Tag Archives: mental health

Anorexia and Autism?

A new study lead by Professor Simon Baron-Cohen of Cambridge University suggests that girls with anorexia have a higher than average “number of autistic traits” (University of Cambridge, 2013). These traits include an “above average interest in systems” and a below average empathy score (ibid). Considering the rigid personality, attitudes and behaviours of anorexics and their obsessive thought patterns in relation to body weight, body image and eating patterns it is not difficult to see how they can be interpreted as typical of autism.













n the study, first published the Journal of Molecular Autism, Baron-Cohen et al. assessed 66 girls between the ages of 12 and 18 with anorexia but no history of autism for autistic traits. A control group of over 1,600 neurotypical teens in the same age group were also given the same assessments including the the Autism Spectrum Quotient (AQ), Systemising Quotient (SQ) and the Empathy Quotient (EQ). Results showed that compared with the control group, the anorexic girls were five times more likely to score in the autistic spectrum. More than 50% of the anorexic girls fell into the “broader autism phenotype” compared with only 15% of the control (ibid). Furthermore, the anorexic girls also scored a higher SQ and lower EQ which also points towards an autistic personality.

As interesting as these results are there is indeed a practical application. Cases of autism are far more prevalent in males; however, Baron-Cohen’s findings show that perhaps autism in young girls is being overshadowed by a diagnosis of anorexia. Dr Tony Jaffa, co-leader of the study confirms that the new correlation between autistic traits and anorexia will give health professionals and researchers a new means to help those suffering from the eating disorder. He remarks:

“For example, shifting their interest away from body weight and dieting on to a different but equally systematic topic may be helpful. Recognising that some patients with anorexia may also need help with social skills and communication, and with adapting to change, also gives us a new treatment angle”

Mental Health Stigma

mentalillnessThis will be my fiftieth post on Cognitive Consonance and because I wanted to make it special by posting something engrossing and clever, I just ended up not posting anything at all. I put far too much pressure on myself, argh! Instead of trying so hard, I am just going to discuss something really important to me personally.

As I think is quite common with people interested in the field of psychology, I have and still continue struggle with depression and anxiety. I am not trying to evoke pity or sympathy because in actual fact, I am quite proud of how far I have come in the past 2 years. It takes quite a long time to learn to accept that you have a disease or disorder and that it is not just all in your head (ha, a pun! :P). Allowing yourself to be treated might make you feel like a failure; like there is something wrong with you because you just can’t get over your problems by yourself. It takes a great deal of strength to recognise that something is wrong.  I believe this is true for more than just mental disorders. Suffers of any ailment go through a period of denial. In fact, denial is the only stage of the Kuebler-Ross model that has been proven to be universal. I believe that the first step of any form of recovering or acceptance is recognising that something is wrong because it means admitting that you are vulnerable. Personally, I struggled with feelings of guilt. I felt like I had no reason to feel unhappy or anxious and that I should just get over myself. The truth is that a mental disorder, like any other medical ailment, needs to be treated. Treatment of course does not always mean in the form of medication. In fact, numerous types of mood disorders as well neuroses, have been treated very successful with cognitive-behavioural therapy.

mentalillness1I digress, in November I posted an ‘Inspiring Video‘ on schizoaffective disorder by a youtuber called Jonny Benjamin as part of the “I’m JustHuman Project.” In the video he discusses his experience with schizoaffective disorder and its impact on his life. However, more importantly his video is part of a project to reduce the stigma that surrounds mental health issues. Many people today mistake the symptoms of schizophrenia for depression and those of depression with a physical ailment (Myers 2001). Furthermore, a large majority of the population think that mental illness equals violence. In truth, most people that suffer from mental illness are no more violent than the rest of the population. The differences are easily accounted for by the symptoms of certain kinds of disorders, specifically the paranoia of paranoid schizophrenia or the lack of empathy seen in psychopaths. Just like certain personality types are more likely to engage in criminal behaviour, such as narcissistic or aggressive people, so are people with certain types of disorders. What I am trying to say is that there is no reason for the fear and stigma that surrounds mental illness.

