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Vitamin K for PTSD

2/15/2017        In the News 5 Comments

by Mary Neal Vieten, Ph.D., ABPP


A February 8, 2017 article in Science Daily reports the results of mice research that suggests the chemical ketamine could make soldiers less reactive to the horrors of war. Besides the typical problems associated with translating animal research into human applications, any response to this line of inquiry must include a comment on SCIENCE as well as ETHICS.

In medical research scientific inquiry assumes that the ailment being cured as well as the treatment being offered, are tangible, identifiable things that can be scientifically distinguished from other things. Ketamine is a pharmaceutical, a thing, and distinguishable from other pharmaceuticals. Its powerful anesthetic effects also make it a popularly used recreational drug, under the names Special K, Cat Valium, and Vitamin K.

PTSD on the other hand, is a construct, not a thing, it is loosely defined, and it is the sum of its definition, a definition that is not isolated by science, but rather negotiated and voted into the DSM-5. No one will argue that there is no problematic response in people who are exposed to psychologically traumatic stimuli, however no one can argue that this is a distinguishable medical thing, separated from other things by objective medical/laboratory tests.

PTSD only requires that a sufferer complains of a specific set of predictable emotional responses, after being traumatized to a licensed listener, who agrees (diagnosis/label given) or disagrees (no diagnosis or another label given). Another listener may interpret the suffering differently, and apply no label or another label. Interpretation is subject to culture, religiion, values, the experiences of the listener - the list goes on. Scientifically determined categories of illness are not subject to this latitude: you either have a bacteria, virus, cancer, macular degeneration, fracture, or you don’t. All of this is to say, that PTSD is a construct, not an illness. Think of it like “peace” or “justice.” Everyone knows when they are there, and when they are absent, but they are still the sum of their definition, not objective things.

Using a potentially harmful pharmaceutical like ketamine that is known to be addictive, cause flashbacks, and a host of other undesirable effects to treat a loosely defined construct is not only unworthy of scientific inquiry, it is also unethical. Giving it to our military members for this purpose is unconscionable. Furthermore, even in the case that PTSD was an identifiable discrete illness, discrete from other illnesses, which it is not, the hallmark of PTSD is a person who is suffering because of something horrific that occurred.

We need to consider the ETHICS of injecting humans with a substance with the goal of preventing normal human suffering in the face of horror. If we succeed, what kind of human have we created? Ask yourself if you want to be or live next door to that creation.

Advocating For Those Incarcerated in Mental Hospitals

 

ISEPP's Roland Angle delivered a series of talks on the abuses of people subjected to the mental hospital system. See all five here: https://www.youtube.com/channel/UCacsBeLtugnFlMUodMq6XuA

Blue Illness

1/21/2017        In the News 1 Comment

by Chuck Ruby, Ph.D.


Including "Blue Monday" in the title of this article in The Sun and briefly mentioning it in the first few paragraphs is a way to grab the attention of readers. But in a bait and switch ploy, the bulk of this article reveals the real intention is to spread the propaganda that depression is an illness. Let me assure readers, depression is not a mental "illness".

In trying to distinguish depression from "common and totally normal" sadness, this article describes it as an "immense feeling of sadness that can last for weeks and maybe even months." So, we are told depression isn't just sadness, it is really, really sad sadness. Yet nowhere are we shown the evidence that it is an illness.

For decades, attempts have been made by the mental health industry to prove the brain-pathology basis of depression. Despite the billions of public dollars invested in this research, no such evidence of brain pathology has been discovered. The only thing this research has shown is that our experiences and behaviors are mirrored by changes in the brain. This is something we already knew. Yet, instead of giving up the search and redirecting those monies to more worthy research of real diseases, the mental health industry repeats the worn out pronouncement that discovery is just around the corner! Ironically, if such a discovery came, wouldn't depression then fall within the medical specialty of neurology, the real medical specialty that studies real brain illnesses?

