He went on to describe The Human Connectome Project, through which many teams of neuroscientists around the world are joining efforts to map the neural connections in the human brain, reminiscent of the large-scale initiative to sequence the entire human genome in 2003. His talk covered the basics on what a synapse is and the enormous number of potential applications of this mapping to understand and cure mental disorders. My jaw dropped. Today, three years later, the idea still amazes me, although I’ve grown a little more skeptical.

From genome to connectome

There is a big difference between understanding the synapse between two neurons and being able to say “I am my connectome.” Before exploring what the connectome is, and to what extent it can help us to understand the human mind, let’s go back for a moment to the predecessor that inspired “the connectome.”

A genome is the entire DNA sequence of an organism. In 2003, fifty years after Watson and Crick first described the double helix structure of DNA, the human genome was completely sequenced and all our genes were mapped through a collaborative international effort dubbed The Human Genome Project. Back then, we believed that we had found nature’s recipe for building a human being. Somebody might as well have said: “I am my genome.” But we are not our genomes. We are more than the combined genetic information from an egg and spermatozoid. From the moment we develop as an embryo and throughout all of our lives, the genetic information of our cells can be modified in response to environmental or external factors. These genes go on to code for proteins, and these proteins build all the cells of our bodies. By this theory, genes and their environmental modification should be enough to explain our physical constitution. However, our personalities, mental faculties, and emotions are a special combination of genes and environment and they represent a more complex system of specialized cellular structure, interaction, and function. This is where the connectome comes in.

Connecting with the connectome

Neurons are the cell type which “conduct” messages, allowing our central nervous system to function. A synapse is the place in which these “messages” pass from one nerve cell to another, in the form of electrical or chemical signals. This impulse transmission is the base of our central nervous system’s functions. This implies a difference between the brain and other organs of our body: brain function relies on not only the cellular processes of individual neurons, but also on the interaction between neurons which can be far from one another. These circuits of neurons are responsible for our capacity to move in and perceive the world. Our mental functions and identities depend on the connections between our neurons.

The term connectome, coined by Olaf Sporns at Indiana University’s Department of Psychological and Brain Sciences, was inspired by the sequencing of the genome. This term refers to the map of all the neural connections within the brain and nervous system. If we see the mind as a system for the flow of information, the connectome would be the circuitry that keeps this information moving. Interestingly, the connectome is the product of both genetic connection patterns and environmental effects which influence this initial circuitry. Although an important part of our brain’s connections is determined by genetics, our connectomes change over time through learning and experience.

Our brains are elastic: synapses are continuously created and eliminated according to use and experience, thus modifying the connectome. For instance, you have probably made new synapses while reading this article. If we believe that the mind emerges from the brain, and that it is in constant flux, we may also believe, like Seung, that the “connectome” is a determinant of who we are.

Explaining mental disorders

The connectome has been seen as a potential pathway to additional insight into mental disorders. When studying some psychiatric illnesses, we have to take into account that there are often no visible morphologic alterations in the brains of people with these conditions. However, the biological theories of many conditions including schizophrenia, bipolar disorder, eating disorders, and autism today include the concept of “disordered connectivity.”
In the words of Alan Evans , a professor of neurology at McGillmental disorders “arise from brain function disorganization.” Assessing brain function disorders has historically been difficult because “we didn’t have tools to observe the connectivity and organization of the entire brain as it changes through life.” With the boost in neuroimaging techniques in the last 20 years, this paradigm has changed. We now have machines to observe the structure and function of the brain in real time.

The Human Connectome Project aims to provide answers to these disorders. For instance, Evans uses a variety of neuroimaging techniques to study the brains of infants who have been diagnosed with and without a disorder in the autistic spectrum. Studying the ongoing wiring of infant brains is also important to understanding autism as we know that infancy is one of the most important developmental periods in which brain connections are being established, and one in which the brain is most plastic.

To date, the only connectome that has been completely mapped is that of C. elegans, a tiny worm from the nematode family; a team led by South African biologist and Nobel Laureate Sydney Brenner drew a wiring diagram of this organism’s nervous system. We know today that C. elegans has 302 neurons and about 7,000 neural connections. In contrast, the human brain has about 100 million neurons and the number of connections is astronomical. Mapping this number of connections is no easy task and the brain sections of the worm can obviously not be applied to the human being. Instead, through the use of new neuroimaging techniques, powerful data-analysis technologies, and the construction of open-source databases, the endeavour is starting to seem feasible. In addition, collaboration between international laboratories in the recent Human Connectome Project, funded by the National Institute of Health in the U.S., have some scientists believing that we may fulfill this goal much sooner than expected.

