Cardiometabolic Disease in Parkinson's Disease High ... - Springer Link

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Sep 26, 2014 - Conflict of Interest Quincy J. Almeida received a grant from Canada. Foundation for Innovation, received honoraria from Parkinson's Society.
Curr Cardiovasc Risk Rep (2014) 8:404 DOI 10.1007/s12170-014-0404-7

PHYSICAL ACTIVITY (D WARBURTON, SECTION EDITOR)

Cardiometabolic Disease in Parkinson’s Disease High or Low Risk — A Risk Worth Protecting? Quincy J. Almeida

Published online: 26 September 2014 # Springer Science+Business Media New York 2014

Abstract Parkinson’s disease (PD) is the most common neurodegenenerative movement disorder known to man, representing a number of Parkinsonian syndromes whose sufferers are faced with similar symptomatology and challenges to mobility, independence and quality of life. With a growing aged population, and no cure for PD, it has become increasingly important to identify risk factors (and approaches to modifying these risk factors) that contribute to morbidity in these populations. This article considers the cyclical nature of whether the cardinal symptoms of PD lead to cardiometabolic decline, or whether the factors that are associated with cardiometabolic disease put people at higher risk for developing PD. Then, we examine the risk of developing cardiometabolic disease in PD compared to the general population. Finally, interventions and physical activity recommendations are reviewed, as well as healthcare management strategies to protect from cardiometabolic disease in PD. These recommendations are likely applicable to other Parkinsonian movement disorders as well. Keywords Parkinson’s disease . Physical inactivity . Cardiometabolic disease . Prevention Parkinson’s disease (PD) is considered the most common movement disorder, affecting over 5 million people beyond the age of 50. This number is expected to double by the year 2030. Due to the degenerative nature of the disease, progression of the typical motor symptoms can often lead to physical inactivity. For example, cardinal symptoms such as This article is part of the Topical Collection on Physical Activity Q. J. Almeida (*) Sun Life Financial Movement Disorders Research and Rehabilitation Centre, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario N2L 3C5, Canada e-mail: [email protected]

bradykinesia (slowness), and rigidity (stiffness) will often limit the opportunity for vigorous physical activity, while postural instability and the associated fear of falling can also lead to a self-regulated decrease in the amount of physical activity occurring outside the home. Interestingly, even the embarrassment of a resting tremor in the hand or head, can cause individuals to remain within the confines of their own home, which has also been argued to contribute to an inactive/ sedentary lifestyle. Thus, it is important to consider the potential for secondary cardiometabolic issues that might be expected to go hand-in-hand with PD. Given that the prevalence of PD is expected to double, it may be equally important to identify preventative strategies that will help combat cardiometabolic disease in PD.

The Cyclical Nature of Secondary Cardiometabolic Disease in Parkinson’s While not entirely unexpected, comorbidities can be multidirectional in PD. Factors such as increasing age, diabetes and depression have all been identified as risk factors associated with PD [24]. More interestingly, not only can other diseases increase the likelihood of PD, but PD has been identified as a risk factor for numerous other ailments including cardiometabolic disease. As such, prevention of cardiometabolic issues in movement disorders such as Parkinson’s disease will become an even more pressing concern and the risk factors for cardiometabolic disease should be carefully considered (see Fig. 1). In addition to the physical inactivity/sedentary lifestyle that typically accompanies PD, a number of risk factors are known to increase the risk of cardiometabolic disease, including: smoking, inflammatory markers, age, race/ethnicity, gender, and family history. Smoking is particularly interesting, since retrospective studies have argued that a history of smoking

404, Page 2 of 6 Fig. 1 The cyclical interaction between Parkinson’s disease and cardiometabolic disease

Curr Cardiovasc Risk Rep (2014) 8:404

CARDIOMETABOLIC DISEASE

Late-onset Diabetes

Hyperlipidemia

PARKINSON’S DISEASE

Bradykinesia

Overweight/

Postural Instability

PHYSICAL INACTIVITY

Obesity

Rigidity

Increased Age

reduces the risk of PD [10]. However, caution should be used when interpreting these results since there is no neuroprotective effect of current smoking on PD symptom progression. According to the definition of cardiometabolic syndrome operationalized by the World Health Organization, an accumulation of at least two cardiometabolic abnormalities is required (see Table 1). Meeting any of these criteria also puts an individual at an increased cardiometabolic risk, meaning that the individual may be more susceptible to type II diabetes, cardiovascular disease and ultimately cardiovascular mortality [11, 19]. Again, due to the cyclical nature of the relationship between PD and cardiometabolic disease, it may be important to consider how peripheral neuropathy which often accompanies late-stage diabetes may lead to balance and gait issues. These symptoms can often be confused with increased progression of PD, or lack of a response to dopaminergic medications, when in fact they symptoms are more related to the peripheral neuropathy. Nevertheless, these sorts of mobility issues can further reduce physical activity levels. Furthermore, given that between 50 and 80 % of all individuals with PD will suffer from dementia-like cognitive symptoms, it is important to consider the identified link between increased visceral adipose tissue distribution around the waist and cognitive decline. Atherosclerosis, high blood pressure, insulin resistance, and hyperglycemia are all factors linked to intra-abdominal visceral adipose tissue, and have been argued to be precursors to the onset of cognitive decline/ neurodegeneration and peripheral vascular diseases [7]. Hypertension is not only a risk factor for stroke, but it facilitates development of white matter hypertensive lesions in brain imaging studies, providing a further link to cognitive dysfunction. In contrast, low diastolic pressure, which is often the result of blood pressure medication has been shown to decrease cerebral perfusion. This is a particularly important finding since the gold standard and most commonly used treatment for PD (dopaminergic agents such as levodopacarbidopa), often has the side effect of lowering blood pressure [1].