mentalillness2Lastly, I want to say that mental illness in most cases is something that you cannot see from outside. Just like many who suffer from autism express frustration with the fact that they look normal but feel different, this frustration

is also common with people suffering from mental disorders. Those of us who have suffered from anxiety and depression learn how to conceal the truth. One of my closest friends showed up at the same mood disorder support meeting as me. Neither one of us had any clue the other person was going through the same thing. I believe that says a lot because the truth of the matter is that we are not so different from anyone else. Keeping that in mind, I feel it is important to be kind, supportive and patient to whomever you can because you never truly know what people are going through. Dealing with disorders such as depression, panic disorder, generalised anxiety disorder, OCD, etc. can easily be concealed and is a personal issue, but at the same time there is no reason to feel ashamed. We are in fact just like everybody else, the only difference is that we have deal with issues that impact our day-to-day lives. It is a struggle but one that is more than worth enduring.

Spotlight Study: SITran Identifies Promising New Parkinson’s Drug

As I will be starting my second year at the University of Sheffield this year I very proud to present this article to you! I hope you enjoy:

A new drug has been identified by the Sheffield Institute for Translation Neuroscience (SITraN), which shows potential of being able to “stop faulty brain cells dying and slow down the progression of Parkinson’s” disease (University of Sheffield, 2013). This synthetic drug called ursodeoxycholic acid (UDCA) was one of the 2,000 tested by the researchers, which could make faulty mitochondria healthy again. These faulty mitochondria are one the “main reasons why brain cells die” in Parkinson’s disease (University of Sheffield, 2013). One of the most promising aspects of UDCA is that it has already been in used to treat forms of liver disease, meaning clinical trails to test the drug as a Parkinson’s treatment can begin right away.

UCDA offers new hope for the millions of people affected with Parkinson’s disease, a basal ganglia disorder affecting basic movement leading to depression, anxiety and basic dysfunction. This new drug, unlike those before, will be able to treat the disease itself rather than the symptoms.

According to ScienceDaily, Parkinson’s UK believes this drug brings us closer to a cure for Parkinson’s.


University of Sheffield. “Ground breaking research identifies promising drugs for treating Parkinson’s.” ScienceDaily, 3 Sep. 2013. Web. 20 Sep. 2013.

Mental Retardation and Dendritic Spines


Dendrite is Greek for “tree-like” and to explain what they do in the simplest terms possible, they receive electrochemical signals from other neurons and then pass these signal down to the soma or neural cell body. Dendrites play a critical role in determining the frequency of the action potential, which drives the electrical signal down axons of the body of the neuron towards the axon terminals. Dendrites are so essential that their architecture is a great indicator of the complexity of our neural connections. In fact, our brain function depends on strong synaptic connections, connections which are cultivated during infancy and early childhood.

Unfortunately, as with all things complex, sometimes something goes wrong in the developing process. Mental retardation occurs when there is a disruption in this early refinement of dendrites that results in cognitive impairment severe enough to disrupt adaptive behaviour. There is a wide array of genetic disorders and poor environmental conditions that can result in mental retardation. For example, Down Syndrome and PKU (both genetic disorders), accidents during pregnancy and childbirth, maternal infections with rubella, Fetal Alcohol Syndrome and environmental impoverishment. Poor environmental conditions in young children such as poor nutrition, isolation and neglect can even result in brain damage severe enough to cause damage to these sensitive dendrites.

spine 2

Healthy dendrites have spines that look like small balloons that hang of the dendrite. In cases of mental retardation dendritic spines are very thin and long, resembling the dendritic spines of a fetus. This is clearly seen in the top most image, a) and c) are healthy dendrites. This clear difference reflects the failure of normal circuits in the brain’s development. Studies by Marin-Padilla and Purpura have discovered a correlation between extent of dendritic spine damage and degree of mental retardation.


Bear, Mark F., Barry W. Connors, and Michael Paradiso. “Neurons and Glia.”Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. 43. Print.