Are we our connectome?

While the idea of the connectome and Sebastian Seung’s TED talk still amazes me, I cannot help but question his claims that the connectome is the ultimate answer to understanding someone’s personality. Eventhough the circuitry of the nervous system is important, it is not the whole story. It is another example of focusing on the “where” things happen while forgetting the “how” a recurring weakness of neuroscience more broadly. The processes and the kind of information being conveyed by individual connections and groups of synapses are also fundamental. In the case of C. elegans, our tiny worm, mapping the entirety of its neural connections did not per se explain the whole repertoire of its behaviours. Rather, the diagram served as a starting point for generating hypotheses of functions for the mapped neural circuits, giving rise to many experiments that slowly began to explain the organism’s behaviour. Twenty-five years after the worm’s connectome was mapped, scientists now understand how it responds to temperature and mechanical stimulations, but they’re still using the connectivity diagram to conduct experiments, looking to advance our understanding of its nervous system and behaviour. If a nervous system composed of 302 neurons is so hard to understand, even with a full map of its connections, what can we expect of the human nervous system with its immense number of connections? The evidence points one way: We are not merely our connectomes. However, mapping our connectomes, in combination with other approaches to brain and mind functioning, seems a worthy endeavour to help us to explain who we are.

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In modern psychiatry, schizophrenia is viewed as a continuum, and belongs to a group of conditions called psychotic disorders. Psychosis, by which psychotic disorders are characterized, is a state in which one detaches from reality and experiences objectively false beliefs (delusions) and altered perceptions (hallucinations) that one believes to be the absolute truth. While going through psychosis, most people with schizophrenia will experience distressing emotions such as anger or uncontrollable fear due to the intensity or the content of psychosis. This can potentially lead them to engage in behaviours they would not normally do in a non-psychotic state. Other common symptoms are disorganized speech and catatonia, the apparent unresponsiveness to external stimuli and emotional flatness.

To be diagnosed with schizophrenia, the aforementioned symptoms have to be present for at least six months and cause significant distress, impairing the patient’s life. Due to the potential of severe effects on patients, doctors and researchers have long dedicated their efforts to try to find a clear cause of and thus a potential treatment for schizophrenia. So far, the only treatments we have are palliative – they treat the symptoms of psychosis, not schizophrenia per se, and have many potential adverse effects.

Nature or nurture?
Since the term was coined, the cause of schizophrenia has been the subject of heated debate. Some psychiatrists in the beginning of the 20th century, such as Bleuler and Carl Jung, believed there to be important sociological and environmental factors, while others such as the eugenicist Emil Kraepelin thought that the cause was solely genetic. This controversy still exists today, although the contemporary neuroscientific view of the disease considers both biological and environmental risk factors. The biological side considers genetics to be a predisposing factor that, when combined with environmental stresses, can trigger symptoms. With advances in genetics, neuroimaging, and molecular pathology, today most scientists and psychiatrists consider schizophrenia as a disorder of brain development. Genes influence the way our brains develop in utero, telling our neurons where and when to migrate to settle in their final spot in the central nervous system. Afterward, external factors like obstetric complications, perinatal incidents, urban residence, famines, and others sources of stress also contribute to this change in brain development and can affect our mental health.

Genes: where are we so far?
Genetics is a particularly appealing approach to diseases we do not understand completely, because it may shed light on causal biological mechanisms. Furthermore, in the case of schizophrenia, heritability is a clear trait of the disorder, as concordance rates of schizophrenia for monozygotic twins have been found to be about 40 to 50 per cent, and heritability – the probability of a child having the same condition as their parents – is estimated to be around 80 per cent. However, the link between particular genes and the disorder is hard to establish given that schizophrenia does not have any single defining symptom or sign, and no known diagnostic laboratory tests can identify it so far.

In 2014, the biggest GWAS to date compared the genomes of nearly [150,000] people, finding 128 gene variants associated with schizophrenia.

Genome-wide association studies (GWAS) – made possible by the Human Genome Project – look for markers of common variation across the human genome, and can compare people that are diagnosed with the disorder to those who are not. In 2014, the biggest GWAS to date compared the genomes of nearly 37,000 people with schizophrenia with more than 113,000 people without the disorder, finding 128 gene variants associated with this condition. This study reinforced two ideas: the role of genetics in the development of schizophrenia and the polygenic and complex nature of this role.

