Self-Compassion May Help Protect People from the Harmful Effects of Perfectionism

Perfectionism has increased among young people since 1980, as has been shown recently. Perfectionism does have a healthier strain, but it should be noted that it can also be quite unhealthy. The self-compassion must allow people to more easily forgive themselves for not always being perfect.

perfectionism-and-compassion

Relating to oneself in a healthy way can help weaken the association between perfectionism and depression, according to a study published February 21, 2018 in the open-access journal PLOS ONE by Madeleine Ferrari from Australian Catholic University, and colleagues.

Perfectionistic people often push themselves harder than others to succeed, but can also fall into the trap of being self-critical and overly concerned about making mistakes. When the perfectionist fails, they often experience depression and burnout. In this study, Ferrari and colleagues considered whether self-compassion, a kind way of relating to oneself, might help temper the link between perfectionist tendencies and depression.

The researchers administered anonymous questionnaires to assess perfectionism, depression, and self-compassion across 541 adolescents and 515 adults. Their analyses of these self-assessments revealed that self-compassion may help uncouple perfectionism and depression.

The replication of this finding in two groups of differently-aged people suggests that self-compassion may help moderate the link between perfectionism and depression across the lifespan. The authors suggest that self-compassion interventions could be a useful way to undermine the effects of perfectionism, but future experimental or intervention research is needed to fully assess this possibility.

“Self-compassion, the practice of self-kindness, consistently reduces the strength of the relationship between maladaptive perfectionism and depression for both adolescents and adults,” says lead author Madeleine Ferrari.

The increases in perfectionism among young people since 1980 are probably caused by the policies of neoliberalism, which began to be implemented much more around 1980 and basically represent undermining mechanisms of social solidarity in society. Also, this is what I wrote when addressing perfectionism and neoliberalism last month: “I have thought for years now that there is generally too much competition and not enough cooperation in society today, which is part of the reason I advocate for reforms such as increasing the use of democratic co-operatives.”

My other advice to people who have struggled with unhealthy variants of perfectionism in the past — as I have — is to simply try to first do well, but maybe not quite to the highest standard you know you’re capable of, and then after that decide if you want to improve what you were doing any further. There are times when it’s much better to do something at 80 to 90 percent of your potential instead of not doing it at all. Experiences (and doing something at 80 to 90 percent rather than not at all is an experience) can be immensely valuable, and based on the findings that show a lot of millennials are prioritizing experiences over traditional gifts, there should be an improving understanding of this.

Article: Is everything you think you know about depression wrong?

This new book further confirms the falsehood that is chemical imbalances in the brain causing depression. Additionally, the author has an interesting perspective in that he was on antidepressants for years, which drove him to uncover many real answers about depression. I also didn’t expect to read about democratic co-operatives being described positively, as I didn’t think the author was likely to even mention them, but it doesn’t actually surprise me that much in hindsight. More people are waking up to how the undemocratic division between employer and employee is one of the most core problems in society.

In the 1970s, a truth was accidentally discovered about depression – one that was quickly swept aside, because its implications were too inconvenient, and too explosive. American psychiatrists had produced a book that would lay out, in detail, all the symptoms of different mental illnesses, so they could be identified and treated in the same way across the United States. It was called the Diagnostic and Statistical Manual. In the latest edition, they laid out nine symptoms that a patient has to show to be diagnosed with depression – like, for example, decreased interest in pleasure or persistent low mood. For a doctor to conclude you were depressed, you had to show five of these symptoms over several weeks.

The manual was sent out to doctors across the US and they began to use it to diagnose people. However, after a while they came back to the authors and pointed out something that was bothering them. If they followed this guide, they had to diagnose every grieving person who came to them as depressed and start giving them medical treatment. If you lose someone, it turns out that these symptoms will come to you automatically. So, the doctors wanted to know, are we supposed to start drugging all the bereaved people in America?

The authors conferred, and they decided that there would be a special clause added to the list of symptoms of depression. None of this applies, they said, if you have lost somebody you love in the past year. In that situation, all these symptoms are natural, and not a disorder. It was called “the grief exception”, and it seemed to resolve the problem.

