Megan Barrett

I’m not going to lie, I do enjoy films like ‘Fight Club’ and ‘Me, Myself and Irene’, and I agree that ‘Dr Jekyll and Mr Hyde’ is a classic novel which should be read by all. But putting entertainment aside, presenting those with schizophrenia as violent individuals with split personalities does not help public understanding of the illness. Such widely believed misconceptions are only amplified further by the media. A prime example was the recent story in The DailyMail about a paranoid schizophrenic who murdered a young man. The paper nicknamed the perpetrator the ‘cannibal killer’; a catchy title which leaves no doubt in the reader’s mind that individuals with schizophrenia are a danger to others. But these views are both mistaken and highly damaging to the 21 million individuals living with schizophrenia around the world today. Hopefully the evidence presented here can go a little way towards dispelling these misconceptions.

Misconception number 1: people with schizophrenia have a split personality

The most common misconception about schizophrenia is that people with the illness have a split personality; that is, they may be their normal selves one minute and then seem like a completely different person the next. In a survey carried out by the National Alliance on Mental Illness (NAMI), 64% of Americans said that they share this belief.

However, what people are actually describing when they talk about a split personality is a condition known as dissociative identity disorder (DID; previously multiple personality disorder). People with DID generally present with around 13–15 different personalities and, in some cases, have even been known to have up to 100! Those with schizophrenia, on the other hand, tend to suffer from hallucinations and paranoia, often hearing voices or believing that someone is ‘out to get them’. The two conditions are very different and should not be confused.

Of course, this misunderstanding is not helped by fact that the term ‘schizophrenia’ means ‘split mind’ in Greek. The name was, however, coined a long time ago, before the symptoms of schizophrenia were properly understood. A significant number of experts in the illness now believe this term is inappropriate and agree that schizophrenia should be renamed.

Misconception number 2: all people with schizophrenia are violent

The belief that all people who suffer from schizophrenia are violent is another widely held misconception. Going back to NAMI’s survey, around 60% of Americans identified violent behaviour as a symptom of schizophrenia. Why is this the case?

Putting aside the obvious influence of films and media, there are studies which have found a correlation between mental illness and violence. Swanson, for instance, concluded in his 1994 study that those with a mental illness, including schizophrenia, were twice as likely to be violent as the general population. This correlation, however, could be explained by the presence of co-existing substance abuse, rather than the mental illness itself. In fact, only 7% of the individuals in the study who had a mental illness but did not use drugs had shown violent behaviour.

More recent investigations by Swanson (2002) and Elbogen (2009) further support the argument that factors other than mental illness may predispose an individual to violence. These studies found that, apart from substance abuse, factors associated with violence in the mentally ill included homelessness, physical abuse and unemployment. Mental illness alone was found to be unrelated to violence and those without any co-existing risk factors were no more likely to be violent than someone from the general population.

On the same topic, the belief that individuals with schizophrenia are violent towards others is not necessarily the case either. In fact, people with schizophrenia are more likely to hurt themselves than those around them, having an 8.5 fold higher suicide risk than the general population.

This is certainly not the first article hoping to dispel the misconceptions that people with schizophrenia are violent or have a split personality, nor will it be the last. But with popular films, such as ‘Fight Club’ and ‘Me, Myself and Irene’, and headline news stories reinforcing these misperceptions, it’s going to take a lot of work to change public view of schizophrenia. Perhaps the introduction of a new name could help dissociate schizophrenia from these stereotypical portrayals, allowing us to be entertained by stories like ‘Fight Club’ or ‘Dr Jekyll and Mr Hyde’, without letting them shape an inaccurate public perception of a mental illness.

Post by: Megan Barrett

We all feel a little ‘blue’ over the winter period. With the days getting shorter and cold setting in, it’s no wonder we find it harder to be our usual ‘perky’ selves. But for some people, this feeling is far more extreme. For those with seasonal affective disorder (or SAD for short), the winter months each year mean a period of significant depression, fatigue and a loss of interest in the activities they would usually enjoy.

