Suicide nation: What’s behind the need to numb and to seek a final escape?

Suicide rates in the U.S. have increased nearly 30 percent in less than 20 years, the Centers for Disease Control and Prevention reported June 7. These mind-numbing statistics were released the same week two very famous, successful and beloved people committed suicide – Kate Spade, a tremendous entrepreneur, trendsetter and fashion icon, and Anthony Bourdain, a distinguished chef and world traveler who took us on gastronomic journeys to all corners of the world through his TV shows.

Their tragic deaths, and others like them, have brought new awareness to the rapidly growing public health problem of suicide in the U.S. These deaths have renewed the country’s conversation about the scope of the problem. The sad truth is that suicide is the 10th leading cause of death among all Americans, and among youth and young adults, suicide is the third leading cause of death.

I believe it’s time for us to pause and to ask the question why? Why are the suicide rates increasing so fast? And, are the increasing suicide rates linked to the seeming increase in demand for drugs such as marijuana, opioids and psychiatric medicine? As a public health researcher and epidemiologist who has studied these issues for a long time, I think there may be deeper issues to explore.

Suicide: More than a mental health issue

Suicide prevention is usually focused on the individual and within the context of mental health illness, which is a very limited approach. Typically, suicide is described as an outcome of depression, anxiety and other mental health concerns including substance use. And, these should not be trivialized; these conditions can be debilitating and life-threatening and should receive treatment. (If you or someone you know need help, call the National Suicide Prevention Lifeline at 1-800-273-8255).

The fact that so many Americans have mental illnesses is critically important as 1 in 6 Americans takes a psychiatric drug, most commonly antidepressants, anxiety relievers and antipsychotics. In addition, more than 1 in 3 U.S. adults are also prescribed pain reliever for physical pain. And, physical pain substantially increases risk for suicide.

In our national discussion of this issue, we raise important questions about the potential failure of our mental health system, its infrastructure and the stigma around mental health diagnoses, substance use and treatment. We also talk about the treatment gap, meaning the difference between those who need treatment versus those who can access and get treatment.

These are all valid concerns and critically important to address, but they are only part of the problem. As the CDC pointed out in its report, more than half of the suicide deaths in the U.S. did not have a known diagnosed mental health condition. So, while there are many reasons for raising concerns about our fragmented mental health system, the treatment gap and associated factors, I don’t think it is sufficient to understand our increasing suicide rates. One needs to look more broadly at underlying factors to understand why the suicide rate is increasing so significantly.

Suicide and substance use

The CDC report noted that among those suicide deaths which had a toxicology test, nearly 80 percent had one or more substance in their system, with alcohol being the most common, followed by opioids, benzodiazepines, cocaine, amphetamines, marijuana and antidepressants. More troubling, “the mortality rate from drug poisoning, alcohol poisoning, and suicide increased by 52 percent between 2000 and 2014,” according to a separate report by Carsey Research. Perhaps that provides some insight into what may be driving the increase in suicide rates. Research shows that many suicide deaths are caused by a substance overdose, but alcohol and substance abuse and addiction are also key risk factors for suicide.

Overall in the U.S., illicit drug use has been increasing. Marijuana use in particular has increased rapidly and doubled in the last decade. Currently nearly 10 percent of adults use marijuana and a third of these users meet criteria for a substance use disorder. This increase in marijuana use may not be surprising given that 30 states and the District of Columbia now have some form of legalized marijuana, allowing millions of people to legally access and use the drug.

Opioid use is also increasing dramatically. Just last year, the U.S. declared the opioid epidemic a public health emergency. In 2016, 42,249 people in the U.S. died from an opioid overdose. That’s nearly as many as those who died from suicide that year. The current opioid epidemic, which comprises both prescription pain relievers as well as illicit drugs like heroin and synthetic opioids such as fentanyl, has raised alarms across the country. Isn’t it time that we ask why there is such high demand for these drugs?

Taken together, it seems that the majority of our U.S. population is currently under the influence of some form of psychoactive substance or drug, whether prescribed or not, or whether legally used or not, that changes brain function, mood, consciousness and behavior. And, let’s not forget alcohol in this context since 70 percent of U.S. adults drink alcohol, and more than 1 in 4 binge drink.

What drives the demand for these psychoactive substances? And can the increasing demand and prevalence of both illicit and licit substance help explain the rising rates of suicides?

Research that seeks to understand the reasons for prescription misuse finds that people who report misusing prescription drugs such as tranquilizers do it because they want to relax or relieve tension; those who misuse stimulants state they need to stay alert; and those who misuse sedatives state it helps with sleep.

I believe it’s also worth considering whether higher levels of stress are driving more Americans to take psychoactive substances and, in extreme cases, take their own lives. Last year, 8 in 10 U.S. adults reported feeling stressed during their day, and 44 percent reported that their stress levels had increased over the past five years. Most people state their stress is due to concerns about the future, money, work, the political climate, and violence and crime.

In addition to our high stress levels, it turns out that only about 1 in 3 Americans are happy.

This is happening as U.S. performance on a range of health and social measures has been deteriorating, which has led some to compare America to a developing country. Most other developed countries score better than we do on a range of quality of life indices and markers of health and longevity, including life expectancy, working conditions, mothers’ well-being, school performance, crime rates and violent death rates to mention a few. Could these factors explain our high stress levels and low levels of happiness?

It is not clear what exactly drives the demand for the psychoactive substances and what has driven the increase in suicides. But I think it’s worth speculating whether a perceived low quality of life for many Americans, marked by high stress and low levels of happiness, is contributing.

Americans stand out from people in other countries with respect to their focus on individualism. Americans believe that success is determined by our own control and that it is very important to work hard to get ahead in life. Perhaps it is this focus on our own achievements, successes and work culture that have created an environment that is no longer sustainable – it has become too stressful.

What other options do we have in a culture where we are also expected to solve our own problems? I believe that for many, the use of substances and suicides may tragically be the only available coping mechanism.

Digital mental health drug raises troubling questions

Moments after Neo eats the red pill in “The Matrix,” he touches a liquefied mirror that takes over his skin, penetrating the innards of his body with computer code. When I first learned about the controversial new digital drug Abilify MyCite, I thought of this famous scene and wondered what kinds of people were being remade through this new biotechnology.

Otsuka Pharmaceuticals and Proteus Digital Health won Food and Drug Administration approval to sell Abilify MyCite in late 2017. This drug contains a digital sensor embedded within the powerful antipsychotic drug Abilify, the brand name for aripiprazole, which is used to treat schizophrenia, bipolar disorder and major depressive disorder. The goal of the digital sensor is for doctors to monitor their patients’ intake of Abilify MyCite remotely and ensure that the patient is adhering to the correct drug dose and timing.