Images courtesy of google images.


Cocaine and the Brain


As part of a new series on drugs that affect the nervous system, I thought I would begin with cocaine. Unlike many other drugs for some reason cocaine is associated with the rich, famous and successful rather than with troubled teenagers and the homeless. Despite its allure cocaine is a highly additive and highly deadly substance. As a powerful stimulant the powerful high can last anywhere from 15-30  minutes up to an hour. Surprisingly, at least to me, approximately 14% of the American population has tried cocaine (WedMD, 2013) with the largest demographic being males between the age of 18 to 25.


Cocaine like most other recreational drugs affects the brain; if it didn’t there would not be much allure to them really. Most people are after all drawn to drugs because of the escape they offer. Unfortunately, no drugs that play with the mind are to be trusted. As a class A drug, the side effects more than out weighs the highs. Cocaine affects the the neurochemical pathways by blocking the re-uptake of neurotransmitters such as norepinephrine, serotonin, and dopamine.


As it blocks these three common neurotransmitters it is called a triple re-uptake inhibitor. Drugs that increase the concentration of these specific neurotransmitters are said to be positively reinforcing meaning they create a pleasurably feeling that can become addicting. Addictions such as sex, gambling, eating, etc. can become addictive because they also produce pleasurable feelings that can be self-reinforcing.

The High 

In cocaine users these highs are described as euphoric with accompanying feelings of supremacy, positive mood and also an increase in energy and alertness. You can see why famous detective Sherlock Holmes may have been drawn to such a drug. However, sometimes the high can result in increased levels of anxiety, restlessness, paranoia and irritability. Such symptoms illustrate the dangers of playing with our neurochemical balance; we cannot be certain the pathways we affect are going to result in positive feelings. People with a family history of mental illness are increasingly vulnerable to the effects of cocaine use because such a major flux in their brain chemistry can trigger the onset of disorders ranging from bipolar disorder to schizophrenia.

Physiological Symptoms 


The dangers of cocaine abuse are not just limited to the brain. Travelling through the blood, cocaine can have devastating effects of the heart, the kidneys, the respiratory system, the gastrointestinal tract and even sexual function. You can read more about these effects on WedMD.


Extracted from the coca leaf, cocaine or benzoylmethylecgonine is a crystalline tropane alkaloid (-ine suffix) meaning that it has a crystal-like and nitrogen-based structure that occurs naturally. The coca leaf is mostly found and cultivated in the Andes of South America. From the coca extract the two major forms of cocaine are crack cocaine and powdered cocaine.


Crack cocaine is the free-base from of the drug meaning it still in its crystalline structure making it possible to be melted down to be smoked.  Powdered cocaine can be dissolved into water or inhaled.

A major danger with cocaine is that it contains a lipophilic group, a hydrophilic group, and an aliphatic group. Meaning it can pass through polar and non-polar membranes, specifically the blood-brain barrier.

Cocaine Addiction 

Over time the reward-system established by frequent cocaine abuse causes damage to the dopamine pathway. This damage means that the pleasure experienced becomes diminished and for the person to experience the same high they must now increase their dosage. Increased cocaine dosage obviously increases the physiological and psychological effects of cocaine addiction.


Physiological and psychological effects of addiction:

  1. Mood swings
  2. High blood pressure
  3. Panic attacks
  4. Cognitive impairment
  5. Changes in personality
  6. Psychosis: including tactile hallucinations (“coke bugs” or formication)
  7. Paranoia
  8. Insomnia
  9. Tachycardia (increased heart rate)

Symptoms of cocaine withdrawal include:

  1. Depression
  2. Paranoia
  3. Exhaustion
  4. Mood swings
  5. Itching
  6. Anxiety
  7. Insomnia
  8. Craving

Cocaine Overdose and Treatment 

Due to the serious nature of the effects of cocaine abuse, cocaine overdose is common amongst users. The most common cause of death due to overdose is tachycardia, and is a result of the body weakening due to the drug rather than an a lethal dosage. As such, cocaine related deaths are frequently accidental. The increased heart rate elevates blood pressure to the point of  respiratory failure, stroke, cerebral hemorrhage, or heart-failure.


