Its authors said they were “shocked and surprised” by the results, and called for the development of new classes of medication.
However, in the absence of better drugs, they do not want current prescribing practice to be changed because the trial also showed sertraline is effective in reducing anxiety, which often accompanies depression.
The new trial is by far the largest to be conducted without the involvement of the pharmaceutical industry.
It is also the most in-depth examination of sertraline – a type of selective serotonin reuptake inhibitor (SSRI) – in patients with a range of depression severities, rather than just in severely depressed patients in specialist mental health units.
The study included 654 people aged 18 to 74 who were given either the antidepressant for 12 weeks or a placebo.
The results showed depressive symptoms were five per cent lower after six weeks in the sertraline group, which was “no convincing evidence” of an effect.
After 12 weeks, there was a 13 per cent reduction, a finding the experts described as “weak”.
But the drug did offer clear benefits in reducing anxiety, with a 21 per cent reduction in symptoms at six weeks and 23 per cent at 12 weeks.
This is likely to explain why patients taking sertraline were twice as likely to say they felt generally better compared to the placebo group, even once questioned on specific symptoms of depression the benefit was far weaker.
Symptoms of depression include poor concentration, low mood, trouble with sleep, lack of enjoyment, whereas anxiety is presents as worry, nervousness, irritability and restlessness.
In the U.S., an estimated 17.3 million American adults (7.1% of the adult population), experienced at least one major depressive episode in 2017.1 The highest rates are reported among those aged between 18 and 25.2 However, not only is there evidence that depression is vastly overdiagnosed, but there’s also evidence showing it’s routinely mistreated.
With regard to overdiagnosis, one 2013 study3 found only 38.4% of participants with clinician-identified depression actually met the DSM-4 criteria for a major depressive episode, and only 14.3% of seniors 65 and older met the criteria.
As for treatment, the vast majority are prescribed antidepressant drugs, despite the fact there’s virtually no evidence to suggest they provide meaningful help, and plenty of evidence showing the harms are greater than patients are being told.
According to a 2017 study,4 1 in 6 Americans between the ages of 18 and 85 were on psychiatric drugs, most of them antidepressants, and 84.3% reported long-term use (three years or more). Out of 242 million U.S. adults, 12% were found to have filled one or more prescriptions for an antidepressant, specifically, in 2013.
According to data5 presented by a watchdog group, hundreds of thousands of toddlers are also being medicated with powerful psychiatric drugs, raising serious ethical questions, along with questions about the future mental and physical health of these children.
Recent studies are also shedding much needed light on the addictive nature of many antidepressants, and demonstrate that the benefits of these drugs have been overblown while their side effects — including suicidal ideation — and have been downplayed and ignored for decades, placing patients at unnecessary risk.
The Chemical Imbalance Myth
One researcher responsible for raising awareness about these important mental health issues is professor Peter C. Gøtzsche, a Danish physician-researcher and outspoken critic of the drug industry (as his book, “Deadly Medicines and Organized Crime: How Big Pharma Has Corrupted Healthcare,”6 suggests).
Over the past several years, Gøtzsche has published a number of scientific papers on antidepressants and media articles and a book discussing the findings. In a June 28, 2019 article,7 Gøtzsche addresses “the harmful myth” about chemical imbalances — a debunked hypothesis that continues to drive the use of antidepressants to this day. He writes, in part:8
“Psychiatrists routinely tell their patients that they are ill because they have a chemical imbalance in the brain and they will receive a drug that fixes this …
Last summer, one of my researchers and I collected information about depression from 39 popular websites in 10 countries, and we found that 29 (74%) websites attributed depression to a chemical imbalance or claimed that antidepressants could fix or correct that imbalance …
It has never been possible to show that common mental disorders start with a chemical imbalance in the brain. The studies that have claimed this are all unreliable.9
A difference in dopamine levels, for example, between patients with schizophrenia and healthy people cannot tell us anything about what started the psychosis … [I]f a lion attacks us, we get terribly frightened and produce stress hormones, but this does not prove that it was the stress hormones that made us scared.
People with psychoses have often suffered traumatic experiences in the past, so we should see these traumas as contributing causal factors and not reduce suffering to some biochemical imbalance that, if it exists at all, is more likely to be the result of the psychosis rather than its cause.10
The myth about chemical imbalance is very harmful. It makes people believe there is something seriously wrong with them, and sometimes they are even told that it is hereditary.
The result of this is that patients continue to take harmful drugs, year after year, perhaps even for the entirety of their lives. They fear what would happen if they stopped, particularly when the psychiatrists have told them that their situation is like patients with diabetes needing insulin.”
Real Cause of Depression Is Typically Ignored
According to Gøtzsche, there is no known mental health issue that is caused by an imbalance of brain chemicals. In many cases, the true cause is unknown, but “very often, it is a response to unhealthy living conditions,” he writes.11
He also cites the book,12 “Anxiety — The Inside Story: How Biological Psychiatry Got It Wrong,” written by Dr. Niall McLaren, in which the author shows that anxiety is a major factor in and trigger of most psychiatric disorders.
