Exercise is Medicine for Schizophrenia - Sasja Zethof



Exercise is Medicine for SchizophreniaReview Sasja ZethofIntroductionExercise as a treatment option is currently gaining popularity for a wide range of various illnesses and disorders. Exercise is Medicine (EIM) is a United States health initiative that was launched in 2007 by the American Medical Association and the American College of Sports Medicine (What is Exercise is Medicine, 2016). Since its launch, EIM has reached beyond the United States with currently 43 national centers around the globe (What is Exercise is Medicine, 2016). There is a website dedicated to the initiative with public access to about how exercise can benefit both mental and physical health. The following is a review investigating how this idea, EIM, may be a treatment option for individuals with schizophrenia. Schizophrenia is a complex mental health disorder with interventions that are inadequate in treating all the symptoms and deficits that characterize it. Evidence points to exercise as being a strong contender as an intervention option with results showing improvements in many areas for these individuals and although barriers to exercise participation are numerous, they are solvable.What is Schizophrenia?As before, schizophrenia is a very complex mental health disorder. It affects approximately 1% of the population with consistent values across the globe (“Section-G Schizophrenia”, 2015). Men and women seem to be affected equally with the onset occurring between late teens and mid-30’s (“Section-G Schizophrenia”, 2015). Men, however, typically have an earlier onset than women (“Section-G Schizophrenia”, 2015). Schizophrenia is characterized by varying degrees of negative and positive symptoms, which comprise a continuum (“Section-G Schizophrenia”, 2015). Currently, there are five known sub-disorders that fall on this continuum: catatonic schizophrenia, disorganized schizophrenia, paranoid schizophrenia, undifferentiated schizophrenia and residual schizophrenia (“Section-G Schizophrenia”, 2015). Negative symptoms are regarded as a flattened affect, lack of emotions, and social withdrawal (“Section-G Schizophrenia”, 2015). These symptoms begin early and typically remain consistent for the course of the illness (Malchow et al, 2013). Catatonic schizophrenia sits at this extreme of the continuum. Positive symptoms, on the other hand, are typically delusions and hallucinations (“Section-G Schizophrenia”, 2015). Delusions are irrational beliefs an individual may have, such as believing someone or something is watching, or following them. Hallucinations are sensory-based experiences such as hearing something or seeing something that is not there. Paranoid schizophrenia sits at this extreme of the continuum. These symptoms are also compounded with cognitive deficits, which also begin early and remain stable for the duration of the disorder (Malchow et al, 2013). Most individuals with schizophrenia have difficulties with memory (particularly short-term memory), attention, executive functioning and perceptual processing (Malchow et al, 2013). These symptoms represent the core features of the disease and usually embody the predictors for social functioning (Malchow et al, 2013). Others have expressed both negative symptoms and cognitive deficits as causing the most disability (Vancampfort et al, 2014). This disease can and very often does, lead to lifelong disabilities, which in term puts a large amount of stress and burden on patients, families and health care systems (Malchow et al, 2013). During 2004, schizophrenia was actually regarded as one of the top 10 leading causes of disability worldwide (“Section-G Schizophrenia”, 2015). Causes of SchizophreniaThe cause of schizophrenia is still widely unknown. There seems to be a genetic component as individuals who are first-degree biological relatives (father, mother, sibling) with someone suffering from schizophrenia are 10 times more likely to also develop the disorder (“Section-G Schizophrenia”, 2015). The environment too has been implicated as a cause of schizophrenia. In particular, prenatal exposure to influenza and other environmental insults have been linked to a significantly increased chance of the child developing schizophrenia (“Section-G Schizophrenia”, 2015; Wolf, Melnik & Kempermann, 2011). Infection-induced increases of pro-inflammatory cytokines within the pregnant mother could be one of the key events leading to the enhanced risk of a number of neuropsychiatric disorders in their offspring (Wolf et al, 2011). Despite these unknowns, there is one thing that seems morphologically consistent across these individuals; decreased