Pills with embedded sensors mark a new era in digital health and, I believe, herald the arrival of a new kind of digital cyborg identity, which sociologist Deborah Lupton defines as “the body that is enhanced, augmented or in other ways configured by its use of digital media technologies.” Drugs are cybernetic technologies in that we absorb pharmaceuticals through metabolic processes that biochemically recode our brains and bodies.

The figure of the cyborg helps us recognize the potential of digital health technologies for enhancing human health, while at the same time critique how the practices of digital health can work to coerce, marginalize or transform individual people and entire social groups. In my view, having pills that connect us to our doctor and pharmaceutical companies via an app is dehumanizing and reduces patients’ psychic lives to a digital readout.

The ethics of a digital pill

Digital mental health drug raises troubling questions
AbilifyMyCite

The sensor, made up of copper, magnesium and silicon, functions like a battery by releasing an electric signal when it has reached the acid in your stomach. The signal sends information about the date and time you took the pill, blood pressure, temperature and level of activity to an adhesive patch worn on the skin. The patch relays this data to your smartphone app, into which users can add their self-reported mental health data about how they are feeling. Users consent to allow their doctor and up to four other caretakers to view their digital pill data, which resides in a cloud-based system.

As a sociologist, I am concerned about the formation of new pharmaceutical persons who are digitally enhanced to be compliant with the profit motives of corporations and the directives of health providers and drug companies. While all sorts of technologies monitor patients’ bodies, this is the first pharmaceutical to do so. The fact that the drug is Abilify, which is prescribed to people who experience serious mental distress, should raise many ethical red flags.

These concerns are especially relevant because the patent for the original Abilify drug expired in 2016, and this new drug technology represents a potentially lucrative new product in the global pharmaceutical armory. Based on my research on the corporate development of new drug combinations for metabolic syndrome – a constellation of major risk factors for heart disease, stroke and diabetes – I think that the new digital version of Abilify represents what I call a “killer application” for mental illness. Killer apps are essentially about profiting from the hottest new technology; their effectiveness for health is determined not in the clinic but in the marketplace. My concern is that as a popular killer app, the company will be motivated to profit from the technology as much as possible, regardless of whether the drug actually improves health.

To sell their drugs as killer applications, corporations create a rhetoric about digital health as progressive, clinically effective and safe. The Abilify MyCite promotional video portrays the drug as a revolutionary method of doctor-patient communication that combines both objective and self-reported data. I believe this promissory rhetoric must be challenged in light of corporate ideologies that offer technological fixes for ensuring that patients take pharmaceuticals, or drug adherence, which is fundamentally a social and not a medical problem.

Digital mental health drug raises troubling questions
If your medicine had a chip embedded in it – that tracked and reported when you took it – would you be more likely to take it as the doctor prescribed? By haryigit/shutterstock.com

More human contact, not less

Nonadherence is described in medical literature as leading to poor health outcomes, increased mortality, invalidation of clinical trials and increased health costs. But, adherence is not simply a matter of taking a medication or not. Having the ability or desire to adhere to a medical plan also involves cultivating adequate levels of social and financial support, robust human communication between the doctor and patient, and sound health care beliefs. The digital pill offers the new possibility of distant and mediated interaction between doctors and patients, thereby decreasing the need for face-to-face communication. This means that patients will have fewer opportunities to tell their doctor why they do not adhere to a drug treatment plan.

Research exploring why patients deviate from treatment plans shows that many feel they have a lack of control over their medical lives and therefore reject elements of treatment as an act of defiance. Patients often express that they have negative experiences with drug dosages and side effects but lack sufficient means of communication with their doctor to articulate and resolve this problem.

Will Abilify MyCite really solve these problems? I seriously doubt it given the lack of medical evidence that digital pills actually increase adherence to drug regimens or that they can be used to change drug doses – a remarkable fact that is printed directly on the drug information insert in plain language.

As a society, we should be moving away from a technologically centered framework for treating mental health and toward one in which patients’ interests and agency are positioned at the center of care. This requires a more critical analysis of how the global pharmaceutical industry has taken over mental health care and what kinds of cyborg-like people they are trying to make through their products.

This article was written in full collaboration with Sophia Mara Ptacek.

Mind molding psychedelic drugs could treat depression, and other mental illnesses

It seems that psychedelics do more than simply alter perception. According to the latest research from my colleagues and me, they change the structures of neurons themselves.

My research group has been studying the effects of psychedelics on neuronal structure and function, and we found that these compounds cause neurons to grow. A lot. Many of these compounds are well-known and include lysergic acid diethylamide (LSD), psilocin (from magic mushrooms), N,N-dimethyltryptamine (DMT, from ayahuasca) and 3,4-methylenedioxymethamphetamine (MDMA, aka ecstasy).

These are among the most powerful drugs known to affect brain function, and our research shows that they can alter the structure of the brain as well. Changes in neuronal structure are important because they can impact how the brain is wired, and consequently, how we feel, think and behave.

Prior to our study, there were relatively few compounds known to have such drastic and rapid effects on neuronal structure. One of those compounds was ketamine – a dissociative anesthetic and quite possibly the best fast-acting antidepressant that we have available to us at the moment.

If you think of a neuron like a tree, then its dendrites would be the large branches, and its dendritic spines – which receive signals from other neurons – would be the small branches. Some of these small branches might have leaves, or synapses in the case of a neuron. In fact, neuroscientists often use terms like “arbor” and “pruning” much like a horticulturist would. When we grew neurons in a dish – which is not unlike growing a plant in a pot – and fed them psychedelic compounds, the neurons sprouted more dendritic branches, grew more dendritic spines, and formed more connections with neighboring neurons.

Mind molding psychedelic drugs could treat depression, and other mental illnesses
The rainbow-colored neuron was treated with LSD, while the purple neuron was the control. LSD altered the structure of the neuron, allowing it to grow more branches and develop a more complex structure. Calvin Ly and Joanne Ly, CC BY-ND

Rethinking depression

Thanks to studies on ketamine, slow-acting antidepressants and chronic stress models of depression, scientists now know that depression is not simply the result of a “chemical imbalance,” as pharmaceutical companies like to suggest. It is far more complicated and involves structural changes in key neural circuits that regulate emotion, anxiety, memory and reward.

One of the hallmarks of depression is the atrophy of neurons in the prefrontal cortex – a region of the brain that controls anxiety and regulates mood among other things. Basically, these branches and spines shrivel up, disconnecting from other neurons in the brain. One hypothesis for why ketamine is so effective is because it can rapidly regrow the arbors and spines of these critical neurons.

Like ketamine, psychedelics have shown promise in the clinic for treating neuropsychiatric diseases. The DMT-containing herbal tea known as ayahuasca produces fast-acting antidepressant effects within a day, psilocybin eases the anxiety of terminally ill cancer patients and MDMA can reduce fear in those suffering from post-traumatic stress disorder (PTSD). Our recent papers suggest the intriguing possibility that psychedelic compounds and ketamine might share a common therapeutic mechanism.

