Tag Archives: Suicide

CHILDHOOD TRAUMA AND MENTAL ‘ILLNESS’. Beyond the smoke – Johann Hari.

Depression isn’t a disease; depression is a normal response to abnormal life experiences.

The medical team, and all their friends, expected these people, who had been restored to health to react with joy. Except they didn’t react that way. The people who did best, and lost the most weight were often thrown into a brutal depression, or panic, or rage. Some of them became suicidal.

Was there anything else that happened in your life when you were eleven? Well, Susan replied that was when my grandfather began to rape me.

“Overweight is overlooked, and that’s the way I need to be.”

What we had perceived as the problem, major obesity, was in fact, very frequently, the solution to problems that the rest of us knew nothing about. Obesity, he realized, isn’t the fire. It’s the smoke.

For every category of traumatic experience you go through as a kid, you are radically more likely to become depressed as an adult. The greater the trauma, the greater your risk of depression, anxiety, or suicide.

Emotional abuse especially, is more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents is the biggest driver of depression, out of all these categories.

We have failed to see depression as a symptom of something deeper that needs to be dealt with. There’s a house fire inside many of us, and we’ve been concentrating on the smoke.

When the women first came into Dr. Vincent Felitti’s office some of them found it hard to fit through the door. These patients weren’t just a bit overweight: they were eating so much that they were rendering themselves diabetic and destroying their own internal organs. They didn’t seem to be able to stop themselves. They were assigned here, to his clinic, as their last chance.

It was the mid-1980s, and in the California city of San Diego, Vincent had been commissioned by the not-for-profit medical provider Kaiser Permanente to look into the fastest-growing driver of their costs, obesity. Nothing they were trying was working, so he was given a blank sheet of paper. Start from scratch, they said. Total blue-sky thinking. Figure out what we can do to deal with this. And so the patients began to come. But what he was going to learn from them led, in fact, to a major breakthrough in a very different area: how we think about depression and anxiety.

As he tried to scrape away all the assumptions that surround obesity, Vincent learned about a new diet plan based on a maddeningly simple thought. It asked: What if these severely overweight people simply stopped eating, and lived off the fat stores they’d built up in their bodies until they were down to a normal weight? What would happen?

In the news, curiously, there had recently been an experiment in which this was tried, eight thousand miles away, for somewhat strange reasons. For years in Northern Ireland if you were put in jail for being part of the Irish Republican Army’s violent campaign to drive the British out of Northern Ireland, you were classed as a political prisoner. That meant you were treated differently from people who committed (say) bank robberies. You were allowed to wear your own clothes, and you didn’t have to perform the same work as other inmates.

The British government decided to shut down that distinction, and they argued that the prisoners were simply common criminals and shouldn’t get this different treatment anymore. So the prisoners decided to protest by going on a hunger strike. They began, slowly, to waste away.

So the designers of this new diet proposal looked into the medical evidence about these Northern Ireland hunger strikers to find out what killed them. It turns out that the first problem they faced was a lack of potassium and magnesium. Without them, your heart stops beating properly. Okay, the radical dieters thought, what if you give people supplements of potassium and magnesium? Then that doesn’t happen. If you have enough fat on you, you get a few months more to live, until a protein deficiency kills you.

Okay, what if you also give people the supplements that will prevent that? Then, it turns out, you get a year to live, provided there’s enough fat. Then you’ll die from a lack of vitamin C, scurvy, or other deficiencies.

Okay, what if you give people supplements for that, too? Then it looks as though you’ll stay alive, Vincent discovered in the medical literature, and healthy, and you’ll lose three hundred pounds a year. Then you can start eating again, at a healthy level.

All this suggested that in theory, even the most obese person would be down to a normal weight within a manageable time. The patients coming to him had been through everything, every fad diet, every shaming, every prodding and pulling. Nothing had worked. They were ready to try anything. So, under careful monitoring, and with lots of supervision, they began this program. And as the months passed, Vincent noticed something. It worked. The patients were shedding weight. They were not getting sick, in fact, they were returning to health. People who had been rendered disabled by constant eating started to see their bodies transform in front of them.

Their friends and relatives applauded. People who knew them were amazed. Vincent believed he might have found the solution to extreme overweight. “I thought my god, we’ve got this problem licked,” he said.

And then something happened that Vincent never expected.

In the program, there were some stars, people who shed remarkable amounts of weight, remarkably quickly. The medical team, and all their friends, expected these people who had been restored to health to react with joy. Except they didn’t react that way.

The people who did best, and lost the most weight were often thrown into a brutal depression, or panic, or rage. Some of them became suicidal. Without their bulk, they felt they couldn’t cope. They felt unbelievably vulnerable. They often fled the program, gorged on fast food, and put their weight back on very fast.

Vincent was baffled. They were fleeing from a healthy body they now knew they could achieve, toward an unhealthy body they knew would kill them. Why? He didn’t want to be an arrogant, moralistic doctor, standing over his patients, wagging his finger and telling them they were ruining their lives, that’s not his character. He genuinely wanted to help them save themselves. So he felt desperate. That’s why he did something no scientist in this field had done with really obese people before. He stopped telling them what to do, and started listening to them instead. He called in the people who had panicked when they started to shed the pounds, and asked them: What happened when you lost weight? How did you feel?

There was one twenty-eight-year-old woman, who I’ll call Susan to protect her medical confidentiality. In fifty-one weeks, Vincent had taken Susan down from 408 pounds to 132 pounds. It looked like he had saved her life. Then, quite suddenly, for no reason anyone could see, she put on 37 pounds in the space of three weeks. Before long, she was back above 400 pounds. So Vincent asked her gently what had changed when she started to lose weight. It seemed mysterious to both of them. They talked for a long time. There was, she said eventually, one thing. When she was very obese, men never hit on her, but when she got down to a healthy weight, one day she was propositioned by a man, a colleague who she happened to know was married. She fled, and right away began to eat compulsively, and she couldn’t stop.

This was when Vincent thought to ask a question he hadn’t asked his patients before. When did you start to put on weight? If it was (say) when you were thirteen, or when you went to college, why then, and not a year before, or a year after?

Susan thought about the question. She had started to put on weight when she was eleven years old, she said. So he asked: Was there anything else that happened in your life when you were eleven? Well, Susan replied that was when my grandfather began to rape me.

Vincent began to ask all his patients these three simple questions. How did you feel when you lost weight? When in your life did you start to put on weight? What else happened around that time? As he spoke to the 183 people on the program, he started to notice some patterns. One woman started to rapidly put on weight when she was twenty-three. What happened then? She was raped. She looked at the ground after she confessed this, and said softly: “Overweight is overlooked, and that’s the way I need to be.”

“I was incredulous,” he told me when I sat with him in San Diego. “It seemed every other person I was asking was acknowledging such a history. I kept thinking, it can’t be. People would know if this was true. Somebody would’ve told me. Isn’t that what medical school is for?” When five of his colleagues came in to conduct further interviews, it turned out some 55 percent of the patients in the program had been sexually abused, far more than people in the wider population. And even more, including most of the men, had had severely traumatic childhoods.

Many of these women had been making themselves obese for an unconscious reason: to protect themselves from the attention of men, who they believed would hurt them. Being very fat stops most men from looking at you that way. It works. It was when he was listening to another grueling account of sexual abuse that it hit Vincent. He told me later:

“What we had perceived as the problem, major obesity, was in fact, very frequently, the solution to problems that the rest of us knew nothing about.”

Vincent began to wonder if the anti-obesity programs, including his own, had been doing it all wrong, by (for example) giving out nutritional advice. Obese people didn’t need to be told what to eat; they knew the nutritional advice better than he did. They needed someone to understand why they ate. After meeting a person who had been raped, he told me, “I thought with a tremendously clear insight that sending this woman to see a dietitian to learn how to eat right would be grotesque.”

Far from teaching the obese people, he realized they were the people who could teach him what was really going on. So he gathered the patients in groups of around fifteen, and asked them: “Why do you think people get fat? Not how. How is obvious. I’m asking why. What are the benefits?” Encouraged to think about it for the first time, they told him. The answers came in three different categories. The first was that it is sexually protective: men are less interested in you, so you are safer. The second was that it is physically protective: for example, in the program there were two prison guards, who lost between 100 and 150 pounds each. Suddenly, as they shed their bulk, they felt much more vulnerable among the prisoners, they could be more easily beaten up. To walk through those cell blocks with confidence, they explained, they needed to be the size of a refrigerator.

And the third category was that it reduced people’s expectations of them. “You apply for a job weighing four hundred pounds, people assume you’re stupid, lazy,” Vincent said. If you’ve been badly hurt by the world, and sexual abuse is not the only way this can happen, you often want to retreat. Putting on a lot of weight is, paradoxically, a way of becoming invisible to a lot of humanity.

“When you look at a house burning down, the most obvious manifestation is the huge smoke billowing out,” he told me. It would be easy, then, to think that the smoke is the problem, and if you deal with the smoke, you’ve solved it. But “thank God that fire departments understand that the piece that you treat is the piece you don’t see, the flames inside, not the smoke billowing out. Otherwise, house fires would be treated by bringing big fans to blow the smoke away. [And that would] make the house burn down faster.”

Obesity, he realized, isn’t the fire. It’s the smoke.

One day, Vincent went to a medical conference dedicated to obesity to present his findings. After he had spoken, a doctor stood up in the audience and explained: “People who are more familiar with these matters recognize that these statements by patients describing their sexual abuse, are basically fabrications, to provide a cover for their failed lives. It turned out people treating obesity had noticed before that a disproportionate number of obese people described being abused. They just assumed that they were making excuses.

Vincent was horrified. He had in fact verified the abuse claims of many of his patients, by talking to their relatives, or to law enforcement officials who had investigated them. But he knew he didn’t have hard scientific proof yet to rebut people like this. His impressions from talking to individual patients, even gathering the figures from within his group, didn’t prove much. He wanted to gather proper scientific data. So he teamed up with a scientist named Dr. Robert Anda, who had specialized for years in the study of why people do self-destructive things like smoking. Together, funded by the Center for Disease Control, a major US. agency funding medical research, they drew up a way of testing all this, to see if it was true beyond the small sample of people in Vincent’s program.

They called it the Adverse Childhood Experiences (ACE) Study, and it’s quite simple. It’s a questionnaire. You are asked about ten different categories of terrible things that can happen to you when you’re a kid, from being sexually abused, to being emotionally abused, to being neglected. And then there’s a detailed medical questionnaire, to test for all sorts of things that could be going wrong with you, like obesity, or addiction. One of the things they added to the list, almost as an afterthought, was the question: Are you suffering from depression?

This survey was then given to seventeen thousand people who were seeking health care, for a whole range of reasons, from Kaiser Permanente in San Diego. The people who filled in the form were somewhat wealthier and a little older than the general population, but otherwise fairly representative of the city’s population.

When the results came in, they added them up, at first, to see if there were any correlations.

It turned out that for every category of traumatic experience you went through as a kid, you were radically more likely to become depressed as an adult. If you had six categories of traumatic events in your childhood, you were five times more likely to become depressed as an adult than somebody who didn’t have any. If you had seven categories of traumatic events as a child, you were 3,100 percent more likely to attempt to commit suicide as an adult.

“When the results came out, I was in a state of disbelief,” Dr. Anda told me. “I looked at it and I said, really? This can’t be true.” You just don’t get figures like this in medicine very often. Crucially, they hadn’t just stumbled on proof that there is a correlation, that these two things happen at the same time. They seemed to have found evidence that these traumas help cause these problems. How do we know? The greater the trauma, the greater your risk of depression, anxiety, or suicide. The technical term for this is “dose-response effect.” The more cigarettes you smoke, the more your risk of lung cancer goes up, that’s one reason we know smoking causes cancer. In the same way, the more you were traumatized as a child, the more your risk of depression rises.

Curiously, it turned out emotional abuse was more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents was the biggest driver of depression, out of all these categories.

When they showed the results to other scientists, including the Centers for Disease Control (CDC), who cofunded the research, they too were incredulous. “The study shocked people,” Dr. Anda told me. “People didn’t want to believe it. People at the CDC didn’t want to believe it. There was resistance within the CDC when I brought the data around, and the medical journals, initially, didn’t want to believe it, because it was so astonishing that they had to doubt it. Because it made them challenge the way they thought about childhood. It challenged so many things, all at one time.” In the years that followed, the study has been replicated many times, and it always finds similar results. But we have barely begun, Vincent told me, to think through its implications.

So Vincent, as he absorbed all this, came to believe that we have been making the same mistake with depression that he had been making before with obesity. We have failed to see it as a symptom of something deeper that needs to be dealt with. There’s a house fire inside many of us, Vincent had come to believe, and we’ve been concentrating on the smoke.

Many scientists and psychologists had been presenting depression as an irrational malfunction in your brain or in your genes, but he learned that Allen Barbour, an internist at Stanford University, had said that depression isn’t a disease; depression is a normal response to abnormal life experiences. “I think that’s a very important idea,” Vincent told me. “It takes you beyond the comforting, limited idea that the reason I’m depressed is I have a serotonin imbalance, or a dopamine imbalance, or what have you.” It is true that something is happening in your brain when you become depressed, he says, but that “is not a causal explanation”; it is “a necessary intermediary mechanism.”

Some people don’t want to see this because, at least at first, “it’s more comforting,” Vincent said, to think it’s all happening simply because of changes in the brain. “It takes away an experiential process and substitutes a mechanistic process.” It turns your pain into a trick of the light that can be banished with drugs. But they don’t ultimately solve the problem, he says, any more than just getting the obese patients to stop eating solved their problems. “Medications have a role,” he told me. “Are they the ultimate be and end-all? No. Do they sometimes short-change people? Absolutely.”

To solve the problem for his obese patients, Vincent said, they had all realized, together, that they had to solve the problems that were leading them to eat obsessively in the first place. So he set up support groups where they could discuss the real reasons why they ate and talk about what they had been through. Once that was in place, far more people became able to keep going through the fasting program and stay at a safe weight. He was going to start exploring a way to do this with depression, with startling results.

More than anyone else I spoke to about the hidden causes of depression, Vincent made me angry. After I met with him, I went to the beach in San Diego and raged against what he had said. I was looking hard for reasons to dismiss it. Then I asked myself. Why are you so angry about this? It seemed peculiar, and I didn’t really understand it. Then, as I discussed it with some people I trust, I began to understand.

If you believe that your depression is due solely to a broken brain, you don’t have to think about your life, or about what anyone might have done to you. The belief that it all comes down to biology protects you, in a way, for a while. If you absorb this different story, though, you have to think about those things. And that hurts.

I asked Vincent why he thinks traumatic childhoods so often produce depressed and anxious adults, and he said that he honestly doesn’t know. He’s a good scientist. He didn’t want to speculate. But I think I might know, although it goes beyond anything I can prove scientifically.

When you are a child and you experience something really traumatic, you almost always think it is your fault. There’s a reason for this, and it’s not irrational; like obesity, it is, in fact, a solution to a problem most people can’t see. When I was young, my mother was ill a lot, and my father was mostly gone, usually in a different country. In the chaos of that, I experienced some extreme acts of violence from an adult in my life. For example, I was strangled with an electrical cord on one occasion. By the time I was sixteen, I left to go and live in another city, away from any adults I knew, and when I was there, I found myself, like many people who have been treated this way at a formative age, seeking out dangerous situations where I was again treated in ways I should not have been treated.

Even now, as a thirty-seven-year-old adult, I feel like writing this down, and saying it to you, is an act of betrayal of the adult who carried out these acts of violence, and the other adults who behaved in ways they shouldn’t have.

I know you can’t figure out who these people are from what I’ve written. I know that if I saw an adult strangling a child with an electrical cord, it would not even occur to me to blame the child, and that if I heard somebody try to suggest such a thing, I would assume they were insane. I know rationally where the real betrayal lies in this situation. But still, I feel it. It’s there, and that feeling almost stopped me from saying this.