“A psychiatrist I respect highly, who only uses psychiatric drugs in rare cases … has said that most people are depressed because they live depressing lives,” Gøtzsche writes.
“No drug can help them live better lives. It has never been shown in placebo-controlled trials that a psychiatric drug can improve people’s lives — e.g., help them return to work, improve their social relationships or performance at school, or prevent crime and delinquency. The drugs worsen people’s lives, at least in the long run.13“
Gøtzsche rightfully points out that antipsychotic drugs create chemical imbalances; they don’t fix them. As a group, they’re also somewhat misnamed, as they do not address psychotic states. Rather, they are tranquilizers, rendering the patient passive. However, calming the patient down does not actually help them heal the underlying trauma that, in many cases, is what triggered the psychosis in the first place.
As noted in one 2012 meta-analysis14 of studies looking at childhood trauma — including sexual abuse, physical abuse, emotional/psychological abuse, neglect, parental death and bullying — and subsequent risk of psychosis:
“There were significant associations between adversity and psychosis across all research designs … Patients with psychosis were 2.72 times more likely to have been exposed to childhood adversity than controls … The estimated population attributable risk was 33% (16%-47%). These findings indicate that childhood adversity is strongly associated with increased risk for psychosis.”
Economy of Influence in Psychiatry
A related article,15 written by investigative journalist Robert Whitaker in 2017, addresses the “economy of influence” driving the use of antidepressant drugs in psychiatric treatment — and the “social injury” that results. As noted by Whitaker, mental disorders were initially categorized according to a disease model in 1980 by the American Psychiatric Association.
“We’re all familiar with the second ‘economy of influence’ that has exerted a corrupting influence on psychiatry — pharmaceutical money — but I believe the guild influence is really the bigger problem,” he writes.
Whitaker details the corruption within the APA in his book “Psychiatry Under the Influence,” one facet of which is “the false story told to the public about drugs that fixed chemical imbalances in the brain.” Other forms of corrupt behavior include:
The biased designs of clinical trials to achieve a predetermined result
Spinning results to support preconceived conclusions
Hiding poor long-term outcomes
Expanding diagnostic categories for the purpose of commercial gain
Creating clinical trial guidelines that promote drug use
In his article, Whitaker goes on to dissect a 2017 review16 published in the American Journal of Psychiatry, which Whitaker claims “defends the profession’s current protocols for prescribing antipsychotics, which includes their regular long-term use.”
As Whitaker points out, there’s ample evidence showing antipsychotic drugs worsen outcomes over the long term in those diagnosed with psychotic disorders such as schizophrenia.
The review in question, led by Dr. Jeffrey A. Lieberman, was aimed at answering persistent questions raised by the mounting of such evidence. Alas, their conclusions dismissed concerns that the current drug paradigm might be doing more harm than good.
“In a subsequent press release and a video for a Medscape commentary, Lieberman has touted it as proving that antipsychotics provide a great benefit, psychiatry’s protocols are just fine, and that the critics are ‘nefarious’ individuals intent on doing harm,” Whitaker writes.17
The Scientific Bias of Psychiatric Treatment
Five of the eight researchers listed on the review have financial ties to drug companies, three are speakers for multiple drug companies and all eight are psychiatrists, “and thus there is a ‘guild’ interest present in this review, given that they are investigating whether one of their treatments is harmful over the long-term,” Whitaker notes.18
Not surprisingly, the review ignored studies showing negative effects, including studies showing antipsychotics have a detrimental effect on brain volume. What’s more, while withdrawal studies support the use of antipsychotics as maintenance therapy over the long term, these studies do not address how the drugs affect patients’ long-term health.
“They simply reveal that once a person has stabilized on the medication, going abruptly off the drug is likely to lead to relapse,” Whitaker writes.19 “The focus on long-term outcomes, at least as presented by critics, provides evidence that psychiatry should adopt a selective-use protocol.
If first-episode patients are not immediately put on antipsychotics, there is a significant percentage that will recover, and this ‘spontaneous recovery’ puts them onto a good long-term course. As for patients treated with the medications, the goal would be to minimize long-term use, as there is evidence that antipsychotics, on the whole, worsen long-term outcomes.”
Vast Majority of Psychotic Patients Are Harmed, Not Helped
In his deconstruction of Lieberman’s review, Whitaker details how biased thinking influenced the review’s conclusions. It’s a rather long article, but well worth reading through if you want to understand how a scientific review can be skewed to accord with a preconceived view.
Details I want to highlight, however, include findings relating to the number needed to treat (NNT) and the percentage of patients harmed by the routine use of antipsychotic drugs as a first-line treatment.
As noted by Whitaker, while placebo-controlled studies reveal the effectiveness of a drug compared to an inert substance, they do not effectively reveal the ratio of benefit versus harm among the patient population. NNT refers to the number of patients that have to take the drug in order to get one positive response.