Then, as the years and decades passed, doctors on the frontline started to come back with another question. All over the world, they were being encouraged to tell patients that depression is, in fact, just the result of a spontaneous chemical imbalance in your brain – it is produced by low serotonin, or a natural lack of some other chemical. It’s not caused by your life – it’s caused by your broken brain. Some of the doctors began to ask how this fitted with the grief exception. If you agree that the symptoms of depression are a logical and understandable response to one set of life circumstances – losing a loved one – might they not be an understandable response to other situations? What about if you lose your job? What if you are stuck in a job that you hate for the next 40 years? What about if you are alone and friendless?

The grief exception seemed to have blasted a hole in the claim that the causes of depression are sealed away in your skull. It suggested that there are causes out here, in the world, and they needed to be investigated and solved there. This was a debate that mainstream psychiatry (with some exceptions) did not want to have. So, they responded in a simple way – by whittling away the grief exception. With each new edition of the manual they reduced the period of grief that you were allowed before being labelled mentally ill – down to a few months and then, finally, to nothing at all. Now, if your baby dies at 10am, your doctor can diagnose you with a mental illness at 10.01am and start drugging you straight away.

Dr Joanne Cacciatore, of Arizona State University, became a leading expert on the grief exception after her own baby, Cheyenne, died during childbirth. She had seen many grieving people being told that they were mentally ill for showing distress. She told me this debate reveals a key problem with how we talk about depression, anxiety and other forms of suffering: we don’t, she said, “consider context”. We act like human distress can be assessed solely on a checklist that can be separated out from our lives, and labelled as brain diseases. If we started to take people’s actual lives into account when we treat depression and anxiety, Joanne explained, it would require “an entire system overhaul”. She told me that when “you have a person with extreme human distress, [we need to] stop treating the symptoms. The symptoms are a messenger of a deeper problem. Let’s get to the deeper problem.”

*****

I was a teenager when I swallowed my first antidepressant. I was standing in the weak English sunshine, outside a pharmacy in a shopping centre 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 and I had told him – crouched, embarrassed – that pain was leaking out of me uncontrollably, like a bad smell, and I had felt this way for several years. In reply, he told me a story. There is a chemical called serotonin that makes people feel good, he said, and some people are naturally lacking it in their brains. You are clearly one of those people. There are now, thankfully, new drugs that will restore your serotonin level to that of a normal person. Take them, and you will be well. At last, I understood what had been happening to me, and why.

However, a few months into my drugging, something odd happened. The pain started to seep through again. Before long, I felt as bad as I had at the start. I went back to my doctor, and he told me that I was clearly on too low a dose. And so, 20 milligrams became 30 milligrams; the white pill became blue. I felt better for several months. And then the pain came back through once more. My dose kept being jacked up, until I was on 80mg, where it stayed for many years, with only a few short breaks. And still the pain broke back through.

I started to research my book, Lost Connections: Uncovering The Real Causes of Depression – and the Unexpected Solutions, because I was puzzled by two mysteries. Why was I still depressed when I was doing everything I had been told to do? I had identified the low serotonin in my brain, and I was boosting my serotonin levels – yet I still felt awful. But there was a deeper mystery still. Why were so many other people across the western world feeling like me? Around one in five US adults are taking at least one drug for a psychiatric problem. In Britain, antidepressant prescriptions have doubled in a decade, to the point where now one in 11 of us drug ourselves to deal with these feelings. What has been causing depression and its twin, anxiety, to spiral in this way? I began to ask myself: could it really be that in our separate heads, all of us had brain chemistries that were spontaneously malfunctioning at the same time?

To find the answers, I ended up going on a 40,000-mile journey across the world and back. I talked to the leading social scientists investigating these questions, and to people who have been overcoming depression in unexpected ways – from an Amish village in Indiana, to a Brazilian city that banned advertising and a laboratory in Baltimore conducting a startling wave of experiments. From these people, I learned the best scientific evidence about what really causes depression and anxiety. They taught me that it is not what we have been told it is up to now. I found there is evidence that seven specific factors in the way we are living today are causing depression and anxiety to rise – alongside two real biological factors (such as your genes) that can combine with these forces to make it worse.