Psychedelics vs. psychoplastogens

Strictly speaking, a psychedelic is a “mind-manifesting” drug – a definition that’s open to interpretation. They tend to produce perceptual distortions or hallucinations by activating 5-HT2A receptors. Our research group has found that compounds typically regarded as psychedelics, like LSD and DMT, as well as those that are sometimes called psychedelics, like MDMA, and those that are not usually called psychedelics, like ketamine, are all capable of profoundly impacting neuronal structure.

Our group has coined the term “psychoplastogen” to refer to such compounds, and we believe that these molecules may hold the key to treating a wide variety of brain diseases.

Our studies on neurons grown in dishes, as well as experiments performed using fruit flies and rodents, have demonstrated that several psychoplastogens, including psychedelics and ketamine, encourage neurons to grow more branches and spines. It seems that all of these compounds work by activating mTOR – a key protein involved in cell growth.

The biochemical machinery that regulates mTOR activity is intricate. As we tease apart how psychedelics and other psychoplastogens turn on mTOR signaling, we might be able to engineer compounds that only produce the therapeutic effects on neuronal growth while bypassing pathways that lead to undesired hallucinations.

Mind molding psychedelic drugs could treat depression, and other mental illnesses
This figure shows the effects of three psychedelics and one control (VEH) on cortical neurons. These neurons were treated for 24 hours before being visualized using super-resolution microscopy. The colors represent proteins found in specific locations of the neuron. Orange protrusions from the purple dendrite indicate dendritic spines. Ly et al., CC BY-ND

The field has known for some time now that psychedelics can produce lasting positive effects on brain function, and it’s possible that these long-lasting changes result from the psychoplastogenic effects of these drugs. If true, this would suggest that psychoplastogens might be used to repair circuits that are damaged in mood and anxiety disorders.

Panacea or poison?

Many diseases, such as depression and anxiety disorders, are characterized by atrophy of dendritic branches and spines. Therefore, compounds capable of rapidly promoting dendritic growth, like psychedelics, have broad therapeutic potential. The number of papers demonstrating that psychedelics can produce therapeutic effects continues to grow every year.

However, we should temper our enthusiasm because we do not yet know all of the risks associated with using these drugs. For example, it’s possible that promoting neuronal growth during development could have negative consequences by interfering with the normal processes by which neural circuits are refined. We just don’t know, yet.

Similarly, it is unclear what effects psychoplastogens will have on the aging brain. It’s important to keep in mind that excessive mTOR activation is also associated with a number of diseases including autism spectrum disorder (ASD) and Alzheimer’s disease.

To me, it’s obvious that we need to understand how these powerful compounds affect the brain, in both positive and negative ways, if we hope to fully comprehend the fundamental laws governing how the nervous system works and how to fix it when it doesn’t.

Stress is bad for your body, but how? Studying piglets may shed light

Stress affects most of us to one degree or another, and that even includes animals. My lab studies early-life stress in pigs and how it impacts their health later in life, specifically in the gastrointestinal (GI) tract. Pigs, whose GI tracts are extremely similar to those of humans, may be one of the clearest windows we have into researching stress, disease, and new therapies and preventatives – both in livestock and people.

In my study of how stress makes humans and pigs vulnerable to disease, I have seen the profound impact that stress-related chemical substances, such as hormones and peptides, can have on a body’s tissues. I’m hopeful that our research in piglets could eventually lead to treatments for both people and animals designed to mitigate the adverse effects of stress on the GI health.

How stress can save your life

Not all stress is bad. When we perceive a threat, our hypothalamus – one of our most basic parts of the brain – kicks in to protect us by triggering what many recognize as the “fight or flight” response. It is a primal evolutionary response programmed in our brains to help us first survive and then restore us to a normal set point, or what feels like stability.

Stress is bad for your body, but how? Studying piglets may shed light
The stress response is essential to helping escape a dangerous situation, such as an attacking dog. Dmitri Ma/Shutterstock.com

What actually is happening has to do with something called the hypothalamic-pituitary-adrenal (HPA) axis, which is at the core of the stress response. During stress, the hypothalamus, a region in the brain, makes and sends out a chemical called corticotrophin-releasing factor, which signals for the pituitary gland to release another chemical, adrenocorticotrophic hormone.

This stimulates the adrenal gland to release adrenalin and cortisol. Adrenalin and cortisol, two of the most well-known stress hormones, power our bodies to react during the fight or flight response. They can heighten our response time in a fight. They can pump blood to our extremities when we flee. They can boost our immune system to protect against pathogens. That stress response gives us what we need to resolve the situation.

How stress can harm your life

Fortunately for many of us, we don’t have to deal with life-threatening situations on a regular basis. However, we still experience stress. This stress can be chronic, due to a specific situation or overall lifestyle.

But, our stress response is meant for short-term resolvable conflict. So, in a way, the stress response is misplaced in today’s world of enduring stressors. Danger comes when we experience repeated elevations of these stress hormones, or when we are exposed to too much of these stress hormones at a young age. Instead of physical threats, many of us experience psychosocial stress, which triggers a similar stress response but is often not resolvable.

For example, stress in the workplace, such as feeling overworked or undervalued, could be perceived as a threat and in turn activate the stress response. However, in these situations, the survival aspects of the stress response, such as increased heart rate and immune activation, is not effective in resolving this threat.

This results in continued production and higher levels of these stress chemicals in the body. They bind to target receptors in many organs, which can have profound effects on physiology and function.

Stress is bad for your body, but how? Studying piglets may shed light
Stress is particularly damaging to the developing brain. Mcimage/Shutterstock.com

High levels of stress are also especially harmful when they occur at a young age, when many of the body’s important stress regulatory systems – for example, the brain and nervous systems – are still developing. Exposure to stress in early life can alter the normal development and physiology of many organ systems, resulting in increased sensitivity to stress and lifelong health risks in offspring.

Also, a mother’s stress during pregnancy can be “transmitted” to the fetus, resulting in permanent changes to the stress response system and health in offspring.

This early-life stress can fuel a constant stress response inside the body. This can include inflammation, or increased activity of the immune system, or immune suppression as its new “normal.”

Inflammation and immune suppression are unpredictable and can manifest in many parts of our body, with different consequences. For example, stress and inflammation near blood vessels can cause blood vessels to constrict. This causes elevated blood pressure, which can lead to a slew of other conditions like coronary artery disease and heart attack.

Immune suppression can reduce the body’s ability to heal wounds and make it more susceptible to other pathogens. Inflammation and immune suppression can affect anything, including our mental health. Chronic stress can traffic immune cells into the brain, where they can cause neuroinflammation, which can affect our mood and fuel diseases like depression and anxiety.