Despite some ongoing cynicism, SAD is classified as a medical condition by the American Psychiatric Association – though the individual must already be diagnosed with a major depressive or bipolar disorder and should have experienced SAD symptoms for at least two consecutive years [1,2]. What is interesting about SAD, however, is that in contrast to the typical symptoms of depression, individuals with SAD often experience hypersomnia (an increased desire to sleep) rather than insomnia and a heightened rather than reduced appetite, resulting in weight gain [1,2].

So far there is no consensus as such on the causes of SAD but it is generally agreed that seasonal changes, primarily shorter light periods and lower levels of environmental light available, play a significant part. This is supported by the use of light therapy to successfully treat up to 70% of individuals with SAD [1]. But how does a lack of light translate into SAD?

One of the major theories relating light to SAD involves our circadian system, known more anecdotally as our ‘biological clock’. This system controls our daily (and seasonal) cycle, dictating when we feel alert and sleepy, when we get hungry, and being responsible for the onset of hibernation in certain (some may argue more sensible) animals. Our circadian system responds to environmental cues, principally light, using these signals to sync our body clocks to the outside world through the release of chemicals which indicate when it is most appropriate to eat, be active or sleep [3]. In individuals with SAD, this delicate and complex system is believed to be disrupted, leading these people to become ‘out of phase’ with their environment, upsetting their sleep and eating patterns and causing them to become depressed.

Much of the research behind the circadian theory to date has focused on melatonin, one of the key components of our circadian systems and the chemical responsible for making us sleepy. Under normal circumstances, our bodies release melatonin at night and stop in the morning in response to light. This allows us to sleep when it is most appropriate. In some people with SAD, however, this cycle appears to be out of sync, with melatonin being released either earlier or later than usual [4]. By normalising this release pattern using either light therapy or the administration of melatonin itself, it may be possible to relieve the symptoms of SAD, and a number of studies have been carried out which support this hypothesis [3,4].

A second theory linking light and SAD looks at the eyes, or more specifically the retinas, of people with SAD, suggesting a lower sensitivity of these structures to light. Under normal circumstances, our retinas increase their sensitivity in response to low light conditions, i.e. dark winter days. In individuals with SAD, however, this may not happen [2]. Studies designed to test retinal function by measuring the electrical response of the retina to light have found that the retinas of some people with SAD are less responsive to light in the winter compared to the summer and in relation to healthy controls, lending support to this theory [3,4].

The third and final theory we’ll discuss in this article involves a family of signalling chemicals found in our brains, known as monoamine neurotransmitters. Members of this family, namely serotonin and noradrenaline, are known to affect our mood, eating and sleeping habits, making it logical to suggest they may be involved in the biological basis of SAD [1]. They also appear to respond to light availability and time of year. Our serotonin levels, for instance, are higher in summer than winter [3,4]. In some people with SAD, levels of serotonin and noradrenaline seem to be lower than in healthy controls. Increasing these back to the norm using either light therapy or drugs which promote serotonin or norepinephrine production has been shown to improve mood in these individuals and relieve their SAD symptoms [3,4].

As is so often the case with medical conditions, particularly those involving our mental health, our understanding of the causes behind SAD is still somewhat hazy. However, irregular responses to low-light environments found in SAD sufferers, whether it be through abnormal melatonin production disturbing their circadian systems, less sensitive retinas, or atypical levels of neurotransmitters, does seem to be a major factor. Both time and further investigation are needed to understand fully the biological causes of SAD and improve therapy options. Nevertheless, for those suffering with this condition, rest assured there is light at the end of the tunnel (do excuse the pun).