Why do so many people who experience violence in childhood feel the same way? Why does it lead many of them to self-destructive behavior, like obesity, or hard core addiction, or suicide? I have spent a lot of time thinking about this. When you’re a child, you have very little power to change your environment. You can’t move away, or force somebody to stop hurting you. So you have two choices. You can admit to yourself that you are powerless, that at any moment, you could be badly hurt, and there’s simply nothing you can do about it. Or you can tell yourself it’s your fault. If you do that, you actually gain some power, at least in your own mind. If it’s your fault, then there’s something you can do that might make it different. You aren’t a pinball being smacked around a pinball machine. You’re the person controlling the machine. You have your hands on the dangerous levers.

In this way, just like obesity protected those women from the men they feared would rape them, blaming yourself for your childhood traumas protects you from seeing how vulnerable you were and are. You can become the powerful one. If it’s your fault, it’s under your control.

But that comes at a cost. If you were responsible for being hurt, then at some level, you have to think you deserved it. A person who thinks they deserved to be injured as a child isn’t going to think they deserve much as an adult, either.

This is no way to live. But it’s a misfiring of the thing that made it possible for you to survive at an earlier point in your life.

You might have noticed that this cause of depression and anxiety is a little different from the ones I have discussed up to now, and it’s different from the ones I’m going to discuss next.

As I mentioned before, most people who have studied the scientific evidence accept that there are three different kinds of causes of depression and anxiety, biological, psychological, and social. The causes I’ve discussed up to now, and will come back to in a moment, are environmental. I’ll come to biological factors soon.

But childhood trauma belongs in a different category. It’s a psychological cause. By discussing it here, I’m hoping childhood trauma can indicate toward the many other psychological causes of depression that are too specific to be discussed in a big, broad way. The ways our psyches can be damaged are almost infinite. I know somebody whose wife cheated on him for years with his best friend and who became deeply depressed when he found out. I know somebody who survived a terror attack and was almost constantly anxious for a decade after. I know someone whose mother was perfectly competent and never cruel to her but was relentlessly negative and taught her always to see the worst in people and to keep them at a distance. You can’t squeeze these experiences into neat categories, it wouldn’t make sense to list “adultery,” “terror attacks,” or “cold parents” as causes of depression and anxiety.

But here’s what we know.

Psychological damage doesn’t have to be as extreme as childhood violence to affect you profoundly. Your wife cheating on you with your best friend isn’t a malfunction in your brain. But it is a cause of deep psychological distress, and it can cause depression and anxiety. If you are ever told a story about these problems that doesn’t talk about your personal psychology, don’t take it seriously.

Dr. Anda, one of the pioneers of this research, told me it had forced him to turn his thinking about depression and other problems inside out.

“When people have these kind of problems, it’s time to stop asking what’s wrong with them,” he said, “and time to start asking what happened to them.”

from

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions

by Johann Hari

get it at Amazon.com

MIGRAINE AND DEPRESSION: It’s All The Same Brain – Gale Scott * Migraine May Permanently Change Brain Structure – American Academy of Neurology * Migraine: Multiple Processes, Complex Pathophysiology – Rami Burstein, Rodrigo Noseda, and David Borsook.

The symptoms that accompany migraine suggest that multiple neuronal systems function abnormally. Neuroimaging studies show that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs. As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally.

Migraine tends to run in families and as such is considered a genetic disorder. Genetic predisposition to migraine resides in multiple susceptible gene variants, many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity.

Migraine is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual. 40% of migraine patients are also depressed.

Migraine and Depression: It’s All The Same Brain

Gale Scott

When a patient suffers from both migraines and depression or other psychiatric comorbidities, physicians have to treat both. It’s a common situation, since 40% of migraine patients are also depressed. Anxiety is even more prevalent in these patients. An estimated 50% of migraine patients are anxious whether with generalized anxiety, phobias, panic attacks. or other forms of anxiety, said Mia Minen, MD Director of Headache Services at NYU Langoni Medical Center.

Health care costs in treating these co-morbid patients are 1.5 times higher than for migraine patients without accompanying psychiatric disorders.

But sorting out whether one problem is causing the other is not always easy, she said in a recent interview at NYU Langone. “it’s really interesting, which came first,” she said, “We really don’t know.”

There may be a bidirectional relationship with depression. Anxiety may precede migraines, then depression may follow.

Fortunately, she said, the question of which problem came first doesn’t really matter that much.

“It’s all one brain, one organ, and some of the same neurotransmitters are implicated in both disorders.” Serotonin is affected in migraine just as it is in depression and anxiety, she said. Dopamine and norepinephrine are also related both to migraines and psychiatric comorbidities.

“So it’s really one organ that’s controlling all these things,” Minen said.

The first step in treatment is having patients keep a headache diary to track the intensity and frequency and what they take when they feel it coming on.

For a mild migraine that might be ibuprofen or another over-the-counter pain killer.

If the migraine is moderately severe there are 7 migraine-specifuc medications that are effective, she said. There are oral, nasal, and injectable forms of triptans a family of tryptamine-based drugs. “We sometimes tell patients to combine the triptan with Naprosyn,” she said.

If triptans are contraindicated because the patient has other health problems, there are still more pharmaceutical options.

Those include some classes of beta blockers, antiseizure medications, and tricyclic antidepressants at low doses.

The drug regimen may vary with the particular comorbidity. For instance, for migraines with anxiety, venlafaxine might work. If patients have sleep disturbances, amitriptyline might be effective. “Lack of sleep is also a trigger for migraine,” she noted.

The toughest co-morbidity to treat in patients with migraine is finding a regimen that works for patients who are taking a lot of psychiatric medications, like SSRIs and antipsychotics.

For older patients with migraines plus cardiovascular disease, drug choices are also limited.

Botox injections seem promising, but Minen is cautious. “It’s a great treatment for patients with chronic migraines but they have to have failed 2 or 3 medications before they qualify for Botox.” Treatment involves 31 injections over the forehead, the back of the head and the neck. Relief lasts about 3 months, she said.

In addition to pharmaceutical treatment, there are cognitive behavior approaches that can work, like biofeedback and progressive muscle relaxation therapy.

Opioids are not the treatment of choice, she said. They have not been shown to be effective, Minen said and reduce the body’s ability to respond to triptans.

“For chronic migraine, studies don’t show opioids enable patients to return to work; there is no objective study showing they work,” and their uses raises other problems. Patients used to taking opioids who go to an emergency room and request them may find themselves suspected of drugseeking behavior. “It’s hard for doctors and patients,” she said, when patients ask for opioids “It puts doctors in a predicament.”

New drugs are on the horizon, she said. “Calcitonin gene related peptide antagonists look good,” and unlike triptans are not contraindicated for people at risk of strokes or heart attacks.

For now, said Minen, treating migraine and comorbidities “is more an art than a science,” she said, “But a large majority of patients do get better.”

Migraine May Permanently Change Brain Structure

American Academy of Neurology

Migraine may have longlasting effects on the brain’s structure, according to a study published in the August 28, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain,” said study author Messoud Ashina, MD, PhD, with the University of Copenhagen in Denmark. “Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways.”

The study found that migraine raised the risk of brain lesions, white matter abnormalities and altered brain volume compared to people without the disorder. The association was even stronger in those with migraine with aura.

Migraine with aura
A common type of migraine featuring additional neurological symptoms. Aura is a term used to describe a neurological symptom of migraine, most commonly visual disturbances.
People who experience ‘migraine with aura’ will have many or all the symptoms of a ‘migraine without aura‘ and additional neurological symptoms which develop over a 5 to 20 minute period and last less than an hour.
Visual disturbances can include: blind spots in the field of eyesight, coloured spots, sparkles or stars, flashing lights before the eyes, tunnel vision, zig zag lines, temporary blindness.
Other symptoms include: numbness or tingling, pins and needles in the arms and legs, weakness on one side of the body, dizziness, a feeling of spinning (vertigo).
Speech and hearing can be affected and some people have reported memory changes, feelings of fear and confusion and, more rarely, partial paralysis or fainting.
These neurological symptoms usually happen before a headache, which could be mild, or no headache may follow.

For the meta-analysis, researchers reviewed six population-based studies and 13 clinic-based studies to see whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans compared to those without the conditions.

The results showed that migraine with aura increased the risk of white matter brain lesions by 68 percent and migraine with no aura increased the risk by 34 percent, compared to those without migraine. The risk for infarct-like abnormalities increased by 44 percent for those without aura. Brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.

“Migraine affects about 10 to 15 percent of the general population and can cause a substantial personal, occupational and social burden,” said Ashina. “We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease. We also want to find out how these lesions may influence brain function.”

The study was supported by the Lundbeck Foundation and the Novo Nordisk Foundation.

To learn more about migraine, please visit American Academy of Neurology.

Migraine: Multiple Processes, Complex Pathophysiology

Rami Burstein (1,3), Rodrigo Noseda (1,3) and David Borsook (2,3)
1 – Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston
2 – Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children’s Hospital
3 – Harvard Medical School

Migraine is a common, multifactorial, disabling, recurrent, hereditary neurovascular headache disorder. It usually strikes sufferers a few times per year in childhood and then progresses to a few times per week in adulthood, particularly in females. Attacks often begin with warning signs (prodromes) and aura (transient focal neurological symptoms) whose origin is thought to involve the hypothalamus, brainstem, and cortex.

Once the headache develops, it typically throbs, intensifies with an increase in intracranial pressure, and presents itself in association with nausea, vomiting, and abnormal sensitivity to light, noise, and smell. It can also be accompanied by abnormal skin sensitivity (anodynia) and muscle tenderness.

Collectively, the symptoms that accompany migraine from the prodromal stage through the headache phase suggest that multiple neuronal systems function abnormally.

As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally. These molecular, anatomical, and functional abnormalities provide a neuronal substrate for an extreme sensitivity to fluctuations in homeostasis, a decreased ability to adapt, and the recurrence of headache.

Homeostasis is the state of steady internal conditions maintained by living things.

Advances in understanding the genetic predisposition to migraine, and the discovery of multiple susceptible gene variants (many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity) define the most compelling hypothesis for the generalized neuronal hyperexcitability and the anatomical alterations seen in the migraine brain.

Regarding the headache pain itself, attempts to understand its unique qualities point to activation of the trigeminovascular pathway as a prerequisite for explaining why the pain is restricted to the head, often affecting the periorhital area and the eye, and intensities when intracranial pressure increases.

Introduction

Migraine is a recurrent headache disorder affecting 15% of the population during the formative and most productive periods of their lives, between the ages of 22 and 55 years. It frequently starts in childhood, particularly around puberty, and affects women more than men.

It tends to run in families and as such is considered a genetic disorder.

In some cases, the headache begins with no warning signs and ends with sleep. In other cases, the headache may be preceded by a prodromal phase that includes fatigue; euphoria; depression; irritability; food cravings; constipation; neck stiffness; increased yawning; and/or abnormal sensitivity to light, sound, and smell and an aura phase that includes a variety of focal cortically mediated neurological symptoms that appear just before and/or during the headache phase. Symptoms of migraine aura develop gradually, feature exeitatory and inhibitory phases, and resolve completely. Positive (gain of function) and negative (loss of function) symptoms may present as scintillating lights and scotomas when affecting the visual cortex; paresthesia, and numbness of the face and hands when affecting the somatosensory cortex; tremor and unilateral muscle weakness when affecting the motor cortex or basal ganglia; and difficulty saying words (aphasia) when affecting the speech area.

The pursuant headache is commonly unilateral, pulsating, aggravated by routine physical activity, and can last a few hours to a few days (Headache Classification Committee of the International Headache Society, 2013). As the headache progresses, it may be accompanied by a variety of autonomic symptoms (nausea, vomiting, nasallsinus congestion, rhinorrhea, lacrimation, ptosis, yawning, frequent urination, and diarrhea), affective symptoms (depression and irritability), cognitive symptoms (attention deficit, difficulty finding words, transient amnesia, and reduced ability to navigate in familiar environments), and sensory symptoms (photophobia, phonophobia, osmophobia, muscle tenderness, and cutaneous allodynia).

The extent of these diverse symptoms suggests that migraine is more than a headache. It is now viewed as a complex neurological disorder that affects multiple cortical, subcortical, and brainstem areas that regulate autonomic, affective, cognitive, and sensory functions. As such, it is evident that the migraine brain differs from the non-migraine brain and that an effort to unravel the pathophysiology of migraine must expand beyond the simplistic view that there are “migraine generator” areas.

In studying migraine pathophysiology, we must consider how different neural networks interact with each other to allow migraine to commence with stressors such as insufficient sleep, skipping meals, stressful or post stressful periods, hormonal fluctuations, alcohol, certain foods, flickering lights, noise, or certain scents, and why migraine attacks are sometimes initiated by these triggers and sometimes not.

We must tackle the enigma of how attacks are resolved on their own or just weaken and become bearable by sleep, relaxation, food, and/or darkness. We must explore the mechanisms by which the frequency of episodic migraine increases over time (from monthly to weekly to daily), and why progression from episodic to chronic migraine is uncommon.

Disease mechanisms

In many cases, migraine attacks are likely to begin centrally, in brain areas capable of generating the classical neurological symptoms of prodromes and aura, whereas the headache phase begins with consequential activation of meningeal nociceptors at the origin of the trigeminovascular system.

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain. If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called nociception.
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The meninges are the three membranes that envelop the brain and spinal cord. In mammals, the meninges are the dura mater, the arachnoid mater, and the pia mater. Cerebrospinal fluid is located in the subarachnoid space between the arachnoid mater and the pia mater. The primary function of the meninges is to protect the central nervous system.

While some clues about how the occurrence of aura can activate nociceptors in the meninges exist, nothing is known about the mechanisms by which common prodromes initiate the headache phase or what sequence of events they trigger that results in activation of the meningeal nociceptors. A mechanistic search for a common denominator in migraine symptomatology and characteristics points heavily toward a genetic predisposition to generalized neuronal hyperexcitability. Mounting evidence for alterations in brain structure and function that are secondary to the repetitive state of headache can explain the progression of disease.

Prodromes

In the context of migraine, prodromes are symptoms that precede the headache by several hours. Examination of symptoms that are most commonly described by patients point to the potential involvement of the hypothalamus (fatigue, depression, irritability, food cravings, and yawning), brainstem (muscle tenderness and neck stiffness), cortex (abnormal sensitivity to light, sound, and smell), and limbic system (depression and anhedonia) in the prodromal phase of a migraine attack. Given that symptoms such as fatigue, yawning, food craving, and transient mood changes occur naturally in all humans, it is critical that we understand how their occurrence triggers a headache; whether the routine occurrence of these symptoms in migraineurs (i.e., when no headache develops) differs mechanistically from their occurrence before the onset of migraine; and why yawning, food craving, and fatigue do not trigger a migraine in healthy subjects.

Recently, much attention has been given to the hypothalamus because it plays a key role in many aspects of human circadian rhythms (wake sleep cycle, body temperature, food intake, and hormonal fluctuations) and in the continuous effort to maintain homeostasis. Because the migraine brain is extremely sensitive to deviations from homeostasis, it seems reasonable that hypothalamie neurons that regulate homeostasis and circadian cycles are at the origin of some of the migraine prodromes.