Unfortunately, even when a person overdosing is brought to an emergency room not much can be done except treat the symptoms. As of right now there is no antidote for cocaine. However, it is still important that these symptoms are treated as it may be able to prevent the above listed causes of cocaine-related deaths.

The symptoms to look for include:

  1. Nausea
  2. Chest pain
  3. Increased heart rate
  4. Fever
  5. Tremors
  6. Vomiting
  7. Seizures
  8. Paranoia
  9. Hallucinations
  10. Delirium


Thank you for reading! Please comment with any drug you would like to learn about next.


“Cocaine Overdose Symptoms and Treatment.” Cocaine Overdose Symptoms, Signs, and Treatment. Project Know, 2013. Web. 16 Aug. 2013. <http://www.projectknow.com/research/cocaine-overdose/&gt;.

“Cocaine Use and Its Effects.” WebMD. WebMD, n.d. Web. 16 Aug. 2013. <http://www.webmd.com/mental-health/cocaine-use-and-its-effects&gt;.

“DrugFacts: Cocaine.” National Institute on Drug Abuse. NIH…Turning Discovery Into Health®, Apr. 2013. Web. 16 Aug. 2013. <http://www.drugabuse.gov/publications/drugfacts/cocaine&gt;


Depression: Symptoms, Aetiology and Treatment Options


Depression is a serious affective disorder that affects millions of people in the world, approximately 5% of the population. In the United States alone approximately 33 million people will suffer from depression at some point in their life (Bear, 2007). In addition, the disorder is the leading cause of suicide. Despite its high prevalence, however, stigma still also remains high. A primary reason for the stigma surrounding any mental disorder is a misunderstanding of the symptoms and causes.


Even though depression strikes people differently, the cardinal symptoms are lowered mood and feelings of dejection, a lack of pleasure or interest rather than sadness. Accompanying symptoms include changes in appetite, fatigue, insomnia or hypersomnia, diminished concentration, feelings of worthlessness and/or guilt and recurrent thoughts of death and/or suicide (Bear, 2007). Depression can be one half of bipolar disorder but also occur on its own and in varying degrees of severity. Usually, for a diagnosis of major depression, the cardinal symptoms of depression must be present every day for approximately 2 weeks. Importantly, the cause of depression cannot be linked to a bereavement. This clear distinction is what separates depression from sadness.

Types of depression include chronic depression of dysthymia, major or clinical depression, atypical depression and manic depression. Chronic depression or dysthymia is usually less severe than major or clinical depression; however, it can be more disabling in that the symptoms are long-term (2 years+) or recurrent throughout a lifetime. Major or clinical depression is more severe; however, the symptoms do not last longer than 2 years and is not typically recurrent. Approximately 17% of sufferers have chronic symptoms.  It is important to note, however, that when depression is left untreated, recurrence is far more likely. Manic depression is found in bipolar disorder, to find out more click here. Finally, atypical depression is when a person suffers from the accompanying symptoms rather than the cardinal symptoms.

Aetiology and Treatment Options 

Biological basis 

Affective or mood disorders such as depression alter the typical function of the brain. Many different parts of the brain are usually affected at the same time, but the major system involved is the hypothalamic-pituitary-adrenal system (HPA). Exaggerated activity in the HPA system is common in people with anxiety and affective disorders. Specific to depression, blood cortisol levels are heightened as is the concentration of corticotropin-releasing hormones (CRH) in the cerebrospinal fluid.