Post by: Megan Barrett

References
Gupta A, Sharma P, Garg V, et al. Role of serotonin in seasonal affective disorder. Eur Med Pharmacol Sci 2013; 17: 49–55.
Roecklein K & Wong P. Seasonal affective disorder. In: Gellman M & Turner J (eds.). Encyclopedia of behavioural medicine. New York: Springer; 2013. p1722–4.
Danilenko K & Levitan R. Seasonal affective disorder. In: Schlaepfer T & Nemeroff (eds.). Handbook of Clinical Neurology, Vol. 106: Neurobiology of psychiatric disorders. 3rd series. Amsterdam: Elsevier; 2012. p279–90.
Rohan K, Roechlein K, Haaga K, et al. Biological and psychological mechanisms of seasonal affective disorder: a review and integration. Curr Psychiatry Rev 2009; 5: 37–47.

You’d be hard pushed nowadays to find anyone unaware of the “five-a-day” rule surrounding fruit and vegetables in our diets. Green vegetables, in particular, are associated with numerous health benefits, such as reduced risk of coronary heart disease.¹ Yet consuming enough of these foods on a daily basis can be hard, especially if you find greens like Brussels sprouts unpleasantly bitter. But why do some of us find these vegetables less palatable? And can anything help make sprouts more appetising? Scientists in the fields of genetics and food science (or bromatology) are working to find the answers.

We all carry a unique set of instructions within our genes, defining who and what we are. Our genes encode the protein building blocks that form our bodies, including protein receptors (or sensors) within our taste buds. These receptors interact with food passing through our mouths telling us how bitter, salty, sweet, sour or umami it tastes. A special group of genetically determined receptors, known as the TAS2R group, detect bitter tastes, meaning that our genes play a key role in determining how bitter our food tastes.

The genetics behind bitterness is complex, but scientists have established a common test to explain why some people experience certain foods as being more bitter than others. This test involves the TAS2R38 bitter taste receptors and two substances they detect, phenylthiocarbamine (PTC) and 6-n-propylthiouracil (PROP). In general, the functionality of a person’s TAS2R38 receptors determines to what degree they taste PTC or PROP as bitter, with people being divided into three groups: non-tasters with non-functional TAS2R38 receptors (PTC and PROP do not taste bitter), medium tasters (PTC and PROP taste slightly bitter) and “super tasters” (PTC and PROP taste very bitter).^2,3 But what does this have to do with green vegetables?

In 2006, a lab group from Yale and Connecticut Universities set out to investigate PROP as a marker for bitterness in green vegetables (Brussels sprouts, kale and asparagus) and whether this related to peoples’ intake and preference. 110 individuals were asked to rate these vegetables, along with PROP, for bitterness and likability whilst also being asked to complete a questionnaire regarding their daily diet.

Interestingly, the results showed that people who tasted PROP as most bitter (i.e. super tasters) also found the green vegetables very bitter, inferring PROP could be a marker of bitterness for this food group as well and suggesting TAS2R38 receptors may be involved in green vegetables’ bitterness.² These people also tended to dislike greens more and eat less of them, suggesting a strong (and logical) relationship between a food’s bitterness and a lack of it in one’s diet. Thus, it seems for super tasters our genetic predisposition to produce functional TAS2R38 receptors may be working against us getting our five a day; making us find green vegetables bitter and unpalatable.

But all is not lost! Food scientists are now working on a solution to the super taster’s quandary. Mastaneh Sharafi and colleagues from the Allied Health Sciences Department at Connecticut University recently investigated the use of additives (aspartame, sodium chloride and sodium acetate) in a pilot study aimed at reducing or ‘masking’ green vegetables’ bitterness. Sharafi began by grouping 37 participants into non-, medium and super taster groups using PROP. They were then asked to rate plain and bitter green vegetables (asparagus, Brussel sprouts and kale), served together with one of the above masking agents, for likability.