Your GI tract and you

The GI tract is our largest interface with the outside world. If you think about it, your GI system is “outside” your body; it experiences many of the pathogens and other foreign entities with which we come into contact. If you unfolded your entire GI system, it would cover a tennis court. The GI system also contains just as many neurons as your spinal cord and houses the largest collection of immune cells in the body. A system of that size is as powerful as it is susceptible.

Chronic stress that affects your GI tract can manifest as abdominal pain, diarrhea or constipation and can lead to common diseases such as irritable bowel syndrome or inflammatory bowel disease.

Early-life stress is especially concerning; scientists only now are beginning to understand the long-term consequences. My research demonstrates the impacts of early-life stress on animal health and productivity, as well as human health. In pigs, this stress can result from early weaning and other management practices. In humans, it could be from physical or emotional trauma like abuse or neglect.

What we can learn from piglets

Pigs and humans have similar digestive tracts, making pigs an excellent model for human GI disease. My research team has demonstrated early stress in piglets results in GI symptoms (e.g. diarrhea, GI infections) that are remarkably similar to stress-related GI disorders in people: Irritable bowel syndrome, inflammatory bowel disease and food allergies are examples.

Through my lab’s research of piglets and early-life stress, we have been able to significantly lower the stress and GI disease that they experience through their life by eliminating individual early-life stressors.

Much of their stress is caused through early weaning, social change due to maternal separation and mixing with unfamiliar pigs. These pigs then experience a higher rate of gastrointestinal and respiratory diseases, as well as reduced growth performance and feed efficiency into adulthood.

We also learned that a particular type of immune cell, called the mast cell, becomes highly activated during stress, which in turn causes much of the stress-associated GI disease. By focusing on animal welfare and implementing new management practices to eliminate individual stressors or intervene therapeutically with mast cell blockers, we can lower the overall threshold of stress that the piglets experience.

This basic research could result in future breakthroughs regarding how we combat stress in humans. Maybe with more fundamental research in animal models, we can develop a therapy to help lessen the impact of bad stress on our bodies.

In the meantime, those of us experiencing stress can take action. If you experience a lot of stress on a daily basis, focus on what you can and cannot control, and then apply your energy to the things within your control while taking care of your body by eating properly, getting enough sleep, and maintaining some level of physical activity. Then, learn to cope with the things you cannot control through therapy, meditation and other stress management practices.

Bourdain, Spade suicides show how even those at the top can know the lows of depression


Bourdain, Spade suicides show how even those at the top can know the lows of depression
Anthony Bourdain in a July 17, 2017, photo at the screening of ‘An Inconvenient Sequel: Truth to Power.’ Evan Agostin/Invision/AP Photos

We struggle to comprehend the loss of Kate Spade and Anthony Bourdain. Sudden deaths are shocking. It’s doubly shocking when the deaths are by suicide. Sudden suicide by people who seemingly have it all: That’s a triple whammy.

Of course, as humans, we try to make sense of it all. We say depression and suicide can strike anyone. We cite U.S. statistics of a sharply rising toll of depression and suicide. We point out that what a person shows on the outside can mask deep pain on the inside.

These explanations are true as far as they go. They just don’t go very far. And they dodge the most nagging question: Shouldn’t having great money, fame, and power insulate a person from severe depression?

As a psychologist who spent years researching the origins of the contemporary depression epidemic and writing a book on that topic, my answer is no. While money can summon therapists, fame can bring admirers, and power can remove many mundane hardships, none of these resources turn off the fundamental psychological drivers of depression in Western societies.

Carrots and Camaros

A first driver goes by the fancy name of hedonic adaptation, which basically means that pleasures inevitably fade. This process flows from evolutionary imperatives to survive and reproduce. Bunnies are built to seek carrots. Pleasure rewards the bunny for finding the carrot. But the satisfaction cannot last. It’s only the end of pleasure and the promise of more that gets the bunny hopping off to find more carrots and ultimately to survive long enough to make more bunnies.

So, too, humans restlessly seek power, fame and money in a race to survive and reproduce. Intuitively, we think the pleasure of having a billion dollars, living in a castle, or having servants should never fade. In reality, all fade as reliably as a good carrot. The wealthy, famous and powerful may fight harder to stave off hedonic adaptation, but data show such efforts are basically futile. Whether you buy one fancy sports car, or 10 of them, any boost to mood quickly subsides.

The mirage of pleasure

Seeking rewards may be natural, but when it comes to the moods we want, millions seek a mirage. Hedonic adaptation cruelly mandates that intense pleasures will not last, at the same moment survey data show Westerners are seeking these states. Hence, there’s a yawning gap between what we want to feel and what we actually feel – a chronic dissatisfaction that breeds depression. In fact, there is evidence that the people who value happiness the most are actually the most depressed.

Are the famous, rich and powerful immune from unrealistic mood standards? No. If anything, people who have “everything” on paper should be even more tempted to ask the question “Why am I not happier?” and set out to grasp an unattainable mood.

Bourdain, Spade suicides show how even those at the top can know the lows of depression
Sharing images of blissful vacations and a nearly perfect life may be adding to feelings of failure or inadequacy, the author writes. NadyaEugene/Shutterstock.com

The widespread use of social media outlets like Facebook and Instagram may be adding social pressure not only to experience unrealistic mood states but also to project these mood states outwardly. The new psychological race to keep up with the Joneses is relentlessly documenting the bliss from fancy vacations, newly acquired possessions, and parties with friends, with the rest of life largely edited out. Perhaps not surprisingly, constantly referencing other people’s highlight reels on social media is associated with depression.

People with money, fame or power cannot easily avoid being swept up in the process of constant upward social comparison. People who “have it all” can become trapped in their own social media webs. Living up to a carefully curated image of a perfect life may bring with it greater pressure to conceal depression, and to push away the support that comes from admitting vulnerability. Social media bubbles burst only when it is too late.

For sure, being rich, powerful and famous has its perks, including preferred access to mental health care. Generally, people in such favored positions don’t wish to swap places with the poor, weak and obscure. That said, the core psychological processes that are breeding depression and suicide in the U.S. are penetrating every ZIP code. At present, no one gets to opt out.

Having an explanation is not the same as solace. In this case, I believe understanding the bigger picture is more unnerving than it is soothing. Because if those at the top of the social pyramid are subject to universal processes at work in an escalating epidemic of depression and suicide, our society can expect that more Spades and Bourdains are yet to come. I hope we will take their deaths as a urgent call, and marshal a more robust public health response to these twin epidemics. And I hope we never become inured to the shock if we do not.

If you are having thoughts of suicide, please know that you are not alone. If you are in danger of acting on suicidal thoughts, call 911. For support and resources, call the National Suicide Prevention Lifeline at 1-800-273-8255 or text 741-741 for the Crisis Text Line.