GWAS do not identify specific genes. Rather, they pinpoint bigger areas of the genome that contribute to risk. This kind of research has been useful in the past to detect causes for other complex diseases, such as diabetes or Crohn’s disease, but the lack of biological markers for mental illness futher complicates schizophrenia.

Synapses and genes
Finding genes that are associated with a disorder does not mean that we understand how they are implicated in its development. Nonetheless, this year, a team of scientists from the Broad Institute and Harvard Medical School participated in what could be a breakthrough in schizophrenia genetics. This team found the strongest association between a single gene and schizophrenia so far.

In previous GWAS, one of the genomic regions associated with schizophrenia was a region in our sixth chromosome. Each region has many genes. In this study, researchers decided to focus on a single gene within this region, the so-called C4 gene. In order to understand and corroborate what this gene does to our brain, the researchers conducted genetic experiments; comparing what would happen to mice that had this gene “blocked” (the so-called knockout mice).
We should not forget that the genome is like a recipe for building living machines: every gene codes for a protein with a specific function. C4 codifies two proteins localized in neurons. These proteins eliminate the synapses (neural connections) that are not needed during postnatal brain development. This process is called synaptic pruning. The greatest rate of synaptic pruning in humans, at least in the prefrontal cortex – which is important for executive processes, judgement, and decision making – happens during the teenage years. Our brain connections are constantly developing and are critical to becoming who we are. Synaptic pruning helps to eliminate those connections that are redundant or that we do not need.

The discovery of the C4 gene accounts for the first time that a single gene with a specific function in the brain has fit the biological theories of schizophrenia – which focus on brain development and maturation – as well as neuroimaging findings – which report neural connection patterns in patients – and with schizophrenia presentation – with symptoms beginning in the late teen years. These exciting results have led to many scientific articles claiming we may be closer to explaining schizophrenia.

However exciting these results may be, this is only one gene of the 128 that have been associated with the disease so far. Schizophrenia heritability is not monogenic, but a complex, polygenic disorder, the biology of which is far from being well understood. Furthermore, we should not forget that genetic risk assesses only one side of the disorder development model, and it happens to be the one factor we cannot change. At the same time that we develop research to advance our biological understanding of schizophrenia, we should also study the equally complex characteristics of environmental and other external factors involved. In the meantime, working on the development of better intervention strategies and building education campaigns to reduce stigma will assure a safer and more inclusive environment for people living with schizophrenia and other psychotic disorders.

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What is ALS

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s Disease, was first described by Jean-Martin Charcot – considered the founder of neurology – in a series of studies conducted between 1865 and 1869. ALS is a neurological disease that consists of progressive degeneration of motor neurons in the brain and spinal cord. Upper motor neurons reside in the cerebral cortexand brain stem, and use axons (the wires of the nervous system) to transmit signals to the spinal cord, where the lower motor neurons reside. From the spinal cord, the axons of lower motor neurons send electric impulses to different muscles in the body, allowing some muscular groups to contract and release for movement. ALS affects both upper and lower motor neurons, causing damage and neural death. When these neurons die, they leave voluntary muscles paralyzed. We use these types of muscles not only to move, but also to speak, eat, and breathe – thus patients with ALS suffer a loss of mobility, loss of speech and eventually loss of breathing  ability.

Even though there is pharmacological treatment to slow the diseaseís progression, there is still no known cure to this illness, almost 250 years since its first description. According to the ALS society of Canada, approximately 2,500 to 3,000 people in Canada are living with ALS; 1,000 will succumb to the disease and 1,000 will be newly diagnosed each year. It is a terminal disease with a lifespan after diagnosis of two to five years on average.

ALS awareness

ALS is commonly associated with Lou Gehrig – the deceased baseball player from whom the disease took its name – and the physicist, cosmologist, and science writer Stephen Hawking, who has shown an atypical course of his disease, surviving more than fifty years since the diagnosis. Last summer, millions of people started talking about ALS thanks to the “Ice Bucket Challenge,” which encouraged participants to film themselves while they had a bucket of ice water poured on their heads to raise awareness and funds for ALS research. The phenomenon quickly went viral on the internet, leading to more than 2.4 million tagged videos circulating Facebook, thrusting the disease into the foreground of public knowledge. In August, the ALS Association announced that their total donations since July 29 had exceeded $100 million. The ALS Association is just one of several ALS-related charities that have benefited from this awareness.

A breakthrough

In September 2015, a group of researchers from the U.S. National Institutes of Health (NIH) published an article in Science Translational Medicine titled “Human endogenous retrovirus-K contributes to motor neuron disease”, the findings indicate that a retrovirus could be implicated in the course of this mysterious disease.