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In contrast, more recent research has argued that decreased body mass index (BMI) may be an equally strong predictor of cognitive decline in PD. In a study of 104 PD patients followed over 3 years, patients whose BMI decreased in the first 6month post-PD diagnosis revealed significantly more cognitive impairment than those who’s BMI did not change. MiniMental State Exam performance not only revealed poorer cognitive function than the stable group after 6 months, but a greater rate of decline was also identified over the 3 year period [13]. Thus, monitoring changes to BMI and cognitive performance within the first six months of diagnosis is highly recommended. Despite the controversy in the literature between reports of high visceral adipose tissue and low BMI in PD, it is generally agreed upon that PD have a higher incidence of being overweight and/or obese (50 % greater than the general population); yet it is puzzling that individuals with PD tend to be less susceptible to cardiovascular disease. A study by Cereda et al. [6•] found that individuals with PD have lower cardiometabolic risk (compared to a healthy control population), independent of nutritional status, body composition, and fat distribution. This is in spite of the fact that nutritional status can be closely related to neurodegenerative diseases including PD [4]. While obesity is more common in PD, generally speaking, Table 1 World Health Organization criterion for cardiometabolic disease Symptom

Positive test value

Hypertension

>160 mmHg systolic or >90 mmHg diastolic plasma triglyceride ≥1.7 mmol/L low HDL cholesterol high BMI or waist to hip ratio

Dyslipidemia Obesity Microalbuminuria Hyperglycemia/high fasting blood sugar Insulin resistance

Curr Cardiovasc Risk Rep (2014) 8:404

progressive weight loss is often observed as PD progresses. Weight loss may be due to a number of factors including, slower mastication and intestinal digestion, difficulty swallowing, loss of appetite and depression. Unfortunately, most of these factors worsen as PD progresses. Additionally, the use of dopaminergic medications often results in motor fluctuations and dyskinesia [1], which ultimately increases basal metabolic rate and resting energy expenditure. It should also be noted that the well-documented ‘shaking palsy’ or rest tremor seen in PD, is considered one of the least responsive symptoms to dopaminergic treatment. Thus, this ‘hyperactive’ symptom would also be expected to increase overall energy expenditure. A study by Capecci et al. [5] examined 58 PD subjects, after excluding conditions known to influence metabolism (i.e., dysphagia, severe tremor, etc.), subjects underwent resting energy expenditure measurements via indirect calorimetry during ON and OFF dopaminergic treatment (generally OFF referes to a minimum 12-hour withdrawal from dopaminergic medication). The study found that in OFF medication state, PD patients demonstrated an increased resting energy expenditure which correlated with disease duration and rigidity. Interestingly, while rigidity is generally considered a symptom that slows and stiffens movement, the underlying mechanism of co-contraction of agonist and antagonist muscles that causes the cogwheel rigidity may in fact increase energy expenditure (considering the muscle pairs are essentially working against each other). In the ON medication state, resting energy expenditure decreased by ~8 %, and this was independent of disease duration. Body mass index was demonstrated to be inversely related to disease duration as well as motor symptom severity (according to the UPDRS motor score) in the OFF state; yet directly related to UPDRS motor score in the ON state. These results would seem to suggest that basal metabolic rate is negatively influence by neurodgeneration, although dopaminergic medication may be able to partially compensate for lower energy expenditure. Thus, body weight fluctuations in PD need to be carefully monitored by a holistic and interdisciplinary health care team, and may be best achieved through consultation with a nutritionist (to balance energy consumption/expenditure), as well as a movement disorders-trained neurologist (to optimize the effectiveness of dopaminergic medications). We often recommend taking dopaminergic medications at least 30 minutes prior to any meals, to avoid interaction with dietary proteins, since this can decrease the effectiveness of the medication.

Diabetes and Parkinson’s Disease It has been well established that as age increases, the coexistence of PD and type 2 diabetes mellitus also increases. Yet it is uncertain whether they may be independently associated with increased age, or whether there is a true relationship to

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chronic neurodegeneration. Scheuing et al. [23••] reported 0.3–2.4 % of PD patients being additionally affected by diabetes mellitus, and that this subgroup tended to be significantly older, while younger PD patients (