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Applying Motivational Theory to Module PNP3002

10 Dec

According to Ryan and Deci (2000) intrinsic motivation is doing something for the pleasure that doing that actual thing gives to an individual.  They also stated that a person has the most self-motivation when they are independently doing what they want (Ryan & Deci, 2000). I found that a major motivational factor for writing blogs was being able to further investigate topics of personal choice and interest. This meant that motivation to do the blogs was highly intrinsic, compared to writing about set subjects, which may not be of personal interest. The motivation to do these would have mainly been extrinsic, which is doing the work for an outside goal, in this case a good grade.

Deci and Ryan (1985) claimed that a major indicator of intrinsic motivation is an interest in the work being done. This was also supported by Krapp (1999) who stated that when working on a task, intrinsic motivation was produced from the person being interested in the task they’re doing. Intrinsic motivation has been found to be more beneficial than extrinsic motivation, with at times, extrinsic motivation being detrimental to not only the work being done, but to future work (Benabou & Tirole, 2003).

It has also been found that intrinsic motivational factors, such as enjoying the work being done and self-efficacy, produce more knowledge sharing (Lin, 2007). Alongside this, it was found that knowledge sharing was not influenced by extrinsic rewards, such as in this case, good grades (Lin, 2007). This indicates that as well as blog writing providing higher motivation to do the work, it also provides more motivation for the blog authors to actively share the knowledge that they acquired whilst writing the blog. I found that this was true of myself and other friends who took the Emotion and Motivation module, as each of us got excited about interesting research we found that we were writing about, and told others about it. This means that whilst I learnt about things that I was interested in, I also learnt new things whilst my friends were researching.

Overall I really enjoyed writing blogs, for the above reasons, but also for the fact that I found that having my work published on the internet, and others reading it gave me more motivation to find topics which interested me the most. I also appreciate that my blog could potentially be used to show to future employees.

 

 

References:

Benabou, R., & Tirole, J. (2003). Intrinsic and Extrinsic Motivation. The Review of Economic Studies, 70(3), 489- 520. doi: 10.1111/1467-937X.00253

Deci, E.L., & Ryan, R.M. (1985). Intrinsic motivation and self-determination in human behavior. London: Plenum.

Krapp, A. (1999). Interest motivation and learning: An educational-psychological perspective. European Journal of Psychology of Education, 34(1), 23-40. Retrieved from http://www.unibw.de/sowi1_1/interesse/pdfneu/krapp1999a

Lin, H-F. (2007). Effects of extrinsic and intrinsic motivation on employee knowledge sharing intentions. Journal of Information Science, 33(2), 135- 149. doi: 10.1177/0165551506068174

Ryan, R. M., & Deci, E. L. (2000). Self-determination theory and the facilitation of intrinsic motivation, social development and well-being. American Psychologist, 55(1), 68- 78. doi:10.1037//0003-­‐066x.55.1.68           

 

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Depersonalisation- emotional dissociation?

4 Dec

“I want to feel things like everyone else again, but I’m deadened and numb. I can laugh or cry but it’s intellectual, my muscles move but I feel nothing.”- Greg (Simeon & Abugel, 2006)

Depersonalization (DP) is a dissociative disorder, and can be explained as feelings of unreality (Sierra & Berrios, 2000). The American Psychiatric Association (1994) defined depersonalization in the DSM-IV as the ’alteration in the perception or experience of the self so that one feels detached from and as if one is an outside observer of ones mental processes or body (e.g. feeling as if one is in a dream)’. Depersonalization is thought to be prevalent in up to 20% of the population (Simeon et al., 1997). It can be a disorder of its own but can also be an effect of depression, anxiety, and other psychological disorders such as schizophrenia (Baker et al., 2003; Nuller, 2007; Roth, 1959). It may also have resulted from prolonged trauma and substance abuse (Simeon et al., 1997; Cohen & Cocores, 1997; Mathew, Wilson, Humphreys, Lowe & Weithe, 1993; Wenzel et al, 1996). This blog is going to discuss the effects of DP on emotions, and briefly evaluate treatment available.

Sierra and Berrios (2000) have suggested that depersonalization has two distinctive effects on the sufferer; these are a lack of emotional processing and a higher level of alertness. Individuals with DP commonly report a lack of emotional response and feeling (Sierra & Berrios, 1998). This is termed by Davidson (1966) as de-affectualization and involves a loss of affection and pleasure, emotional numbing, lack of emotional colouring, changes to the individual’s perceptions and cognitions and a lack of aversion to fearful or disgustful situations (Ackner, 1954; Mayer-Gross, 1935; Roth, 1959; Sapperstein 1949; Sierra & Berrios, 2000). This lack of emotion has been put down to the fact individuals affected with DP do not feel as though they are in reality (Lewis, 1934), but fMRI studies suggest that it could be due to neural differences in the brain.

