The last in our 3 part series addressing psychological and psychiatric disorders associated with psoriasis.
| Psychological and Psychiatric Disorders –
Substance dependence of abuse
1, 2, 3
It is thought that psoriasis has a direct effect on the development of sleep disorders due to the cutaneous (skin) symptoms of the condition. The skin is the primary circadian mediator of core body temperature (CBT), and a decrease in CBT in the late evening is an important mechanism for sleep initiation. Psoriasis has been associated with problems with thermoregulation and researchers have indicated that the reduced ability to dissipate heat is one factor in the inability to initiate sleep. Pruritus (itch) is another contributor to sleep disturbance and it is also regulated by circadian mechanisms. The threshold for pruritus is lowered in the evening due to complex circadian-mediated factors such as lower cortisol levels, decreased epidermal barrier function, and increased distal-to-proximal (distant limbs-to-body centre) gradient in skin temperature. Thus pruritus in psoriasis typically manifests or exacerbates mainly in the evening and worsens at night. 4,5,6
The inflammatory biological mechanism(s) that lead to initiation and exacerbation of psoriasis, also contribute to the development of systemic diseases e.g. depressive disease, hypertension (blood pressure), adverse cardiac events, diabetes, metabolic syndrome and obesity. All of these conditions are known to indirectly give rise to sleep-disordered breathing. The heightened pro-inflammatory state in conditions such as obstructive sleep apnoea syndrome (OSAS) and insomnia could in turn lead to exacerbations of psoriasis.4,5,6
A systematic review of the literature on the relationship between psoriasis, PsA, and formal sleep disorders identified an increased prevalence of OSAS with a 36-81% prevalence in psoriasis versus 2% for women and 4% for men in the general population.4,5 In one study researchers found that some patients with chronic psoriasis and concurrent OSAS showed improvement of their psoriatic lesions while on nasal continuous positive airway pressure (CPAP).6 OSAS leads to severe physical and, possibly, psychological stress to the body, e.g., by hypoxemia (low blood oxygen levels), increased blood pressure, tachycardia (fast or irregular heart rate), sleep fragmentation, reduction of deep sleep, reduction of REM sleep, hypersomnia (excessive sleepiness), and insomnia. It is known that OSAS also dysregulates the function of the patient’s autonomic nervous system and hormone system. It is felt that this might alter the homeostasis of the immune neuroendocrine network in the skin and may cause the initiation of psoriasis in the genetically predisposed individuals.4,5,6
Somatoform Disorders – psychosomatic symptoms
Somatization is the manifestation of psychological distress by the presentation of bodily symptoms such as feeling nausea due to anxiety, stress headaches, falling ill after a trauma and inability to cope with a disease.
Patients with psoriasis exhibit higher scores of hypochondriasis, hysteria, and somatization. As previously exposed hypochondriasis and hysteria may be connected with specific personality traits of patients with psoriasis of late-onset. Psychosomatic factors, namely stressful life events, lack of social support, and attachment insecurity, may explain why patients with psoriasis have greater scores of somatization. Moreover, the presence of depression in psoriasis may modulate itch perception and then exacerbate symptoms of pruritus.7 (Refer to Part 1 of this series) A systematic review of the psychosocial burden of psoriasis found that social stigmatization, high stress levels, physical limitations, depression, employment problems and other psychosocial co-morbidities experienced by patients with psoriasis are not always proportional to, or predicted by, other measurements of disease severity such as body surface area involvement or plaque severity. Some psoriasis patients had, even when their lesions were small and mild, levels of stress and loss of confidence that was not in keeping with the severity of their condition – which leads to the conclusion that they had maladaptive coping mechanisms in play e.g. self blame, blaming parents, social phobia, avoidance behaviours, substance and alcohol abuse etc. 9
Substance – Dependence of Abuse
In our previous blog Psoriasis and Alcohol (ethanol), we stated that patients with psoriasis experience considerable emotional distress, depression and social isolation due to the visibility of skin lesions, especially when the lesions are widespread and severe. Whilst it would be demeaning to state that all psoriasis patients with mild to severe psoriasis suffer from alcoholism, it has been confirmed in several Quality of Life studies that the percentage of psoriasis patients who admit to having a drinking problem may be as high as 32%. Research indicates that men are more likely to use alcohol excessively as a coping mechanism with the psychosocial burden of psoriasis. Consequently they are at a higher risk of developing depression – with the alcohol misuse and psoriasis as underlying causes. 4 Another study indicated that for women, excessive alcohol intake above a certain threshold (?30.0 g/d), may be associated with a significantly increased risk of Psoriatic Arthritis (PsA).5
Alcohol is known to inhibit inflammation and immune responses; however acute and chronic alcohol consumption have opposite effects on inflammatory cell activation. Results indicate that acute alcohol exposure is inhibitory, whereas chronic alcohol exposure leads to an increase in inflammatory cell responses.6
Research has confirmed that alcoholics are more susceptible to infections, as streptococcal infections are trigger factors for psoriasis, this increased susceptibility may be involved in the onset and progress of the disease. It is also known that measurable quantities of ingested ethanol are secreted through human skin. Transdermal ethanol derives from two processes: active secretion by eccrine glands, primarily sweat glands, and passive diffusion through the lipid layers of the skin. Ethanol disrupts the dermal barrier enhancing skin permeability for numerous chemicals and increases the solubility of penetrating chemical compounds.6
Research into the the use of illicit drugs and psoriasis is extremely limited. Methylenedioxymethamphetamine (MDMA), also called Ecstasy, has been reported to initiate Guttate Psoriasis. The researchers theorized that “While MDMA [the main ingredient in ecstasy] is taken for its psychomimetic effect, pharmacologically it increases the level of noradrenaline, serotonin and dopamine by inhibiting the reuptake mechanism. It is known that Patients with psoriasis already have increased levels of noradrenaline.”7 There are also anecdotal stories on support websites where psoriasis sufferers have spoken about the exacerbation of their psoriasis with the use of “meth” (Methamphetamine, Ice). Within our clinic we have had several patients whose psoriasis was initiated and exacerbated by the use of cannabis (street not medicinal), once they ceased the use of cannabis their psoriasis resolved. As long as they did not use cannabis they remained free of any psoriatic lesions.
- Susskind W. and McGuire R.J.: The Emotional Factor in Psoriasis; Scot. med, J., 1959,4:503
- Kessler R. C. et al.; Epidemiology of Anxiety Disorders; M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences 2, DOI 10.1007/7854_2009_9, # Springer?Verlag Berlin Heidelberg 2009, published online 3 September 2009
- Nasreen S. et al.; Frequency and Magnitude of Anxiety and Depression in Patients with Psoriasis Vulgaris; Journal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 397-400
- Brenaut E. et al.; Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venerol. 2013 Aug;27 Suppl 3:30-5. doi: 10.1111/jdv.12164.
- Shaowei Wu et al.; Alcohol Intake and Risk of Incident Psoriatic Arthritis in Women; J Rheumatol. 2015 May ; 42(5): 835–840. doi:10.3899/jrheum.140808.
- Farkas A, Kemény L.; Psoriasis and alcohol: is cutaneous ethanol one of the missing links?; • British Journal of Dermatology 2010 162, pp711–716
- Tan B., Foley P.; Guttate psoriasis following Ecstasy ingestion; Australasian Journal of Dermatology45(3):167-9 September 2004?