Malady of the Mind. Correlations and Possible Causes of Schizophrenia

Essay , 2015 , 8 Seiten

Psychologie - Klinische Psychologie, Psychopathologie, Prävention

The history of schizophrenia forms the mental image of a jigsaw puzzle with at least half the pieces missing. It does not appear throughout much of human history and lacks detailed accounts. There are writings that describe schizophrenic-like symptoms in patients of antiquity but the first recognized cases in both medical and psychiatric literature were not published until 1809. It took another century for the illness to be officially named; schizophrenia, from the Greek “splitting of the mind”, chosen to articulate the separation of the patient’s mind from reality in both perception and thinking. Our knowledge of the illness’s existence does not even stretch back to the time of the French Revolution. When viewed through this perspective the lack of definitive knowledge surrounding cause, treatment and prevention seems expected, or at least understandable.

Diagnosing schizophrenia is a complicated process. An initial requirement is the presence of symptoms such as delusions and hallucinations as well as the significant impairment of social/occupational functioning for a period of six months. It’s difficult to imagine that by the time one is officially diagnosed as schizophrenic their life is not already in complete disarray. It is a life destroying illness.

Malady of the Mind: Correlates and Possible Causes of Schizophrenia Nick Brandtmeier

Penn State University

According to the National Alliance on Mental Illness, schizophrenia affects about 1% of the American population, close to 3 million people (Schizophrenia). The onset of schizophrenia is almost always in the late teens/early twenties for men and slightly later for women; the illness is also a notoriously difficult one to accurately diagnose with there being no physical or lab test to confirm positive results (Schizophrenia). It is widespread and devastating to the individuals that suffer from it but we still have neither a definite etiological path nor an effective treatment without major drawbacks. Research has demonstrated associations with drug use, genetics, environment and brain chemistry in the onset of schizophrenia but none of these has shown to be causal (Schizophrenia). How can this gap in scientific knowledge exist? It is my intent to review scientific literature on the onset of schizophrenia, known correlates to it, and what characteristics seem to be the most prevalent in those who contract it. A cure must start with a cause and if there is a future ahead of us where this terrible illness can be cured then knowledge is our most powerful tool.

The history of schizophrenia forms the mental image of a jigsaw puzzle with at least half the pieces missing. It does not appear throughout much of human history and lacks detailed accounts. There are writings that describe schizophrenic-like symptoms in patients of antiquity (Evans & McGrath & Milns, 2003) but the first recognized cases in both medical and psychiatric literature were not published until 1809 (Heinrichs, 2003). It took another century for the illness to be officially named; schizophrenia, from the Greek “splitting of the mind”, chosen to articulate the separation of the patient’s mind from reality in both perception and thinking (Kuhn, 2004). Our knowledge of the illness’s existence does not even stretch back to the time of the French Revolution. When viewed through this perspective the lack of definitive knowledge surrounding cause, treatment and prevention seems expected, or at least understandable.

Diagnosing schizophrenia is a complicated process. An initial requirement is the presence of symptoms such as delusions and hallucinations as well as the significant impairment of social/occupational functioning for a period of six months (American Psychiatric Association 2013). It’s difficult to imagine that by the time one is officially diagnosed as schizophrenic their life is not already in complete disarray. It is a life destroying illness.

With a definite cause still unknown we can only look to the many correlates that have been found with schizophrenia to form an image of this illness’s process of engagement in the human mind. There are several correlates that have been documented and heavily researched in a variety of avenues, the majority focusing on common characteristics of those afflicted around the time of, and prior to, onset of the illness. Two of the most prominent include: the role of the mother, specifically during pregnancy and early childhood (Betts & Williams & Najman & Scott & Alati, 2014; Davidsen & Harder & MacBeth & Lundy & Gumley, 2015; Keskinen et al., 2015) and adolescent substance use (Kuepper & Van Os & Lieb & Wittchen & Höfler & Henquet, 2011; Large & Sharma & Compton & Slade & Nielssen, 2011).