Unraveling the mechanisms by which hypothalamic and brainstem neurons can trigger a headache is central to our ability to develop therapies that can intercept the headache during the prodromal phase (i.e., before the headache begins. The ongoing effort to answer this question focuses on two very different possibilities (Fig. 1). The first suggests that hypothalamic neurons that respond to changes in physiological and emotional homeostasis can activate meningeal nociceptors by altering the balance between parasympathetic and sympathetic tone in the meninges toward the predominance of parasympathetic tone. Support for such a proposal is based on the following: (1) hypothalamic neurons are in a position to regulate the firing of preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN) and sympathetic preganglionic neurons in the spinal intermediolateral nucleus. (2) the SSN can stimulate the release of acetylcholine, vasoactive intestinal peptide, and nitric oxide from meningeal terminals of postganglionic parasympathetic neurons in the Spheno palatine ganglion (SPG), leading to dilation of intracranial blood vessels, plasma protein extravasation, and local release of inflammatory molecules capable of activating pial and dural branches of meningeal nociceptors; (3) meningeal blood vessels are densely innervated by para sympathetic fibers. (4) activation of SSN neurons can modulate the activity of central trigeminovascular neurons in the spinal trigeminal nucleus. (5) activation of meningeal nociceptors appears to depend partially on enhanced activity in the SPG. (6) enhanced cranial parasympathetic tone during migraine is evident by lacrimation and nasal congestion, and, finally, (7) blockade of the sphenopalatine ganglion provides partial or complete relief of migraine pain.

The second proposal suggests that hypothalamic and brainstem neurons that regulate responses to deviation from physiological and emotional homeostasis can lower the threshold for the transmission of nociceptive trigeminovascular signals from the thalamus to the cortex, a critical step in establishing the headache experience. This proposal is based on understanding how the thalamus selects, amplifies, and prioritizes information it eventually transfers to the cortex, and how hypothalamic and brainstem nuclei regulate relay thalamocortical neurons. It is constructed from recent evidence that relay trigeminothalamic neurons in sensory thalamie nuclei receive direct input from hypothalamic neurons that contain dopamine, histamine, orexin, and melanin concentrating hormone (MCH), and brainstem neurons that contain noradrenaline and serotonin. In principle, each of these neuropeptides/neurotransmitters can shift the activity of thalamic neurons from burst to tonic mode if it is excitatory (dopamine, and high concentration of serotonin, noradrenaline, histamine, orexin, and from tonic to burst mode if it is inhibitory (MCH and low concentration of serotonin). The opposing factors that regulate the firing of relay trigeminovascular thalamic neurons provide an anatomical foundation for explaining why prodromes give rise to some migraine attacks but not to others, and why external (e.g., exposure to strong perfume) and internal conditions (e.g., skipping a meal and feeling hungry, sleeping too little and being tired, or simple stress) trigger migraine attacks so inconsistently.

In the context of migraine, the convergence of these hypothalamic and brainstem neurons on thalamic trigeminovascular neuruns can establish high and low set points for the allostatic load of the migraine brain. The allostatic load, defined as the amount of brain activity required to appropriately manage the level of emotional or physiological stress at any given time, can explain why external and internal conditions only trigger headache some of the times, when they coincide with the right circadian phase of cyclic rhythmicity of brainstem, and hypothalamic and thalamic neurons that preserve homeostasis.

Cortical spreading depression

Clinical and preclinical studies suggest that migraine aura is caused by cortical spreading depression (CSD), a slowly propagating wave of depolarization/excitation followed by hyperpolarization/inhibition in cortical neurons and glia. While specific processes that initiate CSD in humans are not known, mechanisms that invoke inflammatory molecules as a result of emotional or physiological stress, such as lack of sleep, may play a role. In the cortex, the initial membrane depolarization is associated with a large efflux of potassium; influx of sodium and calcium; release of glutamate, ATP, and hydrogen ions; neuronal swelling ; upregulation of genes involved in inflammatory processing; and a host of changes in cortical perfusion and enzymatic activity that include opening of the megachannel Panxl, activation of caspase-1, and a breakdown of the blood brain barrier.

Outside the brain, caspase-1 activation can initiate inflammation by releasing high mobility group protein B1 and interleukin-1 into the CSF, which then activates nuclear factor KB in astrocytes, with the consequential release of cyclooxygenase-2 and inducible nitric oxide swithase (iNOS) into the subarach noid space. The introduction into the meninges of these proinflammatory molecules, as well as calcitonin gene related peptide (CGRP) and nitric oxide, may be the link between aura and headache because the meninges are densely innervated by pain fibers whose activation distinguishes headaches of intracranial origin (e.g., migraine, meningitis, and subaraeh noid bleeds) from headaches of extracranial origin (e.g., tension type headache, cervicogenic headache, or headaches caused by mild trauma to the cranium).

Anatomy and physiology of the trigeminovascular pathway: from activation to sensitization

Anatomical description

The trigeminovascular pathway conveys nociceptive information from the meninges to the brain. The pathway originates in trigeminal ganglion neurons whose peripheral axons reach the pia, dura, and large cerebral arteries, and whose central axons reach the nociceptive dorsal horn laminae of the SpV. In the SpV, the nociceptors converge on neurons that receive additional input from the periorbital skin and pericranial muscles. The ascending axonal projections of trigeminovascular SpV neurons transmit monosynaptic nocieeptive signals to (1) brainstem nuclei, such as the ventro lateral periaqueductal gray, reticular for mation, superior salivatory, parabrachial, cuneiform, and the nucleus of the solitary tract; (2) hypothalamic nuclei, such as the anterior, lateral, perifornical, dorsome dial, suprachiasmatic, and supraoptic; and (3) basal ganglia nuclei, such as the caudate putamen, globus pallidus, and sub stantia innominata. These projections maybe critical for the initiation of nausea, vomiting, yawning, lacrimation, urination, loss of appetite, fatigue, anxiety, irritability, and depression by the headache itself.

Additional projections of trigeminovascular SpV neurons are found in the thalamic ventral posteromedial (VPM), posterior (PO), and parafascicular nuclei. Relay trigeminovascular thalamic neurons that project to the somatosensory, insular, motor, parietal association, retrosplenial, auditory, visual, and olfactory cortices are in a position to construct the specific nature of migraine pain (i.e., location, intensity, and quality) and many of the cortically mediated symptoms that distinguish between migraine headache and other pains. These include transient symptoms of motor clumsiness, difficulty focusing, amnesia, allodynia, phonophobia, photophobia, and osmophobia. Figure 2A illustrates the complexity of the trigeminovascular pathway.

Activation

Studies in animals show that CSD initiates delayed activation (Fig. 2D, 2B,C) and immediate activation (Fig. 2D) of peripheral and central trigeminovascular neurons in a fashion that resembles the classic delay and occasional immediate onset of headache after aura, and that systemic administration of the M type potassium channel opener KCNQ2/3 can prevent the CSD induced activation of the nociceptors.

These findings support the notion that the onset of the headache phase of migraine with aura coincides with the activation of meningeal nociceptors at the peripheral origin of the trigeminovascular pathway. Whereas the vascular, cellular, and molecular events involved in the activation of meningeal nocieeptors by CSD are not well under stood, a large body of data suggests that transient constriction and dilatation of pial arteries and the development of dural plasma protein extravasation, neurogenic inflammation, platelet aggregation, and mast cell degranulation, many of which may be driven by CSD dependent peripheral CGRP release, can introduce to the meninges proinflammatory molecules, such as histamine, bradykinin, serotonin, and prostaglandins (prostaglandin E2), and a high level of hydrogen ions thus altering the molecular environment in which meningeal nociceptors exist.

Sensitization

When activated in the altered molecular environment described above, peripheral trigeminovascular neurons become sensitized (their response threshold decreases and their response magnitude increases) and begin to respond to dura stimuli to which they showed minimal or no response at base line. When central trigeminovascular neurons in laminae I and V of SpV (Fig. 2F) and in the thalamic PO/VPM nuclei (Fig. 2G) become sensitized, their spontaneous activity increases, their receptive fields expand, and they begin to respond to innocuous mechanical and thermal stimulation of cephalic and extracephalic skin areas as if it were noxious. The human correlates of the electrophysiological measures of neuronal sensitization in animal studies are evident in contrast analysis of BOLD signals registered in MRI scans of the human trigeminal ganglion (Fig. 2H), spinal trigeminal nucleus (Fig. 2I), and the thalamus (Fig. 2J), all measured during migraine attacks.

The clinical manifestation of peripheral sensitization during migraine, which takes roughly 10 mins to develop, includes the perception of throbbing headache and the transient intensiflcation of headache while bending over or coughing, activities that momentarily increase intracranial pressure.

The clinical manifestation of sensitization of central trigeminovascular neurons in the SpV, which takes 30-60 min to develop and 120 min to reach full extent, include the development of cephalic allodynia signs such as scalp and muscle tenderness and hypersensitivity to touch. These signs are often recognized in patients reporting that they avoid wearing glasses, earrings, hats, or any other object that come in contact with the facial skin during migraine.

The clinical manifestation of thalamic sensitization during migraine, which takes 2-4 h to develop, also includes extracephalic allodynia signs that cause patients to remove tight clothing and jewelry, and avoid being touched, massaged, or hugged.

Evidence that triptans, 5HT agonists that disrupt communications between peripheral and central trigeminovascular neurons in the dorsal horn, are more effective in aborting migraine when administered early (i.e., before the development of central sensitization and allodynia) rather than late (i.e., after the development of allodynia) provides further support for the notion that meningeal nociceptors drive the initial phase of the headache. Further support for this concept was provided recently by studies showing that humanized monoclonal antihodies against CGRP, molecules that are too big to penetrate the bloodbrain barrier and act centrally (according to the companies that developed them), are effective in preventing migraine. Along this line, it was also reported that drugs that act on central trigeminovascular neurons, e.g., dihydroergotamine (DHE), are equally effective in reversing an already developed central sensitization a possible explanation for DHE effectiveness in aborting migraine after the failure of therapy with triptans.

Genetics and the hyperexcitable brain

Family history points to a genetic predisposition to migraine. A genetic association with migraine was first observed and defined in patients with familial hemiplegic migraine (FHM).

The three genes identified with FHM encode proteins that regulate glutamate availability in the synapse. FHM1 (CACNAIA) encodes the pore-forming a1 subunit of the P/Q type calcium channel; FHM2 (ATP1A2) encodes the 112 subunit of the Na+/K+ ATPase pump; and the FHM3 (SCNIA) encodes the a1 sub unit of the neuronal voltage gated Nav1.1 channel.

Collectively, these genes regulate transmitter release, glial ability to clear (reuptake) glutamate from the synapse, and the generation of action potentials.

Since these early findings, large genome wide association studies have identified 13 susceptibility gene variants for migraine with and without aura, three of which regulate glutaminergic neurotransmission (MTDH/AEG-1 downregulates glutamate transporter, LPRI modulates synaptic transmission through the NMDA receptor, and MEF-2D regulates the glutamatergic excitatory synapse), and two of which regulate synaptic development and plasticity (ASTN2 is involved in the structural development of cortical layers, and FHI5 regulates cAMP sensitive CREB proteins involved msynaptic plasticity).

These findings provide the most plausible explanation for the “generalized” neuronal hyperexcitability of the migraine brain.

In the context of migraine, increased activity in glutamalergic systems can lead to excessive occupation of the NMDA receptor, which in turn may amplify and reinforce pain transmission, and the development of allodynia and central sensitization. Network wise, wide spread neuronal hyperexcitability may also be driven by thalamocortical dysrhythmia, defective modulatory brainstem circuits that regulate excitability at multiple levels along the neuraxis; and inherently improper regulation/habituation of cortical, thalamic, and brainstem functions by limbic structures, such as the hypothalamus, amygdala, nucleus accumbens, caudate, putamen, and globus pallidus. Given that 2 of the 13 susceptibility genes regulate synaptic development and plasticity, it is reasonable to speculate that some of the networks mentioned above may not be properly wired to set a normal level of habituation throughout the brain, thus explaining the multi factorial nature of migraine. Along this line, it is also tempting to propose that at least some of the structural alterations seen in the migraine brain may be inherited and, as such, may be the “cause” of migraine, rather than being secondary to (i.e., being caused by) the repeated headache attacks. But this concept awaits evidence.

Structural and functional brain alterations

Brain alterations can be categorized into the following two processes: (1) alteration in brain function and (2) alterations in brain structure (Fig. 3). Functionally, a variety of imaging techniques used to measure relative activation in different brain areas in migraineurs (vs control subjects) revealed enhanced activation in the periaqueductal gray; red nucleus and substantia nigra; hypothalamus; posterior thalamus; cerebellum, insula, cingulate and prefrontal cortices, anterior temporal pole, and the hippocampus; and decreased activation in the somatosensory cortex, nucleus cuneiformis, caudate, putamen, and pallidum. All of these activity changes occurred in response to nonrepetitive stimuli, and in the cingulate and prefrontal cortex they occurred in response to repetitive stimuli.

Collectively, these studies support the concept that the migraine brain lacks the ability to habituate itself and consequently becomes hyperexcitable. It is a matter of debate, however, if such changes are unique to migraine headache. Evidence for nearly identical activation patterns in other pain conditions, such as lower back pain, neuropathic pain, Hbromyalgia, irritable bowel syndrome, and cardiac pain, raises the possibility that differences between somatic pain and migraine pain are not due to differences in central pain processing.

Anatomically, voxel based morphometry and diffusion sensor imaging studies in migraine patients (vs control subjects) have revealed thickening of the somatosensory cortex; increased gray matter density in the caudate; and gray matter volume loss in the superior temporal gyms, inferior frontal gyms, precentral gyms, anterior cingulate cortex, amygdala, parietal operculum, middle and inferior frontal gyrus, inferior frontal gyrus, and bilateral insula.

Changes in cortical and subcortical structures may also depend on the frequency of migraine attacks for a number of cortical and subcortical regions. As discussed above, it is unclear whether such changes are genetically predetermined or simply a result of the repetitive exposure to pain/stress. Favoring the latter are studies showing that similar gray matter changes occurring in patients experiencing other chronic pain conditions are reversible and that the magnitude of these changes can be correlated with the duration of disease.

Further complicating our ability to determine how the migraine brain differs from the brain of a patient experiencing other chronic pain conditions are anatomical findings showing decreased gray matter density in the prefrontal cortex, thalamus, posterior insula, secondary somatosensory cortex, precentral and posteentral gyms, hippocampus, and temporal pole of chronic back pain patients; anterior insula and orbitofrontal cortex of complex regional pain syndrome patients; and the insula, midanterior cingulate cortex, hippocampus and inferior temporal coxtex in osteoarthritis pa tients with chronic back pain.

Whereas some of the brain alterations seen in migraineurs depend on the sex of the patient, little can he said about the role played by the sex of patients who experience other pain conditions.

Treatments in development

Migraine therapy has two goals: to terminate acute attacks; and to prevent the next attack from happening. The latter can potentially prevent the progression from episodic to chronic state. Regarding the effort to terminate acute attacks, migraine represents one of the few pain conditions for which a specific drug (i.e., triptan) has been developed based on understanding the mechanisms of the disease. In contrast, the effort to prevent migraine from happening is likely to face a much larger challenge given that migraine can originate in an unknown number of brain areas (see above), and is associated with generalized functional and structural brain abnormalities.

A number of treatments that attract attention are briefly reviewed below.

Medications The most exciting drug currently under development is humanized monoclonal antibodies against CGRP. The development of these monoclonal antibodies are directed at both CGRP and its receptors. The concept is based on CGRP localization in the trigeminal ganglion and its relevance to migaine patho-physiology. In recent phase II randomized placebo-controlled trials, the neutralizing humanized monoclonal antibodies against CGRP administered by injection for the prevention of episodic migraine, showed promising results. Remarkably, a single injection may prevent or significantly reduce migraine attacks for 3 months.

Given our growing understanding of the importance of prodromes (likely representing abnormal sensitivity to the fluctuation in hypothalamically regulated homeostasis) and aura (likely representing the inherited conical hyperexcitability) in the pathophysiology of migraine, drugs that target ghrelin, leptin, and orexin receptors may be considered for therapeutic development which is based on their ability to restore proper hypothalamic control of stress, hyperphagia, adiposity, and sleep. All may be critical in reducing allostatic load and, consequently, in initiating the next migraine attack.