To the researchers surprise, it seemed the masking agent’s effectiveness differed depending on both the vegetable and whether participants were non-, medium or super tasters. For super tasters, for instance, the two salt solutions reduced bitterness in asparagus but not sprouts or kale. Aspartame decreased bitterness across all the vegetables for super and medium tasters but had no effect for non-tasters. Participants with a significant dislike of greens and subsequent lack of these in their diets, reported improved likability with aspartame, suggesting masking agents could be useful to increasing green vegetable intake in disinclined individuals.³

So, it appears green veg haters can take some comfort in knowing that their dislike of sprouts is more likely due to their genetics than a desire to be difficult at dinnertime. And that masking these unpleasantly bitter tastes may hold the key to a palatable and balanced diet. Shafari’s small, yet noteworthy experiment certainly shows good prospects for aspartame and salt-based masking additives, but further work is still needed before us super tasters can comfortably achieve our “five-a-day”.

Post by: Megan Barrett

Megan is currently working as an associate writer at a medical communication company. You can follow her on Twitter @Meg_an12.

1. Drewnowski A, Gomez-Carneros C. 2000. Bitter taste, phytonutrients, and the consumer: a review. Am J Clin Nutr. 72(6): 1424-35. http://www.ncbi.nlm.nih.gov/pubmed/11101467
2. Dinehart M, Hayes J, Bartoshuk L, et al. 2006. Bitter taste markers explain variability in vegetable sweetness, bitterness, and intake. Physiol Behav. 87(2): 304-13. http://www.ncbi.nlm.nih.gov/pubmed/16368118
3. Sharafi M, Hayes J, Duffy V. 2013. Masking vegetable bitterness to improve palatability depends on vegetable type and taste phenotype. Chem. Percept. 6:8-19. http://link.springer.com/10.1007/s12078-012-9137-5

Stem cell researchers have been exploring ways of converting human body cells into neural cells specific to dopamine, an important chemical in the brain. Now it seems they may have found one mix of factors that stimulates this conversion directly. It is hoped that one day such cells may be suitable to replace neurons lost through neurodegeneration in Parkinson’s disease (PD).

PD is becoming a growing threat to today’s aging population, with 127,000 people living with this disease in the UK alone. Characterised by the progressive deterioration of dopamine neurons in an area of the brain called the substantia nigra, patients with PD suffer from debilitating movement difficulties that worsen over time. With no cure known and only a few drugs- e.g. levadopa, a dopamine source – to manage patient symptoms, stem cell research has offered a promising new platform towards finding an effective PD treatment.

Numerous studies so far have shown successful generation of dopamine neurons by reprogramming existing donor cells, using specific proteins called transcription factors. When transplanted into rodent and primate models of Parkinson’s disease, these neurons can help alleviate symptoms.

Unfortunately, the two donor cell types suggested for cell conversion until now face various issues. Embryonic stem cell (ESC) use is ethically controversial, while manipulating mature cells- for instance, fibroblasts – to dedifferentiate first to become induced pluripotent stem cells (iPSCs) is time consuming and expensive.

One potential solution? – Cut out the middle men (the iPSCs).

Xinjian Liu and his team at the Radiation Oncology department at Colorado University, have been working to generate dopamine neurons directly from human fibroblasts, without producing iPSCs first.  And it seems they may have identified a suitable combination of transcription factors that makes this happen.

Liu’s group applied transcription factors, Mash1, Ngn2, Sox2, Nurr1 and Pitx3 to human fibroblasts, and found that dopamine neuron-like cells were produced directly. These cells stained positive for dopamine neuron-specific markers and took up and released radioactively-labelled dopamine, just as the control dopamine neurons. When transplanted into rat PD models, the rats’ symptoms improved, with the animals’ rotational behaviour (a measure for their motor abilities) recovering.

Of course, the reality of generating new dopamine neurons that successfully transplant into patients with PD is still far from becoming a viable clinical treatment. Nevertheless, the discovery that Liu’s mix of transcription factors is sufficient to reprogram already mature cells directly into dopamine neuron-like cells presents an exciting step forward towards treating this devastating disorder.

Post by Megan Barrett

Reference: Cell Research, DOI: 10.1038/cr.2011.181

Megan is currently working as an associate writer at a medical communication company. You can follow her on Twitter @Meg_an12.