On an fMRI task, individuals with DP showed a loss in brain activity when the intensity of happy and sad emotional expressions increased, which is opposite to those who do not have DP (Lemche et al., 2008). The same has been found when DP patients viewed aversive stimuli, as they were found to show lower brain activity in areas that are known to be sensitive to emotions, for example the insula and the posterior occipital temporal cortex (Phillips et al., 2001). It has been suggested that individuals with DP actually process aversive stimuli a different way than typical people (Medford et al., 2006). Alongside this, when presented with an aversive stimuli, they showed an increase in brain activity in the inferior and lateral frontal cortex; an area which is associated with the regulation of emotion (Phillips et al., 2001). This higher level of emotional regulation explains the self-reported loss in emotions.

This increase in emotional regulation in individuals with DP can be linked to the suggestion that depersonalization is used as a coping defense when daily stresses become too much to handle (Golembiewski, Munzenrider & Stevenson, 1986). To support this suggestion, it has been found that a higher number of stressors led to a more serious depersonalization (Zapf, Seifert, Schmutte, Mertini & Holz, 2001). This implies that the increased emotional regulation, which leads to a lack of response to aversive situations, is an innate system, designed to help people with stress, anxiety and depression cope with life.

Currently, there is no treatment for DP that has been found to be effective (Pini & Cassano, 2007). Medical treatments including the use of Serotonin Reuptake Inhibitors and Opioid Antagonists have been researched, and found to be helpful is some patients, but not a significant percentage (Pini & Cassano, 2007). Psychotherapeutic techniques, including cognitive-behavioral therapy (CBT) have been implemented (Simeon, 2004). Whilst the results of these studies have produced mixed results, they appear to be more effective than the use of medication, with one study claiming that CBT use over six months cleared the DP symptoms in 29% of the patients (Hunter, Baker, Phillips, Sierra & David, 2005). The higher effectiveness of therapy than medication could be explained regarding the idea of depersonalization being a coping mechanism, referring to the idea that therapy would target the underlying stress, rather than the after effects. It could be debated that the use of medication could be harmful to the individual as it could leave the underlying cause of the depersonalization untreated.

References:

Ackner, B. (1954) Depersonalization I. Aetiology and phenomenology. Journal of Mental Science, 100(421), 838. doi:10.1192/bjp.100.421.838

American Psychiatric Association. (1994). Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington, DC: American Psychiatric Press.

Baker, D., Hunter, E., Lawrence, E., Medford, N., Patel, M., Senior, C., Sierra, M., Lambert, M. V., Phillips, M. L., & David, A. S. (2003). Depersonalisation disorder: clinical features of 204 cases. The British Journal of Psychiatry, 182(1), 428-433. doi: 10.1192/bjp.02.399

Cohen, R. S., & Cocores, J. (1997). Neuropsychiatric manifestations following the use of 3,4-methylenedioxymethamphetamine (MDMA: “ecstasy”). Progress in Neuropsychopharmacology and Biological Psychiatry, 21(4), 727– 734.

Davidson, P. W. (1966). Depersonalization phenomena in 214 adult psychiatric in-patients. Psychiatric Quarterly, 40(1-4), 702–722. doi:10.1007/BF01562791

Golembiewski R.T, Munzenrider R.F., & Stevenson J.G. (1986) Stress in Organizations: Toward a Phase Model of Burnout. Praeger: New York.

Hunter, E. C. M., Baker, D., Phillips, M. L., Sierra, M., & David, A. S. (2005). Cognitive-behaviour therapy for depersonalisation disorder: an open study. Behaviour Research and Therapy, 43(9), 1121- 1130. Retrieved from http://www.sciencedirect.com/science/article/pii/S0005796704002153

Lemche, E., Anilkumar, A., Giampietro, V. P., Brammer, M. J., Surguladze, S. A., Lawrence, N. S., Gasston, D., Chitnis, X., Williams, S. C. R., Sierra, M., Joraschky, P., & Phillips, M. L. (2008). Cerebral and autonomic responses to emotional facial expressions in depersonalisation disorder. The British Journal of Psychiatry, 193(3), 222-228. doi: 10.1192/bjp.bp.107.044

Lewis, A. J. (1934). Melancholia: Clinical Survey of Depressive States. Journal of Mental Science, 80, 277- 378. doi: 10.1192/bjp.80.329.277

Mayer-Gross, W. (1935) On depersonalization. British Journal of Medical Psychology, 15(2), 103- 122. doi:10.1111/j.2044-8341.1935.tb01140.x

Matthew, R. J., Wilson, W. H., Humphreys, D., Lowe, J. V., & Weithe, K. E. (1993). Depersonalisation after Marijuana Smoking. Biological Psychiatry, 33(6), 431- 441.