In order to understand this, we must remember what viruses are: tiny infectious agents that are everywhere around us and inside us. They are considered “at the edge of life” because, despite having genes and evolving by natural selection, they cannot replicate on their own. They need the cell machinery of other species to replicate their genes and assemble their protective coats made of proteins, called capsids.

After infecting the cells of a bigger organism, viruses use cell organelles to build other viruses. Some types of viruses, such as retroviruses, will actually insert their genes in the host’s DNA in order to reproduce. Retroviruses are characterized by the presence of reverse transcriptase, an enzyme that allows them to insert copies of their genes into host chromosomes. Retroviruses are more prone to mutation than most viruses: one of the most common of these is the human immunodeficiency virus (HIV). HIV is the infectious cause of AIDS, which is treated with antiretroviral drugs that target reverse transcriptase enzymes. This is an example of an exogenous retrovirus, which means for infection to occur, transmision between humans must occur.

In contrast, endogenous retroviruses are remnants of ancient viruses that inserted their genes into human DNA long ago and persist through inheritance, generation to generation. This might sound surprising, but up to five per cent of the human genome consists of endogenous retrovirus genes. One of such viral gene sequences in our DNA is called human endogenous retrovirus-K (HERV-K), which  is the virus that scientists from  the NIH recently found to be related to ALS.

Retroviruses and ALS

Avindra Nath, the main investigator of the NIH group, started suspecting a link between a retrovirus and ALS after seeing a patient with AIDS and ALS whose neurological symptoms improved with antiretroviral drugs. This led Nath to look in the medical literature about ALS, where it was found that reverse transcriptase – the enzyme that characterizes retroviruses – had been found in the blood of ALS patients in various reports.

No exogenous retrovirus had been linked to ALS, so the researchers began looking into possible endogenous retroviral genes. When, in 2011, they finally found elevated levels of HERV-K in the brain tissue of 11 ALS deceased patients, they decided to test their hypothesis through more experiments. They found that the gene was present in cortical and spinal neurons of ALS patients,  but not in healthy controls. They also inserted these genes into cultured human neurons, causing damage and death. Furthermore, they found a way for mice to express HERV-K. These mice developed classic symptoms of ALS: muscle atrophy, progressive paralysis, and death. The strength of this evidence finally convinced the scientific community of a link between these viral genes and the development of ALS, although the exact link remains unclear.

The future of ALS

What does all this mean in terms of treatment or detection of the illness? There are two steps after this discovery. The first one focuses on  treatment: antiretroviral drugs similar to those used to treat HIV may be used in addition to the usual drug to slow the diseases progression. The second implication regards early diagnosis. If these sequences can be detected in patients’ DNA or blood, the retrovirus DNA could serve as a biomarker – a measurable indicator of the severity or presence of this disease – which could then lead to earlier intervention.

Although the “Ice Bucket Challenge” may have seemed silly, raising awareness for this disease and increasing funding for ALS research will surely continue to be fruitful in the future, guided by the light of this provocative discovery. However, we should never cast skepticism aside:  Nath admits that the increase of HERV-K in ALS patients could be the result of something else that’s causing the disease. As Raymond Roos, a neurologist at the University of Chicago, has pointed out, “a link does not imply causality.” Finding these associations doesn’t mean that the genes cause the disease, but rather that they can be implicated in the development of the disease, accelerating ALS.

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I will never forget the way those rats behaved after 36 straight hours of intense light exposure. In my eyes, food and water deprivation, isolation, and sudden tilting or wetting of the cages did not have as strong of an effect on their behaviour as the continuous light exposure. When I would come in to the lab to turn the lights off, I would find restless, aggressive rats, attacking each other and running desperately across their cages. Who would have thought that animals could be so vulnerable to changes in light?

Coming from Mexico City, where the seasonal change is almost nonexistent and the difference in daylight hours between summer and winter is less than three hours, my first November in Canada overwhelmed me.

I felt like one of these rats myself when I first arrived in Canada. Once the trees lost their beautiful autumn colours and the branches started waving naked toward the skies, dancing to the song of chilly winds, we all changed our clocks to wintertime. This meant that sunlight would be over at around 4:30 p.m.. Lights off in the middle of the afternoon. Coming from Mexico City, where the seasonal change is almost nonexistent and the difference in daylight hours between summer and winter is less than three hours, my first November in Canada overwhelmed me. After the time change, I would wake up with heavy feet; sleepiness would be my companion for the whole day. Coming home after work at 6 p.m., I would only feel like getting into my bed and letting the world around me disappear. It was as if the day was over as soon as the lights went off.

