Psoriasis and Cardiovascular Disease
Everyday Choices Make a Difference
As life-changing as a moderate-to-severe case of psoriasis can be, the chronic inflammatory and autoimmune disease is itself not life-threatening. That may be small comfort for the individual with moderate to severe symptoms, but evidence is gathering that this systemic inflammatory disease does carry a greater risk than previously thought. The good news in this evidence is that some of the factors conveying this additional risk relate to lifestyle choices, and patient, deliberate attention to these choices can be the proverbial stone with a better chance at hitting two birds at once. Changes in diet, in levels of stress, in smoking and alcohol consumption, and exercise are primary actions that can lower the risk of developing many diseases. Such intentional lifestyle changes are likely to impart a significant benefit for the individual with psoriasis, in both a direct treatment regimen but also in reducing one's risk for other inflammatory conditions that are life-threatening—in particular, cardiovascular disease.
Systemic Inflammation, CVD, and Psoriasis—Interacting Genetics and Lifestyle
A body of literature has been growing that associates the severity of psoriasis in an individual to a higher risk for cardiovascular disease (CVD). The risk factors that are common to an array of coronary and vascular conditions are seen to be common to psoriasis as well. In fact, a leading cause of death in psoriasis sufferers is CVD. High blood pressure, high cholesterol, smoking, diabetes, and obesity are more prevalent in psoriasis sufferers than in those without psoriasis, as well as being the primary risk factors for heart disease.
These are non-disease-specific risk factors because individuals with either incipient or full-blown heart disease, but no sign of psoriasis, often bear these risk factors. Nor are those with any of these risks guaranteed further illness, although the likelihood of disease is certainly greater. As modifiable risks, lifestyle changes reduce one's risk to not just one condition, but to all that can arise from inattention to the dangers they pose to an individual's health. The systemic inflammation of psoriasis, a result of interacting genetic and environmental components of the disease, appears to be exacerbated by these factors in ways not entirely clear, but which are likely to yield some of their influence in psoriasis when healthy changes in lifestyle are made and patiently adhered to.
Specific Behaviors/Specific Responses
Smoking is a known risk factor for a number of cardiovascular diseases and directly connected with high mortality from them. Cigarette smoke has been seen to induce changes in both the form and function of white blood cells (leukocytes), mediator cells in the body's immune response, and to also increase production of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), a key inflammation signal in psoriasis. A 2005 study examined the effects of smoking on severity of psoriasis and found an increased risk was dependent on the number of cigarettes smoked in a day, and the effect was more prevalent among women smokers with psoriasis than among men. While addiction to tobacco can be a difficult habit to kick, doing so is well known to show health benefits in a number of ways, likely including one's psoriasis.
Metabolic Syndrome and Psoriasis
In a similar way, the constellation of features associated with metabolic syndrome—obesity, dyslipidemia (abnormal blood lipid levels, including HDL and LDL cholesterol ratios and triglyceride levels), hypertension (high blood pressure), and insulin resistance—are more prevalent in psoriasis sufferers. As problematic inflammatory components, each of these is also a risk factor for both type 2 diabetes and cardiovascular disease.
While an association between psoriasis and metabolic syndrome is reported in the literature, the actual mechanisms for this association have yet to be elucidated, although a great deal of work is being done in this area. One connection appears to exist in the high levels of the hormone leptin seen in both psoriasis patients and overweight individuals.
Leptin, Insulin, Inflammation, and Psoriasis
Leptin is a hormone discovered in 1994 that stimulates endocrine activity in adipose tissue (fatty tissue). It plays an active role in regulating energy levels, metabolism, and immune-inflammatory responses, as well as appetite and satiety. Expressed in the body by the obese gene (ob), circulating levels of this hormone are in direct relation to both the mass of adipose tissue in the body and insulin, a crucial hormone necessary to maintaining normal blood sugar levels.
Regulating energy and metabolism, leptin works by modulating food intake, fat storage, and body weight through the hypothalamus, and participates in many biological processes, including glucose metabolism. While it is not clear how, elevated levels of leptin (hyperleptinemia) in psoriasis tend toward dysfunctional metabolic processes and inflammation. Whether a causal link exists between psoriasis and excess leptin is not known, but the association is relevant to both inflammation and a healthy metabolism.