A meta-analysis cited in Lieberman’s review had an NNT of 6, meaning that six patients must take the drug in order for one to benefit from the treatment. The remaining five patients — 83% — are potentially harmed by the treatment. As noted by Whitaker:20
“The point … is this: reviewers seeking to promote their drug treatment as effective will look solely at whether it produces a superior response to placebo. This leads to a one-size-fits-all protocol.
Reviewers that want to assess the benefit-harm effect of the treatment on all patients will look at NNT numbers. In this instance, the NNT calculations argue for selective use of the drugs …”
Antidepressants Are Not Beneficial in the Long Term
While typically not as destructive as antipsychotics, antidepressants also leave a trail of destruction in their wake. A systematic review21 by Gøtzsche published in 2019 found studies assessing harm from selective serotonin reuptake inhibitors (SSRIs) fail to provide a clear and accurate picture of the harms, and therefore “cannot be used to investigate persistent harms of antidepressants.”
In this review, Gøtzsche and colleagues sought to assess “harms of SSRIs … that persist after end of drug intake.” The primary outcomes included mortality, functional outcomes, quality of life and core psychiatric events. In all, 22 papers on 12 SSRI trials were included. Gøtzsche found several distinct problems with these trials. For starters, only two of the 12 trials had a drop-out rate below 20%.
Gøtzsche and his team also note that “Outcome reporting was less thorough during follow-up than for the intervention period and only two trials maintained the blind during follow-up.” Importantly, though, all of the 22 papers came to the conclusion that “the drugs were not beneficial in the long term.”
Another important finding was that all trials either “reported harms outcomes selectively or did not report any,” and “Only two trials reported on any of our primary outcomes (school attendance and number of heavy drinking days).”
Antidepressants Are More Addictive Than Admitted
In a June 4, 2019, article,22 “The Depression Pill Epidemic,” Gøtzsche writes that antidepressant drugs:
“… do not have relevant effects on depression; they increase the risk of suicide and violence; and they make it more difficult for patients to live normal lives.23 They should therefore be avoided.
We have been fooled by the drug industry, corrupt doctors on industry payroll, and by our drug regulators.24 Surely, many patients and doctors believe the pills are helpful, but they cannot know this, because people tend to become much better with time even if they are not treated.25
This is why we need placebo-controlled trials to find out what the drugs do to people. Unfortunately, virtually all trials are flawed, exaggerate the benefits of the drugs, and underestimate their harms.26“
Addictive Nature of Antidepressants Skews Results
In his article,27 Gøtzsche reviews several of the strategies used in antidepressant drug trials to exaggerate benefits and underestimate the harms. One little-known truth that helps skew study results in the drug’s favor is the fact that antidepressants tend to be far more addictive than officially admitted. He explains how this conveniently hides the skewing of results as follows:28
“Virtually all patients in the trials are already on a drug similar to the one being tested against placebo. Therefore, as the drugs are addictive, some of the patients will get abstinence symptoms … when randomized to placebo …
These abstinence symptoms are very similar to those patients experience when they try to stop benzodiazepines. It is no wonder that new drugs outperform the placebo in patients who have experienced harm as a result of cold turkey effects.
To find out how long patients need to continue taking drugs, so-called maintenance (withdrawal) studies have been carried out, but such studies also are compromised by cold turkey effects. Leading psychiatrists don’t understand this, or they pretend they don’t.
Most interpret the maintenance studies of depression pills to mean that these drugs are very effective at preventing new episodes of depression and that patients should therefore continue taking the drugs for years or even for life.”
Scientific Literature Supports Reality of User Complaints
Over the years, several studies on the dependence and withdrawal reactions associated with SSRIs and other psychiatric drugs have been published, including the following:
• In a 2011 paper29 in the journal Addiction, Gøtzsche and his team looked at the difference between dependence and withdrawal reactions by comparing benzodiazepines and SSRIs. Benzodiazepines are known to cause dependence, while SSRIs are said to not be addictive.
Despite such claims, Gøtzsche’s team found that “discontinuation symptoms were described with similar terms for benzodiazepines and SSRIs and were very similar for 37 of 42 identified symptoms described as withdrawal reactions,” which led them to conclude that:
“Withdrawal reactions to selective serotonin re‐uptake inhibitors appear to be similar to those for benzodiazepines; referring to these reactions as part of a dependence syndrome in the case of benzodiazepines, but not selective serotonin re‐uptake inhibitors, does not seem rational.”
• Two years later, in 2013, Gøtzsche’s team published a paper30 in the International Journal of Risk & Safety in Medicine, in which they analyzed “communications from drug agencies about benzodiazepine and SSRI withdrawal reactions over time.”
By searching the websites of drug agencies in Europe, the U.S., UK and Denmark, they found that it took years before drug regulators finally acknowledged the reality of benzodiazepine dependence and SSRI withdrawal reactions and began informing prescribers and patients about these risks.