Medford, N., Brierley, B., Brammer, M., Bullmore, E. T., David, A. S., & Phillips, M. L. (2006). Emotional memory in depersonalization disorder: A functional MRI study. Psychiatry Research: Neuroimaging, 148(2-3), 93- 102. Retrieved from http://www.sciencedirect.com/science/article/pii/S0925492706000941

Nuller, Y. L. (1982). Depersonalisation – symptoms, meaning, therapy. Acta Psychiatrica Scandinavica, 66(6), 451- 458. doi: 10.1111/j.1600-0447.1982.tb04502.x

Phillips, M. L., Medford, N., Senior, C., Bullmore, E. T., Suckling, J., Brammer, M. J., Andrew, C., Sierra, M., Williams, S. C. R., & David, A. S. (2001). Depersonalization disorder: thinking without feeling. Psychiatry Research. Neuroimaging, 108(3), 145–160. doi: 10.1016/S0925-4927(01)00119-6

Pini, M. M. S., & Cassano, G. B. (2007). The neurobiology and clinical significance of depersonalization in mood and anxiety disorders: A critical reappraisal. Journal of Affective Dissorders, 99(1-3), 91-99. doi:http://dx.doi.org/10.1016/j.jad.2006.08.025

Roth, M. (1959). The Phobic Anxiety-depersonalization Syndrome. Proc R Soc Med., 52(8): 587–595. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1870046/?page=1

Saperstein, J. L. (1949). On the phenomena of depersonalization. Journal of Nervous and Mental Disorders, 110(3), 236–251.

Sierra, M., & Berrios, G. E. (1998). Depersonalization: neurobiological perspectives. Biological Psychiatry, 44(9), 898- 908. Retrieved from http://www.sciencedirect.com/science/article/pii/S0006322398000158

Sierra, M., & Berrios, G. E. (2000). The Cambridge Depersonalisation Scale: a new instrument for the measurement of depersonalization. Psychiatry Research, 93(2), 153- 164.

Simeon, D. (2004). Depersonalisation Disorder. CNS Drugs, 18(6), 343- 354. doi:10.2165/00023210-200418060-00002

Simeon, D., & Abugel, J. (2006). Feeling Unreal; Depersonalisation Disorder and the Loss of the Self. New York: Oxford University Press.

Simeon, D., Gross, S., Guralnik, O., Stein, D. J., Schmeidler, J., & Hollander, E. (1997). Feeling unreal: 30 cases of DSM-III-R depersonalization disorder. American Journal of Psychiatry, 154, 1107–1113. Retrieved from http://www.pn.psychiatryonline.org/data/Journals/AJP/3679/1107.pdf

Wenzel, K., Bernstein, D. P., Handelsman, L., Rinaldi, P., Ruggiero, J., & Higgins, B. (1996). Levels of dissociation in detoxified substance abusers and their relationship to chronicity of alcohol and drug use. Journal of Nervous and Mental Disease, 184(4), 220–227. doi: 10.1097/00005053-199604000-00004

Zapf, D., Siefert, C., Schutte, B., Mertini, H., & Holz, M. (2001). Emotion work and job stressors and their effects on burnout. Psychology & Health, 16(5), 527- 545. doi:10.1080/08870440108405525

Does the Illegal Drug LSD Have the Potential to Treat Depression?

20 Nov

Lysergic acid diethylamide (LSD), more commonly known as acid, was first synthesized in 1938 by Albert Hofmann (Stoll, 1947 as cited in Clark & Del Giudice, 1970). Due to the popularity of LSD as a recreational drug, it became illegal in the United Kingdom in 1966, with medical research and use being forced to stop in 1973 due to bad publicity (DrugScope, 2004). Before this date, LSD was used clinically on humans, with plenty of benefits to mental health reported. In recent years, rules have slackened, and LSD is making a comeback into Psychological and Medical research (Sessa, 2005). This blog is going to discuss the potential of LSD being used medically to treat mental health problems, in particular depression.

LSD psychotherapy can be administered in two separate ways, the first is known as Psychedelic therapy, and involves the individual being exposed to one single dose of the drug in carefully controlled settings (Perrine, 1996). The aim of this is to give them one experience that would help to alter their perceptions (Perrine, 1996). The other is Psycholytic therapy; this entails moderate doses being given, alongside other, more regular, psychoanalytic techniques (Perrine, 1996). Mental disorders treated by these therapies include anxiety disorders, depression and obsessive-compulsive disorders (Vanggard, 1964 ; Moreno, Wiegand, Taitano & Delgado, 2006). The general after effects of taking LSD include decreasing unhappiness, compulsive habits, anxiety, and increasing extraversion and self- realization (Savage, Savage, Fadiman & Harman, 1964).

Studies involving terminally ill cancer patients showed that taking LSD removed their fear of dying (Pahnke, 1969) and was effective at treating depression and anxiety (Pahnke & Kurland, 1970; Kurland, 1985). Even at doses which did not bring on a psychedelic state, LSD has been found to be as effective as opiates in reducing pain, but longer lasting (Kast, 1967). This has been put down to a decrease in anxiety, and therefore less distress about the pain, rather than less pain (Kast, 1967). Research proposes the idea that psychedelic drugs, such as LSD, affect the serotonin system in the same way as antidepressants (Riedlinger & Riedlinger, 1994), aiding explanation as to why it decreases depression and anxiety.