Why predicting suicide is a difficult and complex challenge


Why predicting suicide is a difficult and complex challenge
Anthony Bourdain, left, and Kate Spade, right. The Conversation with images from PeabodyAwards/flickr, CC BY-SA

Who is going to die by suicide? This terrible mystery of human behavior takes on particular poignance in the wake of suicides by high-profile and much-beloved celebrities Kate Spade and Anthony Bourdain. It is only natural that people want to know why such tragedies occur. Those closest to those who take their lives are often tormented, wondering if there is something they could have – or should have – known to prevent their loved one’s suicide.

As a scientist who has focused on this question for the past decade, I should have a pretty good idea of who is and isn’t going to die by suicide. But the sad truth is, I don’t. The sadder truth is, neither do any other suicide experts, psychiatrists or physicians. The sum of the research on suicide shows that it does not matter how long we’ve known someone or how much we know about them. In my research, my colleagues and I have shown that we can only predict who is going to die by suicide slightly more accurately than random guessing.

The need for answers

The fact that suicide is so hard to predict unfortunately took about 50 years for most scientists to appreciate. About the same time that this recognition became widespread a few years ago, a new hope emerged: a form of artificial intelligence called machine learning. As several research groups have demonstrated in recent years, machine learning may be able to predict who is going to attempt or die by suicide with up to 90 percent accuracy.

To understand why this is, and why we humans won’t ever be able to accurately predict suicide on our own, one needs to take a step back and understand a little more about the nature of human cognition, suicide and machine learning.

As humans, we love explanations that have two qualities. First, explanations should be simple, meaning that they involve one or a small number of things. For example, depression is a simple explanation for suicide.

Second, explanations should be determinate, meaning that there is one set explanation that accounts for all or most of something. For example, the idea that depression causes most suicides is a determinate explanation. This simple and determinate explanatory style is highly intuitive and very efficient. It’s great for helping us to survive, procreate, and get through our days.

But this style of thinking is terrible for helping us understand nature. This is because nature is not simple and determinate. In recent decades, scientists have come to recognize that nearly everything – from physics to biology to human behavior – is complex and indeterminate. In other words, a very large number of things combined in a complex way are needed to explain most things, and there’s no set recipe for most physical, biological or behavioral phenomena.

I know that this latter idea of indeterminacy is especially counterintuitive, so let me provide a straightforward example of it. The math equation X plus Y equals 1 is indeterminate. As humans, we instinctively try to find one solution to this equation (e.g., X equals 1, Y equals 0). But there is no set recipe for solving this equation; there are nearly infinite solutions to this equation. Importantly, however, this does not mean that “anything goes.” There are also near infinite values for X and Y that do not solve this equation. This indeterminate middle ground between “one solution” and “anything goes” is difficult for most humans to grasp, but it’s how much of nature works.

The sum of our scientific evidence indicates that, just like most other things in nature, the causes and predictors of suicide are complex and indeterminate. Hundreds, and maybe thousands, of things are relevant to suicide, but nothing predicts suicide much more accurately than random guessing. For example, depression is often considered to be an extremely important predictor of suicide. But about 2 percent of severely depressed people eventually die by suicide, which is only slightly higher than the 1.6 percent of people from the general United States population who eventually die by suicide. Such a pattern is consistent with complexity because it suggests that we must put a lot of factors together to account for suicide.

Empathy will always matter

So how should we put all of these factors together? One intuitive solution is to add many of these factors together. But even when summing hundreds of factors, this doesn’t work – prediction is still only slightly more accurate than random guessing.

A much better solution would be to somehow find an optimized combination of tens or even hundreds of factors. How can we do this? One promising answer is machine learning. In short, machine learning programs can process a large amount of data and learn an optimal combination of factors for a given task. For example, most existing machine learning studies have used data from electronic health records, spanning hundreds of factors related to mental health diagnoses, physical health problems, medications, demographics and hospital visit patterns. Results from several groups in recent years have shown that this approach can consistently predict future suicide attempts and death with 80-90 percent accuracy. Multiple groups are currently working on applying these algorithms to actual clinical practice.

One important thing to keep in mind is that there isn’t, and never will be, a single algorithm or recipe for suicide prediction. This is because suicide is indeterminate, much like the X plus Y equals 1 equation. There are likely near-infinite algorithms that could predict suicide with 80-90 percent accuracy, as a number of studies have shown. Research has already demonstrated that no particular factors are necessary for a good algorithm, and many different types of algorithms can produce accurate prediction. But again, this indeterminacy also means that there are near-infinite bad algorithms, too.

Why predicting suicide is a difficult and complex challenge
About 2 percent of severely depressed people die by suicide. Fure/Shutterstock.com

All of this research shows that suicide is unfortunately too complex and indeterminate for humans to predict. Neither I nor anyone else can accurately predict who is going to die by suicide or truly explain why a particular person died by suicide (this includes the suicide decedents themselves). Machine learning can do a much better job of approximating the complexity of suicide, but even it falls far short. Although it can accurately predict who will eventually die by suicide, it cannot yet tell us when someone will die by suicide. This “when” dimension of prediction is critical, and we are likely still many years away from accounting for it.

In the meantime, what can we humans do? While we don’t have the ability to know whether someone is going to die by suicide or not, we do have the ability to be supportive and caring. If you believe that someone may be struggling, talk with them and let them know about resources such as the US National Suicide Prevention Lifeline (1-800-273-8255).

If this article has raised issues for you or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Neurons made from blood cells – a new tool for understanding brain diseases

Our team at Stanford University has just figured out the recipe for converting blood cells from adults directly into nerve cells, or neurons.

You may be wondering why anyone would want to convert blood into brain cells. Researchers like myself would like to gain a better understanding of what causes brain diseases such as autism, schizophrenia or major depression. But it is difficult to study complex diseases like these in the lab.

Our new procedure should make this research easier because we can collect blood cells from a patient with schizophrenia, for example, and see whether disease processes that happens in an individual’s brain can be replicated in blood-derived neurons in the petri dish. This research will not only provide insights into how diseases develop but will also create a way to test new therapies before they are given to patients.

Why are neuropsychiatric diseases so difficult to study?

What makes brain diseases hard to study is that every person has a unique genetic makeup which means that the same disease – autism or schizophrenia or depression – manifests differently in every individual. In addition, only a small percentage of patients have mutations in a single gene that appears to be responsible for the disease.

When the DNA of hundreds of patients with neuropsychiatric diseases and healthy individuals was screened for disease-causing genes, certain versions of genes were more common in patients versus the healthy population, suggesting they may play a role in causing the disease.

This suggests that the majority of patients carry multiple genes that all contribute to their condition. The contribution of each gene is small, but the combination of dozens of genetic variations add up to a severe disease.

For this reason, it is challenging to assess the role of these minor genes in the whole disease process, figure out which ones are key players and determine the critical combination of genetic variations necessary to trigger disease. Because we don’t know the key genes involved, we cannot engineer mice that accurately mimic the disease process in humans, and we can’t test therapies to address these illnesses.