Brain modification

Neuroimaging studies showing that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs justify attempts to develop therapies that widely modify brain networks and their functions. Transcranial magnetic stimulation, which is thought to modify cortical hyperexcitability, is one such approach. Another approach for generalized brain modification is cognitive behavioral therapy.

Conclusions

Migraine is a common and undertreated disease. For those who suffer, it is a major cause of disability, including missing work or school, and it frequently has associated comorbidities such as anxiety and depression. To put this in context, it is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual.

There is currently no objective diagnosis or treatment that is universally effective in aborting or preventing attacks. As an intermittent disorder, migraine represents a neurological condition wherein systems that continuously evaluate errors (error detection) frequently fail, thus adding to the allostatic load of the disease.

Given the enormous burden to society, there is an urgent imperative to focus on better understanding the neurobiology of the disease to enable the discovery of novel treatment approaches.

AN ANXIOUS PARADISE. Crisis in New Zealand mental health services as depression and anxiety soar – Eleanor Ainge Roy * World in mental health crisis of monumental suffering – Sarah Broseley.

System neglects ‘missing middle’ of the population who face common problems.
50-80% of New Zealanders experience mental distress or addiction challenges at some point in their lives, while each year one in five people experience mental illness or significant mental distress.

A landmark inquiry has found New Zealand’s mental health services are overwhelmed and geared towards crisis care rather than the wider population who are experiencing increasing rates of depression, trauma and substance abuse.

It has urged the government to widen provision of mental health care from 3% of the population in critical need to “the missing middle” – the 20% of the population who struggle with “common, disabling problems” such as anxiety.

New Zealand has one of the highest rates of suicide in the OECD, especially among young people. In 2017, 20,000 people tried to take their own life.

. . . The Guardian

Also on TPPA = CRISIS

World in mental health crisis of ‘monumental suffering’, say experts – Sarah Broseley.

“Mental health problems kill more young people than any other cause around the world.” Prof. Vikram Patel, Harvard Medical School
Lancet report says 13.5 million lives could be saved every year if mental illness addressed.

Global warming will drive up suicide rates, study warns – Sharon Kirkey * How Climate Change Affects Mental Health – Katherine Schreiber * Mental Health and our Changing Climate, A Primer – APA.

The health, economic, political, and environmental implications of climate change affect all of us. The tolls on our mental health are far reaching. They induce stress, depression, and anxiety; strain social and community relationships; and have been linked to increases in aggression, violence, and crime.

Heat profoundly affects the human mind. The more neurotransmitters needed to cool the body, the less available to suppress emotions like aggression, impatience or violence. Heat increases circulating levels of the stress hormone, cortisol. Psychiatric hospital visits increase during hotter weather.

Virtually everywhere around the world we’re facing warmer temperatures, and there is a lot of evidence of direct effects of warming on mental health.

Although the psychological impacts of climate change may not be obvious, they are no less serious because they can lead to disorders, such as depression, antisocial behavior, and suicide. Therefore, these disorders must be considered impacts of climate change as are disease, hunger, and other physical health consequences.

Of the 36% of Americans who are personally concerned a great deal about climate issues, 72% are Democrats, and 27% are Republicans (PEW Research).

Sharon Kirkey

It was Raymond Chandler who wrote of nights with a hot wind blowing into Los Angeles, a wind that makes “your nerves jump.”

“On nights like that every booze party ends in a fight,” he wrote. “Meek little wives feel the edge of the carving knife and study their husbands’ necks. Anything can happen.”

Now there’s research that says climate change may damage our mental health, just like Chandler’s hot wind from the Santa Ana Mountains.

Last week, a team of 28 specialists convened by the Lancet medical journal listed climate change among the greatest threats to mental health globally.

Ferocious storms and more frequent weather extremes will affect the human psyche in costly ways, some scientists predict, from more depression and anxiety to increased suicide rates.

One working theory is that some of the same neurotransmitters used by the brain to regulate the body’s temperature are also used to control emotions. The more neurotransmitters needed to cool the body, the less available to suppress emotions like aggression, impatience or violence.

. . . National Post

How Climate Change Affects Mental Health.

A new report shows global warming affects our psyches just as much as our earth.

Katherine Schreiber

When we talk about climate change, we tend to think about its effects on our environment, melting polar ice caps, extreme swings in weather, more frequent droughts, flooding, and higher incidences of natural disasters. But what about the effect on our moods, thoughts, and feelings? A new report written by the American Psychological Association, Climate for Health, and ecoAmerica argues that our mental wellbeing is just as vulnerable to global warming as is our earth.

. . . Psychology Today

MENTAL HEALTH AND OUR CHANGING CLIMATE:

IMPACTS IMPLICATIONS, AND GUIDANCE

WHY WE OFFER THIS REPORT

When you think about climate change, mental health might not be the first thing that comes to mind. Americans are beginning to grow familiar with climate change and its health impacts: worsening asthma and allergies; heat-related stress: foodborne, waterborne, and vector-borne diseases; illness and injury related to storms; and floods and droughts. However, the connections with mental health are not often part of the discussion.

It is time to expand information and action on climate and health, including mental health. The health, economic, political, and environmental implications of climate change affect all of us. The tolls on our mental health are far reaching. They induce stress, depression, and anxiety; strain social and community relationships; and have been linked to increases in aggression, violence, and crime. Children and communities with few resources to deal with the impacts of climate change are those most impacted.

To compound the issue, the psychological responses to climate change, such as conflict avoidance, fatalism, fear, helplessness, and resignation are growing. These responses are keeping us, and our nation, from properly addressing the core causes of and solutions for our changing climate, and from building and supporting psychological resiliency.

To help increase awareness of these challenges and to address them, the American Psychological Association and ecoAmerica sponsored this report, Mental Health and Our Changing Climate: Impacts, Implications, and Guidance. This is an updated and expanded version of our 2014 report, Beyond Storms & Droughts: The Psychological Impacts of Climate Change, which explored how climate change can impact mental health and provided guidance to engage the public. This updated report is intended to further inform and empower health and medical professionals, community and elected leaders, and the public. Our websites offer webinars and other resources to supplement this report.

On behalf of the authors, the many professionals who contributed directly and indirectly to this work, and all those involved in expanding awareness of and action on climate and mental health, thank you for taking the time to review and share this important resource.

We invite your feedback, and as the field continues to grow, we’ll continue to update this work.

EXECUTIVE SUMMARY

Thus far, most research and communications on the impacts of climate change have emphasized the physical health effects, while mental health has been secondary. Building upon Beyond Storms and Droughts: The Psychological Impacts of Climate Change, the goal of this updated report is to increase awareness of the psychological impacts of climate change on human mental health and well-being. The report provides climate communicators, planners, policymakers, public health professionals, and other leaders the tools and tips needed to respond to these impacts and bolster public engagement on climate solutions.

The impacts of climate change on people’s physical, mental, and community health arise directly and indirectly. Some human health effects stem directly from natural disasters exacerbated by climate change, like floods, storms, wildfires, and heatwaves. Other effects surface more gradually from changing temperatures and rising sea levels that cause forced migration. Weakened infrastructure and less secure food systems are examples of indirect climate impacts on society‘s physical and mental health.

Some communities and populations are more vulnerable to the health-related impacts of climate change. Factors that may increase sensitivity to the mental health impacts include geographic location. presence of pre-existing disabilities or chronic illnesses, and socioeconomic and demographic inequalities, such as education level, income, and age.

In particular, stress from climate impacts can cause children to experience changes in behavior, development, memory, executive function, decision-making, and scholastic achievement.

The connection between changes in the climate and impacts on a person can be difficult to grasp. Although people’s understanding and knowledge of climate change can increase by experiencing the effects directly, perception, politics, and uncertainty can complicate this link. Psychological factors (like psychological distance), a political divide, uncertainty, helplessness, and denial influence the way people comprehend information and form their beliefs on climate change. Research on the impacts of climate change on human well-being is particularly important given the relationship among understanding, experiencing, and comprehending climate change. People’s willingness to support and engage in climate solutions is likely to increase if they can relate them to local experiences or if they see the relevance to their own health and well-being. Additionally, individuals who have higher perceived environmental self-efficacy, or the sense of being able to positively contribute, are more motivated to act on climate solutions.

Climate solutions are available now, are widespread, and support psychological health. Increasing adoption of active commuting, public transportation, green spaces, and clean energy are all solutions that people can choose to support and integrate into their daily lives. These climate solutions, among others, can help to curb the stress, anxiety, and other mental illnesses incurred from the decline of economies, infrastructure, and social identity that comes from damage to the climate.

Major acute mental health impacts include increases in trauma and shock, posttraumatic stress disorder (PTSD), compounded stress, anxiety, substance abuse, and depression. Climate change induced extreme weather, changing weather patterns, damaged food and water resources, and polluted air impact human mental health. Increased levels of stress and distress from these factors can also put strains on social relationships and even have impacts on physical health, such as memory loss, sleep disorders, immune suppression, and changes in digestion.

Major chronic mental health impacts include higher rates of aggression and violence, more mental health emergencies, an increased sense of helplessness, hopelessness, or fatalism, and intense feelings of loss. These feelings of loss may be due to profound changes in a personally important place (such as one’s home) and/or a sense that one has lost control over events in one’s life due to disturbances from climate change. Additionally, a sense of loss regarding one’s personal or occupational identity can arise when treasured objects are destroyed by a disaster or place-based occupations are disrupted by climate change.

Personal relationships and the ways in which people interact in communities and with each other are affected by a changing climate. Compounded stress from a changing environment, ecomigration, and/or ecoanxiety can affect community mental well-being through the loss of social identity and cohesion, hostility, violence, and interpersonal and intergroup aggression.

Psychological well-being includes positive emotions, a sense of meaning and purpose, and strong social connections. Although the psychological impacts of climate change may not be obvious, they are no less serious because they can lead to disorders, such as depression, antisocial behavior, and suicide. Therefore, these disorders must be considered impacts of climate change as are disease, hunger, and other physical health consequences.

Building resilience is essential to address the physical and mental health impacts of climate change. Many local governments within the United States and in other countries have created plans to protect and enhance infrastructure, but these plans tend to overlook the support needed to ensure thriving psychological well-being. There is an opportunity to include the resilience capacity of individuals and communities in the development of preparedness plans.

OUR CHANGING CLIMATE: A PRIMER

Our climate is changing at an accelerated rate and continues to have profound impacts on human health. This change jeopardizes not only physical health but also mental health.

ACCELERATION

From wildfires and drought in California to severe flooding in Maryland to Alaskan communities threatened by rising seas, we are clearly living through some of the most severe weather events in US. history as a result of damage to our climate. Thes impacts on our environment will, in turn, affect human health and community well-being.

CHANGES WORLDWIDE

Climate change is creating visible impacts worldwide, including many here in America. As seen in the tripling of heat waves between 2011 and 2012, weather patterns introduce lasting impacts, such as food insecurity. Similarly, rising sea-surface temperatures have been connected to increasing rates of disease for marine life and humans. Sea levels are estimated to increase anywhere from 8 inches to 6.6 feet due to warmer temperatures by 2100, putting 8 million Americans living in coastal areas at risk for flooding. In terms of our economy, Hurricane Sandy cost the United States around $68 billion in total. Droughts caused by increases in temperature and changing weather patterns cost California $2.7 billion in 2015 and Texas $7.62 billion in 2011. As these climate disturbances become more dramatic and persistent, we must prepare for these climate conditions.

COMMUNITIES ARE IMPACTED

Our communities’ health, infrastructure, and economy are directly connected to our climate. As temperatures increase, we experience higher levels of pollution, allergens, and diseases. Severe weather events threaten our businesses and vulnerable communities. Pollution and drought undermine our food and water supplies, and the latter increases the prevalence of wildfires that can destroy homes and communities. Although all Americans are affected, certain populations of concern will feel the impacts more severely. Together, communities can build resilience to a changing climate.

HEALTH IS IMPACTED

As severe weather events, poorer air quality, degraded food and water systems, and physical illnesses increase, the direct and indirect impacts on health must be understood. The next section highlights the physical health impacts of climate change, and the following sections delve deeper into the mental health impacts, and what can be done to protect human well-being.

THE CLIMATE AND HEALTH IMPACTS ON HUMANS

Health is more than the absence of disease. Health includes mental health, as well as physical well-being, and communities that fail to provide basic services and social support challenge both. As we think about the impacts of climate change on our communities, we need to recognize not only the direct effects but also the indirect consequences for human health based on damage to the physical and social community infrastructure. Regardless of how these impacts surface, whether they occur within a matter of hours or over several decades, the outcomes of climate change are interconnected to all facets of our health.

ACUTE IMPACTS:

DlSASTER-RELATED EFFECTS

Recent increases in natural disasters illustrate the relationship between the acceleration of climate change and severe weather.

Areas that endure a natural disaster face a number of risks and difficulties. Direct physical impacts range from brute physical trauma to more pernicious effects, like increased incidence of infectious disease, asthma, heart disease, and lung problems. These physical health impacts interact with mental health impacts.

Major and minor acute physical injury

Natural disasters lead to increased rates of death and injury. The most common causes of mortality during floods are drowning and acute physical trauma. This past year alone, deaths from flash floods have more than doubled the 10-year average. Many people sustain non-fatal injuries, such as cuts and broken bones.

Infrastructure, food, and water

The direct effect of a natural disaster is often exacerbated by a cascade of indirect consequences that follow. Natural disasters can lead to technological disasters (such as power outages), breakdowns in the water, sewer, and other infrastructure, or urban fires. For instance, the risk of carbon monoxide poisoning related to power outages increases as a result of climate change-induced disasters. Disruptions to medical infrastructure, including the provision of medical supplies, can transform minor issues into major and even fatal problems. In addition, disruptions in other types of services (e.g., cell phone communication, transportation, or waste management) add stress and difficulty during the aftermath of a disaster. These disruptions may impact people’s physical health by making it more difficult to access health care or by potentially increasing exposure to pests or hazardous substances (e.g., when there is no garbage pick-up. Loss of income while businesses are closed due to natural disasters can be a major threat to food security, especially for non-professionals or small business owners.

After effects

Additional health threats follow in the wake of a disaster. Floodwater has been shown to introduce toxic materials, water-borne diseases (e.g., respiratory illnesses, skin infections, and neurologic and gastrointestinal illness where there are poor hygiene resources), and vector-borne illnesses (e.g., West Nile). Other after effects of flooding include heart attack, heat stroke, dehydration, and stroke, particularly when the affected areas lack the necessary medical supplies. In addition, post-flood mold due to fungal growth inside houses can worsen allergy or asthma symptoms.

MORE GRADUAL HEALTH EFFECTS

Ongoing effects of climate change include rising sea levels, increases in temperature, and changes in precipitation that will affect agricultural conditions. The impacts on human health are less dramatic in the short term but in the long run can affect more people and have a fundamental impact on society.

Severe and changing weather

Periods of higher-than-normal heat result in higher rates of heat exhaustion, heat cramps, heat stroke, hospital admission for heart-related illnesses, and death.

It’s estimated that the average American citizen will experience between 4 and 8 times as many days above 95 degrees Fahrenheit each year as he or she does now by the end of the century. This increase will likely push Arizona’s above-95-degree days from 116 today to as many as 205 by 2099. In contrast, extreme winter storms can expose people to hypothermia and frostbite. Altered growing seasons and ocean temperatures change the timing and occurrence of diarrhea, fever, and abdominal cramps from pathogen transmissions in raw food. Additionally, changing weather patterns influence the expansion of the migration patterns of animals and insects. This expansion has already begun to result in the spread of vector-borne illness, such as Lyme disease, malaria, dengue fever, plague, and Zika virus to new U.S. geographic areas. For example, vector-borne illnesses carried by mosquitoes can capitalize on receding floodwater for mosquito breeding.