A significant part of the problem, they found, is that drug agencies rely on spontaneous reporting of adverse effects, which “leads to underestimation and delayed information about the problems.”
In conclusion, they state that “Given the experience with the benzodiazepines, we believe the regulatory bodies should have required studies from the manufacturers that could have elucidated the dependence potential of the SSRIs before marketing authorization was granted.”
• A 2019 paper31 in the Epidemiology and Psychiatric Sciences journal notes “It took almost two decades after the SSRIs entered the market for the first systematic review to be published.” It also points out that reviews claiming withdrawal effects to be mild, brief in duration and rare “was at odds with the sparse but growing evidence base.”
In reality, “What the scientific literature reveals is in close agreement with the thousands of service user testimonies available online in large forums. It suggests that withdrawal reactions are quite common, that they may last from a few weeks to several months or even longer, and that they are often severe.”
Antidepressants Increase Your Risk of Suicide and Violence
In his June 4 article,32 Gøtzsche also stresses the fact that antidepressants can be lethal. In one of his studies,33 published in 2016, he found antidepressants “double the occurrence of events that can lead to suicide and violence in healthy adult volunteers.”
Other research34 has shown they “increase aggression in children and adolescents by a factor of 2 to 3 — an important finding considering the many school shootings where the killers were on depression pills,” Gøtzsche writes.
In middle-aged women with stress urinary incontinence, the selective serotonin and norepinephrine reuptake inhibitor (SNRI) duloxetine, which is also used to treat incontinence, has been shown to double the risk of a psychotic episode and increase the risk of violence and suicide four to five times,35 leading the authors to conclude that harms outweighed the benefits.
“I have described the dirty tricks and scientific dishonesty involved when drug companies and leading psychiatrists try convincing us that these drugs protect against suicide and other forms of violence,36“ Gøtzsche writes.37“Even the FDA was forced to give in when it admitted in 2007, at least indirectly, that depression pills can cause suicide and madness at any age.
There is no doubt that the massive use of depression pills is harmful. In all countries where this relationship has been examined, the sharp rise in disability pensions due to psychiatric disorders has coincided with the rise of psychiatric drug usage, and depression pills are those which are used the most by far. This is not what one would expect if the drugs were helpful.”
Drugmaker Lied About Paxil’s Suicide Risk
In 2017, Wendy Dolin was awarded $3 million by a jury in a lawsuit against GlaxoSmithKline, the maker of Paxil. Dolin’s husband committed suicide six days after taking his first dose of a Paxil generic, and evidence brought forth in the case convincingly showed his suicide was the result of the drug, not emotional stress or mental illness.38
The legal team behind that victory, Baum Hedlund Aristei Goldman, is also representing other victims of Paxil-induced violence and death. At the time, attorney R. Brent Wisner said:39
“The Dolin verdict sent a clear message to GSK and other drug manufacturers that hiding data and manipulating science will not be tolerated … If you create a drug and know that it poses serious risks, regardless of whether consumers use the brand name or generic version of that drug, you have a duty to warn.”
GSK’s own clinical placebo-controlled trials actually revealed subjects on Paxil had nearly nine times the risk of attempting or committing suicide than the placebo group. To gain drug approval, GSK misrepresented this shocking data, falsely reporting a higher number of suicide attempts in the placebo group and deleting some of the suicide attempts in the drug group.
An internal GSK analysis of its suicide data also showed that “patients taking Paxil were nearly seven times more likely to attempt suicide than those on placebo,” Baum Hedlund Aristei Goldman reports, adding:40
“Jurors in the Dolin trial also heard from psychiatrist David Healy, one of the world’s foremost experts on Paxil and drugs in its class … Healy told the jurors that Paxil and drugs like it can create in some people a state of extreme ’emotional turmoil’ and intense inner restlessness known as akathisia …
‘People have described it like a state worse than death. Death will be a blessed relief. I want to jump out of my skin,’ Dr. Healy said. Healthy volunteer studies have found that akathisia can happen even to people with no psychiatric condition who take the drug …
Another Paxil side effect known to increase the risk of suicide is emotional blunting … apathy or emotional indifference … [E]motional blunting, combined with akathisia, can lead to a mental state in which an individual has thoughts of harming themselves or others, but is ‘numbed’ to the consequences of their actions. Drugs in the Paxil class can also cause someone to ‘go psychotic, become delirious,’ Dr. Healy explained.”