Once I learned this, I was able to see that a very different set of solutions to my depression – and to our depression – had been waiting for me all along.

To understand this different way of thinking, though, I had to first investigate the old story, the one that had given me so much relief at first. Professor Irving Kirsch at Harvard University is the Sherlock Holmes of chemical antidepressants – the man who has scrutinised the evidence about giving drugs to depressed and anxious people most closely in the world. In the 1990s, he prescribed chemical antidepressants to his patients with confidence. He knew the published scientific evidence, and it was clear: it showed that 70% of people who took them got significantly better. He began to investigate this further, and put in a freedom of information request to get the data that the drug companies had been privately gathering into these drugs. He was confident that he would find all sorts of other positive effects – but then he bumped into something peculiar.

We all know that when you take selfies, you take 30 pictures, throw away the 29 where you look bleary-eyed or double-chinned, and pick out the best one to be your Tinder profile picture. It turned out that the drug companies – who fund almost all the research into these drugs – were taking this approach to studying chemical antidepressants. They would fund huge numbers of studies, throw away all the ones that suggested the drugs had very limited effects, and then only release the ones that showed success. To give one example: in one trial, the drug was given to 245 patients, but the drug company published the results for only 27 of them. Those 27 patients happened to be the ones the drug seemed to work for. Suddenly, Professor Kirsch realised that the 70% figure couldn’t be right.

It turns out that between 65 and 80% of people on antidepressants are depressed again within a year. I had thought that I was freakish for remaining depressed while on these drugs. In fact, Kirsch explained to me in Massachusetts, I was totally typical. These drugs are having a positive effect for some people – but they clearly can’t be the main solution for the majority of us, because we’re still depressed even when we take them. At the moment, we offer depressed people a menu with only one option on it. I certainly don’t want to take anything off the menu – but I realised, as I spent time with him, that we would have to expand the menu.

This led Professor Kirsch to ask a more basic question, one he was surprised to be asking. How do we know depression is even caused by low serotonin at all? When he began to dig, it turned out that the evidence was strikingly shaky. Professor Andrew Scull of Princeton, writing in the Lancet, explained that attributing depression to spontaneously low serotonin is “deeply misleading and unscientific”. Dr David Healy told me: “There was never any basis for it, ever. It was just marketing copy.”

[…]

So, what is really going on? When I interviewed social scientists all over the world – from São Paulo to Sydney, from Los Angeles to London – I started to see an unexpected picture emerge. We all know that every human being has basic physical needs: for food, for water, for shelter, for clean air. It turns out that, in the same way, all humans have certain basic psychological needs. We need to feel we belong. We need to feel valued. We need to feel we’re good at something. We need to feel we have a secure future. And there is growing evidence that our culture isn’t meeting those psychological needs for many – perhaps most – people. I kept learning that, in very different ways, we have become disconnected from things we really need, and this deep disconnection is driving this epidemic of depression and anxiety all around us.

Let’s look at one of those causes, and one of the solutions we can begin to see if we understand it differently. There is strong evidence that human beings need to feel their lives are meaningful – that they are doing something with purpose that makes a difference. It’s a natural psychological need. But between 2011 and 2012, the polling company Gallup conducted the most detailed study ever carried out of how people feel about the thing we spend most of our waking lives doing – our paid work. They found that 13% of people say they are “engaged” in their work – they find it meaningful and look forward to it. Some 63% say they are “not engaged”, which is defined as “sleepwalking through their workday”. And 24% are “actively disengaged”: they hate it.

Most of the depressed and anxious people I know, I realised, are in the 87% who don’t like their work. I started to dig around to see if there is any evidence that this might be related to depression. It turned out that a breakthrough had been made in answering this question in the 1970s, by an Australian scientist called Michael Marmot. He wanted to investigate what causes stress in the workplace and believed he’d found the perfect lab in which to discover the answer: the British civil service, based in Whitehall. This small army of bureaucrats was divided into 19 different layers, from the permanent secretary at the top, down to the typists. What he wanted to know, at first, was: who’s more likely to have a stress-related heart attack – the big boss at the top, or somebody below him?