Respiratory issues and allergens

People exposed to ozone air pollution, which is emitted mostly by cars and industrial facilities and is intensified by warmer temperatures, are more likely to visit the hospital for respiratory issues, suffer from asthma, and die prematurely of strokes or heart attacks. Hotter and drier summers increase the frequency and intensity of large wildfires that contribute to smoke inhalation. Pollution contributes to higher levels of pollen and translates into longer and more prevalent allergy seasons.

Fetal and child development

CIimate-driven physical stress on mothers can cause adverse birth outcomes, such as preterm birth and low birth weight. Scientific research shows that children and developing fetuses are at particular risk from air pollution, heat, malnutrition, infectious diseases, allergies, and mental illnesses, which have detrimental impacts on development.

Water and food supply

Nutrition and food safety can be affected because climate change can lower crop yields, reduce the nutritional quality of food, interrupt distribution chains, and reduce access to food because families lose income. For example, higher C02 concentrations lower the levels of protein and essential minerals of widely consumed crops such as wheat, rice, and potatoes. Barriers to food transport, such as damage to infrastructure and displacement of employees, affect food markets by increasing food costs. Droughts, floods, and changes in the availability of fertile land lead to hunger and malnutrition, though these changes are less likely in wealthy countries, such as the United States. Nevertheless, there will be an increased likelihood of a global food market crisis as climate change accelerates. A two-degree Celsius increase in temperature places 100-400 million people at risk of hunger, according to the World Bank.

General fitness

Increased average temperatures and decreased air quality also lead to changes in the type of activities that people engage in, particularly outdoor activities and recreation. These changes, in turn, may be associated with increased rates of obesity and cardiovascular disease. Although people may compensate by exercising in indoor environments, reduced access to the restorative potential of outdoor environments may indirectly increase stress and bypass the long-term emotional benefits of taking physical activity outdoors.

LINKING PHYSICAL IMPACTS, MENTAL HEALTH, AND COMMUNITY WELL-BEING

MENTAL HEALTH

The ability to process information and make decisions without being disabled by extreme emotional responses is threatened by climate change. Some emotional response is normal, and even negative emotions are a necessary part of a fulfilling life. In the extreme case, however, they can interfere with our ablllty to think rationally, plan our behavior, and consider alternative actions. An extreme weather event can be a source of trauma, and the experience can cause disabling emotions. More subtle and indirect effects of climate change can add stress to people’s lives in varying degrees. Whether experienced indirectly or directly, stressors to our climate translate into impaired mental health that can result in depression and anxiety. Although everyone is able to cope with a certain amount of stress, the accumulated effects of compound stress can tip a person from mentally healthy to mentally ill. Even uncertalnty can be a source of stress and a risk factor for psychological distress. People can be negatively affected by hearing about the negative experiences of others, and by fears, founded or unfounded, about their own potential vulnerability.

PHYSICAL HEALTH AND MENTAL HEALTH

Compromised physical health can be a source of stress that threatens psychological well being. Conversely mental health problems can also threaten physical health, for example, by changing patterns of sleep, eating, or exercise and by reducung immune system function.

COMMUNITY HEALTH

Although resndents‘ mental and physical health affect communlties, the impacts of climate on community health can have a particularly strong effect on community fabric and interpersonal relationships. Altered environmental condtions due to climate change can shift the opportunities people have for social interaction, the ways in which they relate to each other. and their connectlons to the natural world.

COMPREHENDING CLIMATE CHANGE

Witnessing the visible impacts of climate change may help people overcome barriers to grasping the problem; however, comprehension has many facets.

PERCEPTION IS DIFFICULT

Although most people are generally aware that climate change is occurring, it continues to seem distant: something that will happen to others, in another place, at some unspecified future date. Psychologists refer to this idea as psychological distance. Terms such as “climate change” and “global warming” draw attention to the global scale rather than the personal impacts. Additionally, the signal of climate change is obscured by the noise of daily and seasonal weather variation. All this makes the issue easier for people to push aside, particularly when faced with other pressing life issues. When people learn about and experience local climate impacts, their understanding increases. Local effects of climate change are often more personally relevant than the general phenomenon of a warming climate, and particularly when knowledge of direct effects is combined with news stories of the imminent risks of climate change. Perceived experience of impacts is associated with increased concern and awareness about climate change, direct experience also increases people’s understanding of climate change. However, direct experience does not necessarily lead to behavior change. For example, experiencing water shortages may increase behavior changes in water use but not encourage other sustainable behavior. Similarly, research suggests experiencing temperature change has no impact on water use behavior.

A PARTISAN ISSUE

Politically polarized in the United States, climate change is perceived as an issue that belongs with the political left, which can suppress belief and concern and discussions about solutions. For example, of the 36% of Americans who are personally concerned a great deal about climate issues, 72% are Democrats, and 27% are Republicans. Political orientation can make open conversations about climate impacts and solutions difficult, and make those who are concerned about climate change feel isolated or paranoid in some circles.

Concerns about health impacts provide common ground for discussion with both ends of the political spectrum. Describing the health-related impacts of climate change and the relevant benefits of taking action to address the impacts can inspire hope among those who dismiss climate change. For instance, conservatives showed decreased support for climate action when the negative health effects were described as affecting people in a faraway country as opposed to people who live in the United States. Listing several health impacts is overwhelming, causing fatalism and diminished engagement.

UNCERTAINTY AND DENIAL

People feel uncertain about the threat of climate change and how to minimize the damage. The media have been criticized for promoting an inaccurate perception of climate change: for example, that there is more scientific controversy about climate change than actually exists. In some cases, information that increases perceptions of the reality of climate change may feel so frightening that it leads to denial and thus a reduction in concern and support for action. In addition, communicating scientific information is not easy; this complexity itself may be a problem. One study showed that people who received more complex information on environmental problems 1) felt more helpless and more inclined to leave the problem to the government; and 2) those who felt ignorant about the topic were more likely to want to avoid hearing about more negative information.

Worldviews and ideologies act as filters to help increase or decrease concern about climate change and motivate action toward solutions. People do not perceive the world neutraly. Instead, through directionally motivated cognition, individuals strive to maintain a world consistent with the ideology and values of their social groups. Because of this, individuals whose worldviews conflict with climate change realities actually may not perceive certain climate effects. Myers, Maibach, Roser-Renouf, Akerlof, and Leiserowitz (2012) found that individuals who were 1) either very concerned about or skeptical of climate change tended to report personal experience with climate change (or lack thereof) based on their pre-existing beliefs about its existence; and 2) individuals less engaged with the issue of climate change changed their beliefs about the existence of climate change based on perceived personal experience with its impacts. Ideologies of climate change and action may also contribute to widespread psychological denial. The distress of climate change can manifest in negative reactions to climate activism. These reactions are reflected in outlets such as social media, and researchers believe this behavior shifts others to denial.

CLIMATE SOLUTIONS BENEFIT MENTAL HEALTH

Physical commuting enhances a sense of well-being. Choosing to bike and/or walk (assuming it is safe and practical to do so) is one individual step that can help reduce the use of climate change-driving fossil fuels. Physical commuting also directly impacts depression, anxiety, PTSD, and other mental illnesses. People who bike and walk to work, school, appointments, and other activities not only reduce emissions and improve their physical health but also experience lower stress levels than car commuters. For instance, individuals who utilized the Washington DC. bikeshare program reported reduced stress levels and weight loss. Similarly, adolescents who actively commute to school show not only lower levels of perceived stress but also increased cardiovascular fitness, improved cognitive performance, and higher academic achievement.

Public transportation invigorates community mental health. Moving people from individual cars to public transit also results in lower greenhouse gas emissions. In addition, several studies have shown that using public transportation leads to an increase in community cohesion, recreational activities, neighborhood walkability, and reduced symptoms of depression and stress associated with less driving and more exercise. Meanwhile, traffic driving worsens air quality and contributes to reduced productivity and increased healthcare costs. Sound transportation systems and urban planning should be expanded as they lead to beneficial mental health and climate outcomes. Green spaces diminish stress. Parks and green corridors have been connected to improved air quality and can increase mental well-being. For example, trees sequester carbon, and green spaces absorb less heat than paved surfaces and buildings. More time spent interacting with nature has been shown to significantly lower stress levels and reduce stress-related illness. Interestingly, this evidence is supported across socioeconomic status, age, and gender. Likewise, individuals who move to areas with access to more green space showed sustained mental health improvements, while individuals who moved to areas with less access to green space experienced substantial negative mental health impacts. However, although a person’s physical and mental health is determined to a large degree by the neighborhood in which he or she lives, relocating to a greener neighborhood isn’t always an option. As planners and policymakers make decisions that will reshape the landscapes of our cities and communities, it is important to recognize the significance and role green areas have in improving air quality, reducing stress, and ensuring a healthy living environment for everyone.

Clean energy reduces health burdens. Wind, solar, hydro, and other clean energy as well as energy efficiency are not only climate-friendly; they also reduce particulates and pollution in the air. Studies on air quality and children’s lung development have shown that as air pollution is reduced, children display significant lung function improvements. Further research revealed that children exposed to higher levels of urban pollution are more likely to develop attention problems and symptoms of anxiety and depression, as well as lower academic performance and brain function. Clean energy provides an opportunity to protect populations of concern, such as children, who experience these impacts more severely.

Although the co-benefits are clear, more comprehensive research on the positive mental health outcomes of climate solutions is needed to bolster support. Research can further promote dynamic solutions as opportunities to improve our health. It is important to increase awareness of the daily choices we make, from how to get to work to the sources of energy to, the more climate-friendly behaviors become mainstreamed, the more they help populations of concern: children, elderly, sick, low income, etc. Fortunately, tangible and effective climate solutions are available today to implement and build upon.

MENTAL HEALTH IMPACTS

The mental health effects of Climate change are gaining public attention. A 2071 government report (US. Global Change Research Program) reviewed a large body of research to summarize the current state of knowledge. This report builds on that knowledge, and considers the direct and indirect effects of Climate change on mental health.

We start by describing the mental health effects on individuals, both short and long term, acute and chronic, the stressors that accumulate in the aftermath of a disaster, and the impacts that natural disasters have on social relationships, with consequences for health and well-being. We move on to discussing the individual-level impacts of more gradual changes in climate, including impacts on aggression and violence, identity, and the long-term emotional impacts of Climate change. Next, we discuss the impacts of climate change on communities and on intergroup and international relationships. Finally, we address the problem of inequity, the fact that certain populations are relatively more vulnerable to these mental health impacts compared to others.

IMPACTS ON INDIVIDUALS

Climate change has acute and chronic impacts, directly and indirectly, on individual well-being. Acute impacts result from natural disasters or extreme weather events. Chronic impacts result from longer term changes in climate. This discussion emphasizes the impacts experienced directly by individuals; however, it also touches on indirect impacts (witnessing others being impacted), which have profound implications for mental health.

ACUTE IMPACTS

Trauma and shock

Climate change-induced disasters have a high potential for immediate and severe psychological trauma from personal injury, injury or death of a loved one, damage to or loss of personal property (e.g., home) and pets, and disruption in or loss of livelihood. An early meta-analysis of studies on the relationship between disasters and mental health impacts found that between 7% and 40% of all subjects in 36 studies showed some form of psychopathology. General anxiety was the type of psychopathology with the highest prevalence rate, followed by phobic, somatic, and alcohol impairment, and then depression and drug impairment, which were all elevated relative to prevalence in the general population. More recent reviews concluded that acute traumatic stress is the most common mental health problem after a disaster. Terror, anger, shock, and other intense negative emotions are likely to dominate people’s initial response. Interview participants in a study about flooding conducted by Carroll, Morbey, Balogh, and Araoz (2009) used words such as “horrifying,” “panic stricken,” and “petrified“ to describe their experience during the flood

Post-traumatic stress disorder (PTSD)

For most people, acute symptoms of trauma and shock are reduced after conditions of security have been restored. However, many continue to experience problems as PTSD manifests as a chronic disorder. PTSD, depression, general anxiety, and suicide all tend to increase after a disaster.

For example, among a sample of people living in areas affected by Hurricane Katrina, suicide and suicidal ideation more than doubled, one in six people met the diagnostic criteria for PTSD, and 49% of people living in an affected area developed an anxiety or mood disorder such as depression. Similarly, 14.5% showed symptoms of PTSD from Hurricane Sandy, and 15.6% of a highly affected community showed symptoms of PTSD several years after experiencing extreme bushfire. PTSD is often linked to a host of other mental health problems, including higher levels of suicide, substance abuse, depression, anxiety, violence, aggresson, interpersonal difficulties, and job-related difficulties.

Incidence of PTSD is more likely among those who have lost close family members or property. Individuals who experience muitiple or long-lasting acute events, such as more than one disaster or multiple years of drought, are likely to experience more severe trauma and may be even more susceptible to PTSD and the other types of psychiatric symptoms described above. For example, a study showed that refugees exposed to multiple traumatic events experienced a higher rate of immediate and lifetime PTSD and had a lower probability of remission than refugees who had experienced few traumatic events. The likelihood of suicide is higher among those who have been exposed to more severe disasters.

Compounded stress

In general, climate change can be considered an additional source of stress to our everyday concerns, which may be tolerable for someone with many sources of support but can be enough to serve as a tipping point for those who have fewer resources or who are already experiencing other stressors. Stress manifests as a subjective feeling and a physiological response that occur when a person feels that he or she does not have the capacity to respond and adapt to a given situation. Thus, climate-related stress is likely to lead to increases in stress-related problems, such as substance abuse, anxiety disorders, and depression. These problems often carry economic costs incurred by lost work days, increased use of medical services, etc, which, in turn, create additional stress for individuals and society and have their own impacts on mental and physical health. Stress can also be accompanied by worry about future disasters and feelings of vulnerability, helplessness, mourning, grief, and despair. Following disasters, increased stress can also make people more likely to engage in behavior that has a negative impact on their health (e.g., smoking, risky behavior, and unhealthy eating habits; e.g. Stain et al. (2011) found that people living in a drought-affected area who had also recently experienced some other adverse life event were more likely to express a high degree of worry about the ongoing drought conditions. Although not as dramatic and acute a disaster as a hurricane, drought is associated with psychological distress, and one study found increased rates of suicide among male farmers in Australia during periods of prolonged drought. Several studies have found that many victims of a flood disaster express psychological distress even years after the flood.

Impacts of stress on physical health

High levels of stress and anxiety also appear to be linked to physical health effects.

For example, chronic distress results in a lowered immune system response, leaving people more vulnerable to pathogens in the air and water and at greater risk for a number of physical ailments. Sleep disorders also increase in response to chronic distress. Doppelt (2016) has described potential physiological responses to the stress of climate change, such as increased levels of the stress hormone cortisol, which, if prolonged, can affect digestion, lead to memory loss, and suppress the immune system. The World Heart Federation (2016) lists stress as a serious risk factor in developing cardiovascular disease.

Strains on social relationships

Particularly in home environments, disasters precipitate a set of stressors that can strain interpersonal interactions. A review of research on the impacts of natural disasters identified problems with family and interpersonal relations, as well as social disruption, concerns about the wider community, and feelings of obligation to provide support to others. Families whose homes are damaged by a flood, storm, or wildfire may need to be relocated, sometimes multiple times, before settling permanently. Family relationships may suffer. Separation from one another and from their systems of social support may occur. Children may have to attend a new school or miss school altogether; parents may find themselves less able to be effective caregivers. In addition, even those who are able to remain in their own home may still lose a sense of their home as a safe and secure environment. This has implications for interpersonal connections, as a home provides the context for social relationships. When the physical home is damaged, it changes the dynamic of the social relationships, often negatively. Domestic abuse, for example, including child abuse, often increases among families who have experienced disasters, such as Hurricane Katrina or the Exxon Valdez oil spill.