We are also told in this article, "Some people think depression is trivial and not a genuine health condition. They're wrong - it is a real illness with real symptoms." This is the set up: present a false dichotomy straw man argument with those who believe depression is an illness on one side and those who think it is trivial on the other (I don't know of anyone who thinks it is trivial). This doesn't represent ISEPP's critique, nor many others' critiques, of the conventional medical model view of depression. It falsely categorizes those of us who say depression is not a real illness as people who think it is a trivial matter.

Nothing can be further from the truth, but it is the typical way those in power try to discredit organizations like ours and perpetuate the myth. ISEPP considers depression serious and potentially dangerous. But we see it for what it is: a natural and expected human reaction to intense emotional pain, not a sign of brain pathology. There is absolutely no evidence it is caused by real biological defects of the brain. Therefore, medical interventions, such as the prescription of chemicals and sending electrical currents through the brain, are not the answer.

In truth, depression is an insidious strategy adopted in an attempt to escape painful emotions. This is done in various ways such as remaining in bed, not answering the phone, not eating, not leaving the house, and generally trying to back out of life and to shut down. All these are attempts to sooth through escape.

The problem with the strategy of depression is that it doesn't work, other than in the very short term. Remaining in bed, for instance, can be very soothing. But once you wake up, your life is still there, and you might also now feel guilty and lethargic about having stayed in bed all day. As another example, turning down a social engagement provides immediate relief, but in the long run this can also lead to feelings of guilt and increasing social isolation. In short, the paradox of depression is that while it is intended to soothe, it actually adds more emotional pain to life, from which further and further attempts to escape are made, spiraling the person down into despair.

The answer to depression is in allowing emotions to be felt and "heard”, sometimes with the help of so-called professionals but sometimes just with the aid of an understanding friend. The process can be a long one, and it certainly isn't fixed by simplistic mechanical or chemical interventions. Emotions are how humans know what is important. The brain evolved to react to certain significant situations such as loss (sadness) and danger (fear). We experience these emotions when those things are happening and it is important to heed the messages, not avoid them.

This article is just one of thousands of others spread across the internet, which perpetuate the myth of mental illness. It is time to think critically about how basic human struggles have been inappropriately medicalized and subjecting people to the inhumane and harmful mental health industry.

In Search of a Scapegoat

1/12/2017        In the News 0 Comments

by Chuck Ruby, Ph.D.


A recent CNN report is the latest in a long line of horrific shootings and the unfortunately misinformed and misunderstood calls to deny gun ownership to those with "psychiatric problems". NIMH estimates that around 1 in 5 adults are diagnosed with "psychiatric problems" each year. This doesn't include substance abuse "psychiatric problems" and it doesn't include children or teenagers. Further it only includes people who have been formally diagnosed and not those who choose to stay out of the psychiatric system (probably a good choice for them). Lastly, this is only an annual prevalence; each year additional people can be diagnosed, effectively increasing the number of those who have had "psychiatric problems". So if we were to deny all those people the right to have a gun, we're talking about a very large proportion of the population, and many of those calling on gun restrictions would be surprised to find out they are among those with "psychiatric problems".

The problem with gun violence is not "psychiatric problems". Research fails to show a relationship between a diagnosis of mental disorder and risk of violence. Mental disorder diagnoses are merely very loose ways to categorize people with various emotional and behavioral dilemmas. They do not map onto actual neurobiological illnesses that cause violence. There is no such illness. Problem yes, illness no.

But the important thing to remember about gun violence is that a diagnosis is not a way to weed out people who are at risk. There are fairly robust factors that increase one's risk of violence, but the ever-inclusive label of "psychiatric problems" is not one of them. You can see a summary of this issue here: http://psychintegrity.org/wp-content/uploads/2015/08/The-Role-of-Mental-Illness-in-Violent-Behavior-July-2-2014.pdf, which includes how conventional mental health treatment can increase the risk of violence, and in particular how psychiatric drug use can increase the risk as shown here: http://psychintegrity.org/wp-content/uploads/2015/08/White-Paper-Psychiatric-Drugs-and-Violence.pdf.