Hundreds of Thousands of Toddlers on Psychiatric Drugs
Considering the many serious psychological and physical risks associated with psychiatric drugs, it’s shocking to learn that hundreds of thousands of American toddlers are on them. In 2014, the Citizens Commission on Human Rights, a mental health watchdog group, highlighted data showing that in 2013:41
274,000 babies aged 1 and younger were given psychiatric drugs — Of these, 249,699 were on anti-anxiety meds like Xanax; 26,406 were on antidepressants such as Prozac or Paxil, 1,422 were on ADHD drugs such as Ritalin and Adderall, and 654 were on antipsychotics such as Risperdal and Zyprexa
In the toddler category (2- to 3-year-olds), 318,997 were on anti-anxiety drugs, 46,102 were on antidepressants, 10,000 were prescribed ADHD drugs and 3,760 were on antipsychotics
Among children aged 5 and younger, 1,080,168 were on psychiatric drugs
These are shocking figures that challenge logic. How and why are so many children, babies even, on addictive and dangerously mind-altering medications? Considering these statistics are 6 years old, chances are they’re even higher today. Just what will happen to all of these youngsters as they grow up? As mentioned in the article:42
“When it comes to the psychiatric drugs used to treat ADHD, these are referred to as ‘kiddie cocaine’ for a reason. Ritalin (methylphenidate), Adderall (amphetamine) and Concerta are all considered by the federal government as Schedule II drugs — the most addictive.
ADHD drugs also have serious side effects such as agitation, mania, aggressive or hostile behavior, seizures, hallucinations, and even sudden death, according to the National Institutes of Health …
As far as antipsychotics, antianxiety drugs and antidepressants, the FDA and international drug regulatory agencies cite side effects including, but not limited to, psychosis, mania, suicidal ideation, heart attack, stroke, diabetes, and even sudden death.”
Children Increasingly Prescribed Psych Drugs Off-Label
Making matters even worse, recent research shows the number of children being prescribed medication off-label is also on the rise. An example offered by StudyFinds.org,43 which reported the findings, is “a doctor recommending antidepressant medication for ADHD symptoms.”
The study,44 published in the journal Pediatrics, looked at trends in off-label drug prescriptions made for children under the age of 18 by office-based physicians between 2006 and 2015. Findings revealed:
“Physicians ordered ≥1 off-label systemic drug at 18.5% of visits, usually (74.6%) because of unapproved conditions. Off-label ordering was most common proportionally in neonates (83%) and in absolute terms among adolescents (322 orders out of 1000 visits).
Off-label ordering was associated with female sex, subspecialists, polypharmacy, and chronic conditions. Rates and reasons for off-label orders varied considerably by age.
Relative and absolute rates of off-label orders rose over time. Among common classes, off-label orders for antihistamines and several psychotropics increased over time …
US office-based physicians have ordered systemic drugs off label for children at increasing rates, most often for unapproved conditions, despite recent efforts to increase evidence and drug approvals for children.”
The researchers were taken aback by the findings, and expressed serious concern over this trend. While legal, many of the drugs prescribed off-label have not been properly tested to ensure safety and efficacy for young children and adolescents.
As noted by senior author Daniel Horton, assistant professor of pediatrics and pediatric rheumatologist at Rutgers Robert Wood Johnson Medical School, “We don’t always understand how off-label medications will affect children, who don’t always respond to medications as adults do. They may not respond as desired to these drugs and could experience harmful effects.”
Educate Yourself About the Risks
If you, your child, or another family member is on a psychiatric drug, I urge you to educate yourself about the true risks, and to consider switching to safer alternatives. When it comes to children, I cannot fathom a situation in which a toddler would need a psychiatric drug and I find it shocking that there are so many doctors out there that, based on a subjective evaluation, would deem a psychiatric drug necessary.
With pharmaceutical and even robotic “cures” in the works for loneliness – a condition once considered part of the normal human emotional range but now framed as a health risk – we risk losing the ability to be alone at all.
The pathologization of emotion has been on the march for decades, especially in the US, where fully one sixth of the adult population takes an antidepressant or other psychiatric drug. Now the mental-health industry has a new target – loneliness.
Nearly half of Americans polled last year by health insurer Cigna said they lacked meaningful relationships or companionship. A solutions-based society might examine why so many people feel alienated from their peers despite the constant connectivity of smartphones and internet. A symptom-focused model, however, simply looks to stop them from feeling that way by any means necessary.
Loneliness is “worse than obesity,” according to a raft of studies that have emerged linking the emotion to increased risk of premature death, and even rivals smoking. And like obesity – big business for Big Pharma, gastric bypass surgeons and weight-loss gurus – it requires medical intervention.
THERE’S A PILL FOR THAT
The University of Chicago’s Brain Dynamics Laboratory recently began an eight-week trial of the hormone pregnenolone, rounding up volunteers with “off-the-chart” scores on a psychological loneliness scale. Based on animal studies suggesting the chemical can reduce the exaggerated threat reactions that researchers say characterize loneliness, they hope to normalize the lonely person’s self-centered hyper-vigilance that drives them to both desire human connection and deal poorly with it.
Researchers insist the intention is not to cure loneliness with a pill, but the trial sets a precedent for doing just that – with another psychiatric drug, if pregnenolone doesn’t work out. Antidepressants, for example, have for years been used (and abused) to treat conditions other than depression, with the largest pharmaceutical industry lawsuits targeting overprescribing and off-label prescribing.