Everybody told him: you’re wasting your time. Obviously, the boss is going to be more stressed because he’s got more responsibility. But when Marmot published his results, he revealed the truth to be the exact opposite. The lower an employee ranked in the hierarchy, the higher their stress levels and likelihood of having a heart attack. Now he wanted to know: why?

And that’s when, after two more years studying civil servants, he discovered the biggest factor. It turns out if you have no control over your work, you are far more likely to become stressed – and, crucially, depressed. Humans have an innate need to feel that what we are doing, day-to-day, is meaningful. When you are controlled, you can’t create meaning out of your work.

Suddenly, the depression of many of my friends, even those in fancy jobs – who spend most of their waking hours feeling controlled and unappreciated – started to look not like a problem with their brains, but a problem with their environments. There are, I discovered, many causes of depression like this. However, my journey was not simply about finding the reasons why we feel so bad. The core was about finding out how we can feel better – how we can find real and lasting antidepressants that work for most of us, beyond only the packs of pills we have been offered as often the sole item on the menu for the depressed and anxious. I kept thinking about what Dr Cacciatore had taught me – we have to deal with the deeper problems that are causing all this distress.

I found the beginnings of an answer to the epidemic of meaningless work – in Baltimore. Meredith Mitchell used to wake up every morning with her heart racing with anxiety. She dreaded her office job. So she took a bold step – one that lots of people thought was crazy. Her husband, Josh, and their friends had worked for years in a bike store, where they were ordered around and constantly felt insecure, Most of them were depressed. One day, they decided to set up their own bike store, but they wanted to run it differently. Instead of having one guy at the top giving orders, they would run it as a democratic co-operative. This meant they would make decisions collectively, they would share out the best and worst jobs and they would all, together, be the boss. It would be like a busy democratic tribe. When I went to their store – Baltimore Bicycle Works – the staff explained how, in this different environment, their persistent depression and anxiety had largely lifted.

It’s not that their individual tasks had changed much. They fixed bikes before; they fix bikes now. But they had dealt with the unmet psychological needs that were making them feel so bad – by giving themselves autonomy and control over their work. Josh had seen for himself that depressions are very often, as he put it, “rational reactions to the situation, not some kind of biological break”. He told me there is no need to run businesses anywhere in the old humiliating, depressing way – we could move together, as a culture, to workers controlling their own workplaces.

*****

With each of the nine causes of depression and anxiety I learned about, I kept being taught startling facts and arguments like this that forced me to think differently. Professor John Cacioppo of Chicago University taught me that being acutely lonely is as stressful as being punched in the face by a stranger – and massively increases your risk of depression. Dr Vincent Felitti in San Diego showed me that surviving severe childhood trauma makes you 3,100% more likely to attempt suicide as an adult. Professor Michael Chandler in Vancouver explained to me that if a community feels it has no control over the big decisions affecting it, the suicide rate will shoot up.

[…]

After I learned all this, and what it means for us all, I started to long for the power to go back in time and speak to my teenage self on the day he was told a story about his depression that was going to send him off in the wrong direction for so many years. I wanted to tell him: “This pain you are feeling is not a pathology. It’s not crazy. It is a signal that your natural psychological needs are not being met. It is a form of grief – for yourself, and for the culture you live in going so wrong. I know how much it hurts. I know how deeply it cuts you. But you need to listen to this signal. We all need to listen to the people around us sending out this signal. It is telling you what is going wrong. It is telling you that you need to be connected in so many deep and stirring ways that you aren’t yet – but you can be, one day.”

If you are depressed and anxious, you are not a machine with malfunctioning parts. You are a human being with unmet needs. The only real way out of our epidemic of despair is for all of us, together, to begin to meet those human needs – for deep connection, to the things that really matter in life.

Prozac and Chemical Imbalances in the Brain — The False Narrative

There are admittedly probably a few people with actual chemical imbalances in the brain that cause depression, but for the most part, I think the commonly false chemical imbalance narrative is a ploy pushed by pharmaceutical companies to make profits. I lived years of my life with pretty severe depression and I knew that antidepressants wouldn’t remedy that — if anything, they would have made it worse. I learned that sleeping enough, exercising fairly often, finding some satisfying sex life (ideally finding a lover), limiting or avoiding drug intake, having a healthy diet, having good friends, and doing work that is fulfilling and meaningful are much better types of solutions than relying on a pill. The underlying problem has to be fixed for real happiness — it shouldn’t be artificially made with drugs.