Reprogramming the cell

Cellular reprogramming, the ability to convert one cell type into another, offers a possible solution to this problem. In 2006, scientists showed that skin cells could be transformed into pluripotent stem cells – cells that have the potential to develop into many cell types – which in turn could be coaxed into neurons. A few years later, in 2010, we simplified this two-step process and discovered a way to convert skin cells directly into neurons.

But obtaining skin cells is not straightforward and involves a painful procedure. Moreover, the skin cells have to be grown before they are converted into other cells, which can introduce artificial mutations not relevant to causing the disease.

With our approach, we can take just a few drops of blood and generate tens of thousands of neurons.

We can complete this shape-shifting transformation of one cell type into another by adding just four specific proteins – which we determined play vital roles in brain development – to freshly drawn or stored blood cells. These four factors are enough to rapidly reprogram these cells and transform them into neurons within a few weeks of treatment.

Over this period the white blood cells change shape, from a ball-shaped cell to a neuron with delicate tentacle-like branches. They display proteins that typically decorate the surface of neurons, and in our experiments they behaved like neurons and transmitted electrical signals. Compared to neurons in the brain the “induced” neurons appear less mature. Our technique is already useful for some applications, for others that require mature neurons it still needs to be refined.

Our strategy allows scientists to generate neurons from patients affected with a disease of interest which harbor all the genetic elements that actually cause the condition. We will still need to create neurons from many patients and healthy subjects and analyze the genes that are active in each group before we can determine which genes are involved in all forms of the disease. Through this method, we will be hopefully be able to identify the most relevant genes which should be good targets for disease-modifying medicines.

Tom Südhof, professor of molecular and cellular physiology at Stanford University, also contributed to this article and owns shares of Neucyte, Inc.

Why Mister Rogers’ message of love and kindness is good for your health

The release of the Mister Rogers documentary, “Won’t You Be My Neighbor?” calls to mind the essential message of Rogers’ long-running children’s program, “Mister Rogers’ Neighborhood.” Fred McFeely Rogers, who died in 2003, was also an ordained Presbyterian minister. Over the course of three decades on public broadcasting, he brought to millions of children what his faith’s General Assembly referred to as “unconditional love.”

In preaching love, Rogers wasn’t just attending to the moral character of his youthful audience. He believed that he was also promoting their health. As he said in 1979, “My whole approach in broadcasting has always been, ‘You are an important person just the way you are. You can make healthy decisions.’ Maybe I’m going on too long, but I just feel that anything that allows a person to be more active in the control of his or her life, in a healthy way, is important.”

Since Rogers’ death, evidence has mounted that he was on to something – namely, that love and kindness truly are healthful, and that people who express them regularly really do lead healthier lives. Simply put, people who are generous and volunteer their time for the benefit of others seem to be happier than those who don’t, and happy people tend to have fewer health complaints and live longer than those who are unhappy.

Love gave rise to a calling

Born in Pennsylvania in 1928, as a young minister Rogers regretted the messages television was conveying to children in the 1960s. He said, “I went into television because I hated it so, and I thought there’s some way of using this fabulous instrument to nurture those who would watch and listen.” “Mr. Rogers’ Neighborhood” debuted nationally in 1968 and won its creator and host many accolades, including a Presidential Medal of Freedom, two Peabody Awards, and over 40 honorary degrees.

Why Mister Rogers' message of love and kindness is good for your health
Fred Rogers with Pres. George W. Bush, who is about to place the Presidential Medal of Freedom on Rogers in a July 9, 2002 ceremony. Kenneth Lambert/AP Photo

Rogers believed that the need to love and be loved was universal, and he sought to cultivate these capacities through every program, saying in a 2004 documentary hosted by actor Michael Keaton, one of his former stagehands, “You know, I think everybody longs to be loved, and longs to know that he or she is lovable. And consequently, the greatest thing we can do is to help somebody know they’re loved and capable of loving.”

Love and health

As it turns out, there are many ways in which love and kindness are good for health. For one thing, they tend to reduce factors that undermine it. Doing something nice for someone causes the release of endorphins, which help to relieve pain. People who make kindness a habit have lower levels of stress hormones such as cortisol. Intentionally helping others can even lower levels of anxiety in individuals who normally avoid social situations.

Carrying out acts of kindness, or even merely witnessing them, also increases levels of oxytocin, a hormone with health benefits as diverse as lowering blood pressure, promoting good sleep and reducing cravings for drugs such as cocaine and alcohol. That oxytocin should have so many health benefits is not so surprising when we recall its central role in stimulating uterine contractions during birth, the letdown of milk during lactation, the pleasure associated with orgasm and pair bonding.

Acts of generosity and compassion also appear to be good for mood. A 2010 study showed that while people with money tend to be somewhat happier than those without it, people who spend money on others report even greater levels of happiness, an effect that can be detected even in toddlers. When people give money to others, areas of the brain associated with pleasure are activated, and this response is greater when the transfer is voluntary rather than mandatory.

Such happiness can have big benefits in longevity. For example, a review of 160 published studies concluded that there is compelling evidence that life satisfaction and optimism are associated with better health and enhanced longevity. Another study of older people showed that, even after correcting for other factors such as age, disease and health habits, those who rated their happiness highest were 35 percent less likely to die in five years than those who were least content.

What would Mister Rogers say?

Of course, Rogers would remind us that there are reasons to be committed to love and kindness that extend far beyond their health benefits. Rogers was, after all, not a physician but a minister, and ultimately he was ministering to an aspect of human wholeness that cannot be analyzed by blood tests or visualized with CT scans. In a commencement address at Dartmouth College in 2002, he focused less on the body than what he might have called the spirit:

“When I say it’s you I like, I’m talking about that part of you that knows that life is far more than anything you can ever see or hear or touch. That deep part of you that allows you to stand for those things without which humankind cannot survive. Love that conquers hate, peace that rises triumphant over war, and justice that proves more powerful than greed.”

Why Mister Rogers' message of love and kindness is good for your health
A pair of Mister Rogers’ sneakers at the LBJ Library exhibition to celebrate the 50th anniversary of Pres. Johnson signing the public broadcasting act in 1967. Jay Godwin/LBJ Foundation

When Rogers encouraged children to be kinder and more loving, he believed that he was not only promoting public health but also nurturing the most important part of a human being – the part that exhibits a divine spark. As Rogers indicated in another commencement speech the year before at Middlebury College, “I believe that appreciation is a holy thing, that when we look for what’s best in the person we happen to be with at the moment, we’re doing what God does; so in appreciating our neighbor, we’re participating in something truly sacred.”

In expressing such deeply religious sentiments, Rogers was not trying to undermine a concern with bodily health. In fact, he regularly encouraged his viewers to adopt healthy life habits, and Rogers himself was a committed vegetarian and lifelong swimmer who maintained a low body weight his entire life. Yet he also believed that health alone does not a full life make, and he regarded the soundness of the body as but part of the wellness of whole persons and communities, which may explain why he was able to face his own mortality with such equanimity.