CHRONIC IMPACTS

Aggression and violence

The psychological impacts of warmer weather on aggression and violence have been extensively studied. Lab-based experiments and field-based surveys have demonstrated a causal relationship between heat and aggression. In other words, as the temperature goes up, so does aggression. This influenced researcher Craig Anderson (2012) to predict a demonstrable increase in violence associated with increased average temperatures. The relationship between heat and violence may be due to the impacts of heat on arousal, which results in decreases in attention and self-regulation, as well as an increase in the availability of negative and hostile thought, effect on cognitive function, which may reduce the ability to resolve a conflict without violence. Although this impact can manifest as an acute impact (e.g., as a result of a heat wave), due to the pervasive warming trends, and the shifting of climate zones, it is listed under chronic impacts.

Mental health emergencies

There is evidence that increases in mean temperature are associated with increased use of emergency mental health services. This is true not only in hot countries, like Israel and Australia, and in parts of the United States but also in relatively cooler countries, such as France and Canada. Higher temperatures have been linked to increased levels of suicide. It appears that the distress of feeling too hot can overwhelm coping ability for people who are already psychologically fragile. Climate emergencies can also exacerbate preexisting symptoms and lead to more serious mental health problems.

Loss of personally important places

Perhaps one of the best ways to characterize the impacts of climate change on perceptions is the sense of loss. Loss of relationship to place is a substantial part of this. As climate change irrevocably changes people‘s lived landscapes, large numbers are likely to experience a feeling that they are losing a place that is important to them, a phenomenon called solastalgia. This psychological phenomenon is characterized by a sense of desolation and loss similar to that experienced by people forced to migrate from their home environment. Solastalgia may have a more gradual beginning due to the slow onset of changes in one’s local environment. Silver and Grek-Martin (2015) described the emotional pain and disorientation associated with changes in the physical environment that were expressed by residents of a town damaged by tornadoes, even by residents who had not experienced personal loss.

Loss of place is not a trivial experience. Many people form a strong attachment to the place where they live, finding it to provide a sense of stability, security, and personal identity. People who are strongly attached to their local communities report greater happiness, life satisfaction, and optimism; whereas work performance, interpersonal relationships, and physical health can all be negatively affected by disruption to place attachment. For instance, Scannell and Gifford (2016) found that people who visualized a place to which they were attached showed improved self-esteem and sense of belonging relative to those who visualized a place to which they were not attached.

Climate change is likely to have a significant effect on human well-being by increasing migration. When people lose their home to rising sea levels, or when a home becomes unsuitable for human habitation due to its inability to support food crops, they must find another place to live. Although it is difficult to identify climate change as the causal factor in a complex sequence of events affecting migration, a common prediction is that 200 million people will be displaced due to climate change by 2050. Migration in and of itself constitutes a health risk. Immigrants are vulnerable to mental health problems, probably due to the accumulated stressors associated with the move, as well as with the condition of being in exile. Adger, Barnett, Brown, Marshall, and O‘Brien (2013) found being forced to leave one‘s home territory can threaten one’s sense of continuity and belonging. Because of the importance of connection to place in personal identity, such displacement can leave people literally alienated, with a diminished sense of self and increased vulnerability to stress. Although empirical research on the psychological impacts of migration is rare, Tschakert, Tutu, and Alcaro (2013) studied the emotional experience among residents of Ghana who were forced to move from the northern region of the country to the capital, Accra, because local conditions no longer supported their farming practices. Also, respondents expressed nostalgia and sadness for the home left behind and helplessness due to changes in their environments, such as deforestation, that were described as sad and scary.

Loss of autonomy and control

Climate change will intensify certain daily life inconveniences, which can have psychological impacts on individuals’ sense of autonomy and control. The desire to be able to accomplish basic tasks independently is a core psychological need, central to human well-being, and basic services may be threatened due to dangerous conditions. This may make mobility a challenge, particularly for the elderly and those with disabilities. Exposure to unwanted change in one’s environment can also reduce one’s sense of control over one’s life, which, in turn, has negative impacts on mental health.

Loss of personal and occupational identity

A more fundamental loss is the loss of personal identity tied to mundane aspects of daily life. Losing treasured objects when a home is damaged or destroyed is one way in which climate change can significantly impair an individual’s sense of self and identity. This is because objects help provide a continuing sense of who we are, particularly objects that represent important moments in life (e.g., journals), relationships (e.g., gifts or photographs), or personal family history (e.g., family heirlooms). Interviewees in a study conducted by Carroll et al. (2009) indicated that flood victims were particularly troubled by the loss of personal possessions, such as things they had made themselves or special things they had spent time and effort to procure or maintain. Although this may seem acute, the losses are permanent; the impacts are persistent and therefore become chronic.

A loss of identity associated with climate change is also sometimes attributable to its effect on place-bound occupations. This is likely due to the close relationship between identity and place-based occupations, like farming and fishing. Because severe storms and high temperatures disrupt economic activity climate change may have an effect on occupational identity in general. Loss of occupation has been associated with increased risk of depression following natural disaster.

Helplessness, depression, fear, fatalism, resignation, and ecoanxiety

Gradual, long-term changes in climate can also surface a number of different emotions, including fear, anger, feelings of powerlessness, or exhaustion. A review by Coyle and Van Susteren (2011) described cases in which fear of extreme weather approaches the level of phobia and the “unrelenting day-by-day despair” that can be experienced during a drought. Watching the slow and seemingly irrevocable impacts of climate change unfold, and worrying about the future for oneself, children, and later generations, may be an additional source of stress. Albrecht (2011) and others have termed this anxiety ecoanxiety. Qualitative research provides evidence that some people are deeply affected by feelings of loss, helplessness, and frustration due to their inability to feel like they are making a difference in stopping climate change. Some writers stress the possible detrimental impact of guilt, as people contemplate the impact of their own behavior on future generations. Although the impacts of climate change are not always visible, they perpetuate a delayed destruction that, like the damage to climate, are incremental and can be just as damaging as acute climate impacts.

IMPACTS ON COMMUNITY AND SOCIETY

In addition to the effects on individual health and wellbeing, climate change affects how individuals interact in communities and relate to each other. For example, natural disasters can have a negative impact on community bonds. A changing climate will likely affect aspects of community wellbeing, including social cohesion, aggression, and social relationships.

SOCIAL COHESION AND COMMUNITY CONTINUITY

Compounded stress from climate change has been observed among various communities. For example, CunsoLo Willox et al. (2013) examined the impacts of climate change on a small Inuit COMMUNITY. Members of the community, who all reported a strong attachment to the land, said they had noticed changes in the local climate and that these changes contributed to negative effects on themselves. As a result of altered interactions with the environment, community members reported food insecurity, sadness, anger, increased family stress, and a belief that their sense of self-worth and community cohesion had decreased. Elders expressed specific concern for the preservation of Inuit language and culture as they directly influence mental wellbeing and social cohesion.

Social cohesion and social capital can protect communities against mental and physical health impacts during a climate related disaster. Regardless of socioeconomic or cultural backgrounds, communities with high levels of social capital and community leadership experience the quickest recoveries after a disaster and the highest satisfaction with community rebuilding.

When locaI conditions become practically uninhabitable, ecomigration, leading to environmental refugees, can result. Such migrations erode social networks, as communities disperse in different directions. Because social networks provide important practical and emotional resources that are associated with health and wellbeing, the loss of such networks places people’s sense of continuity and belonging at risk. The current Syrian conflict, which has resulted in mass migration, may partially stem from climate change driven precipitation changes, rising mean sea levels, and a decrease in soil moisture. These climate impacts were exacerbated during the drought from 2007 to 2010 due to human disruptions within natural systems, leading to crop failure and large-scale conflict, hunger, and desperation. Although such civil unrest cannot be attributed to a single cause, recent evidence suggests climate-change caused drought may have played a significant role in the unraveling of an already vulnerable political and ecological climate.

AGGRESSION

Heightened anxiety and uncertainty about one’s own future can reduce the ability to focus on the needs of others, negatively impacting social relationships with friends and co-workers, as well as attitudes toward other people in general.

Interpersonal violence

High temperatures associated with climate change may increase people‘s aggressive tendencies. Aggression can also be exacerbated by decreased access to stress reducing green spaces and supportive social networks. Rising levels of frustration in society consequently lead to interpersonal aggression (such as domestic violence, assault, and rape). Ranson (2012) calculated that between 2010 and 2099, climate change would cause an estimated additional 30,000 murders, 200,000 cases of rape, and 3.2 million burglaries due to increased average temperatures.

Intergroup aggression

Climate change may increase conflict through several mechanisms. Violence may increase when competition for scarce natural resources increases or when ecomigration brings formerly separate communities into contact and they compete for resources, like jobs and land. In a recent metaanalysis, Hsiang, Burke, and Miguel (2013) found evidence that climate change can contribute to the frequency of intergroup violence (ie. political conflict and war). For example, in Houston, Texas, crime rates increased significantly following Hurricane Katrina, although Katrina migrants have not been definitively sourced as the cause. Meanwhile, restraints on crime weaken when existing social institutions are disrupted, thus increasing the probability of criminal behavior. For example, when government resources are devoted to damaged infrastructure from natural disasters, those resources may be diverted away from criminal justice systems, mental health agencies, and educational institutions, all of which tend to help mitigate crime. Agnew (2012) further pointed out that the effects of climate chanqe are likely to promote crime by “increasing strain, reducing social control, and weakening social support.”

Intergroup attitudes can also be negatively impacted by climate change. In a recent study, survey respondents displayed more negative attitudes toward policies to support minorities and immigrants when temperatures were high. An experimental study showed that people who were thinking about climate change became more hostile to individuals outside their social group (that is, people they consider to be unlike them) and more likely to support the status quo and its accompanying social inequities. Hostility toward individuals outside one’s social group can be a way of affirming one’s own group identity in the face of a perceived threat. In a vicious cycle, lower levels of social cohesion and connectedness, greater social inequalities, lack of trust between community members and for institutions, and other factors that inhibit community members from working together are associated with intergroup aggression.

THE PROBLEM OF INEQUITY

The impacts of climate change are not distributed equally. Some people will experience natural disasters firsthand, some will be affected more gradually over time, and some will experience only indirect impacts. This section describes some of the populations that are more vulnerable to the mental health impacts of climate change, including people who live in risk-prone areas, indigenous communities, low-income groups, certain communities of color, women, children, older adults, and people with disabilities or chronic illnesses. A thorough review of demographic differences in vulnerability to climate change can be found in Dodqen et al. (2016).

RISK-PRONE AREAS

Communities in which people’s livelihoods are directly tied to the natural environment, through agriculture, fishing, or tourism, are at greater risk. Some parts of the world are geologically more vulnerable to storms, rising seas, wildfires, or drought. There are detailed reports of farmers in Australia who have been negatively affected by prolonged periods of drought caused by changing weather patterns. Additionally, communities in low-lying areas, such as coastal Louisiana and islands in the Chesapeake Bay, are losing their land to erosion and rising seas. This past year, residents of Isle de Jean Charles, Louisiana, became the first climate refugees in the United States; a $48 million budget was allocated to relocate residents to a less flood-prone area, inhabitants of indigenous communities often depend on natural resources for their livelihoods and are located in geographically vulnerable regions.

Communities that lack resources, both physical and financial, can experience climate impacts more severely. This can be demonstrated by higher incidents of extreme weather within impoverished communities. In disasters, socioeconomically disadvantaged communities often suffer the most. For example, following Hurricane Sandy, lower income residents reported weak or absent social support networks and had the greatest percentages of severe mental distress and diagnosis of depression or anxiety after the hurricane. Furthermore, 35% of children living in a household that earns less than $20,000 annually experienced feelings of sadness, depression, fear, or nervousness following the hurricane.

INDIGENOUS COMMUNITIES

Indigenous communities are at risk of losing their cultural heritage, as well as their homes. Imperiled indigenous communities are found around the world, including the United States. In Alaska, for example, some native Alaskans have seen their villages literally vanish due to the thawing permafrost, and others are facing a similar outcome in the near future. For indigenous communities, climate change may threaten not oniy their physical home but also their lifestyle, including access to traditional food and culturally meaningful practices. Chief Albert Naquin of a Louisiana tribal community threatened by climate change stated, ”We’re going to lose all our heritage, all our culture”. Cunsolo, Willox et al. (2013) reviewed case studies of several Inuit communities and reported weakening social networks, increased levels of conflict, and significant stress associated with relocation or even thinking about relocation. In evocative language, Inuit community members interviewed by Durkalec et al. (2015) reported that an inability to go out on the sea ice (due to a changing climate) would make them feel like they “have no health” and ”can’t breathe,“ and they would ”be very sad,” “be lost,” or ”go crazy”.

The loss of any community is tragic, but the impact on native communities is particularly notable because it diminishes the cultural heritage and because indigenous communities are often defined by a special connection to the natural environment. This connection includes traditional patterns of behavior and environmental knowledge about the specific local ecosystem, knowledge that is disappearing, and about how to adapt to changing environments that could help us as a broader society as we adapt to the consequences of climate change.

CHILDREN AND INFANTS

Climate change has a big impact on young people. Children are more vulnerable to many of the effects due to their small size, developing organs and nervous systems, and rapid metabolisms. Children are more sensitive to temperature, because their physiological regulatory systems may be less effective (e.g., they sweat less) and because they are more likely to depend on others to help them regulate their behavior. Their small size makes very young children more susceptible to dehydration, and children under age five living in poverty represent 80% of victims of sanitation-related illnesses and diarrheal disease.

Climate impacts may have long-term and even permanent effects, such as changing the developmental potential and trajectory of a child. Currie and Almond (2011) reviewed evidence that even minor disturbances during childhood may have effects on health and earning potential that last into adulthood. Studies have shown that children who experience a flood or a drought during key developmental periods are shorter, on average, as adults. Fetuses are vulnerable to heat waves, with research shows that exposure to heat waves especially during the second and third trimesters of pregnancy leads to a lower average birth weight and possibly a greater incidence of preterm birth. Malnourishment or severe threat to health during the early years is associated with fewer years of schooling and reduced economic activity as adults, as well as with behavioral and motor problems and reduced IQ. Additionally, early exposure to disease provoked by climate change can have a major and permanent impact on neurological development, as can be dramatically seen in children exposed prenatally to the Zika virus.

Children can experience PTSD and depression following traumatic or stressful experiences with more severity and prevalence than adults. After climate events, children typically demonstrate more severe distress than adults. Furthermore, the prevalence of distress is also higher; higher rates of PTSD were found in children two years after a flood. Children’s mental health can also be affected not only by their experiences of stressors, such as natural disasters, extreme weather, and ecomigration, but also by the mental health of their caregivers. Children also have the potential to be emotionally affected if they become separated from their primary caregivers. Similar to physical experiences, traumatic mental experiences can have lifelong effects. Of course, early childhood is critical for brain development. Studies have documented that high levels of stress during childhood can affect the development of neural pathways, in ways that impair memory, executive function, and decision-making in later life.

Children are also at increased risk from disruptions to the educational system. Natural disasters, in particular can damage or destroy schools or make them inaccessible to teachers and students. After Hurricane Katrina, for example, 196,000 public school students had to change schools, and many of them missed a month or more of schooling. In this case, because the hardest-hit school districts were also some of the worst-performing ones, some students benefitted by transferring to better schools. However the effects on school achievement were negative.

Disasters may cause children to lose their social support networks to a greater extent. During adversity, people draw upon all of their personal resources, emotional and material. Although social networks can fill the gaps when individual resources become depleted during extreme trauma, the resources available from a tight-knit community may not go far, especially if the network is small or the community is poor. When disasters hit an area, they affect everyone and put entire neighborhoods in need of help. A study of children impacted by Hurricane Katrina found that those who were hit hardest by the storm also experienced less social support, likely because people in their immediate support network were themselves suffering.