These bodily symptoms came with negative thoughts, sadness, and irritability. Everything in my life seemed darker, as if the lights in my brain had also been turned off. Obviously, the subsequent drops in temperature into the negative degrees did not help me feel better. I couldn’t fully understand this, seasonal change being a new phenomenon for me.
However, the sensations and feelings that I had that first November – that I wrote off as homesickness, loneliness, and consequences of my adaptation process – kept appearing in the following years when the days became shorter and colder. This group of symptoms, casually referred to as the “winter blues,” is called seasonal affective disorder (SAD). SAD is actually a type of depression that follows a seasonal pattern. This condition exists mostly in higher latitude countries, where there are more significant changes in daylight, temperature, and weather between seasons. According to the Centre for Addiction and Mental Health, up to 15 per cent of Canadians say they experience “winter blues” and 2 to 5 per cent suffer from severe symptoms and are actually diagnosed with SAD.

Susceptibility to SAD

Human beings, like all other mammals, have internal clocks that are sensitive to light. These internal clocks are groupings of interacting molecules in cells throughout the body. They are all coordinated by the suprachiasmatic nucleus – a “master-clock” – which is a group of neurons within the hypothalamus, located in the base of our brains. Our internal clocks generate circadian (daily) rhythms, internal endogenous (self-made) oscillations of about 24 hours that control behavioural patterns of sleep, appetite, as well as patterns of core body temperature, brain wave activity, and hormone production, among others.

Our complex biological clocks do not work on their own, but are rather modulated by the light-dark cycle. Daylight, perceived by the retina, inhibits the production of a hormone called melatonin, produced in the pineal gland. Melatonin is considered one of the main circadian hormones, because its production fits the 24-hour cycle. Its concentrations inform our body of the day-night cycle and thus help to adjust the internal biological clock. In this way, light acts as an external regulator of our circadian rhythms to help us adapt to our adapt to our environment – sleeping during the night and being awake during the day.
Considering this, it is understandable that not receiving daylight signals our bodies are used to may alter our circadian rhythms and have significant effects on our well-being. Several studies have shown that circadian cycles are more irregular in people that suffer from SAD than in people who don’t, deviating from the 24 hour-cycle, with hormones peaking at less predictable times. This is called the “phase-shift” phenomenon.

After my own experiences with SAD, I began to wonder: why are some people more vulnerable to changes in daylight and temperature? Is there a genetic predisposition to this disorder? Which population is more prone to this disorder and why? One possible explanation for is that the lack of sunlight leads to a failure in the production of the hormones we require to feel awake as well as an augmentation of the hormones like melatonin that make us feel tired and sluggish. This eventually leads to a disruption in our sleep-wake cycle and a tendency for low mood and depression. However, other factors may play a role, such as genetic predisposition to depression and the general vulnerability to mental health disorders.

Considering this, it is understandable that not receiving daylight signals our bodies are used to may alter our circadian rhythms and have significant effects on our wellbeing.

Some studies have looked at patterns of SAD in twins and families, revealing that there is a familial tendency to experience SAD. A study published in 2013 in the Journal of Affective Disorders explored SAD prevalence among the indigenous populations of Norway, Finland, Siberia, and Alaska. The research showed lower rates of SAD amongst these populations. It makes sense: residing at high northern latitudes for several generations may have adjusted the molecular mechanisms of their internal clocks, helping those groups to adapt to the reduced daylight of the Arctic Winter.

In 2002, the Norwegian Institute of Public Health conducted the Oslo Immigrants Health Study, and found that five immigrant groups that came from lower latitudes to Norway had a higher incidence of SAD than the native Norwegian and indigenous populations.

For those of us who must continue to grapple with this melancholic winter existence, there are certain ways to fight off the so-called winter blues. It could sound bizarre to say that sitting in front of a shiny box could help you with SAD – and no, I am not talking about your computer, but it works. Light therapy boxes, or phototherapy boxes are a special kind of lamp that have been proven effective in treating SAD. The therapy consists of sitting in front of the light box for 30 minutes to 2 hours – depending on the light intensity – to compensate for the lack of light on short winter days. Outside of these lamps, waking up early to catch some sun light, exercise, and the presence of plants can also help improve the mental health of those grappling with SAD. All in all, it is important that we who are dealing with SAD take care of ourselves, never ignoring symptoms that could be signs of decreasing mental health, and somehow find joy in this dark, depressing season.