With 2012 being the year of the Olympics, many of us will have noticed the various campaigns pushing us to get out and get fit. We receive regular updates on the benefits of exercise to our health and have become increasingly familiar with phrases like ‘30 minutes a day’ and ‘at least 3 times a week.’ Now, there is growing evidence to suggest that regular physical activity may also benefit Multiple Sclerosis (MS) sufferers – lessening their fatigue, aiding walking mobility and improving their quality of life.

MS is one of the most common neurological disorders affecting young adults today. Approximately 250 million people from around the world currently suffer from this disease; including some well-known faces from the Olympic sporting community itself. Some may recall the 4-times Olympic Gold medallist, Betty Cuthbert for instance, who was diagnosed with MS back in her thirties.

MS is a chronic autoimmune disease, where the bodies own immune system targets and damages the sufferers nervous tissue. The disease specifically targets the fatty covering which surrounds most nerve fibres (called myelin). Myelin is necessary for nerve cells to communicate efficiently over long distances, meaning that nerve fibres of MS sufferers are significantly less efficient at sending messages around the body. As a result, MS sufferers present with a range of symptoms, depending on where the damage is located, including fatigue, muscle weakness and reduced mobility.

Quite understandably, MS sufferers therefore tend to be less active than the general population. Approximately 75-95% of patients with MS report fatigue as their most common symptom, with at least half of suffers classifying it as being the most troublesome. To date no medicines have been approved by drug licensing bodies to treat MS-related fatigue. A number of studies trialling exercise therapy in MS sufferers, however, have yielded promising results…

A few years back in 2009, two independent research groups reviewed the use of physical activity to treat MS-associated fatigue and mobility problems. Maria Garrett and Susan Coote, based at Limerick University’s department of Physiotherapy, reviewed 19 related studies which took place between 2004 and 2008. Whilst Robert Motl and Erin Snook from the University of Illinois, drew evidence from 22 further studies spanning a period of more than 40 years. The type of exercise both groups were interested in consisted of regular and supervised exercise regimes which progressed in intensity over several weeks.

Crucially, the main conclusions that both Garrett’s and Motl’s groups drew from their assessments were that formal exercise programmes can have a positive impact on fatigue and walking mobility in patients with MS. In addition, no harmful effects or exacerbation to symptoms were seen in any of the studies, and patients generally felt their quality of life was improved by the therapy.

Despite a few limitations (such as small sample size), which may have biased the studies, both research groups believed that there was sufficient merit in these findings to justify further research into the area. In their discussions, Garrett and Motl both recommend the development of longer, larger and more controlled trials involving the use of exercise therapy on patients with MS. Unfortunately, while it seems this research may be well worth carrying out, no such studies have yet appeared.

However, just this year Robert Motl from the University of Illinois headed a pilot study on exercise intervention for MS. This research, published in the March 2012 edition of the Journal of Neurologic Physical Therapy, investigated the effects of an 8-week exercise programme on 13 patients with MS. This regime involved a mixture of aerobic, resistance and balance-based exercises supervised by an experienced physiotherapist. Promisingly, all the patients involved in this trial reported improvements in their walking mobility. Objective measures showing increased walking speeds also supported patient feedback. Looking at these results, one would certainly hope this trial will be a precursor to research on a larger scale.

So perhaps this year, MS sufferers could actually benefit from ‘jumping on the Olympic bandwagon’ to get active and exercise. After all, research so far has implied no harmful effects of using exercise therapy for patients with MS. Not to mention the small but promising number of trials, we have discussed here, which indicate that physical activity may in fact aid fatigue and walking mobility in suffers. Given such evidence, healthcare professionals may also look towards encouraging a change in the behaviour of their MS patients.

Meanwhile, I for one will certainly have my fingers crossed with the hope that Motl’s study is a sign that further and larger-scale research into this area is now on its way…

Post by: Megan Barrett