Some 2,000 years ago, the Ancient Greek scholar Hippocrates argued that all ailments, including mental illnesses such as melancholia, could be explained by imbalances in the four bodily fluids, or “humors.” Today, most of us like to think we know better: Depression—our term for melancholia—is caused by an imbalance, sure, but a chemical imbalance, in the brain.

This explanation, widely cited as empirical truth, is false. It was once a tentatively-posed hypothesis in the sciences, but no evidence for it has been found, and so it has been discarded by physicians and researchers. Yet the idea of chemical imbalances has remained stubbornly embedded in the public understanding of depression.

Prozac, approved by the US Food and Drug Administration 30 years ago today, on Dec. 29, 1987, marked the first in a wave of widely prescribed antidepressants that built on and capitalized off this theory. No wonder: Taking a drug to tweak the biological chemical imbalances in the brain makes intuitive sense. But depression isn’t caused by a chemical imbalance, we don’t know how Prozac works, and we don’t even know for sure if it’s an effective treatment for the majority of people with depression.

One reason the theory of chemical imbalances won’t die is that it fits in with psychiatry’s attempt, over the past half century, to portray depression as a disease of the brain, instead of an illness of the mind. This narrative, which depicts depression as a biological condition that afflicts the material substance of the body, much like cancer, divorces depression from the self. It also casts aside the social factors that contribute to depression, such as isolation, poverty, or tragic events, as secondary concerns. Non-pharmaceutical treatments, such as therapy and exercise, often play second fiddle to drugs.

In the three decades since Prozac went on the market, antidepressants have propagated, which has further fed into the myths and false narratives we tell about mental illnesses. In that time, these trends have shifted not just our understanding, but our actual experiences of depression.

[…]

Both the narrative and the use of drugs to treat symptoms of depression transformed after Prozac—the brand name for fluoxetine—was released. “Prozac was unique when it came out in terms of side effects compared to the antidepressants available at the time (tricyclic antidepressants and monoamine oxidase inhibitors),” Anthony Rothschild, psychiatry professor at the University of Massachusetts Medical School, writes in an email. “It was the first of the newer antidepressants with less side effects.”

Even the minimum therapeutic dose of commonly prescribed tricyclics like amitriptyline (Elavil) could cause intolerable side effects, says Hyman. “Also these drugs were potentially lethal in overdose, which terrified prescribers.” The market for early antidepressants, as a result, was small.

Prozac changed everything. It was the first major success in the selective serotonin reuptake inhibitor (SSRI) class of drugs, designed to target serotonin, a neurotransmitter. It was followed by many more SSRIs, which came to dominate the antidepressant market. The variety affords choice, which means that anyone who experiences a problematic side effect from one drug can simply opt for another. (Each antidepressant causes variable and unpredictable side effects in some patients. Deciding which antidepressant to prescribe to which patient has been described as a “flip of a coin.”)

Rothschild notes that all existing antidepressant have similar efficacy. “No drug today is more efficacious that the very first antidepressants such as the tricyclic imipramine,” agrees Hyman. Three decades since Prozac arrived, there are many more antidepressant options, but no improvement in efficacy of treatment.

Meanwhile, as Lacasse and Leo note in a 2005 paper, manufacturers typically marketed these drugs with references to chemical imbalances in the brain. For example, a 2001 television ad for sertraline (another SSRI) said, “While the causes are unknown, depression may be related to an imbalance of natural chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance.”

Another advertisement, this one in 2005, for the drug paroxetine, said, “With continued treatment, Paxil can help restore the balance of serotonin,” a neurotransmitter.

“[T]he serotonin hypothesis is typically presented as a collective scientific belief,” write Lacasse and Leo, though, as they note: “There is not a single peer-reviewed article that can be accurately cited to directly support claims of serotonin deficiency in any mental disorder, while there are many articles that present counterevidence.”