LSD has also shown promise in the treatment of addiction, in particular alcohol addiction (Abramson, 1967). Results have shown that between 50 and 90% of alcoholics who partook in psychedelic therapy were still abstinent six months later (Sessa, 2005). Another study claimed that 50% of 500 alcoholics were sober a year later, many of which had previously failed with help from Alcoholics Anonymous (Maclean, Macdonald, Ogden & Wilby, 1967). It has been proposed that alcoholism and depression can originate from the same reasons (Swendsen & Merikangas, 2000), suggesting that LSD affects this underlying factor.

Just before LSD became illegal for medical purposes, all doctors who had prescribed this drug to human patients were interviewed (Malleson, 1971). Of these doctors, only 7% said they thought LSD was unsuitable to be used medically, whilst 56% claimed that it was effective and that they would continue using it on their patients (Malleson, 1971). By 1965, there were over 1,000 clinical studies published claiming to have identified beneficial effects of LSD use is more than 40,000 people (Malleson, 1971). Another positive of LSD is that the harmful effects of it on the body are scarce; it is non-addictive, does not cause brain damage, and has very low toxicity (Luscher & Engless, 2006). Whilst anxiety, paranoia and delusions can occur (Passie, Halpern, Stichtenoth, Emrich & Hintzen, 2008), these can be minimized with proper practice (Strassman, 1984) and it has been claimed that overall there are few side effects and it is safe to use (Masters & Houston, 1970).

 Although recent research on the use of LSD in the treatment of depression is scare, previous results show promising outcomes and the idea it effects peoples emotions is well supported. Saying this, medical treatments have advanced greatly since 1973, and with the new drugs available, it is questionable whether the use of LSD would still be beneficial to the clinical scene. More research needs to be done on the clinical use of LSD in altering emotions, to clarify the potential of this drug in medicine.

 

References:

Clark, W. G., & Del Giudice, J. (1970). Principles of Psychopharmacology. Academic Press: London, UK.

DrugScope. (2004). LSD. In DrugScope. Retrieved November 17, 2013, from http://www.drugscope.org.uk/resources/drugsearch/drugsearchpages/lsd

Kast, E. (1967). Attenuation of anticipation: a therapeutic use of lysergic acid diethylamide. Psychiat. Quart., 41(4), 646–57. doi:10.1007/BF01575629.

Kurland, A. A. (1985). LSD in the Supportive Care of the Terminally Ill Cancer Patient. Journal of Psychoactive Drugs, 17(4), 279- 290. doi:10.1080/02791072.1985.10524332

Lüscher, C., & Ungless, M. A. (2006). The Mechanistic Classification of Addictive Drugs. PLoS Med, 3(11), e437. doi:10.1371/journal.pmed.0030437

Maclean, J. R., Macdonald, D. C., Ogden, F., & Wilby, E.  1967. The Use of LSD in Psychotherapy and Alcoholism. Bobbs-Merrill: New York.

Malleson, N. (1971). Acute Adverse Reactions to LSD in Clinical and Experimental Use in the United Kingdom. Br J Psychiatry,118(543), 229–30. doi:10.1192/bjp.118.543.229.

Masters, R. E. L., & Houston, J. (1970). Therapeutic Applications of LSD and Related Drugs. PSYCHEDELICS, The Uses and Implications of Psychedelic Drugs
 (eds B. Aaronson & H. Osmond). Hogarth Press: London.

Moreno, F. A., Wiegand, C. B., Taitano, E. K. & Delgado, P. L. (2006). Safety, tolerability, and efficacy of psilocybin in 9 patients with obsessive-compulsive disorder. Journal of Clinical Psychiatry, 67(11), 1735–1740. doi:10.4088/JCP.v67n1110

Pahnke, W. N. (1969). The Psychedelic Mystical Experience in the Human Encounte with Death. Harvard Theological Review, 62(1), 1- 21. Retrieved from http://csp.org/docs/PahnkeIngersoll1969.pdf

Pahnke, W. N., & Kurland, A. A. (1970). The Experimental Use of Psychedelic (LSD) Psychotherapy. JAMA, 212(11), 1856- 1863. doi:10.1001/jama.1970.03170240060010

Passie, T., Halpern, J. H., Stichtenoth, D. O., Emrich, H. M., & Hintzen, A. (2008). The Pharmacology of Lysergic Acid Diethylamide: a Review. CNS Neuroscience and Therapeutics, 14(4), 295–314. doi:10.1111/j.1755-5949.2008.00059.x.