The mother’s role during pregnancy/early childhood and the later development of schizophrenia is a fascinating association. Maternal infections may be transmitted to the fetus via the placenta, which makes the infant much more susceptible to additional illnesses in early life. Prenatal infections and resulting health problems in infancy positively correlate with the development of schizophrenia (Betts & Williams & Najman & Scott & Alati, 2014). An infant’s early existence revolves around attention, food and security provided by their primary caregiver(s). This relationship is not beneficial just in immediate survival; it provides the basis of what later becomes secure attachment. Research has indicated that parental avoidance (in both physical contact and verbal communication) with infants was linked with not just insecure attachment styles but the child’s later development of schizophrenia (Davidsen & Harder & MacBeth & Lundy & Gumley, 2015). It’s plausible that these biological and familial shortcomings early in life contribute to the development of schizophrenia, but it seems unlikely they alone can serve as a direct cause.

Previous research has established that adolescent substance use is an accurate predictor for the later onset of schizophrenia but this correlation does not stand up to scrutiny. There is decidedly greater number of adolescents who use illicit substances and never develop schizophrenia so there cannot be a direct, causal relationship between the two. The onset of schizophrenia and adolescent substance use appear related solely in correlation with one another through coincidence or the presence of an unknown/unaccounted third factor

Three other well studied correlates of schizophrenia’s onset are genetic/biochemical pathways, environment, and the age of the father at conception. Recent research in the fields of genetics and human biochemistry is especially encouraging and progressive. Certain gene mutations predict other, related mutations and variants that are involved in the heritability of schizophrenia (Kranz et al., 2015). Other studies have emphasized a central role for neural and immune-related pathways in the etiology of schizophrenia (Chang & Fang & Zhang & Wang, 2015) as well as common variants in calcium ion channel genes affecting the onset of schizophrenia (Purcell et al., 2014). The dual influence of genetics and human biochemistry is recognized in many aspects of human health, schizophrenia included. Recognizing markers for heritability and identifying related genomic variants are significant leaps in knowledge of the illness.

Environment, like genetics, has shown throughout human history to be a powerful influence on living biological systems of all kinds. Studies on the role of environment with the onset of schizophrenia have yielded three extremely interesting findings; 1) by percentage afflicted, schizophrenia is more prevalent among minorities; 2) individuals who grow up in an urban setting are more susceptible than those who do not; 3) sufferers of developmental trauma compose another subgroup with greater susceptibility to the illness (Boydell & McKenzie & Allardyce, 2001; Van Os & Driessen & Gunther & Delespaul, 2000; Van Os & Kenis & Rutten, 2010). An especially notable observation of environmental studies: The researchers find interesting, progressive results which validate the influence of environment but still conclude that the most likely course of onset for schizophrenia is a matter of gene-environment interaction.

Maternal age in regard to conception, pregnancy and childbirth is widely acknowledged to have a large influence on the health and upbringing of the child. The many troubles of young mothers are well documented along with the health risks that accompany mothers of older ages. Schizophrenia’s strong associations with the health and role of the mother are important and revealing, but not unanticipated. Conversely, a fascinating and unforeseen (at least for me) correlate is paternity age, which has shown to be a strong indicator in its own right.

Advancing paternal age is a strong correlate to schizophrenia; so strong that it has been observed in families with no history of the illness at an equal rate to families with such a history (Sipos et al., 2004). This association is even more prominent in first-born children than those later in the birth order (Petersen & Mortensen & Pedersen, 2011) and has been shown to carry over more than a single generation (Frans et al., 2011). It’s clear that paternal age has a strong affiliation with schizophrenia but further analysis demonstrates that the relationship may not be particularly unique.