hippocampal volume as compared to healthy individuals (Firth, Cotter, Elliot, French & Yung, 2015; Grace, 2016; Kimhy et al, 2015; Malchow et al, 2013; Nieto, Kukljan & Silva, 2013; Pajonk et al, 2010; Scheewe et al, 2013; Vancampfort et al, 2014; Wolf, Melnik & Kempermann, 2011). It is this hippocampal volume that is not only linked to cognitive deficits but also negative symptoms and positive symptoms. There are a few theories that try to explain why this atrophy occurs. Wolf and colleagues (2011) discuss the possibility of exposure to environmental stresses within the womb impacting telomerase activity, within the progeny, through increased levels for maternal cytokines, therefore causing impaired neurogenesis. Telomerase is an enzyme that maintains genomic stability by adding a six-base DNA repeated sequence to the chromosome ends in order to decrease telomere shortening during the process of mitosis (Wolf et al, 2011). Usually, telomerase is present at high levels in neural precursor cells during development of the brain (Wolf et al, 2011). An accelerated shortening of the peripheral cells such as leukocytes as well as lower telomerase activity has been reported in individuals with schizophrenia (Wolf et al, 2011). If this evidence is consistent within the central nervous system, neurogenesis may be impaired due to this mechanism, causing the hippocampal atrophy. More evidence, however, is in support of the brain-derived neurotrophic factor model for explaining this hippocampal atrophy. Neurotrophins, in general, are proteins that signal neurons to survive, differentiate and grow (Kimhy et al, 2015). In other words, they are very important for neurogenesis and brain plasticity (Kimhy et al, 2015). Brain-derived neurotrophic factor (BDNF), in particular, is one of the most abundant in the growth factor family (Kimhy et al, 2015). It plays a major role in neurogenesis and the protection of neurons within the central nervous system (Kimhy et al, 2015). Schizophrenia is actually associated with lower serum levels of BDNF, which may, in turn, explain this decrease in hippocampal volume (Kimhy et al, 2015). Additionally, synaptic alterations in BDNF expression may also impact the neurotransmitter pathways that were first associated with schizophrenia including dopaminergic and GABAergic systems (Nieto, Kukuljan & Silva, 2013). Overall, it seems as though this decrease in hippocampal volume and other alterations within the hippocampus are the causes of the positive symptoms, the negative symptoms and the cognitive deficits that are typically characterized in this disease (Kimhy et al, 2015). The anterior portion of a human hippocampus in an individual with schizophrenia seems to be hyperactive as compared to healthy individuals (Grace, 2016). This hyperactivity has been correlated with a substantial decrease in the amount of inhibitory paravalbumin-expressing GABAergic interneurons in the hippocampus (Grace, 2016). This loss of paravalbumin interneurons in the limbic system leads to inadequate inhibition and the hyper-responsive dopamine system that underlying the positive symptoms of schizophrenia (Grace, 2016). Likewise, the hippocampus plays a pivotal role in learning, memory, cognition, response to stress, and in the regulation of mood and emotions, in other words negative symptoms and cognitive deficits (Wolf, 2011).Treatment OptionsThere are currently two widely used treatment options for people with schizophrenia and they are often used in tandem: psychotherapy and pharmacological therapy. Types of psychotherapy typically provided to individuals with schizophrenia include cognitive behavioural therapy, family therapy, and skills training (Firth et al, 2015). Although they have been shown to somewhat reduce negative and cognitive symptoms, they can be costly causing poor accessibility (Firth et al, 2015). On the other hand, pharmacological options are effective in treating positive symptoms but come with a whole host of additional problems (Firth et al, 2015). Most of the anti-psychotics on the market today block dopamine D2 receptors at doses found to be effective through clinical trials (Grace, 2016). They typically work to decrease the hypersensitivity to dopamine in order to decrease positive symptoms. The list of side effects involved with these drugs, however, is lengthy; they only increase other health issues both physically and mentally (Firth et al, 2015). Metabolic syndrome is one of the major side effects of anti-psychotics. It is a cluster of co-occurring risk factors for diabetes and cardiovascular disease including obesity, high blood pressure and hyperglycemia (Firth et al, 2015). In