And unlike most regular medical patients, individuals deemed mentally ill tend to remain on medication for years, if not for life.
Mental health professionals writing about the loneliness epidemic discuss behavioral interventions, community programs, and therapy, but the introduction of a pharmaceutical solution may prove too tempting for a profession that has learned to love the quick fix a pill provides. Like depression, loneliness has an infinite number of possible causes, some of which are natural and healthy reactions to major life changes. Other types of loneliness have clear behavioral causes that would (before the magic pill, at least) necessitate clear behavioral solutions. Would a psychiatrist reach to medicate the loneliness of a person who only socializes through Facebook with a pill rather than encourage them to talk to real people?
Studies have shown that just a week away from the platform can bring “significant” improvements in well-being, suggesting that in this case, at least, correlation may indeed equal causation. But why force the patient to change his life when a pill will do the trick?
In a quick-fix society that prefers to treat the symptoms while ignoring the disease, a pill for loneliness may be embraced with all the fervor with which antidepressants were greeted before people began to realize that they cause suicidal and homicidal behavior, sexual dysfunction, weight gain, and a host of other problems – and that they don’t actually cure depression.
A loneliness pill will also not address Americans’ emotionally unhealthy digitally-addicted lifestyles. After all, human contact, including real-life socializing, has become a luxury – so says the New York Times, explaining that humans are expensive, screens and robots are cheap, and expecting the unwashed masses to be able to afford access to living, breathing humans like themselves is simply unrealistic.
BRIDGING THE UNCANNY VALLEY
Because if the “loneliness pill” doesn’t work out, AI is waiting in the wings. Already seen as the future of at-home healthcare for aging populations under the care of cash-strapped governments, friendly, helpful robots could find their way into the homes of the lonely. And while snooping AI “digital assistants” like Amazon’s Alexa tend to creep people out, this new wave of robo-buddies would be framed as medical help. As lonely humans become accustomed to conversing with their robot pals, their expectation for real human contact may diminish, and their sense of loneliness with it. After all, you can’t miss what you never had. Already, given the stunted level of discourse on social media, many of us have found ourselves tricked into talking to bots, sometimes exchanging several messages before realizing our interlocutor is not human.
As the bar for “meaningful relationships” is lowered to the point where chatting with an AI can qualify, the loneliness epidemic vanishes – on paper, at least, and in US public health policy, sometimes that’s all that matters.
LONELY OR JUST ALONE?
The pathologization of loneliness will inevitably elide the difference between being alone and being lonely, as the mental health industry runs out of lonely people to treat with whatever therapeutic weapon wins this particular arms race and is forced to seek more patients. “Loners” – those dangerous types who actually enjoy solitude – are stigmatized as unpredictable weirdos who need to be brought into the fold. The man who shot up a Walmart in El Paso earlier this month was an “extreme loner,” according to media reports. Would we be reading about it if he was an “extreme extrovert”? The myth of the “introvert killer” pops up every time, even though it has been thoroughly debunked.
With no anti-loneliness pill on the market – yet – it is impossible to predict what’s next for the creeping pathologization of the human emotional experience. But Amazon’s Alexa has moved one step closer to the companion-robot model, rolling out a medical feature earlier this year which could conceivably be deployed to “check on” individuals at risk for loneliness.
And with implantable devices like Elon Musk’s Neuralink on the horizon, bringing that AI directly in contact with your mind, you’ll never be able to feel lonely again. Solitude – like privacy and human contact before it – thus becomes the ultimate luxury good.
Helen Buyniski is an American journalist and political commentator, working at RT since 2018
Have you ever wondered why so many people who take antidepressants continue to be depressed? The truth is that like many other drugs for mental disorders, they are not the cures that many people believe them to be. They might address symptoms, but they don’t really do much about the cause of depression – and therein lies an important distinction.
In the Waking Times, author Tracy Kolenchuk looks at the logic of a depression diagnosis. What happens when someone is cured of depression? Let’s say their depression was actually caused by a nutritional deficiency. When the deficiency is corrected, their depression goes away – but did they ever really have depression in the first place, or did they just have malnutrition? She argues that depression was a symptom of malnutrition in such a case rather than a disease.
In the case of depression being caused by drugs or toxic chemical exposure, a similar mechanism is at play: Removing the drugs or chemicals from the equation may cure the person’s feelings of depression, but again, it was just a symptom of some type of poisoning rather than a disease. When depression is caused by abuse and then the person is removed from the abusive situation, it wasn’t a mental disorder – it was abuse.
The same can be said of chronic depression, only in this case, the chronic nature of the cause must be addressed to bring about benefits. If a person is in chronically toxic relationships or chronically deficient in nutrition, it’s these causes that must be addressed – but on a wider scale than in the previous cases. A healthy meal or two may help, but if they’re chronically malnourished, they might also be poor, and then their chronic poverty – and by extension, chronic malnutrition – must also be addressed. That’s a much bigger task, of course.