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But how is it that normal reproductive function can have a consequence on mental health? Is there a clear mechanism that explains how hormones may impact nervous system functioning? Or is it more a question of a biased interpretation of normal bodily processes, the bias arising from physical discomfort and reinforced by the negative view society has on menstruation?

Do PMS and menstruation really affect our brains?

One widely held hypothesis focuses on possible effects of hormones on the nervous system, though it is not very well supported. This hypothesis suggests that severe PMS may be the result of altered activity or sensitivity of certain neurotransmitter systems, caused by changes in steroid hormone concentration.

Evidence cited by proponents of this hypothesis comes from mood changes related to pregnancy, delivery, menopause, and other physiological states in which hormones are shifting dramatically. Postpartum depression and the increased onset of anxiety disorders after menopause would act as examples of hormonal changes that have negative consequences for mental health.

There are issues with this hypothesis, however. We know that brain activity generates and directs the production of all hormones through the neuroendocrine system. This interaction between the nervous system – the brain – and the endocrine system involves different hormone-secreting glands in our bodies. However, this does not explain in any way how the balance between steroid hormones such as estrogen, progesterone, and testosterone can affect neurotransmitter function. So far, there is no evidence of clear molecular or cellular mechanisms to explain a hormonal influence on neurotransmission, nor a clear model of which hormonal profile contributes the most to positive or negative moods.

As a society, we should consider changing the way we view the normal female reproductive function, dropping the misleading notion that it is a “risk factor” for instability, anxiety, depression, and lack of mental control.

Scientists that side with the biological susceptibility hypothesis also claim that it is open to non-biological factors, explaining that the neuroendocrine process related to female reproduction is also vulnerable to changes in psychosocial, environmental, and physiological spheres. But the question remains: why are only female reproductive hormones – and not any of the other axes of the endocrine system – causing these impacts on emotional states?

The bias in our approach to PMS and menstruation

To assess the strength of scientific evidence in support of a well-defined PMS, researchers at the University of Toronto conducted a literature review in 2012 that examined more than 47 scientific studies on the daily reported moods in people who do not look for medical assistance to solve their period-related issues. Surprisingly, the majority of subjects did not regularly experience premenstrual negative moods. Adding to a previous study done by the same group in the same year that failed to find a clear relation between mood and specific hormone concentrations in saliva, blood, and urine, it may well be that the evidence we used to define the existence of mental health disturbances in PMS as a universal phenomenon could have been biased to begin with.

There are several factors that may have lead to bias in studies related to mental health and PMS. First, most of the information gathered about the syndrome comes from those who seek help and do not represent the general population of people who have periods. Also, the more than sixty instruments used to gather information on subject’s moods during the menstrual cycle ask mainly about experiences such as depression, anxiety, and irritability, placing much more emphasis on the negative experiences and thus limiting a complete description of premenstrual mood experiences.

The majority of subjects did not regularly experience premenstrual negative moods.

Interestingly, in 1994, a research group led by Joan Chrisler at Connecticut College created the Menstrual Joy Questionnaire (MJQ) to study how positive moods varied with the menstrual cycle in an attempt to shift the focus from negative phenomena only. Among the forty participants that responded to the questionnaire, about 75 per cent reacted with incredulity, surprise, or thought that the title was ironic – as if, to them, it was impossible to find joy in such a thing.

An interesting point to discuss is the definition that Antonio Damasio, a professor of neuroscience at the University of Southern California, gives for emotions. He explains that feelings arise from a conscious interpretation of purely physical signals of the body reacting to external and internal stimuli. In this case, negative emotions during both PMS and menstruation could arise from the physical discomfort caused by symptoms like bloating, water retention, breast tenderness, and menstrual cramps. To this is added the fact that menstruation is generally looked at in society as negative, even disgusting.

Overall, we find that the evidence for the biological susceptibility hypothesis is not convincing enough to explain a consistent change in neurotransmitters that repeats itself period after period, nor to believe that women’s negative mental states are largely determined by their hormones. However, whether it’s in the media, in the way we talk to each other, or in the way parents teach their children about menstruation, we as a society keep reinforcing this idea by associating the anger or sadness experienced during the menstrual period with hormones, or assuming women’s judgement may be blurred by PMS. Studies on those who do not have PMDD don’t show any consistent patterns of dysfunction due to negative premenstrual moods. So, with 75 per cent of the female population experiencing PMS, and without any evidence of an aberrant function of the hormonal system, should we keep thinking of it as a syndrome or disease? Or, is the idea that it is a well-established disorder misleadingly reinforcing our negative perception of normal body processes? It is true that, for those with PMDD, the symptoms associated with the last phase of the cycle may be a cause of distress and may require medical attention. When people do experience mental and physical health issues as a result of PMDD, it is important we take this seriously, and not write it off as, “Oh, it’s just because of your period, suck it up.” But, among those who have periods and do not suffer from PMDD, menstruation need not continue to be seen as a negative phenomenon that could lead to neurological impairment, such as irrational emotionality, as the science simply does not support this.

