Psychosocial Stress and Exacerbation of Psoriasis
Psychosocial Stress and Exacerbation of Psoriasis
Hippocrates, the father of modern medicine, was the first to allude to a relationship between mind and body. In 1808 Willan described the disease that we now know as psoriasis; however, it was only in the late 19th century that a 'neuropathic hypothesis' of psoriasis was first proposed. This stemmed largely from anecdotal reports of 'nervous upset' precipitating the onset of psoriasis. Wittkower, in 1946, formally investigated the relationship between stress and psoriasis. In his cross-sectional study of military personnel with psoriasis he noted an over-representation of 'emotionally maladjusted individuals'; he postulated that this trauma might have provoked onset of psoriasis. Although this study was retrospective, relied heavily on patient recall and was somewhat speculative in its conclusions, it provided the first evidence of a link between psychosocial factors and psoriasis. In 1954 in the inaugural Watson Smith lecture to the Royal College of Physicians, Ingram stated, 'perhaps the most potent influence on psoriasis is the psychological.' Seville was the first to investigate the temporal relationship between stress and psoriasis onset. He treated 132 patients with dithranol (until clear) and followed them prospectively for 3 years. He showed that 39% of patients recalled a significant stressor (most commonly family upset) within 1 month of the development or relapse of their psoriasis; the incubation period between stress and onset/relapse of psoriasis was between 2 days and 1 month. In a follow-on study he demonstrated that improved prognosis was probably due to patients' insight into the stress-related exacerbation of their disease. Again, both studies may have been subject to recall bias. Fortune et al. found that 60·1% of patients reported that stress played a causative role in the aetiology of psoriasis, with 46% believing that their behaviour could influence the course of psoriasis. Recently, two studies have confirmed these findings. Manolache et al., in a case-controlled study, noted that 54·4% of patients had a stressful – particularly a family-related – event in the year preceding a new onset or recurrence/extension of psoriasis, compared with 19·5% of controls. Verhoeven et al. demonstrated in a prospective study that disease severity and degree of itch in psoriasis corresponded with periods of high daily stress 1 month earlier. Not all authors support these observations. Schuster refutes the findings of Seville's studies, a view supported by Payne et al. in their retrospective case-controlled study, which had a small sample size, utilized postal questionnaires and did not exclude the possibility of a subgroup of patients with stress-responsive disease.
Overall, despite several studies being retrospective and reliant upon patient recall, there is a mounting body of evidence to support the anecdotal patient reports that psychosocial stress has a temporal association with the worsening of psoriasis.
Historical Overview of the Stress–Psoriasis Association
Hippocrates, the father of modern medicine, was the first to allude to a relationship between mind and body. In 1808 Willan described the disease that we now know as psoriasis; however, it was only in the late 19th century that a 'neuropathic hypothesis' of psoriasis was first proposed. This stemmed largely from anecdotal reports of 'nervous upset' precipitating the onset of psoriasis. Wittkower, in 1946, formally investigated the relationship between stress and psoriasis. In his cross-sectional study of military personnel with psoriasis he noted an over-representation of 'emotionally maladjusted individuals'; he postulated that this trauma might have provoked onset of psoriasis. Although this study was retrospective, relied heavily on patient recall and was somewhat speculative in its conclusions, it provided the first evidence of a link between psychosocial factors and psoriasis. In 1954 in the inaugural Watson Smith lecture to the Royal College of Physicians, Ingram stated, 'perhaps the most potent influence on psoriasis is the psychological.' Seville was the first to investigate the temporal relationship between stress and psoriasis onset. He treated 132 patients with dithranol (until clear) and followed them prospectively for 3 years. He showed that 39% of patients recalled a significant stressor (most commonly family upset) within 1 month of the development or relapse of their psoriasis; the incubation period between stress and onset/relapse of psoriasis was between 2 days and 1 month. In a follow-on study he demonstrated that improved prognosis was probably due to patients' insight into the stress-related exacerbation of their disease. Again, both studies may have been subject to recall bias. Fortune et al. found that 60·1% of patients reported that stress played a causative role in the aetiology of psoriasis, with 46% believing that their behaviour could influence the course of psoriasis. Recently, two studies have confirmed these findings. Manolache et al., in a case-controlled study, noted that 54·4% of patients had a stressful – particularly a family-related – event in the year preceding a new onset or recurrence/extension of psoriasis, compared with 19·5% of controls. Verhoeven et al. demonstrated in a prospective study that disease severity and degree of itch in psoriasis corresponded with periods of high daily stress 1 month earlier. Not all authors support these observations. Schuster refutes the findings of Seville's studies, a view supported by Payne et al. in their retrospective case-controlled study, which had a small sample size, utilized postal questionnaires and did not exclude the possibility of a subgroup of patients with stress-responsive disease.
Overall, despite several studies being retrospective and reliant upon patient recall, there is a mounting body of evidence to support the anecdotal patient reports that psychosocial stress has a temporal association with the worsening of psoriasis.
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