Despite the lack of evidence, the theory has saturated society. In their 2007 paper, Lacasse and Leo point to dozens of articles in mainstream publications that refer to chemical imbalances as the unquestioned cause of depression. One New York Times article on Joseph Schildkraut, the psychiatrist who first put forward the theory in 1965, states that his hypothesis “proved to be right.” When Lacasse and Leo asked the reporter for evidence to support this unfounded claim, they did not get a response. A decade on, there are still dozens of articles published every month in which depression is unquestionably described as the result of a chemical imbalance, and many people explain their own symptoms by referring to the myth.

Meanwhile, 30 years after Prozac was released, rates of depression are higher than ever.

[…]

Depression is now a global health epidemic, affecting one in four people worldwide. Treating it as an individual medical disorder, primarily with drugs, and failing to consider the environmental factors that underlie the epidemic—such as isolation and poverty, bereavement, job loss, long-term unemployment, and sexual abuse—is comparable to asking citizens to live in a smog-ridden city and using medication to treat the diseases that result instead of regulating pollution.

Investing in substantive societal changes could help prevent the onset of widespread mental illness; we could attempt to prevent the depressive health epidemic, rather than treating it once it’s already prevalent. The conditions that engender a higher quality of life—safe and affordable housing, counsellors in schools, meaningful employment, strong local communities to combat loneliness—are not necessarily easy or cheap to create. But all would lead to a population that has fewer mental health issues, and would be, ultimately, far more productive for society.

Smartphone Addiction Creates Brain Imbalance, Study Suggests

My advice is to control the phone instead of letting it control you. As with many other parts of life, for some that will be much easier said than done.

Researchers have found an imbalance in the brain chemistry of young people addicted to smartphones and the internet, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA).

According to a recent Pew Research Center study, 46 percent of Americans say they could not live without their smartphones. While this sentiment is clearly hyperbole, more and more people are becoming increasingly dependent on smartphones and other portable electronic devices for news, information, games, and even the occasional phone call.

Along with a growing concern that young people, in particular, may be spending too much time staring into their phones instead of interacting with others, come questions as to the immediate effects on the brain and the possible long-term consequences of such habits.

Hyung Suk Seo, M.D., professor of neuroradiology at Korea University in Seoul, South Korea, and colleagues used magnetic resonance spectroscopy (MRS) to gain unique insight into the brains of smartphone- and internet-addicted teenagers. MRS is a type of MRI that measures the brain’s chemical composition.

The study involved 19 young people (mean age 15.5, 9 males) diagnosed with internet or smartphone addiction and 19 gender- and age-matched healthy controls. Twelve of the addicted youth received nine weeks of cognitive behavioral therapy, modified from a cognitive therapy program for gaming addiction, as part of the study.

[…]

Researchers used standardized internet and smartphone addiction tests to measure the severity of internet addiction. Questions focused on the extent to which internet and smartphone use affects daily routines, social life, productivity, sleeping patterns and feelings.

The researchers performed MRS exams on the addicted youth prior to and following behavioral therapy and a single MRS study on the control patients to measure levels of gamma aminobutyric acid, or GABA, a neurotransmitter in the brain that inhibits or slows down brain signals, and glutamate-glutamine (Glx), a neurotransmitter that causes neurons to become more electrically excited. Previous studies have found GABA to be involved in vision and motor control and the regulation of various brain functions, including anxiety.

The results of the MRS revealed that, compared to the healthy controls, the ratio of GABA to Glx was significantly increased in the anterior cingulate cortex of smartphone- and internet-addicted youth prior to therapy.

Dr. Seo said the ratios of GABA to creatine and GABA to glutamate were significantly correlated to clinical scales of internet and smartphone addictions, depression and anxiety.

Having too much GABA can result in a number of side effects, including drowsiness and anxiety.

More study is needed to understand the clinical implications of the findings, but Dr. Seo believes that increased GABA in the anterior cingulate gyrus in internet and smartphone addiction may be related to the functional loss of integration and regulation of processing in the cognitive and emotional neural network.

The good news is GABA to Glx ratios in the addicted youth significantly decreased or normalized after cognitive behavioral therapy.

“The increased GABA levels and disrupted balance between GABA and glutamate in the anterior cingulate cortex may contribute to our understanding the pathophysiology of and treatment for addictions,” Dr. Seo said.