We cannot deny the highly negative images of menstrual function that still prevail, or the negative side effects of this experience. I have personally experienced discomfort and mood changes at the onset of my period on many occasions. However, given the evidence, I realize the source of these experiences may not be as clear or well-defined as I thought it was. As a society, we should consider changing the way we view the normal female reproductive function, dropping the misleading notion that it is a “risk factor” for instability, anxiety, depression, and lack of mental control. This may not only help people endure their mood changes during their cycle as something normal, but may be the first step toward avoiding the long prevailing negative image of female sexual physiology.

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Logically, this should make sense; you focus all your attention on your goal until, suddenly, there you are: you have succeeded, and thus you will feel happy and free. But the truth is that things do not necessarily happen in this order. After a 12-hour rush in which you force yourself to sit down and do some work, you realize that your strategy was flawed. Stressed and overwhelmed, you find yourself absolutely deprived of ideas, despite your best efforts to dedicate yourself to the given task. Instead of helping you to become more concentrated and mentally sharp, denying yourself pleasure may actually be detrimental for your productivity and motivation.

Several studies have reported on the importance of well-being and happiness to remain motivated, and thus achieve everyday duties. One study published recently in the Journal of Occupational and Environmental Medicine reported that it would be possible for an organization to increase workplace productivity by almost 50 per cent if it addressed certain mental-health related issues, such as unnoticed depression among coworkers. Many books have been written on the strategies, habits, and tools that enable people to work harder and better. However, many of them cannot answer a fundamental question that can be assessed through neuroscience: what exactly is motivation in biological terms? What generates this disposition to do things in terms of the brain, and what mechanisms does it imply?

Our brains have developed a system that adjusts our actions according to biological needs, and this is what orchestrates our behaviour. This system, which consists of an ensemble of neural centers that respond mainly to two neurotransmitters – dopamine and serotonin – is known as the “brain-reward system.” Connected to areas that control memory and behaviour, this complex neural circuitry assesses the potential benefit of every future behaviour, obtaining those that anticipate rewards.

The main goal of the system is to detect rewarding stimuli, which have also been called “reinforcements.” From an evolutionary perspective, this system helps organisms to evaluate different plans of action to guide the body toward those that will give them “primary reinforcements” – for example, food, water, or sex – that will help them survive. By releasing dopamine – which is associated with feelings of pleasure – the system will strengthen the neural connections needed first to activate the behaviours that procure such rewards, and, second, to establish memories of which activities gave us such reinforcements.

Under this view, the reward systems is responsible for goal selection by weighing anticipated risks, costs, and benefits. In other words, motivational states will arise from an anticipation of pleasure.

How does this apply to our everyday productivity? In an ideal situation, the work we have to do would be rewarding enough to keep us motivated and productive. However, this may not always be the case. External pressure, such as a heavy workload or difficult tasks may generate stress, another physiological reaction that our brains identify with aversive stimuli, that threaten our integrity, and thus, should be avoided. Taking this into account, feeling motivated to do something that does not reward us and makes us feel stressed might almost constitute a biological contradiction. Through reinforcements, the brain associates certain behaviours with positive outcomes, and in their absence, our brain won’t do anything to ensure that we will repeat those behaviours in the future. It is illogical that we expect to accomplish our tasks in an efficient way if we force ourselves to avoid pleasure for the sake of the completion of a job and render our only motivation the reward that remains out of reach until the work is done.

Instead of doing this, we could try to take advantage of this neural system that guides our brains toward evolution. Intercalating moments of pleasure into our work schedules could boost our dopamine release levels and activate our reward system, taking us out of the automated state in which we enter as a result of exhaustion, and benefiting our productivity. Some techniques suggest that we take breaks after sprints of productivity – for example, the Pomodoro technique suggests five minutes of rest after every 25 minutes of uninterrupted hard work. When it comes to organization, building a schedule that implies both work periods and leisure time may help to keep our minds sharp during the time we dedicate to our duties, instead of forcing ourselves on them until we have no energy left.