Perrine, D. M. (1996). The Chemistry of Mind-Altering Drugs. American Chemical Society: Washington, DC

Riedlnger, T. J., & Riedlinger, J. E. (1994). Psychedelic and Entactogenic Drugs in the Treatment of Depression. Journal of Psychoactive Drugs, 26(1), 41- 55. doi:10.1080/02791072.1994.10472600

Savage, C., Savage, E., Fadiman, J., & Harman, W. (1964). Therapeutic Effects of the Psychedelic Experience. Psychological Reports, 14, 111-120. Retrieved from http://www.amsciepub.com/doi/pdf/10.2466/pr0.1964.14.1.111

Sessa, B. (2005). Can psychedelics have a role in psychiatry once again? The British Journal of Psychiatry, 186, 457-458. 
doi: 10.1192/bjp.186.6.457

Strassman, R. J. (1984). Adverse Reactions to Psychedelic Drugs: A Review of the Literature. Journal of Nervous and Mental Disease, 172(10), 577- 595. doi:10.1097/00005053-198410000-00001

Swendsen, J. D., & Merikangas, K. R. (2000). The comorbidity of depression and substance use disorders. Clinical Psychology Review, 20(2), 173- 189. doi: http://dx.doi.org/10.1016/S0272-7358(99)00026-4

Vanggard, T. (1964). Indications and Counterindications for LSD Treatment. Acta Psychiatrica Scandinavica, 40, 427- 437. 

Can empathy be facilitated in children with an Autistic Spectrum Disorder?

23 Oct

In the United Kingdom just over one percent of the population is thought to be on the Autistic Spectrum (The National Autistic Society, 2013). Children with Autistic Spectrum Disorder (ASD) commonly demonstrate deficits in three main areas, known as the triad of impairments (Wing & Potter, 2002). These are language and communication, flexibility of thought and imagination, and social and emotional understanding (Wing & Potter, 2002). From a young age, children with ASD respond differently to others emotions than typically developing children do (Beall, Moody, McIntosh, Hepburn and Reed, 2008). This is shown by a lack of empathy (Baron-Cohen, Golan & Ashwin, 2009), defined by an inability to mentally place themselves in another’s position, identify with their emotional state (Baron-Cohen, Leslie & Frith, 1985), or react to it (Baron-Cohen, Golan & Ashwin, 2009). Currently, ASD is an incurable condition (The National Autistic Society, 2013) that compromises the quality of life of sufferers (Lee, Harrington, Louie & Newschaffer, 2008). If empathy in children with ASD were to be increased, it would greatly aid their communication with others.

Harris (1989) claimed that this lack of emotional understanding is not due to an impaired perception of others mental states, but rather the inability to simulate or imagine emotions. To support this, children with ASD can recognize emotions in others faces when they are asked to look for an emotion (Begeer, Rieffe, Terwogt & Stockmann, 2006). However, it was found that the child could not recognize expressions without being asked to look for a specific emotion (Begeer, Rieffe, Terwogt & Stockmann, 2006). This highlights potential problems in applying the teaching of emotions to real world situations.

Many technological interventions for children with ASD have been studied (Goldsmith & LeBlanc, 2004). It has been found that humanoid avatars can be successful in helping children with ASD to identify emotions (Moore, Cheng, McGrath & Powell, 2005). The use of humanoid robots has also been proved to be successful in not only to identifying emotions, but also to social interaction skills, such as turn taking (Robins, Dautenhahn, Boekhorst & Billard, 2010). Other teaching methods that have been found effective in increasing recognition and prediction of others emotional responses are the use of computer programs (Silver & Oakes, 2001) and videotapes (Bernad-Ripoll, 2007).

An animated DVD series called The Transporters has been specially developed, with the aim to help children recognize emotions (The Transporters, 2013). Research into the effects of this program have shown that in four weeks of watching 15 minutes at least three times a week, children with ASD performed as well on tasks relating to emotion than typically developing children who had not watched the animations (Golan et al, 2010). Alongside this, the parents of the children with ASD reported their children to have a higher interest in facial expressions, be more willing to discuss emotions and have change in their behavior and ability to interact with others (Golan et al, 2010). These parental reported effects indicate that the teaching of emotions may be applicable to real life, although they may have been subjective and possibly influenced by the parents increased awareness of their child’s emotional knowledge.

Although results from research appear to be promising in terms of teaching children with ASD emotions, methods used to collect the data, such as using emotional situations and expressions in cartoons, photographs and stories (Silver & Oakes, 2001), question how applicable the results will be to real life situations.  To support this, research suggests that whilst children with ASD can be taught to pass tasks that assess emotion and belief understanding, the teaching effects were not generalisable to other areas in which the children had not been previously taught (Hadwin, Baron-Cohen, Howlin & Hill, 1996). This indicates that the passing of tasks is due to the rules that the children have been taught, rather than understanding the concept of emotion. Whilst it does seem possible to teach emotions to children with autism, it does not seem that they completely understand these emotions at a level to apply them to real life situations.