Advancing paternal age has been revealed to have a similar relationship with Down syndrome, some forms of cancer, offspring with reduced fertility and birth defects, etc. (Bray & Gunnell & Smith, 2006). These findings are quite revealing of advanced paternal age and its relationship with offspring. It’s certainly a positive correlate, or even cause, for a great number of negative health outcomes in offspring, schizophrenia being only one of several. Recent research has failed to demonstrate a discernible relationship between advanced paternal age and proposed genetic correlates of schizophrenia (Jaffe & Eaton & Straub & Marenco & Weinberger, 2014; Malherbe & Roos & Ehlers & Karayiorgou & Roos, 2015), maintaining the status quo of obscurity in moving from correlation to causation.

At this time our understanding of the development and onset of schizophrenia can best be described as limited. The big five correlates of schizophrenia – mother’s health and affect, adolescent substance use, environment, genetic/biochemical avenues, advanced paternal age – are all interesting sources of knowledge and contribute a unique, valuable piece to the developing picture of schizophrenia’s etiology. Reviewing the research concerning each of these correlates provides the means for drawing conclusions about their relevance, specifically in relation to one another, and which areas really stand out as potentially groundbreaking.

In looking specifically for possible causation, adolescent substance use and advanced paternal age do not carry the same weight as the other correlates reviewed. Each of their correlations with schizophrenia have been researched and poured over, not because of a unique, distinct relationship, but because of the scarcity of knowledge regarding schizophrenia. The number and diversity of negative outcomes associated with adolescent substance use and advanced paternal age, respectively, for young adults and offspring, is staggering and a testament to their influence. These factors are so exoteric it’s impossible either could be a direct cause of schizophrenia. The correlational relationships they exhibit with onset are neither dismissed nor doubted but future research would best be served acknowledging their presence, not directed upon it.

I cannot name an illness or disease that has one, specific, solitary cause responsible for its onset and I can’t imagine schizophrenia fits this description either. The most recent schizophrenia-based research is headed in this direction; studies concerned with linking genetic factors and environment, familial and biological variables, etc., to identify specific interactions in hopes of establishing causality. Maternal prenatal infection, youth/adolescent environment and genetic/biochemical pathways are currently the best known correlates for the discovery of a hidden causal relationship(s) and should continue to be researched and reviewed. Although there is undoubtedly a sizable amount of progress to make in fully understanding the etiology of schizophrenia, the task is a worthwhile endeavor with exciting avenues of future research. The cause of schizophrenia is unknown, not impossible to know.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

Betts, K. S., Williams, G. M., Najman, J. M., Scott, J., & Alati, R. (2014). Maternal prenatal infection, early susceptibility to illness and adult psychotic experiences: A birth cohort study. Schizophrenia Research, 156 (2-3), 161-167. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1016/j.schres.2014.04.013

Boydell, J., J., McKenzie, K., Allardyce, J. (2001). Incidence of schizophrenia in ethnic minorities in London: Ecological study into interactions with environment. British Medical Journal, 323(7325), 1336-8.

Bray, I., Gunnell, D., & Davey Smith, G. (2006). Advanced paternal age: How old is too old? Journal of Epidemiology and Community Health, 60 (10), 851-853.

Chang, S., Fang, K., Zhang, K., & Wang, J. (2015). Network-based analysis of schizophrenia genome-wide association data to detect the joint functional association signals. PLoS One, 10 (7) doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1371/journal.pone.0133404

Davidsen, K. A., Harder, S., MacBeth, A., Lundy, J., & Gumley, A. (2015). Mother–infant interaction in schizophrenia: Transmitting risk or resilience? A systematic review of the literature. Social Psychiatry and Psychiatric Epidemiology, doi:http://dx.doi.org/10.1007/s00127-015-1127-x

Evans, K., McGrath, J., Milns, R. (2003). Searching for schizophrenia in ancient Greek and Roman literature: A systematic review. Acta Psychiatrica Scandinavica, 107(5), 323– 330. doi:10.1034/j.1600-0447.2003.00053.x.