Monoamine hypothesis

The monoamine hypothesis of depression states that a deficit in monoamines causes mood disorders. Monoamines include serotonin and catecholamines (inc. dopamine, noradrenaline, norepinephrine).  Current anti-depressants focus on this theory of depression. Anti-depressants inhibit the re-uptake of of monoamines, increasing the concentration of them in the synaptic cleft. The great benefit of anti-depressants is that they promote long-term, adaptive changes in the brain reducing the possibility of another depressive episode. Unfortunately, not all depressed people find anti-depressants effective. This can mean that either the treatment does not work for them at all or they require a greater dosage. Furthermore, it can takes week for depressants to take affect. Lastly, anti-depressants can raise levels of norepinephrine, which makes anti-depressants less effective. As anti-depressants are not always effective,  patients with prolonged depressive episodes may seek alternative treatment. Electroconvulsive therapy (ECT) and therapy are both options. ECT is mainly used in extreme cases because it can offer immediate relief. However, ECT is controversial due to the danger of memory loss. This is not surprising considering ECT is a localised seizure controlled by keeping the patient under anaesthesia. It is unknown exactly how ECT works; however, the hippocampus has been implicated. The hippocampus is involved in regulating CRH levels and the HPA system.

Types of anti-depressants include: selective serotonin re-uptake inhibitors, serotonin-noradrenaline re-uptake inhibitors, tricyclic anti-depressants and monoamine oxidase inhibitors. For people with bipolar disorder, lithium is also used to stabilise mood primarily the mania but has been shown stabilise mood overall.

Diathesis-Stress hypothesis 

The diathesis-stress hypothesis proposes that mental disorders have a genetic component that predisposes us to mental illness. Certain life stressors then makes us susceptible to mental illness actually presenting themselves. As such, traumatic childhoods full of abuse and/or neglect can leave a child at high risk for developing mental disorders. Tragically, children whose poor treatment is due to mentally ill caregivers, this cycle becomes hard to break. However, according to the diathesis-stress model, a trigger is not enough to bring forth mental illness without a genetic foundation. This genetic foundation goes hand in hand with the HPA system. Of course this does not mean that only traumatised children will suffer from mental health disorders. Individuals that have experienced a highly stressful life even such as divorce, moving away from home, changing schools, becoming ill, etc. will also be at risk are they predisposed to mental health issues.


In a healthy individual, cortisol activates hippocampal glucocorticoid receptors, which inhibit the the HPA system. However, in a depressed individual there is a flaw in the feedback system. On a molecular level there is a diminished hippocampal response to cortisol due to reduced number of  glucocorticoid receptors. Here the genetic component of depression comes into play; glucocorticoid receptors are the product of gene expression. Hence, an individual with few glucocorticoid receptors is more susceptible. Fittingly, the amount of glucocorticoid receptors are epigentically influenced, early sensory experience can alter the number as well. This means that a childhood where we are well looked after, loved, cared for, kept safe and happy can protect us from developing depression even if we disposed to at birth. This illustrates how important the interaction of nature and nurture is. Think Voldemort vs Harry Potter. Despite the traumatic death of his parents, the one year of unconditional love and Lily’s sacrifice protected him not just magically but neurologically. Interestingly, in an interview with Oprah Winfrey, JK Rowling discuss this exact point.



Antidepressants . (n.d.). Antidepressants. Retrieved July 18, 2014, from http://www.nhs.uk/conditions/Antidepressant-drugs/Pages/Introduction.aspx

Bear, M. F., Connors, B. W., & Paradiso, M. A. (Eds.). (2007). Neuroscience(Vol. 2). Lippincott Williams & Wilkins.

Pinel, J. P. (2010). Biopsychology (8th ed., International ed.). Harlow: Pearson Education.

What the Heck is an HPA Axis & What Does it Have to do with Stress?. (n.d.). About.com Fibromyalgia & Chronic Fatigue. Retrieved July 18, 2014, from http://chronicfatigue.about.com/od/cfsglossary/g/hpa_axis.htm

Bipolar Disorder

My most recent post showcased the artist Isti Kaldor who has bipolar disorder. This post will explain the basics of the disorder. Quite a few celebrities have come forward stating they have bipolar disorder including Catherine Zeta Jones, Demi Lovato and Stephen Fry. If you want to know the true scope, there is a wikipedia page dedicated to celebrities known to have it. Despite their very public work lives, with our limited insight into their personal lives it is difficult to really know much about the disorder. Stephen Fry, however, did a brilliant documentary on his experiences dealing with his bipolar disorder called Stephen Fry: The Secret Life of the Manic Depressive, which is available in full on YouTube.