References

Baron-Cohen, S., Golan, O., & Ashwin, E. (2009). Can emotion recognition be taught to children with autism spectrum conditions? Philosophical Transactions of The Royal Society of Biological Sciences, 364(1535), 3567-3574. doi: 10.1098/rstb.2009.0191

Baron-Cohen, A. M., Leslie, A. M., Frith, U. (1985). Does the autistic child have a “theory of mind”? Cognition, 21(1), 37- 46. Retrieved from http://autismtruths.org/pdf/3.%20Does%20the%20autistic%20child%20have%20a%20theory%20of%20mind_SBC.pdf

Beall, P. M., Moody, E. J., McIntosh, D. N., Hepburn, S. L., & Reed, C. L. (2008). Rapid facial reactions to emotional facial expressions in typically developing children and children with autism spectrum disorder. Journal of Experimental Child Psychology, 101(3), 206 -223. Retrieved from http://www.sciencedirect.com/science/article/pii/S0022096508000623

Begeer, S., Rieffe, C., Meerum Terwogt, M. & Stockmann, L. (2006). Attention to facial emotional expressions in children with autism. Autism, 10(1), 37-51. doi: 10.1177/1362361306057862

Bernad-Ripoll, S. (2007). Using a Self-as-Model Video Combined With Social Stories™ to Help a Child With Asperger Syndrome Understand Emotions. Focus on Autism and Other Developmental Disabilities, 22(2), 100- 106. doi: 10.1177/10883576070220020101

Golan, O., Ashwin, E., Granader, Y., McClintock, S., Day. K., Leggett, V., & Baron-Cohen, S. (2010). Enhancing Emotion Recognition in Children with Autism Spectrum Conditions: An Intervention Using Animated Vehicles with Real Emotional Faces. Journal of Autism and Developmental Disorders, 40(3), 269- 279. doi: 10.1007/s10803-009-0862-9

Goldsmith, T. R., & LeBlanc, L. A. (2004). Use of Technology in Interventions for Children with Autism. Journal of Early and Intensive Behavioral Intervention, 1(2), 166- 178. Retrieved from citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.95.4813&rep=rep1&type=pdf&embedded=true

Hadwin, J., Baron-Cohen, S., Howlin, P., & Hill, K. (1996). Can we teach children with autism to understand emotions, belief, or pretence? Development and Psychopathology, 8(2), 345- 365. doi: 10.1017/S0954579400007136

Harris, P. L. (1989). Children and Emotion, the Development of Psychological Understanding. Oxford, England: Basil Blackwell Ltd.

Lee, L., Harrington, R. A., Louie, B. B., & Newschaffer, C. J. (2008). Children with Autism: Quality of Life and Parental Concerns. Journal of Autism and Developmental Disorders, 38(6), 1147- 1160. doi:10.1007/s10803-007-0491-0

Moore, D., Cheng, Y., McGrath, P., & Powell, N. J. (2005). Collaborative Virtual Environment Technology for People With Autism. Focus on Autism and Other Developmental Disabilities, 20(4), 231- 243. doi: 10.1177/10883576050200040501

Robins, B., Dautenhahn, K., Boekhorst, R. T., & Billard, A. (2010). Robotic assistants in therapy and education of children with autism: can a small humanoid robot help encourage social interaction skills? Universal Access in the Information Society, 4(2), 105- 120. doi: 10.1007/s10209-005-0116-3

Silver, M., & Oakes, P. (2001). Evaluation of a New Computer Intervention to Teach People with Autism or Asperger Syndrome to Recognize and Predict Emotions in Others. Autism, 5(3), 299- 316. doi: 10.1177/1362361301005003007

The National Autistic Society. (2013). Is there a cure? Retrieved from http://www.autism.org.uk/about-autism/autism-and-asperger-syndrome-an-introduction/what-are-the-causes-is-there-a-cure/is-there-a-cure.aspx

The Transporters. (2001). Retrieved October 21, 2013, from http://www.thetransporters.com/

Wing, L., & Potter, D. (2002). The epidemiology of autistic spectrum disorders: Is the prevalence rising? Mental Retardation and Developmental Disabilities Research Reviews, 8(3), 151–161. doi: 10.1002/mrdd.10029

 

 

Breast is Best?

27 Apr

The subject of breastfeeding is not often talked about, or thought about by people other than expectant mothers and fathers. It is not common to go out in the United Kingdom (UK) and see someone breastfeeding their baby in public. Although it is well known that breast milk is the best start a baby can have, for some reason breastfeeding rates are not high. At one week old, only 35% of babies in the UK are breastfed, and by the time they are five months old this number drops to a mere 3% (UNICEF, 2005). This seems crazy considering the benefits of breast-feeding for both mother and child, and the fact that the price of formula milk costs around £100 per month.

A survey in The United States (US) revealed that 27% of people thought that breastfeeding was embarrassing, and a third of people thought that babies aged one year old or over should not be breastfed (Li, Fridinger & Grummer-Strawn, 2002).  Even breastfeeding mothers reported that they disapproved of breastfeeding in public, and said they were often ridiculed by their own friends, and found a lack of support from some health service providers (Guttman & Zimmerman, 2000). The most negative perceptions of breastfeeding came from people aged 30 and under, and those aged over 65, people will low income and less education (Li, Fridinger & Grummer-Strawn, 2002). Guttman and Zimmerman (2000) suggested that it is these negative perceptions of breastfeeding that discouraged some mothers, who would have liked to have breastfed their babies, from breastfeeding.