These days, especially in a university setting, the prevalent mentality tells us that success and proactivity must take priority over one’s own pleasure and happiness. At the same time, we pertain to a generation that is used to immediate reward, a phenomenon that has been potentiated by technological devices that give us tangible results right away. While the idea of success over self-care can lead us to believe that we need success and results in order to be happy, our expectation of immediate rewards will lead to inevitable frustration and lack of motivation after long periods of working without positive reinforcements. Maybe we should change our minds and stop seeing pleasure as mere distraction, and instead start seeing it as fuel that will boost our way into success.

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Soon after, Jeffrey Lieberman, the former president of the American Psychiatric Association (APA), published a response in Medscape titled “What Does the New York Times Have Against Psychiatry?” Lieberman argues that Luhrmann’s article is unscholarly, and ultimately misinformed. Although Lieberman admits that a wider perspective on mental illness is necessary, he questions the idea that an anthropologist should speak about the medical validity of psychiatric diagnosis. He claims that there is no room for an anthropologist’s opinions in medical specialties like cardiology or gastroenterology, and therefore asks why they should be taken to account in psychiatry.
Is Lieberman right? Has American psychiatry and its Diagnostic and Statistical Manual of Mental Disorders (DSM) succeeded when it comes to characterizing mental illness? Is the biological framework enough to explain mental disorders?

Most medical schools and many psychiatric programs do not include any courses in anthropology, social psychology, or cognitive science. Nor do they try to give students a background on the ancient inquiries of various disciplines that sought an understanding of what the mind is and its relation to the brain and nervous system – the so-called mind-body problem.

Deep down, I think we all know that unlike the functioning of a kidney or a lung, the biology and what we know of the function of the brain are still not enough to explain the mind.

When diagnosing a patient, many psychiatrists rely only on the APA guidelines, which are based only on the presence or absence of certain symptoms, ignoring the fact that that these manifestations do not only depend on biology but on the way patients interpret and understand their own symptoms, as well as on social and interpersonal processes. However, the DSM does not include remarks on the effect patients’ social and cultural contexts (such as their economic status, language, and faith) could have on their mental health.

Deep down, I think we all know that unlike the functioning of a kidney or a lung, the biology and what we know of the function of the brain are still not enough to explain the mind. A mere biological framework is often not enough to explain why cognitive processes deviate and lead to a disturbed mental life, and thus mere biological remedies cannot be enough as treatment.

In the fifties, the development of modern psychopharmacology brought the wonderful hope that people’s psychological suffering would be cured by the swallowing of a pill. Unfortunately, this has not been shown to be the case. It is true that many patients with psychosis acknowledge that their medications make these experiences less frequent, intense or distressing, and help them to go through the day. However, their lives are still often shattered by their alienation from society, and their readaptation to their social environment becomes an additional struggle. Overwhelmed with the enormous amount of work they have in hospitals, psychiatrists do not treat this part of patients’ experiences – social workers, psychologists, and others will often be the ones involved in a patient’s life after the initial prescription of their medications.

It is a huge mistake to disqualify what those in other disciplines may have to say about the mind.

We should also reconsider the arbitrary line society forges between psychiatric patients and so-called normal people. According to the World Health Organization, one in four people will suffer from an episode of mental illness during their lives. As long as these episodes do not disrupt the way a person functions in the world, they will not be classified as “crazy” by their doctors and by society and alienated as psychiatric patients often are. Let’s also consider that, besides suffering when dealing with mental health symptoms, psychiatric patients are told that they are abnormal, permanently ill beings because they may have to take medication for the rest of their lives if they want to be able to take part in society. This is not the case in other contexts, such as in spiritual groups in India in which psychotic experiences can even be considered as “illumination” and bring respect and admiration to people who experience them.

So, while it is true that presenting mental health problems as the product of chemical disturbances has led us a long way in the development of pharmacological compounds and has provided an interesting framework to study these conditions, this view alone has failed to be enough to treat and define mental disease. In fact, the disease rhetoric has contributed to the stigmatization of the population of people who are diagnosed with mental health issues, as it frames these people as being biologically abnormal and inferior.

There is no doubt regarding the importance of psychiatry, and of the fact that we need doctors to treat people whose minds have somehow turned against them. What I would like to question is the narrow vision expressed by Lieberman that argues that mental illness is merely biological and that nobody but medical specialists should authoritatively speak on it.

Humans are living beings immersed in a social and cultural context, and it is a huge mistake to disqualify what those in other disciplines may have to say about the mind. What psychologists, anthropologists, ethologists, philosophers, and even artists have to tell us about the mind and subjective experience represents a richness that will be lost if doctors remain self-righteous and unaware. As French physiologist Claude Bernard observed in the 19th century, a human being is more than just the sum of its parts.

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