Symptoms and Types 

As the title says, bipolar disorder is sometimes also called manic depression, but bipolar disorder is its official name. Characterised as a recurrent mood disorder, it consists of repeated episodes of mania interchanged with episodes of depression. The depressive episodes include similar but less severe symptoms of major depression such as changes in appetite, insomnia or hypersomnia, fatigue, feelings of worthlessness, guilt, inability to concentrate and suicidal thoughts. As such, the symptoms can be managed with anti-depressants. The manic periods, however, are the opposite in some respects. Symptoms consist of grandiosity, decreased need for sleep, talkativeness, flight of ideas, short attention span, and impaired judgement. It is believed that the correlation between bipolar disorder and celebrities is that those with the disorder usually experience these manic highs with bursts of creativity and inspiration. Unfortunately, the manic period can also result in promiscuity and complete loss of inhibition much like the effects of alcohol. As with any disorder, the range and complexity of symptoms varies greatly from person to person.

Bipolar comes in two general forms: type I and type II. Type I is marked by manic episodes (with or without incidents of major depression), and occurs in about 1% of the population, equally among men and women. Type II is marked by hypomania (milder form of mania that is not associated with marked impairments in judgment of performance) and is always followed by milder depressive periods.


Numerous twin studies and most notably the one conducted by McGuffin and colleagues (2003) have shown that there is a high concordance between monozygotic twins with “67% MZ vs. 19% DZ.” Also, even though there is a high correlation with depression and mania, the manic component appears to be significantly more heritable in monozygotic twins. We do know that bipolar disorder affects our neurochemical pathways as treatment of lithium and anti-depressants do help alleviate the drastic mood swings. However, the actual structural component is yet to be properly determined. Studies by Bearden et al., 2001 admit that even though “dysfunction is implicated in bipolar illness patients supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions” there is still not enough conclusive evidence to draw a clear link between right hemisphere dysfunction and bipolar disorder.

Strakowski et al., 2005 on the other hand using MRIs have found compelling examples of damage to the prefrontal cortical areas, striatum and amygdala that predates that onset of symptoms, which suggests that abnormal brain structure could in fact play a quintessential role in onset of the disease. Furthermore, if further studies can confirm these findings, it could offer psychiatrists and neurologists a revolutionary way of pre-symptomatic diagnosis. As of 2012, Strakowski et al. have reached a “general consensus” that bipolar type I occurs due to abnormalities within networks that control emotional behaviour such as the prefrontal cortex and limbic area, specifically the amygdala.


To date the most effective treatments for bipolar disorder include lithium (used to target the manic episodes), anti-depressants such as SSRIs, monoamine oxidase and tricyclics. Other types of medication such as anti-anxieties and anti-psychotics are used in some cases depending on the severity of the symptoms. In addition to medication, therapy has also been proved to significantly reduce the psychological stress of the disorder.


Bear, Mark F., Barry W. Connors, and Michael Paradiso. Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. Print.

Bearden, C. E., Hoffman, K. M. and Cannon, T. D. (2001), The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disorders, 3: 106–150. doi: 10.1034/j.1399-5618.2001.030302.x

Malliaris, Yanni,. “1.7 Aetiology of Bipolar Disorder.” 1.7 Aetiology of Bipolar Disorder. BipolarLab.com, 20 Aug. 2010. Web. 03 Aug. 2013.

Strakowski, S. M., Adler, C. M., Almeida, J., Altshuler, L. L., Blumberg, H. P., Chang, K. D., DelBello, M. P., Frangou, S., McIntosh, A., Phillips, M. L., Sussman, J. E. and Townsend, J. D. (2012), The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disorders, 14: 313–325. doi: 10.1111/j.1399-5618.2012.01022.x