fact, after the first year of taking these medications, the incidence for metabolic syndrome increases five-fold (Firth et al, 2015). The side effect of weight gain also decreases these individuals’ motivation to participate in physical activities leading to further health declines (Firth et al, 2015). Furthermore, both psychotherapy and anti-psychotics are inadequate in dealing with negative symptoms and cognitive deficits, and it is these that cause the most disability within this population (Firth et al, 2015). There is an obvious need for an effective treatment option that will decrease the side effects seen from anti-psychotics, treat the negative and cognitive symptoms, and be cost effective and accessible. Exercise as TreatmentPhysical activity or exercise may be a good treatment option for people with schizophrenia. Not only is it very accessible but it can be low cost as well. Additionally, there is a substantial amount of evidence showing that exercise will not only help with regular fitness and difficulties with weight, but also help with the symptoms of schizophrenia. Prolonged exposure to aerobic running has been shown to increase telomerase levels, which may lead to restored telomere length and therefore maintenance of neurons and possibly an increased or maintained hippocampal volume (Wolf et al, 2011). Aerobic exercise has also been shown to cause an up-regulation in brain-derived neurotrophic factor in humans (Kimhy et al, 2015) as well as an increase in hippocampal blood flow (Wolf et al, 2011). This increase in BDNF, in turn, seems to help with hippocampal atrophy as it signals the increase of cell proliferation and survival (Kimhy et al, 2015). With an increase in hippocampal volume, many of the symptoms and deficits that characterize schizophrenia have also been shown to improve in response. These improvements include better dopamine regulation, which decreases positive symptoms as well as improved negative symptoms, and improved cognitive deficits such as short-term memory difficulties (Pajonk et al, 2010; Vancampfort et al, 2014; Wolf et al, 2011). Specifically, aerobic exercise has led to a 34% improvement in short-term memory for persons with schizophrenia (Vancampfort et al, 2014). These effects were exactly what Pajonk and colleagues (2010) found in their study of individuals with schizophrenia. They conducted a randomized controlled study in which male patients with chronic schizophrenia were matched with healthy subjects. Participants were randomly grouped into two conditions. The experimental condition involved the aerobic exercise of cycling for three months while the control condition consisted of table football participation for three months (Pajonk, 2010). MRI scans were used to measure hippocampal volume and maximum oxygen consumption was used to measure aerobic fitness. Results showed a significant increase in hippocampal volume in both patients and healthy subjects that partook in the experimental condition (Pajonk et al, 2010). These increases in hippocampal volume in the exercise group were correlated with improvements in aerobic fitness (Pajonk et al, 2010). Following this, Firth and colleagues (2015) completed a meta-analysis in which they compared the effects of different types of exercise and dosage. Overall, evidence points to 90 minutes of moderate-to-vigorous aerobic exercise a week as being the best course of action to initiate the effects previously mentioned, with aerobic exercise being cycling, running, sports, or resistance training (Firth et al, 2015). Exercise has also been found to help by providing distraction, drawing attention away from positive symptoms to reconnect individuals with reality (Firth et al, 2016). The exertion and effort being put into the exercise can help ground peoples with schizophrenia (Firth et al, 2016). It may also improve negative symptoms by providing valued social interactions with achievable and fulfilling goals (Firth et al, 2016). Overcoming Barriers Many people of the general public have a hard time participating in exercise. The typical reasons usually include a lack of time, interest and/or motivation. Individuals with schizophrenia combat not only these barriers but also many more specifically related to their disorder. Key barriers for this population include symptoms of paranoia, anxiety, body-image issues (due to weight-gain and cardiovascular anti-psychotic side effects), and boredom (Firth et al, 2016; Kimhy et al, 2015). Using exercise as an intervention for individuals just beginning to show signs of schizophrenia, early intervention for psychosis individuals, may help with some of these barriers (Firth et al, 