate the national average, but it was lower, 149.8mg/day. Our sample was limited to patients already self-selected for medical care in a multispecialty clinic. This bias may have generated the discrepancy. Our sample had a higher percentage of pregnant women than the general population, which consumes less caffeine.’ Alternately, the discrepancy between Barone and Robert’s9 estimation and ours may reflect a decline in American coffee consumption, as noted by others.” Last, the discrepancy may indicate differences in our survey instruments. Unlike Barone and Roberts, we did not ask patients about their coffee brewing method (instant, drip, or perked), or the size of their cup. Not accounting for these variables causes an underestimation of caffeine intake.” We also did not ask subjects about their consumption of chocolate confections or “decaffeinated’ ’ coffee, which contains about 3mg caffeine per 5-0~ cup.” Our study did not control for confounding variables. Schreiber et al” list several confounders associated with caffeine consumption. They report that white men drink 25% more coffee than white women, and smokers drink about 250% more coffee than nonsmokers. The potential interactions between caffeine and nicotine deserve further study. Caffeine consumption is also slightly correlated with alcohol intake, obesity, and other dietary risk factors.12 We found that chronic pain patients consumed 2.6 times more caffeine than control patients, or twice the national average reported by Barone and Roberts.’ We postulate that increased caffeine potentiates chronic back pain. The reverse hypothesis could be true (eg, chronic pain decreases sleep, so patients 2: Consumption

PAIN,

White/Black/Hispanic/ Oriental-Amerlndian Ratio

groups were skewed towards zero, with long right tails (kurtosis of chronic curve = 8.4, of control curve = 6.6). Hence, we also analyzed caffeine consumption using a nonnormal test, the Mann-Whitney U statistic of ranked sums. This test also demonstrated significant differences between the two groups (table 2). The source of most caffeine consumption was coffee or soft drinks. Only 4 patients reported taking caffeinated medications, such as Anacin. Pooling data from 120 charts, we found that men consumed 86% more caffeine per day than women (table 3). The statistical strength of this difference was much weaker than the difference between chronic pain patients and control patients. We found little correlation between patient’s age and caffeine consumption, (Pearson r = ,126).

Table

BACK

Rank Sum of Caffeine Consumption’

4385 2875

CAFFEINE

Table

of Caffeine

by Men

Mean Daily Caffeine Consumption* (Standard Deviation)

Sample Men Women *Mean

3: Consumption

358.5mg 192.2mg values

(485.24mg) (225.31mg)

are significantly

different

AND

CHRONIC

and Women Range of Daily Caffeine Consumption 0 to 2550mg 0 to 1062mg

(t = 2.367,

p = ,021.

about their caffeine habits. We urge patients to wean off excess consumption or avoid it altogether. This recommendation is shared by other clinicians who work with chronic pain patients.5,6,‘3.19 References 1. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988;318: 291-300. 2. James JE. Caffeine and health. London: Academic Press, 1991. 3. Lutz EG. Restless legs, anxiety and caffeinism. J Clin Psycho1 1978; 39:693-K 4.

5. 6. 7. 8. 9.

Young JJ, Brownlee HJ, Delaney R. Caffeine and burning feet. Drug Intel1 Clin Pharm 1982; 16:779-780. Glore S, Ricker A. Trigeminal neuralgia: case study of pain cessation with a low-caffeine diet. J Am Diet Assoc 1991;91:1120-1. Travel JG, Simons DG. Myofascial pain and dysfunction. The trigger point manual, vol 1. Baltimore: Williams and Wilkins, 1983. Lutz EG. Muscular manifestations of caffeinism. J Clin Psych 1982; 43:81. Rosomoff HL, Fishbain DA, Goldberg M, Santana R, Steele-Rosomoff R. Physical findings in patients with chronic intractable benign pain of the neck and/or back. Pain 1989;37:279-87. Barone JJ, Roberts H. Human consumption of caffeine. In: Dews P, editor. Caffeine: perspectives from recent research. Berlin: Springer-Verlag, 1984:59-73.

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10. Gilbert RM. Caffeine consumption. In: Spiller G, editor. Methylxanthine beverages and foods: chemistry, consumption, and health effects. New York: Alan Liss Inc., 1984:185-213. 11. Schreiber GB, Maffeo CE, Robins M, Master MN, Bond AP. Measurement of coffee and caffeine intake: implications for epidemiologic research. Prev Med 1988; 17:280-94. 12. Schreiber GB, Robins M, Maffeo CE, Master MN, Bond AP, Morganstein D. Confounders contributing to the reported associations of coffee or caffeine with disease. Prev Med 1988; 17:295-309. 13. Ochs LA, Holmes GE, Karst RH. Caffeine consumption and disability: clinical issues in rehabilitation. J Rehabil 1992;58:44-50. 14. Holm S, Nachemson A. Nutrition of the intervertebral disc. Acute effects of cigarette smoking. An experimental animal study. Uppsala J Med Sci 1988;93:91-9. 15. Kauppila LI, Tallroth K. Postmortem angiographic findings for arteries supplying the lumbar spine: their relationship to low-back symptoms. J Spinal Disord 1993;6: 124-9. 16. Brust M. Fatigue and caffeine effects in fast-twitch and slow-twitch muscles of the mouse. PAiigers Arch 1976; 367: 189-200. 17. Debrah K, Sherwin RS, Kerr D. Effect of caffeine on the recognition of and physiological responses to hypoglycaemia in insulin-dependent diabetes. Lancet 1996; 347: 19-24. 18. Mense S. Chonsiderations concerning the neurobiological basis of muscle pain. Can J Physiol Pharmacol 1991;69:610-6. 19. Hooshmand H. Chronic pain. Boca Raton: CRC Press, 1993. 20. Svensson HO, Cedin A, Wilhelmsson C, Andersson GBJ. Lowback pain in relation to other diseases and cardiovascular risk factors. Spine 1983;8:277-85. 21. Stephenson PE. Physiologic and psychotropic effects of caffeine on man: a review. J Am Diet Assoc 1977;71:240-7. 22. Lane JD. Caffeine may intensify feelings of workplace stress [abstract]. Am Fam Physician 1994;50:1531. 23. Beers RF, Bassett EG. Mechanisms of pain and analgesic compounds. New York: Raven Press, 1979. Supplier a. Systat, Inc., Evanston, IL.

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