One of the major disadvantages of breastfeeding is the lack of freedom it gives the mother. Mothers who are planning on returning to work or education are often faced with the problem of having to wean their baby off the breast onto a bottle, which can be a challenge. Producing enough expressed milk for the baby to have whilst the mother is not there is also difficult. A mother returning to work is one of the major reasons for the decline in breastfeeding (Van Esterik & Greiner, 1981).  But whilst mothers who have worked and breastfed have reported it as challenging, they have also said that it is rewarding and worth doing (Zafar & Bustamante-Gavino, 2008).

If a breastfeeding mother chooses not to express, or her baby will not take a bottle (which is common with breastfed babies) the mother is pretty much attached to her baby 24 hours a day, every day, which can be very hard work. This also means that the father will not be able to bond with the baby, and unable to settle it. A breastfeeding mother is also advised to drink no alcohol, not to take illegal drugs and certain medication, not smoke, and is provided with a list of foods which may be harmful to the baby, give it colic, or make their milk taste bad. This all limits the freedom which the mother feels.

Around 50% of mothers who did begin breastfeeding their babies said that their reason for stopping feeding was the fact that their milk alone did not satisfy their baby (Li, Fein, Chen & Grummer-Strawn, 2008). The other two top reasons were that the baby began to bite, or lost interest in the breast and began to wean itself (Li, Fein, Chen & Grummer-Strawn, 2008). The reasons for stopping breastfeeding in the first month of the babies life were that the mothers experienced sore nipple, the babies would not latch on correctly, or there was not enough milk for them (Li, Fein, Chen & Grummer-Strawn, 2008).

Image

[Graph above retreived from: http://www.sharontrotter.org.uk/NIP2011-breastfeeding.html%5D

The above graph highlights the fact that most problems which breastfeeding mothers encounter are due to not enough or incorrect support and advice. This means that most problems could actually be stopped altogether.

There are certain medical and health conditions which make a mother unable to breastfeed, but these only account for 2% of women and their babies (Community Midwife, 2011), Apart from these 2% the other valid reasons to not breastfeed seem to be the lack of freedom it gives the mother and the publics perception of breastfeeding. These should not outweigh the emotional and physical benefits which breastfeeding gives to mother and baby.  More needs to be done to promote breastfeeding and to change the public’s opinion of it so that it can be accepted as a social norm.

 

References:

Guttman, N., &Zimmerman, D. R. (2000). Low-income mothers’ views on breastfeeding. Social Science & Medicine, 50(10), 1457- 1473.

Li, R., Fein, S. B., Chen, J., & Grummer-Strawn, L. M. (2008). Why Mothers Stop Breastfeeding: Mothers’ Self-reported Reasons for Stopping During the First Year. Pediatrics, 122(2), 69- 76. doi: 10.1542/peds.2008-1315i

Li, R., Fridinger, F., & Grummer-Strawn. (2002). Public Perceptions on Breastfeeding Constraints. Human Lactation, 18(3), 227-235. doi: 10.1177/089033440201800304

Zafar, N., & Bustamante-Gavino, I. (2008). Breastfeeding and working full time Experiences of nurse mothers in Karachi, Pakistan. International Journal of Caring Sciences, 1(3), 132–139.

Why do men go bald?

25 Mar

By the age of 80, 80% of all men have some hair loss; this balding is called Androgenetic Alopecia (Ellis, Stebbing & Harrap, 2000). Balding is due to the hair follicles on the head shrinking, to eventual become so tiny that they appear to not be there. Balding has been associated with genetic factors for many years, and it often runs in families (Birch & Messenger, 2001). But there could be other factors. Nyholt et al (2003) did genes on identical twins and concluded that 81% of hair loss was due to genetics.

To support the genetic reason of balding, research has shown link between male baldness and the androgen receptor gene (Levy-Nissenbaum et al, 2005). The androgen receptor is a gene that is activated by the binding of testosterone.  It has been suggested that the polymorphism of this gene can cause baldness (Levy-Nissenbaum et al, 2005).

Research in 2008 suggested that baldness could be to do with the weight of the scalp (Tuncay Ustuner, 2008).  Tuncay Ustuner (2008) proposed that as a man got older, the soft tissues around the hair follicles stops working as well as it once did. Therefore the hair follicles become trapped between the scalp and the skull, damaging them and causing baldness.

Stress can also cause some people to go bald. Alopecia Areata is when white blood cells attack the hair follicles, causing boldness in weeks (Scott, 2011). This is not permanent hair loss and treatment can usually get the hair to grow again (Scott, 2011). Telogen Effluvium is also due to stress. This is when the hair just simply stops growing. This is not serious and grows back within a year (Scott, 2011).

In the past testosterone has been said to be linked to balding. The graph below shows how the amount of testosterone decreases with age; as does hair. This suggests that there could be a link but more recent research claims that there is not.