Frans, E. M., McGrath, J. J., Sandin, S., Lichtenstein, P., Reichenberg, A., Långström, N., & Hultman, C. M. (2011). Advanced paternal and grandpaternal age and schizophrenia: A three-generation perspective. Schizophrenia Research, 133 (1-3), 120-124

Heinrichs, R.W. (2003). Historical origins of schizophrenia: Two early madmen and their illness. Journal of the History of the Behavioral Sciences, 39(4), 349– 363. doi:10.1002/jhbs.10152

Jaffe, A. E., Eaton, W. W., Straub, R. E., Marenco, S., & Weinberger, D. R. (2014). Paternal age, de novo mutations and schizophrenia. Molecular Psychiatry, 19 (3), 274-275. doi:http://dx.doi.org/10.1038/mp.2013.76

Keskinen, E., Marttila, A., Marttila, R., Jones, P. B., Murray, G. K., Moilanen, K., . . . Miettunen, J. (2015). Interaction between parental psychosis and early motor development and the risk of schizophrenia in a general population birth cohort. European Psychiatry, 30 (6), 719-727.

Kranz, T. M., Harroch, S., Manor, O., Lichtenberg, P., Friedlander, Y., Seandel, M., . . .

Malaspina, D. (2015). De novo mutations from sporadic schizophrenia cases highlight important signaling genes in an independent sample. Schizophrenia Research, 166 (1-3), 119-124. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1016/j.schres.2015.05.042

Kuepper, R., Van Os, J., Lieb, R., Wittchen, H., Höfler, M., & Henquet, C. (2011). Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study. BMJ: British Medical Journal, 342 (77-96)

Kuhn R. (2004). Eugen Bleuler's concepts of psychopathology. Hist Psychiatry, 15 (3), 361- 366.doi:10.1177/0957154X04044603

Large, M., Sharma, S., Compton, M. T., Slade, T., & Nielssen, O. (2011). Cannabis use and earlier onset of psychosis: A systematic meta-analysis. Archives of General Psychiatry, 68 (6), 555-561. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1001/archgenpsychiatry.2011.5

Malherbe, P. J., Roos, J. L., J., Ehlers, R., Karayiorgou, M., & Roos, J. L. (2015). Phenotypic features of patients with schizophrenia carrying de novo gene mutations: A pilot study. Psychiatry Research, 225 (1-2), 108-114. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1016/j.psychres.2014.10.024

Petersen, L., Mortensen, P. B., & Pedersen, C. B. (2011). Paternal age at birth of first child and risk of schizophrenia. The American Journal of Psychiatry, 168 (1), 82-88. doi:http://dx.doi.org/10.1176/appi.ajp.2010.10020252

Purcell, S. M., Moran, J. L., Fromer, M., Ruderfer, D., Solovieff, N., Roussos, P., . . . Sklar, P. (2014). A polygenic burden of rare disruptive mutations in schizophrenia. Nature, 506 (7487), 185-90.

Schizophrenia. (n.d.). Retrieved December 4, 2015, from https://www.nami.org/Learn- More/Mental-Health-Conditions/Schizophrenia

Sipos, A., Rasmussen, F., Harrison, G., Tynelius, P., Lewis, G., Leon, D. A., & Gunnell, D. (2004). Paternal age and schizophrenia: A population based cohort study. BMJ: British Medical Journal, 329 (7474), 1070. doi:http://dx.doi.org/10.1136/bmj.38243.672396.55

Van Os, J., Driessen, G., Gunther, N., & Delespaul, P. (2000). Neighbourhood variation in incidence of schizophrenia: Evidence for person–environment interaction. The British Journal of Psychiatry, 176, 243-248. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1192/bjp.176.3.243

Van Os, J., Kenis, G., & Rutten, B. P. F. (2010). The environment and schizophrenia. Nature, 468 (7321), 203-212. doi:http://dx.doi.org.ezaccess.libraries.psu.edu/10.1038/nature09563

• Autor: Nick Brandtmeier (Autor:in)
• Erscheinungsjahr: 2015
• Seiten: 8
• Katalognummer: V319582
• ISBN (eBook): 9783668190887
• ISBN (Buch): 9783668190894
• Sprache: Deutsch
• Schlagworte: malady, mind, correlations, possible, causes, schizophrenia