2016). Early intervention psychosis is a critical period within which physical health interventions greatly benefit the prevention of metabolic syndrome (Firth et al, 2016). It has also been found to be the critical time for interventions, which target negative and cognitive symptoms (Firth et al, 2016). Beginning early would also mean gaining control over some of the anti-psychotic side effects such as weight-gain, which can later causes major barriers to participation in physical activity. In a study conducted by Firth and colleagues (2016), they observed greater adherence and retention rates in early intervention psychosis individuals than in previous trials of exercise for schizophrenia. They believe this may be due to the nature of the intervention or the characteristics of the early intervention sample (Firth et al, 2016). Active-play through video games used as aerobic exercise programs may also decrease barriers for this population by making physical activity more fun (Kimhy et al, 2015). Moreover, autonomy and social support within the prescribed programs have been identified by schizophrenic individual’s themselves as critical for effectively engaging people to participate in moderate-to-vigorous activity (Firth et al, 2016). Conclusion and Future StudyIn order to break further barriers to participation, future studies should focus on comparing benefits seen in a predetermined program of moderate-to-vigorous exercise as opposed to a moderate-to-vigorous program chosen by patients themselves. Overall, exercise may help fill in the gaps that other interventions for schizophrenia have left behind. Most notably, exercise increases brain-derived neurotrophins causing an increase in hippocampal volume, which then causes improvements in all areas of this disorder. Moderate-to-vigorous exercise is accessible, affordable, and a feasible treatment option for individuals with schizophrenia. ReferencesFirth, J., Carney, R., Jerome, L., Elliott, R., French, P., & Yung, A. R. (2016). The effects and determinants of exercise participation in first-episode psychosis: a qualitative study.?BMC Psychiatry,?16(1), 1. doi: 10.1186/s12888-016-0751-7Firth, J., Cotter, J., Elliott, R., French, P., & Yung, A. R. (2015). A systematic review and meta-analysis of exercise interventions in schizophrenia patients. Psychological Medicine,?45(07), 1343-1361. doi:10.1017/S0033291714003110 Grace, A. A. (2016). Dysregulation of the dopamine system in the pathophysiology of schizophrenia and depression.?Nature Reviews Neuroscience, 17, 524-532. doi:10.1038/nrn.2016.57Kimhy, D., Vakhrusheva, J., Bartels, M. N., Armstrong, H. F., Ballon, J. S., Khan, S., ... & Castrén, E. (2015). The impact of aerobic exercise on brain-derived neurotrophic factor and neurocognition in individuals with schizophrenia: a single-blind, randomized clinical trial.?Schizophrenia Bulletin,41(4), 859-868. doi:10.1093/schbul/sbv022Malchow, B., Reich-Erkelenz, D., Oertel-Kn?chel, V., Keller, K., Hasan, A., Schmitt, A., ... & Falkai, P. (2013). The effects of physical exercise in schizophrenia and affective disorders.?European Archives of Psychiatry and Clinical Neuroscience,?263(6), 451-467. doi:10.1007/s00406-013-0423-2Nieto, R., Kukuljan, M., & Silva, H. (2013). BDNF and schizophrenia: from neurodevelopment to neuronal plasticity, learning, and memory.?Frontiers In Psychiatry,?4, 45. doi:10.3389/fpsyt.2013.00045Pajonk, F. G., Wobrock, T., Gruber, O., Scherk, H., Berner, D., Kaizl, I., ... & Backens, M. (2010). Hippocampal plasticity in response to exercise in schizophrenia.?Archives of General Psychiatry,?67(2), 133-143. doi: 10.1001/archgenpsychiatry.2009.193.Scheewe, T. W., van Haren, N. E., Sarkisyan, G., Schnack, H. G., Brouwer, R. M., de Glint, M., ... & Cahn, W. (2013). Exercise therapy, cardiorespiratory fitness and their effect on brain volumes: a randomised controlled trial in patients with schizophrenia and healthy controls.?European Neuropsychopharmacology,?23(7), 675-685. doi:10.1016/j.euroneuro.2012.08.008Section-G Schizophrenia [Web page]. (2015). Retrieved from Vancampfort, D., Probst, M., De Hert, M., Soundy, A., Stubbs, B., Stroobants, M., & De Herdt, A. (2014). Neurobiological effects of physical exercise in schizophrenia: a systematic review.?Disability and Rehabilitation,?36(21), 1749-1754. doi:10.3109/09638288.2013.874505Wolf, S. A., Melnik, A., & Kempermann, G. (2011). Physical exercise increases adult neurogenesis and telomerase activity, and improves behavioral deficits in a mouse model of schizophrenia.?Brain,Behavior, and Immunity,?25(5), 971-980. doi:10.1016/j.bbi.2010.10.014 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download