Just a few months before he died, Rogers recorded a message for the many adult fans who had grown up watching “Mister Rogers’ Neighborhood.” In it, he practiced what he preached, saying:

“I would like to tell you what I often told you when you were much younger. I like you just the way you are. And what’s more, I’m so grateful to you for helping the children in your life to know that you’ll do everything you can to keep them safe. And to help them express their feelings in ways that will bring healing in many different neighborhoods. It’s such a good feeling to know that we’re lifelong friends.”

Migrants’ latest health challenge: Scabies


Migrants' latest health challenge: Scabies
Scabies led to the closure of migrant camps such as these in Calais, France, in 2014. Pascal Rossignol/Reuters

Scabies, long considered a disease of the past in the developed world, is making its way back. This highly contagious parasitic skin disease, which is caused by the burrowing itch mite Sarcoptes scabiei var. hominis, is most commonly transmitted through personal contact in close living quarters and institutional settings, such as schools, aged care facilities, hospitals and refugee camps.

We are currently investigating the treatment of scabies in human and animal trials. Our recent study examined scabies outbreaks across the globe in close living quarters and institutional settings.

On the public agenda

After years of absence from the global health agenda, in 2013, scabies was added to the World Health Organization list of neglected tropical diseases. The disease has a significant and widespread health impact that extends far beyond an itchy rash.

Scabies is very common, with a global prevalence at any one time estimated at about 300 million cases, or about 4 percent of the world’s population. The disease is endemic in a number of countries, with an average prevalence of 5-10 percent in children of developing countries.

The highest rates of scabies occur in communities in tropical regions such as Central America, the Pacific islands and Northern Australia, where more than 30 percent of the residents may have scabies. In a national study of Fijian residents incorporating skin examination, 36.5 percent of children below 5 years of age and 43.7 percent of children aged 5 to 9 had scabies. A study of children in two remote Northern Australian Aboriginal communities found that by 1 year of age, 63 percent of children had presented with scabies.

Migrants' latest health challenge: Scabies
A refugee child in Kutapalong, Bangladesh, on Oct. 14, 2017, shows evidence of scabies. Djohan Shahrin/Reuters

Outside of occasional institutional outbreaks, scabies has long been considered a disease of the past in the developed world. However, with the influx of immigrants, mostly from North African and Middle Eastern countries due to socioeconomic and political upheaval, we have seen scabies re-emerge as a modern-day problem.

Morbidity and complications

Scabies infestation occurs when a mite burrows into the outermost layer of our skin, the epidermis. The primary method of scabies mite transmission between humans is prolonged skin-to-skin contact, with about 15-20 minutes of close contact required for successful direct transmission.

In scabies infestation, hypersensitivity to the mite debris, eggs or feces causes severe, persistent itching, which can have an extraordinarily unpleasant and debilitating effect. Intense itching leads to disturbed sleep, which consequently affects school and work attendance and performance.

Furthermore, scabies lesions are often secondarily infected with the bacteria Streptococcus pyogenes (S. pyogenes) or Staphylococcus aureus (S. aureus). These bacteria can cause local skin infections that can be superficial (such as impetigo), or affect the deeper layers of the skin (such as cellulitis).

Infection with S. pyogenes can potentially lead to fatal bloodstream infections (septicaemia) and post-infection complications, including end-stage renal failure and acute rheumatic fever. Repeated episodes of this can lead to rheumatic heart disease, which is estimated to affect at least 2.4 million children worldwide, with 79 percent occurring in developing countries. It is unclear how many cases of scabies lead to acute rheumatic fever and rheumatic heart disease; however, there are significantly higher rates of S. pyogenes infections and rheumatic fever and rheumatic heart disease in communities with ongoing scabies infestations.

In 2010, the direct effects of scabies infestation were estimated to have resulted in more than 1.5 million disability-adjusted life years worldwide. Disability-adjusted life years is defined as years of life lost due to early death plus years lived with disability.

Impact of refugee migration

In recent years, as conflicts and instability in the Middle East and parts of Asia and North Africa have left over 65 million people displaced worldwide, scabies outbreaks have arisen among refugees to the European Union. There have also been health concerns over unscreened illegal immigrants bringing infectious diseases into the United States. For example, in 2014, a U.S. border patrol agent reported a scabies infestation among about 40 immigrants newly arrived by plane.

Refugees seeking asylum are typically being accommodated in overcrowded shelters for extended time periods after having traveled upon overloaded and unsafe boats or trucks. There are reports of significant scabies infestations among migrants traveling by boat, such as seen among the 1,074 migrants rescued at sea off Az Zawiyah, Libya, on Sept. 16, 2017.

Scabies was also the most commonly reported illness in Malaysian immigration detention centers, predominantly those accommodating stateless Muslim Rohingya refugees from Myanmar.

Why is scabies spreading?

Scabies has been recognized as a disease in humans and animals for at least 3,000 years, and was reported in ancient India, China and the Middle East. Aristotle (384-323 B.C.) described it as ‘lice of the flesh,’ and references to disease symptoms are included in the Old Testament.

Today, poor living conditions, lack of access to clean water and overcrowding provide an ideal environment for the spread of scabies in refugee shelters. In fact, media and public health agency reports suggest that scabies is one of the most commonly observed diseases in these refugee populations.

Authors of a recent German study found that, between 2004 and 2014, the number of disease outbreaks per year in centralized homes for asylum seekers increased, rising 10-fold as a contributor to total community shelter outbreaks. Scabies was the third most frequent cause of outbreaks after chickenpox and measles, accounting for 19 percent of the total 615 incidents among 119 reported outbreaks. Additionally, in 2014 there were more reported outbreaks than in the past 10 years, indicating that this public health problem is rapidly growing in relevance.

The French Institute for Public Health Service estimated that scabies accounted for 20 percent of medical diagnoses between the end of 2015 and mid-2016 in the now dismantled refugee camp in Calais, France.

With the continued arrival of new refugees in France and the movement of many of the Calais refugees to the Chapelle camp in Paris, the problem of scabies persists.

Current challenges in managing scabies

Modern treatments for scabies include topical permethrin, topical benzyl benzoate and oral ivermectin for children older than 5.

However, there are a number of challenges associated with these treatment options, including poor adherence with therapy (particularly with the use of topical treatments, which require extensive skin coverage and repeated applications to treat the disease properly), unachievable costs for resource-poor communities (such as refugee populations), and increasing treatment resistance.

The possibility of reinfestation remains high when close contacts are not treated or the disease is endemic in a population.

Also, no currently available treatments possess the combined ability to kill eggs, act as an antibacterial, and have anti-inflammatory/antipruritic (anti-itch) properties. Added to this, they are all ineffective at preventing treatment relapse arising from newly hatched mites and evidence indicates the mites are becoming resistant to existing scabies treatments.