Leptin's role in immunity and in the inflammation response is played out through regulation of the signaling factors in both acute and chronic inflammation, some of the same factors critical in the development of inflammation in psoriasis: TNF-alpha, Th1 and IL-6 cells to name a few. Elevated levels of leptin have been implicated in not just psoriasis but a number of other autoimmune inflammatory conditions, including arthritis and chronic bowel disease. Obesity is characterized by hyperleptinemia, and this may account, in part, for the systemic low-grade inflammation found in obese patients. To complete the circle of risk from low-grade inflammation to disease presentation, persistent low-grade inflammation, such as that promoted by obesity, favors a rise in insulin resistance and metabolic syndrome. Weight loss has been shown to decrease circulating leptin levels and is likely to benefit the psoriasis patient, both through better metabolic regulation and by way of diminishing the leptin-induced inflammatory response.
Stress, Heart Rate, and Psoriasis
Stress has long been implicated as an "environmental" factor in psoriasis outbreaks. In a 2006 study activation of the sympathetic nervous system through induced stress in psoriasis patients showed a "blunted increase in heart rate," and a sharp increase in diastolic blood pressure compared to control individuals. Diastolic blood pressure is the pressure exerted by the heart at the end of the beat, just before the more forceful contraction, or systole, of the heart, from which the systolic reading is determined. The diastolic reading is the lower or bottom value on standard blood pressure readings. An increase in this reading indicates that blood pressure is higher than normal at the end of the heartbeat. A blunted increase in heart rate indicates the heart did not respond normally to the induced stress as would be expected in a sympathetic nervous system response, the system that regulates the fight or flight response.
Thought to be at fault in the psoriasis patient is the low reactivity rate of receptors that regulate heart beat and vasoconstriction. Heart beta1-adrenergic receptors and artery wall beta2-adrenergic receptors activate with signaling from the sympathetic nervous system under normal conditions. One of their functions is to adjust the volume of blood the heart prepares to circulate in a given beat, as well as adjustment of the pressure exerted by the peripheral blood vessels. Dysfunction of these receptors, although in a different manner, is implicated in heart failure progression.
Calming activities, such as meditation, yoga, and breathing techniques are known to increase an individual's tolerance to stress, and are likely to be of benefit in psoriasis by minimizing sympathetic nervous system responses. Exercise is another excellent means to increase an individual's tolerance to stress, while strengthening the heart, lowering blood pressure, and regulating one's weight.
Psoriasis: An Independent Risk Factor for Cardiovascular Disease
While psoriasis shares these modifiable risk factors with cardiovascular disease, research is showing that even after accounting for these risk factors psoriasis is itself, through the systemic inflammation and autoimmunity that characterize the condition, an independent risk factor for cardiovascular disease. The inflammatory pathway that is fairly well understood in the formation of psoriatic plaques is very similar to the pathway of inflammation that occurs in the formation of atherosclerotic plaques in coronary, cerebral, and peripheral blood vessels. Disease-specific risk factors—elevated blood levels of C-reactive protein, infiltration of activated T cells to trouble spots, and elevated levels of inflammatory cytokines—are specific for both psoriasis and CVD.
Inflammation appears to be the pivotal link between psoriasis and cardiovascular disease, as well as other comorbid conditions that are characterized by autoimmunity and chronic inflammation. Comorbid conditions occur simultaneously and often independently of another medical condition. Some of the other comorbidities associated with psoriasis include rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Crohn's disease. Epidemiological studies have provided data supporting the association of cardiovascular events and RA and SLE, and inflammation is increasingly seen as central to the development of atherosclerosis, the formation of fatty plaques lining arteries and infiltrating artery walls.
Changing the Outcome In the Play Between Genes and Environment
The genetic component of psoriasis may enable this disease to pass down through generations of family members, a seemingly inescapable consequence of one's inherited genes. But this does not mean the environmental side of the disease should be discounted and ignored. Increasingly research into the emerging field of science known as epigenetics reveals that environmental factors work upon genetic material to strongly influence long-term health outcome.
Obvious triggers to outbreaks are wisely avoided as a matter of course when possible. Avoiding the less obvious influences of systemic inflammation through deliberate changes in lifestyle is likely to provide a more subtle but perhaps, with time, a very effective means to diminish disease symptoms. Improving one's overall health through a healthy diet, exercise, and stress reduction aims to improve the underlying metabolic processes involved in psoriasis while decreasing the risk of developing life-threatening cardiovascular conditions.
Some elements of one's disease cannot be changed—yet taking charge of those elements that can be changed is both empowering and likely to provide a benefit over the long run.