She says that these concepts also apply to anxiety, psychosis, social anxiety, panic attacks, and hyperactivity. If it can be cured, that can be done by addressing the cause – but in that case, it was never really a mental disorder after all.
Getting relief from depression
Of course, all this is just semantics. A depressed person likely just wants relief and doesn’t care about labels, and many of us – depressed or not – have had it drilled into our heads that antidepressants are really the only option out there. That’s the main reason so many people willingly subject themselves to the side effects of these drugs, which include weight gain, insomnia, loss of sexual desire, nausea, constipation, and suicidal thoughts.
Depression is complex and often has multiple causes, and each of these needs to be addressed to make real progress toward feeling better. For many, it’s not just about cleaning up their diet, even though that can help. Consider this: If malnutrition causes a person to become depressed, they may attract toxic relationships into their lives, which could eventually spur them to turn to toxic drugs in a downward spiral of illness. This, too, can be cured, but it requires addressing all of these factors.
Many people don’t realize the strong connection between the gut and the brain. For example, an inflammatory response that starts in your gut that is connected to a lack of nutrients like omega 3s, probiotics, and magnesium, leads to the inflammation in the brain that is behind depression. Therefore, it shouldn’t too surprising to learn that food supplements such as omega 3s, magnesium, zinc, and vitamin D3 and B vitamins can help improve mood and relieve depression and anxiety.
If you or someone you care about is suffering from depression, share this information with them. It could very well help them avoid dangerous antidepressants and finally find some true relief.
Antidepressants and antihistamines are among the most common types of medications people take, and they belong to a class of drugs known as anticholinergics. These drugs can treat a variety of health problems, including COPD, asthma, depression, dizziness, gastrointestinal problems, overactive bladder, and the symptoms of Parkinson’s. Although they can be effective, a large new study has shown that if you take them, you might just be trading one problem for another, possibly bigger one: dementia.
Although people who suffer from depression may be desperate to get relief from this illness that can have such a negative impact on daily life, tricyclic antidepressants fall into this category, so it’s important to pay attention the concerning new findings if you take medications like Elavil, Deptran, Sinequan, or Silenor. The same can be said for antihistamines like Benadryl, among other drugs.
The study, which was published in BMJ, involved more than 40,000 dementia patients and more than 283,000 people who don’t have dementia and followed them from 2006 to 2015. They found that people who had dementia had a greater likelihood of having taken class 3 anticholinergic drugs prior to developing the illness.
These medications block the actions of acetylcholine in the brain, which can prevent it from causing involuntary movements in the muscles in the lungs, urinary tract, gastrointestinal tract, and other parts of the body.
Although the higher risk varied depending on the drugs, some of them raised the risk by 30 percent. Not every anticholinergic drug had the effect, but using some of them even as far back as 20 years raised a person’s risk of dementia later on. Generally speaking, they believe that a person aged 65 to 70 sees their risk of dementia increase by 19 percent if they’ve used anticholinergic antidepressants. The association with dementia goes up with greater levels of exposure to the meds.
The study was praised by experts for its strength and using U.K. healthcare databases rather than relying on patient recall, which isn’t always dependable.
The drugs are believed to have this effect because anticholinergic medications lower the levels of a chemical called acetylcholine in the brain, which is a crucial messenger in memory pathways. This is a known effect that already stops some doctors from prescribing such drugs to older and more frail patients.
Other studies have reached a similar conclusion about anticholinergic drugs
In a different study involving nearly 3,500 people, researchers reached a similar conclusion, finding that those who used anticholinergic drugs had a greater likelihood of developing dementia, and their risk increased according to their cumulative dose. For example, taking such meds for three years or longer was linked to a 54 percent rise in dementia risk compared to taking the same dose for less than three months.
Experts say such findings are a good reminder that people should evaluate all the medications they’re taking from time to time to see if they are really working for you. For example, if you’re taking antidepressants and are still depressed, the medications may not be helping. Many of these drugs have safer alternatives, including non-medication approaches that could make a difference safely and effectively.
With the number of people suffering from Alzheimer’s expected to triple by 2050, it’s important to do all you can to minimize your risk – and that includes staying away from anticholinergic drugs if possible.
Researchers from the Nordic Cochrane Centre have expressed alarm at research into the effectiveness of antidepressant medication, citing such degrees of widespread bias and systematic distortion that we can’t be certain they work.
“We are not saying (anti-depression medication) doesn’t work. But the studies that have been done are often of poor quality and it’s therefore difficult to say anything about the effect of antidepressants,” said Asger Sand Paludan-Müller, a Ph.D. student and one of the co-authors of the analysis, as cited by Videnskab.
Previous studies show that the medication is effective but don’t really quantify exactly how much more effective they are than a placebo or alternative treatments. In their recent meta analysis, the Danish researchers highlight pervasive positive selection bias, inadequate reporting of side effects as well as systematic distortion of results in up to 79 percent of the studies analyzed.