DISADVANTAGED COMMUNITIES

Some communities of color are prone to experience increased impacts. A persistent reality in American culture is the existence of environmental injustice: Some racial and ethnic groups tend to be more exposed to environmental risks and to have fewer financial and political resources to buffer the impact. This is partly, but not completely, explained by economic status. Communities with fewer resources and greater exposure, for example, in Phoenix, Arizona, are likely to experience greater rates of high temperature impacts than majority groups. Lower-income communities are more likely to have outdated infrastructure, such as a lack of extreme weather warning systems, inadequate storm surge preparedness, and clogged or inadequate storm sewer systems, which places these communities at greater risk for the impacts of climate change. Areas with a high number of residents who lack access to health care or health insurance, or already experience poor health are more likely to be affected by climate change. Communities are also less resilient when they are weakened by social stressors, such as racism, economic inequality, and environmental injustices. Many of the communities in New Orleans that were affected by Hurricane Katrina possessed all of these characteristics, and the effects of racial disparities were clearly visible in the aftermath of the storm.

OCCUPATIONAL GROUPS

Certain lines and fields of work are more directly exposed to the impact of climate change. These occupations may include but not be limited to first responders, construction workers, health care workers, farmers, farm workers, fishermen, transportation workers, and utility workers. Inequitable health outcomes may arise directly through workers’ exposure to increased temperatures, air pollution, and extreme weather, and indirectly through vector-borne diseases, increased use of pesticides, and many other elements. According to the US Environmental Protection Agency, outdoor workers will be the first to endure the effects of climate change, as they will be exposed to extreme heat, which can cause heat stroke, exhaustion, and fatigue. As natural disasters occur more frequently, such as wildfires and flooding, firefighters and paramedics face increased safety risks. Agricultural workers face increased vulnerability to allergens, insects carrying diseases, such as West Nile, and pesticide exposure that are increased by changing weather and insect migration patterns.

ADDITIONAL POPULATIONS OF CONCERN

Individuals of all ages with disabilities or chronic mental or physical health issues may experience climate-related impacts at a greater extent. Often, people living with disabilities have disproportionately far lower access to aid during and after climate-related disasters. Those with mental health disorders can also experience exacerbated symptoms due to natural disasters. Degraded infrastructure creates barriers for people with mental illnesses to receive proper medical attention, leading to additional negative mental and physical health outcomes. For instance, following the 2012 Wisconsin heat wave, 52% of all heat-related deaths were among individuals with at least one mental illness. Half of those suffering from mental illness were taking psychotropic medications, which impede one’s ability to regulate one’s body temperature. These medications that treat mental illness are one of the main underlying causes of heat-related deaths. Additionally, those suffering from ongoing asthma and respiratory illnesses, like chronic obstructive pulmonary disease (COPD), are more sensitive to reduced air quality. Moreover, inequalities in the incidence of those who are chronically ill arise as a result of several socioeconomic factors.

Due to increased health and mobility challenges, the elderly are very susceptible to the risks of climate impacts. Higher rates of untreated depression and other physical illnesses reported among seniors contribute to this increased vulnerability. Research suggests the elderly, in particular, experience declines in cognitive ability when exposed to air pollution over the long ter. A study by Dominelii (2013) found that when infrastructure broke down (e.g., roads were impassable) due to floods. heat waves, or freeze-thaw events (all potentially climate-driven), formal care services were not available to vulnerable people, such as the elderly. They could not get to the services, and their normal services could not come through. Heat can have a particuIarly severe impact on the elderly and on people with pre-existing mental health problems; some of the medications associated with mental illness make people more susceptible to the effects of heat. Extreme temperatures or pollution can also make it more difficult for seniors to engage in regular outdoor activities, thus depriving them of the associated physical and mental benefits.

The stress directly related to supporting a child makes women more affected by climate change. Because of a mother’s frequent caregiver role, and because, on average, women have fewer economic resources than men, women may also be more affected, in general, by the stress and trauma of natural disasters. Possible loss of resources, such as food, water, shelter, and energy, may also contribute to personal stress. Epidemiological studies of post-disaster cohorts and the general population, suggest that women are more likely to experience mental health problems as a result of trauma. For example, the prevalence of PTSD in the general population is reported to be approximately twofold greater in women than in men.

BUILDING RESILIENCE

Developing plans to adapt and cope is critical in addressing the physical and psychological impacts of climate change. Resilience can be defined as the ability of a person (or a community) to cope with, grow through, and transcend adversity.

Climate change is no longer a distant, unimaginable threat; it is a growing reality for communities across the globe. Recognizing the risk, many local governments in the United States (as well as other places around the world) have created preparation or adaptation plans for shoring up physical infrastructure to withstand new weather and temperature extremes. These plans, while an important step, generally overlook the psycho-social impacts of a changing climate and do little to create or support the soft infrastructure needed for community psychological wellbeing. How can communities prepare themselves to minimize suffering and promote resilience in the face of the challenging impacts of climate change? Resilient communities can create the physical and social infrastructure that makes them less susceptible to negative effects.

On an individual level, resilience is built internally and externally through strategies, such as coping and self-regulation, and community social support networks. Most people come through adversity with positive adjustment and without psychopathology. In fact, some individuals may even experience what is called post-traumatic growth and come through a significant disruption with the feeling of having gained something positive, such as stronger social relationships or spectfic skills.

Even so, much can be done to increase the resilience capacity of individuals and communities, particularly in response to climate change.

Download the full report here.

MIT Creates AI that Predicts Depression from Speech – Cami Rosso.

Depression is one of the most common disorders globally that impacts the lives of over 300 million people, and nearly 800,000 suicides annually.

For a mental health professional, asking the right questions and interpreting the answers is a key factor in the diagnosis. But what if a diagnosis could be achieved through natural conversation, versus requiring context from question and answer?

An innovative Massachusetts Institute of Technology (MIT) research team has discovered a way for AI to detect depression in individuals through identifying patterns in natural conversation.

Psychology Today

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions – Johann Hari.

“Even when the tears didn’t come, I had an almost constant anxious monologue thrumming through my mind. Then I would chide myself: It’s all in your head. Get over it. Stop being so weak.”

As she was speaking, I started to experience something strange. Her voice seemed to be coming from very far away, and the room appeared to be moving around me uncontrollably. Then, quite unexpectedly, I started to explode, all over her hut, like a bomb of vomit and faeces. When, some time later, I became aware of my surroundings again, the old woman was looking at me with what seemed to be sad eyes. “This boy needs to go to a hospital,” she said. “He is very sick.

Although I couldn’t understand why, all through the time I was working on this book, I kept thinking of something that doctor said to me that day, during my unglamorous hour of poisoning.

“You need your nausea. It is a message. It will tell us what is wrong with you.”

It only became clear to me why in a very different place, thousands of miles away, at the end of my journey into what really causes depression and anxiety, and how we can find our way back.
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In every book about depression or severe anxiety by someone who has been through it, there is a long stretch of pain-porn in which the author describes, in ever more heightened language, the depth of the distress they felt. We needed that once, when other people didn’t know what depression or severe anxiety felt like. Thanks to the people who have been breaking this taboo for decades now, I don’t have to write that book all over again. That is not what I am going to write about here. Take it from me, though: it hurts.

Prologue: The Apple

One evening in the spring of 2014, I was walking down a small side street in central Hanoi when, on a stall by the side of the road, I saw an apple. It was freakishly large and red and inviting. I’m terrible at haggling, so I paid three dollars for this single piece of fruit, and carried it into my room in the Very Charming Hanoi Hotel. Like any good foreigner who’s read his health warnings, I washed the apple diligently with bottled water, but as I bit into it, I felt a bitter, chemical taste fill my mouth. It was the flavor I imagined, back when I was a kid, that all food was going to have after a nuclear war. I knew I should stop, but I was too tired to go out for any other food, so I ate half, and then set it aside, repelled.

Two hours later, the stomach pains began. For two days, I sat in my room as it began to spin around me faster and faster, but I wasn’t worried: I had been through food poisoning before. I knew the script. You just have to drink water and let it pass through you.

On the third day, I realized my time in Vietnam was slipping away in this sickness-blur. I was there to track down some survivors of the war for another book project I’m working on, so I called my translator, Dang Hoang Linh, and told him we should drive deep into the countryside in the south as we had planned all along. As we traveled around, a trashed hamlet here, an Agent Orange victim there, I was starting to feel steadier on my feet.

The next morning, he took me to the hut of a tiny eighty-seven-year-old woman. Her lips were dyed bright red from the herb she was chewing, and she pulled herself toward me across the floor on a wooden plank that somebody had managed to attach some wheels to. Throughout the war, she explained, she had spent nine years wandering from bomb to bomb, trying to keep her kids alive. They were the only survivors from her village.

As she was speaking, I started to experience something strange. Her voice seemed to be coming from very far away, and the room appeared to be moving around me uncontrollably. Then-quite unexpectedly, I started to explode, all over her hut, like a bomb of vomit and faeces. When, some time later, I became aware of my surroundings again, the old woman was looking at me with what seemed to be sad eyes. “This boy needs to go to a hospital,” she said. “He is very sick.”

No, no, I insisted. I had lived in East London on a staple diet of fried chicken for years, so this wasn’t my first time at the E.coli rodeo. I told Dang to drive me back to Hanoi so I could recover in my hotel room in front of CNN and the contents of my own stomach for a few more days.

“No,” the old woman said firmly. “The hospital.”

“Look, Johann,” Dang said to me, “this is the only person, with her kids, who survived nine years of American bombs in her village. I am going to listen to her health advice over yours.” He dragged me into his car, and I heaved and convulsed all the way to a sparse building that I learned later had been built by the Soviets decades before. I was the first foreigner ever to be treated there. From inside, a group of nurses, half excited, half baffled, rushed to me and carried me to a table, where they immediately started shouting. Dang was yelling back at the nurses, and they were shrieking now, in a language that had no words I could recognize. I noticed then that they had put something tight around my arm.

I also noticed that in the corner, there was a little girl with her nose in plaster, alone. She looked at me. I looked back. We were the only patients in the room.

As soon as they got the results of my blood pressure, dangerously low, the nurse said, as Dang translated, they started jabbing needles into me. Later, Dang told me that he had falsely said that I was a Very Important Person from the West, and that if I died there, it would be a source of shame for the people of Vietnam. This went on for ten minutes, as my arm got heavy with tubes and track marks. Then they started to shout questions at me about my symptoms through Dang. It was a seemingly endless list about the nature of my pain.

As all this was unfolding, I felt strangely split. Part of me was consumed with nausea, everything was spinning so fast, and I kept thinking: stop moving, stop moving, stop moving. But another part of me, below or beneath or beyond this, was conducting a quite rational little monologue. Oh. You are close to death. Felled by a poisoned apple. You are like Eve, or Snow White, or Alan Turing.

Then I thought, is your last thought really going to be that pretentious?

Then I thought, if eating half an apple did this to you, what do these chemicals do to the farmers who work in the fields with them day in, day out, for years? That’d be a good story, some day.

Then I thought, you shouldn’t be thinking like this if you are on the brink of death. You should be thinking of profound moments in your life. You should be having flashbacks. When have you been truly happy? I pictured myself as a small boy, lying on the bed in our old house with my grandmother, cuddling up to her and watching the British soap opera Coronation Street. I pictured myself years later when I was looking after my little nephew, and he woke me up at seven in the morning and lay next to me on the bed and asked me long and serious questions about life. I pictured myself lying on another bed, when I was seventeen, with the first person I ever fell in love with. It wasn’t a sexual memory, just lying there, being held.

Wait, I thought. Have you only ever been happy lying in bed? What does this reveal about you? Then this internal monologue was eclipsed by a heave. I begged the doctors to give me something that would switch off this extreme nausea. Dang talked animatedly with the doctors. Then he told me finally: “The doctor says you need your nausea. It is a message, and we must listen to the message. It will tell us what is wrong with you.”

And with that, I began to vomit again.

Many hours later, a doctor, a man in his forties came into my field of vision and said: “We have learned that your kidneys have stopped working. You are extremely dehydrated. Because of the vomiting and diarrhea, you have not absorbed any water for a very long time, so you are like a man who has been wandering in the desert for days.” Dang interjected: “He says if we had driven you back to Hanoi, you would have died on the journey.”

The doctor told me to list everything I had eaten for three days. It was a short list. An apple. He looked at me quizzically. “Was it a clean apple?” Yes, I said, I washed it in bottled water. Everybody burst out laughing, as if I had served up a killer Chris Rock punch line. it turns out that you can’t just wash an apple in Vietnam. They are covered in pesticides so they can stand for months without rotting. You need to cut off the peel entirely, or this can happen to you.

Although I couldn’t understand why, all through the time I was working on this book, I kept thinking of something that doctor said to me that day, during my unglamorous hour of poisoning.

“You need your nausea. It is a message. It will tell us what is wrong with you.”

It only became clear to me why in a very different place, thousands of miles away, at the end of my journey into what really causes depression and anxiety, and how we can find our way back.

“When I flushed away my final packs of Paxil, I found these mysteries waiting for me, like children on a train platform, waiting to be collected, trying to catch my eye. Why was I still depressed? Why were there so many people like me?”

Introduction: A Mystery

I was eighteen years old when I swallowed my first antidepressant. I was standing in the weak English sunshine, outside a pharmacy in a shopping center in London. The tablet was white and small, and as I swallowed, it felt like a chemical kiss.

That morning I had gone to see my doctor. I struggled, I explained to him, to remember a day when I hadn’t felt a long crying jag judder its way out of me. Ever since I was a small child, at school, at college, at home, with friends, I would often have to absent myself, shut myself away, and cry. They were not a few tears. They were proper sobs. And even when the tears didn’t come, I had an almost constant anxious monologue thrumming through my mind. Then I would chide myself: It’s all in your head. Get over it. Stop being so weak.

I was embarrassed to say it then; I am embarrassed to type it now.

In every book about depression or severe anxiety by someone who has been through it, there is a long stretch of pain-porn in which the author describes, in ever more heightened language, the depth of the distress they felt. We needed that once, when other people didn’t know what depression or severe anxiety felt like. Thanks to the people who have been breaking this taboo for decades now, I don’t have to write that book all over again. That is not what I am going to write about here. Take it from me, though: it hurts.

A month before I walked into that doctor’s office, I found myself on a beach in Barcelona, crying as the waves washed into me, when, quite suddenly, the explanation, for why this was happening, and how to find my way back, came to me. I was in the middle of traveling across Europe with a friend, in the summer before I became the first person in my family to go to a fancy university. We had bought cheap student rail passes, which meant for a month we could travel on any train in Europe for free, staying in youth hostels along the way. I had visions of yellow beaches and high culture, the Louvre, a spliff, hot Italians. But just before we left, I had been rejected by the first person I had ever really been in love with, and I felt emotion leaking out of me, even more than usual, like an embarrassing smell.

The trip did not go as I planned. I burst into tears on a gondola in Venice. I howled on the Matterhorn. I started to shake in Kafka’s house in Prague.

For me, it was unusual, but not that unusual. I’d had periods in my life like this before, when pain seemed unmanageable and I wanted to excuse myself from the world. But then in Barcelona, when I couldn’t stop crying, my friend said to me, “You realize most people don’t do this, don’t you?”

And then I experienced one of the very few epiphanies of my life. I turned to her and said: “I am depressed! It’s not all in my head! I’m not unhappy, I’m not weak, I’m depressed!”

This will sound odd, but what I experienced at that moment was a happy jolt, like unexpectedly finding a pile of money down the back of your sofa.