[image retrieved from: http://www.benbest.com/lifeext/aging.html]

Although there may be other causes of hair loss apart from hereditary, these appear to be either for non- permanent hair loss or are unreliably researched ideas. Unfortunately for some, it appears that some men are destined to baldness.

References:

Birch, M. P., & Messenger, A. G. (2001). Genetic factors predispose to balding and non-balding in men. European Journal of Dermatology. 11(4), 309-14. Retrieved from http://www.jle.com/en/revues/medecine/ejd/e-docs/00/01/88/AE/article.md

Ellis, J. A., Stebbing, M., & Harrap, S. B. (2000). Polymorphism of the Androgen Receptor Gene is Associated with Male Pattern Baldness. Journal of Investigative Dermatology 116, 452–455. doi:10.1046/j.1523-1747.2001.01261.x

Nyholt, D. R., Gillespie, N. A., Heath, A.C., & Martin, N.G. (2003). Genetic basis of male pattern baldness. J Invest Dermatol, 121, 1561-4.

Scott, E. (2011). Stress and Hair Loss: What Are The Causes of Hair Loss? Medical Review Board.

Tuncay Ustuner, E. (2008). Baldness may be caused by the weight of the scalp: Gravity as a proposed mechanism for hair loss. Medical Hypotheses, 71(4), 505- 514. doi:10.1016/j.mehy.2008.05.030

Homosexuality; Nature vs. Nurture

10 Mar

Whilst the American Psychological Association (APA) have changed their original classification of homosexuality from being a mental illness in 1975, it was only in 1994 that the APA put out a statement saying “…homosexuality is neither a mental illness nor a moral depravity. It is the way a portion of the population expresses human love and sexuality” (American Psychological Association, 2010). Today they claim that being homosexual is not a choice and that “…it emerges from most people in early adolescence with no prior sexual experience” (APA, 2010). There are many arguments about whether homosexuality is a consequence of a person’s upbringing, or genetics.

In 1990, Swaab & Hofman discovered that the hypothalamus in homosexual males brains differed to that in a heterosexual’s brain. Other studies have also found this to be true, suggesting that homosexuality is genetic. Twin studies by Bailey and Pillard (1991), discovered that if one identical twin was homosexual, there was a 52% chance of the other one being so too, the chance was lowered to 22% for non- identical twins and only 11% for non- related adopted brothers. This research also suggests that homosexuality is genetic, supporting the nature side of the debate. Then in 1993, Hamer discovered the ‘gay gene’; the X-Chromosome called Xq28. This Chromosome was found to have certain markers in 64% of both homosexual brothers.

Despite sufficient evidence for the nature side of the debate, sociobehaviourists do not agree, claiming that homosexuality is caused by environmental factors, especially in childhood. In 1999, Wickelgren questioned Hamer’s study and concluded that the link is too weak between the Xq28 Chromosome and homosexuality. Parenting has been suggested to cause some people to be homosexual. Factors such as whether boys were allowed to play with dolls, or treated like a ‘sissy’ girl, have been linked to homosexuality, as well as child abuse (Nicolosi, 2002). If someone was to take the view of a Tabula Rasa, a blank slate, then it could be argued that upbringing must be the cause of homosexuality.

[Graph above retrieved from: Satinova, J. (1995). The Complex Interaction Of Genes And Environment: A Model For Homosexuality. Collected Papers from the NARTH Annual Conference.]

The above graph shows some possible environmental effects which could contribute to homosexuality and the percentage of relevant genes inherited. It suggests that both nature and nurture contribute, but neither are essential.

The nature side of thedebate has much more scientific and reliable research conducted in favor of it. Many ‘nurture’ factors could contribute to homosexuality developing, but it is likely that the persons susceptibility to be homosexual is due to genetics and ‘nature’. Whilst genetics may not always be the cause, there is no doubt that the nature side of the debate is a valid theory.

 

References:

Bailey, J. M., & Pillard, R. C. (1991). Genetic Study of Male Sexual Orientation. Arch Gen Psychiatry, 48(12), 1089-1096.

Hamer, D. H., Hu, S., Magnuson, V. L., Hu, N., & Pattatucci, A. M. (1993). A linkage between DNA markers on the X chromosome and male sexual orientation. Science, 261(5119), 321- 327. DOI: 10.1126/science.8332896

Nicolosi, J., & Nicolosi, L. A. (2002). A Parent’s Guide to Preventing Homosexuality. Intervarsity Press.

Publication Manual of the American Psychological Association, 6th ed (2010). Washington, DC: American Psychological Association.

Swaab, D. F., & Hofman, M. A. (1990). An enlarged suprachiasmatic nucleus in homosexual men. Brain Research, 537 (1-2), 141- 14. http://dx.doi.org/10.1016/0006-8993(90)90350-K

Wickelgren, I. (1999). Discovery of ‘Gay Gene’ Questioned. Science, 248(5414), 571. DOI: 10.1126/science.284.5414.571