“Our argument here is that the uncertainty is so great that we think we should be saying that we don’t actually know for sure.”
In many cases within the meta analysis, previous researchers had stated a number of goals prior to conducting their studies but would then omit negative results and only focus on the goals achieved without mentioning where there were shortcomings, greatly inflating the apparent effectiveness of a given medication.
There were also repeated failures in double-blind tests, generally considered the highest standard of medical research, as both patients and doctors could quickly tell whether a placebo had been administered or not due to the appearance of side effects.
“When you experience side effects, it is easy for the subject as well as for the researchers to guess that you get medication, and then it is not blind,” explained lead author Klaus Munkholm.
The researchers suggest more in-depth analysis and new and better studies into the treatment of depression using so-called active placebos, which mimic side effects to a certain degree to guarantee that studies remain double-blind.
“If we do not and just choose to say that we now believe that the medicine works, then we do not find out how to make better trials and perhaps create a better treatment,” Munkholm concludes.
In 1996, a group of European researchers found that a certain gene, called SLC6A4, might influence a person’s risk of depression.It was a blockbuster discovery at the time. The team found that a less active version of the gene was more common among 454 people who had mood disorders than in 570 who did not. In theory, anyone who had this particular gene variant could be at higher risk for depression, and that finding, they said, might help in diagnosing such disorders, assessing suicidal behavior, or even predicting a person’s response to antidepressants.Back then, tools for sequencing DNA weren’t as cheap or powerful as they are today. When researchers wanted to work out which genes might affect a disease or trait, they made educated guesses, and picked likely “candidate genes.” For depression, SLC6A4 seemed like a great candidate: It’s responsible for getting a chemical called serotonin into brain cells, and serotonin had already been linked to mood and depression. Over two decades, this one gene inspired at least 450 research papers.
But a new study—the biggest and most comprehensive of its kind yet—shows that this seemingly sturdy mountain of research is actually a house of cards, built on nonexistent foundations.
Richard Border from the University of Colorado at Boulder and his colleagues picked the 18 candidate genes that have been most commonly linked to depression—SLC6A4 chief among them. Using data from large groups of volunteers, ranging from 62,000 to 443,000 people, the team checked if any versions of these genes were more common among people with depression. “We didn’t find a smidge of evidence,” says Matthew Keller, who led the project.Between them, these 18 genes have been the subject of more than 1,000 research papers, on depression alone. And for what? If the new study is right, these genes have nothing to do with depression. “This should be a real cautionary tale,” Keller adds. “How on Earth could we have spent 20 years and hundreds of millions of dollars studying pure noise?”“What bothers me isn’t just that people said [the gene] mattered and it didn’t,” wrote the psychiatrist Scott Alexander in a widely shared blog post. “It’s that we built whole imaginary edifices on top of this idea of [it] mattering.” Researchers studied how SLC6A4 affects emotion centers in the brain, how its influence varies in different countries and demographics, and how it interacts with other genes. It’s as if they’d been “describing the life cycle of unicorns, what unicorns eat, all the different subspecies of unicorn, which cuts of unicorn meat are tastiest, and a blow-by-blow account of a wrestling match between unicorns and Bigfoot,” Alexander wrote.
Border and Keller’s study may be “bigger and better” than its predecessors, but “the results are not a surprise,” says Cathryn Lewis, a geneticist at Kings College London. Warnings about the SLC6A4/depression link have been sounded for years. When geneticists finally gained the power to cost-efficiently analyze entire genomes, they realized that most disorders and diseases are influenced by thousands of genes, each of which has a tiny effect. To reliably detect these miniscule effects, you need to compare hundreds of thousands of volunteers. By contrast, the candidate-gene studies of the 2000s looked at an average of 345 people! They couldn’t possibly have found effects as large as they did, using samples as small as they had. Those results must have been flukes—mirages produced by a lack of statistical power. That’s true for candidate-gene studies in many diseases, but Lewis says that other researchers “have moved on faster than we have in depression.”
Marcus Munafo from the University of Bristol remembers being impressed by the early SLC6A4 research. “It all seemed to fit together,” he says, “but when I started doing my own studies in this area, I began to realize how fragile the evidence was.” Sometimes the gene was linked to depression; sometimes it wasn’t. And crucially, the better the methods, the less likely he was to see such a link. When he and others finally did a large study in 2005—with 100,000 people rather than the 1,000 from the original 1996 paper—they got nothing.e University, who did early influential work on SLC6A4, notes that the candidate-gene approach has already been superseded by other methods. “The relative volume of candidate-gene studies is going way down, and is highly likely to be trivial indeed,” she says. Border and Keller disagree. Yes, they say, their geneticist colleagues have largely abandoned the approach, which is often seen as something of a historical embarrassment. “But we have colleagues in other sciences who had no idea that there was even any question about these genes, and are doing this research to this day,” Border says. “There’s not good communication between sub-fields.” (A few studies on SLC6A4 and depression have even emerged since their study was published in March.)
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