There is a term for feeling like this! It is a medical condition, like diabetes or irritable bowel syndrome! I had been hearing this, as a message bouncing through the culture, for years, of course, but now it clicked into place. They meant me! And there is, I suddenly recalled in that moment, a solution to depression: antidepressants. So that’s what I need! As soon as I get home, I will get these tablets, and I will be normal, and all the parts of me that are not depressed will be unshackled. I had always had drives that have nothing to do with depression, to meet people, to learn, to understand the world. They will be set free, I said, and soon.

The next day, we went to the Parc Güell, in the center of Barcelona. It’s a park designed by the architect Antoni Gaudi to be profoundly strange, everything is out of perspective, as if you have stepped into a funhouse mirror. At one point you walk through a tunnel in which everything is at a rippling angle, as though it has been hit by a wave. At another point, dragons rise close to buildings made of ripped iron that almost appears to be in motion. Nothing looks like the world should. As I stumbled around it, I thought, this is what my head is like: misshapen, wrong. And soon it’s going to be fixed.

Like all epiphanies, it seemed to come in a flash, but it had in fact been a long time coming. I knew what depression was. I had seen it play out in soap operas, and had read about it in books. I had heard my own mother talking about depression and anxiety, and seen her swallowing pills for it. And I knew about the cure, because it had been announced by the global media just a few years before. My teenage years coincided with the Age of Prozac the dawn of new drugs that promised, for the first time, to be able to cure depression without crippling side effects. One of the bestselling books of the decade explained that these drugs actually make you “better than well”, they make you stronger and healthier than ordinary people.

I had soaked all this up, without ever really stopping to think about it. There was a lot of talk like that in the late 1990s; it was everywhere. And now I saw, at last that it applied to me.

My doctor, it was clear on the afternoon when I went to see him, had absorbed all this, too. In his little office, he explained patiently to me why I felt this way. There are some people who naturally have depleted levels of a chemical named serotonin in their brains, he said, and this is what causes depression, that weird, persistent, misfiring unhappiness that won’t go away. Fortunately, just in time for my adulthood, there was a new generation of drugs, Selective Serotonin Reuptake Inhibitors (SSRIs), that restore your serotonin to the level of a normal person’s. Depression is a brain disease, he said, and this is the cure. He took out a picture of a brain and talked to me about it.

He was saying that depression was indeed all in my head, but in a very different way. It’s not imaginary. It’s very real, and it’s a brain malfunction.

He didn’t have to push. It was a story I was already sold on. I left within ten minutes with my script for Seroxat (or Paxil, as it’s known in the United States).

It was only years later, in the course of writing this book, that somebody pointed out to me all the questions my doctor didn’t ask that day. Like: Is there any reason you might feel so distressed? What’s been happening in your life? Is there anything hurting you that we might want to change? Even if he had asked, I don’t think I would have been able to answer him. I suspect I would have looked at him blankly. My life, I would have said, was good. Sure, I’d had some problems; but I had no reason to be unhappy, certainly not this unhappy.

In any case, he didn’t ask, and I didn’t wonder why. Over the next thirteen years, doctors kept writing me prescriptions for this drug, and none of them asked either. If they had, I suspect I would have been indignant, and said, If you have a broken brain that can’t generate the right happiness, producing chemicals, what’s the point of asking such questions?

Isn’t it cruel? You don’t ask a dementia patient why they can’t remember where they left their keys. What a stupid thing to ask me. Haven’t you been to medical school?

The doctor had told me it would take two weeks for me to feel the effect of the drugs, but that night, after collecting my prescription, I felt a warm surge running through me, a light thrumming that I was sure consisted of my brain synapses groaning and creaking into the correct configuration. I lay on my bed listening to a worn-out mix tape, and I knew I wasn’t going to be crying again for a long time.

I left for the university a few weeks later. With my new chemical armor, I wasn’t afraid. There, I became an evangelist for antidepressants. Whenever a friend was sad, I would offer them some of my pills to try, and I’d tell them to get some from the doctor. I became convinced that I was not merely nondepressed, but in some better state, I thought of it as “antidepression.” I was, I told myself, unusually resilient and energetic. I could feel some physical side effects from the drug, it was true, I was putting on a lot of weight, and I would find myself sweating unexpectedly. But that was a small price to pay to stop hemorrhaging sadness on the people around me. And-look! I could do anything now.

Within a few months, I started to notice that there were moments of welling sadness that would come back to me unexpectedly. They seemed inexplicable, and manifestly irrational. I returned to my doctor, and we agreed that I needed a higher dose. So my 20 milligrams a day was upped to 30 milligrams a day; my white pills became blue pills.

And so it continued, all through my late teens, and all through my twenties. I would preach the benefits of these drugs; after a while, the sadness would return; so I would be given a higher dose; 30 milligrams became 40; 40 became 50; until finally I was taking two big blue pills a day, at 60 milligrams. Every time, I got fatter; every time, I sweated more; every time, I knew it was a price worth paying.

I explained to anyone who asked that depression is a disease of the brain, and SSRis are the cure. When I became a journalist, I wrote articles in newspapers explaining this patiently to the public. I described the sadness returning to me as a medical process, clearly there was a running down of chemicals in my brain, beyond my control or comprehension. Thank God these drugs are remarkably powerful, I explained, and they work. Look at me. I’m the proof. Every now and then, I would hear a doubt in my head, but I would swiftly dismiss it by swallowing an extra pill or two that day.

I had my story. In fact, I realize now, it came in two parts. The first was about what causes depression: it’s a malfunction in the brain, caused by serotonin deficiency or some other glitch in your mental hardware. The second was about what solves depression: drugs, which repair your brain chemistry.

I liked this story. It made sense to me. It guided me through life.

I only ever heard one other possible explanation for why I might feel this way. It didn’t come from my doctor, but I read it in books and saw it discussed on TV. It said depression and anxiety were carried in your genes. I knew my mother had been depressed and highly anxious before I was born (and after), and that we had these problems in my family running further back than that. They seemed to me to be parallel stories. They both said, it’s something innate, in your flesh.

I started work on this book three years ago because I was puzzled by some mysteries, weird things that I couldn’t explain with the stories I had preached for so long, and that I wanted to find answers to.

Here’s the first mystery. One day, years after I started taking these drugs, I was sitting in my therapist’s office talking about how grateful I was that antidepressants exist and were making me better. “That’s strange,” he said. “Because to me, it seems you are still really quite depressed.” I was perplexed. What could he possibly mean? “Well,” he said, “you are emotionally distressed a lot of the time. And it doesn’t sound very different, to me, from how you describe being before you took the drugs.”

I explained to him, patiently, that he didn’t understand: depression is caused by low levels of serotonin, and I was having my serotonin levels boosted. What sort of training do these therapists get, I wondered?

Every now and then, as the years passed, he would gently make this point again. He would point out that my belief that an increased dose of the drugs was solving my problem didn’t seem to match the facts, since I remained down and depressed and anxious a lot of the time. I would recoil, with a mixture of anger and prissy superiority.

“No matter how high a dose I jacked up my antidepressants to, the sadness would always outrun it.”

It was years before I finally heard what he was saying. By the time I was in my early thirties, I had a kind of negative epiphany, the opposite of the one I had that day on a beach in Barcelona so many years before. No matter how high a dose I jacked up my antidepressants to, the sadness would always outrun it. There would be a bubble of apparently chemical relief, and then that sense of prickling unhappiness would return. I would start once again to have strong recurring thoughts that said: life is pointless; everything you’re doing is pointless; this whole thing is a fucking waste of time. It would be a thrum of unending anxiety.

So the first mystery I wanted to understand was: How could I still be depressed when I was taking antidepressants? I was doing everything right, and yet something was still wrong. Why?

“Addictions to legal and illegal drugs are now so widespread that the life expectancy of white men is declining for the first time in the entire peacetime history of the United States.”

A curious thing has happened to my family over the past few decades.

From when I was a little kid, I have memories of bottles of pills laid out on the kitchen table, waiting, with inscrutable white medical labels on them. I’ve written before about the drug addiction in my family, and how one of my earliest memories was of trying to wake up one of my relatives and not being able to. But when I was very young, it wasn’t the banned drugs that were dominant in our lives, it was the ones handed out by doctors: old-style antidepressants and tranquilizers like Valium, the chemical tweaks and alterations that got us through the day.

That’s not the curious thing that happened to us. The curious thing is that as I grew up, Western civilization caught up with my family. When I was small and I stayed with friends, I noticed that nobody in their families swallowed pills with their breakfast, lunch, or dinner. Nobody was sedated or amped up or antidepressed. My family was, I realized, unusual.

And then gradually, as the years passed, I noticed the pills appearing in more and more people’s lives, prescribed, approved, recommended. Today they are all around us. Some one in five US. adults is taking at least one drug for a psychiatric problem; nearly one in four middle-aged women in the United States is taking antidepressants at any given time; around one in ten boys at American high schools is being given a powerful stimulant to make them focus; and addictions to legal and illegal drugs are now so widespread that the life expectancy of white men is declining for the first time in the entire peacetime history of the United States.

These effects have radiated out across the Western world: for example, as you read this, one in three French people is taking a legal psychotropic drug such as an antidepressant, while the UK has almost the highest use in all of Europe. You can’t escape it: when scientists test the water supply of Western countries, they always find it is laced with antidepressants, because so many of us are taking them and excreting them that they simply can’t be filtered out of the water we drink every day. We are literally awash in these drugs.

What once seemed startling has become normal. Without talking about it much, we’ve accepted that a huge number of the people around us are so distressed that they feel they need to take a powerful chemical every day to keep themselves together.

So the second mystery that puzzled me was: Why were so many more people apparently feeling depressed and severely anxious? What changed?

“We’ve accepted that a huge number of the people around us are so distressed that they feel they need to take a powerful chemical every day to keep themselves together.”

Then, when I was thirty-one years old, I found myself chemically naked for the first time in my adult life. For almost a decade, I had been ignoring my therapist’s gentle reminders that I was still depressed despite my drugs. It was only after a crisis in my life, when I felt unequivocally terrible and couldn’t shake it off, that I decided to listen to him. What I had been trying for so long wasn’t, it seemed, working. And so, when I flushed away my final packs of Paxil, I found these mysteries waiting for me, like children on a train platform, waiting to be collected, trying to catch my eye. Why was I still depressed? Why were there so many people like me?

And I realized there was a third mystery, hanging over all of it. Could something other than bad brain chemistry have been causing depression and anxiety in me, and in so many people all around me? If so-what could it be?

Still, I put off looking into it. Once you settle into a story about your pain, you are extremely reluctant to challenge it. It was like a leash I had put on my distress to keep it under some control. I feared that if I messed with the story I had lived with for so long, the pain would be like an unchained animal, and would savage me.

Over a period of several years, I fell into a pattern. I would begin to research these mysteries, by reading scientific papers, and talking to some of the scientists who wrote them, but I always backed away, because what they said made me feel disoriented, and more anxious than I had been at the start. I focused on the work for another book, Chasing the Scream: The First and Last Days of the War on Drugs, instead. It sounds ridiculous to say I found it easier to interview hit men for the Mexican drug cartels than to look into what causes depression and anxiety, but messing with my story about my emotions, what I felt, and why I felt it, seemed more dangerous, to me, than that.

And then, finally, I decided I couldn’t ignore it any longer. So, over a period of three years, I went on a journey of over forty thousand miles. I conducted more than two hundred interviews across the world, with some of the most important social scientists in the world, with people who had been through the depths of depression and anxiety, and with people who had recovered. I ended up in all sorts of places I couldn’t have guessed at in the beginning, an Amish village in Indiana, a Berlin housing project rising up in rebellion, a Brazilian city that had banned advertising, a Baltimore laboratory taking people back through their traumas in a totally unexpected way. What I learned forced me to radically revise my story, about myself, and about the distress spreading like tar over our culture.

“Everything that causes an increase in depression also causes an increase in anxiety, and the other way around. They rise and fall together.”

I want to flag up, right at the start, two things that shape the language I am going to use all through the book. Both were surprising to me.

I was told by my doctor that I was suffering from both depression and acute anxiety. I had believed that those were separate problems, and that is how they were discussed for the thirteen years I received medical care for them. But I noticed something odd as I did my research. Everything that causes an increase in depression also causes an increase in anxiety, and the other way around. They rise and fall together.

It seemed curious, and I began to understand it only when, in Canada, I sat down with Robert Kohlenberg, a professor of psychology. He, too, once thought that depression and anxiety were different things. But as he studied it, for over twenty years now, he discovered, he says, that “the data are indicating they’re not that distinct.” In practice, “the diagnoses, particularly depression and anxiety, overlap.” Sometimes one part is more pronounced than the other, you might have panic attacks this month and be crying a lot the next month. But the idea that they are separate in the way that (say) having pneumonia and having a broken leg are separate isn’t borne out by the evidence. It’s “messy,” he has proved.

Robert’s side of the argument has been prevailing in the scientific debate. In the past few years, the National Institutes of Health, the main body funding medical research in the United States, has stopped funding studies that present depression and anxiety as different diagnoses. “They want something more realistic that corresponds to the way people are in actual clinical practice,” he explains.

I started to see depression and anxiety as like cover versions of the same song by different bands. Depression is a cover version by a downbeat emo band, and anxiety is a cover version by a screaming heavy metal group, but the underlying sheet music is the same. They’re not identical, but they are twinned.

*

from

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions

by Johann Hari

get it at Amazon.com

Anatomy of a teenage suicide: Leo’s death will count – Virginia Fallon.

In the past year, 668 people took their own lives in New Zealand: the highest number since records began and the fourth year in a row the number increased.


In 2016, some time after the magnitude 7.8 Kaikōura earthquake rattled the capital, the 18-year-old took his own life.

Stuff.co.nz

get help

24/7 Lifeline – 0800 543 354

World in mental health crisis of ‘monumental suffering’, say experts – Sarah Broseley.

“Mental health problems kill more young people than any other cause around the world.” Prof. Vikram Patel, Harvard Medical School
Lancet report says 13.5 million lives could be saved every year if mental illness addressed.

Every country in the world is facing and failing to tackle a mental health crisis, from epidemics of anxiety and depression to conditions caused by violence and trauma, according to a review by experts that estimates the rising cost will hit $16tn (£12tn) by 2030.

A team of 28 global experts assembled by the Lancet medical journal says there is a “collective failure to respond to this global health crisis” which “results in monumental loss of human capabilities and avoidable suffering.”

The burden of mental ill-health is rising everywhere, says the Lancet Commission, in spite of advances in the understanding of the causes and options for treatment. “The quality of mental health services is routinely worse than the quality of those for physical health,” says their report, launched at a global ministerial mental health summit in London.

The Guardian

Towards a New Era for Mental Health

Prabha S Chandra, Prabhat Chand
The new Lancet Commission on global mental health and sustainable development raises important issues at a time when many countries in the Global South are re-examining their national priorities in mental health. With its broad vision, the Commission shows why mental health is a public good that is a crucial part of the Sustainable Development Goals (SDGs). The Commission’s report emphasises the need to take a dimensional approach to mental health problems and their treatment; to allocate resources where they will be most cost-effective; to consider a life-course approach; and to build on existing research that will pave the way for better understanding of the causes, prevention, and treatment of mental health problems.

The Lancet

James Reardon: Let’s talk about suicide

Why is New Zealand’s most serious, persistent health problem banished to the coroner’s files?

It prevents nothing, but promotes the myth that suicide is a mysterious, fatal disease that is never talked about, even after death. NZ Herald 

Video: Mike King on Suicide 

​Why do people take their own lives? How do they reach such a place where they decide they no longer want to live. Experts tell us there are so many reasons, that it’s too complicated to pinpoint why, that it’s too difficult to provide an answer for.  This type of diagnosis doesn’t help. All it does is create and fuel judgemental attitudes like: coward, attention seeker, weakling, soft-cock, pussy.  There are 3 reasons, and only 3 reasons why people take their own lives.  If all of us can learn to better understand these reasons, we might just be in a better position to look after those who may just need help. Please watch and share.

Video