Given the current treatment challenges, and the substantial clinical and economic burden of scabies and associated complications in tropical developing countries and resource-poor societies, there have been renewed appeals for coordinated global campaigns. However, it has also been highlighted that any treatment strategies need to be simple and affordable and resonate well with the local challenges and cultures.

While treatment adherence is an important factor in controlling scabies, it must be emphasized that known environmental influences contribute to scabies outbreaks and the endemic nature of the infestation in some populations. Improved living conditions and providing adequate health care and sanitation, particularly in isolated communities and refugee camps, are essential to prevent and control outbreaks, and to reduce the burden of scabies in endemic regions.

Las terribles huellas psicológicas de la deportación

Read in English.

En febrero de 2017 un hombre se suicidió en Tijuana. El joven de 25 años había sido deportado de los Estados Unidos y se arrojó de un puente vehicular en Tijuana, Baja California, a pocos kilómetros de la frontera Estados Unidos-México.

Este penoso caso demuestra la precariedad de las actuales condiciones de vida de los migrantes mexicanos en EEUU como resultado de las severas políticas migratorias impulsadas por la administración de Donald Trump. La vulnerabilidad en la salud mental de esta población ha ido en aumento con la amenaza de la detención y deportación.

Como profesora de psicología, reconozco que el solo hecho de atravesar por el proceso de deportación -lo cual implica estar sujeto a un proceso judicial, acudir a audiencias, solicitar y pagar por asesoría legal profesional, y ser retenido y trasladado de un centro de detención a otro hasta finalmente ser expulsado del país- ya supone un alto nivel de estrés e incertidumbre.

En los refugiados de los conflictos en Medio Oriente, por ejemplo, investigaciones han comprobado que la política de intercepción y detención tiene efectos negativos en el bienestar mental de las personas impactadas por estas actividades.

Las terribles huellas psicológicas de la deportación
Un grupo de hombres deportados, cerca de la doble reja de metal que divide a San Diego y Tijuana. Jorge Duenes/Reuters

El estrés vivido es una realidad inherente para los deportados. Estudios llevados a cabo con hispanos en EUA demuestran que el miedo a la deportación, la discriminación, el dominio del idioma y el estatus migratorio son factores que producen estrés a diario. La ansiedad ante la posible separación forzada de los seres queridos es también una fuente de profunda angustia, así como se evidencia plenamente en un reciente capítulo del show de radio norteamericano This American Life.

Y ello sin contar las redes criminales a las que los migrantes indocumentados se encuentran particularmente expuestos, al entrar y salir del país.

Si a esto se le suma la desesperanza y la frustración de ver truncado el proyecto de vida situado en el país receptor y la falta de oportunidades en el país de origen, la combinación puede resultar letal, así como se vio en Tijuana el mes pasado. Oficiales públicos en zonas fronterizas han advertido que se están preparando para más “casos de esta naturaleza”.

En busca de una vida mejor

Alrededor del mundo, el migrante -legal o indocumentado- ya es un sujeto vulnerable, aun antes de cualquier procedimiento de deportación.

Los patrones migratorios se ven influidos mayormente por factores sociales, económicos y políticos suscitados en el lugar de origen de los migrantes. En Centroamérica y México se incluyen el crimen, la pobreza y el desempleo. En México, la mayor proporción de migrantes son hombres entre 20 a los 24 años de edad, pero las mujeres también huyen de la violencia que las rodea.

En buena medida la demanda de los destinos migratorios se vincula con las valoraciones positivas (fundamentadas o no) del territorio al que los migrantes se piensan desplazar. Según cifras del Instituto Nacional de Estadística y Geografía de México, el trabajo, la familia, los estudios y el matrimonio son los principales motivos por los cuales los ciudadanos van a EU, destino de más del 86% de los mexicanos que emigraron en 2014.

Es decir, la migración en México se vincula con la búsqueda de mejoras en las oportunidades laborales y en las condiciones de vida, y quienes se arriesgan a desplazarse son, en su mayoría, hombres y mujeres jóvenes, en la cúspide de la edad productiva.

Del estatus migratorio dependerán las condiciones de vulnerabilidad y los riesgos a los que los migrantes estarán expuestos. Pero casi todos se enfrentarán a una serie de factores estresantes que podrán repercutir directamente en su estado de salud y en su integridad mental.

Las terribles huellas psicológicas de la deportación
Los migrantes ya son una población vulnerada, aun antes de la amenaza de ser deportados. Jorge Luis Plata/Reuters

El desplazamiento territorial en sí mismo puede ser considerado como un factor estresante, sobre todo si la migración se da en condiciones de incertidumbre, y si el sujeto migrante no cuenta con una red de apoyo o una comunidad receptora instalada previamente en el país de acogida.

El idioma, las diferencias culturales, el nivel educativo, el limitado acceso a servicios y el aislamiento social pueden convertirse en obstáculos que cotidianamente repercutirán en la vida de los migrantes y sus hijos después de llegar.

El trauma de la incertidumbre

Bajo ciertas circunstancias, las personas más marginadas por su nuevo contexto social corren el riesgo de padecer trastornos emocionales y psíquicos de diversa índole y de magnitud variable.

Entre los grupos minoritarios dentro de Estados Unidos se ha observado la aparición de estrés “aculturativo” e insatisfacción, particularmente con respecto al ambiente de residencia; ambos fenómenos pueden asociarse a niveles considerables de ansiedad, fatiga y depresión.

Por otra parte, esta vulnerabilidad se puede manifestar en el uso problemático de sustancias como alcohol y drogas, exacerbando existentes desequilibrios psíquicos y, en consecuencia, en riesgos de salud que impactarán negativamente en la calidad de vida de los migrantes.

Las terribles huellas psicológicas de la deportación
Un mensaje para Donald Trump. Jonathan Earnst/Reuters

La especificidad de las problemáticas psicosociales que enfrentan los migrantes han llevado a los expertos a acuñar el término “síndrome de Ulises”: altos niveles de estrés con duelos crónicos recurrentes y no resueltos, como el constante sentimiento de fracaso, la sensación de soledad, de aislamiento social y, claro, el miedo a ser deportado. Los síntomas físicos se caracterizan por la fatiga crónica acompañada de dolores de cabeza, colitis, gastitis y cansancio.

El suicidio de aquel hombre indocumentado en Tijuana probablemente pudo haber sido evitado con la debida atención psicológica. No obstante, debido a la precariedad de las condiciones de vida de los migrantes indocumentados, el acceso a servicios de salud mental y el adecuado tratamiento representan lujos fuera del alcance de estos sujetos (así como de muchos ciudadanos estadounidenses).

Las políticas de deportación, y la amenaza, estigmatización y precariedad que ejercen sobre las vidas de los indocumentados latinos en EEUU los ha llevado casi al borde de lo indigno.

This article was originally published in English