If we are serious about reducing violence, we should be focusing in the right direction instead of searching for a scapegoat.

Diseasing the Elderly

12/31/2016        In the News 0 Comments

cr-health-hero-why-face-to-face-talks-help-in-dealing-with-depression-12-16Chuck Ruby, Ph.D.


Consumer Reports recently published an article reporting the results of research about how face-to-face interaction reduces the chance of depression in the elderly. There are two problems with this article.

First, the article makes it seem that elderly people are at higher risk of developing “mental illness”, in this case, depression. The problem with this is that the experiences they have as they approach the end of their lives, typically encountering health failures and the deaths of their peers, would reasonably lead to sadness and fear. Sometimes these emotions are so great that they trigger the shutting down of depression in an attempt to soothe. But this is natural, it is not an illness. It is also something I think most reading this article would already know.

Second, the article concludes with a call for screening. Screening for so-called “mental illnesses” is dangerous for two reasons: 1) it is well-known that such screening has large “false positives”; and 2) those identified by screening will then be subjected to the onslaught of the mental health industry, usually consisting of the prescription of toxic psychiatric chemicals that do nothing but sedate and chemically straightjacket.

In the case of low base rate occurrences, like depression, even the best and most precise screening tools will result in a large number of people who are not depressed nevertheless being identified as such. The screening is likely to cause concern in these non-depressed people, convincing them to see a doctor, effectively pulling them into that harmful psychiatric pipeline.

Those among us who are entering the final years will be helped with understanding and a meaningful, not medical, attempt to assuage the anguish.

Stacking the Deck

12/26/2016        In the News 0 Comments

teenager-422197_960_720by Matt Stevenson


Psychology Today reports the results of a study, For Depressed Teens, Therapy Shows No Edge Over Routine Care, concluding that psychotherapy doesn’t work with adolescents. But, this is an example of how the researchers stacked the deck by looking only at short term types of therapy. Such a model of research treats psychotherapy as if it were just another medical intervention that can be “applied”, rather than the interactive, relationship-dependent, and individualistic process that it is.

When people are depressed, there is a reason – usually it relates in large part to depressing events or difficult relationships in that person's life, which have often taken years to develop!

In this particular study, adolescents were only given a small handful of therapy sessions; to quote the article: “The median number of treatment sessions differed significantly between patients in the brief psychosocial intervention group (n=6 [IQR 4–11]), CBT group (n=9 [5–14]), and short-term psychoanalytical therapy group (n=11 [5–23]; p<0·0001), but there was no difference between groups in the average duration of treatment (27·5 [SD 21·5], 24·9 [17·7], 27·9 [16·8] weeks, respectively; Kruskal–Wallis p=0·238).”

Seeing someone 6, 8, or 10 times is likely to be modestly supportive during the limited timeframe the intervention is given, but it's nowhere near long enough to examine in depth the complex life experiences that may have led a person to feel depressed.

Forming a positive therapeutic alliance for a person in a difficult emotional state often takes 6-10 sessions or more on its own, before contributors to the feelings of depression are explored, which might in turn allow a person to gain insights and change their behavior in ways that really allow them to feel better. Thus, we should not be surprised that significant differences did not turn up in this particular study, since the intervention was likely not lengthy or intensive enough to allow significant differences to emerge.

An interesting contrast to this study lies in the meta-analyses of long-term psychotherapy (for 1 year or more) performed by Falk Leichsenring, Paul Knekt, and Barry Duncan:

For example, in Leichsenring's meta-analysis comparing long-term psychotherapies with shorter-term approaches, 96% of patients getting longer-term therapy felt and functioned better than patients in the shorter-term group. See specifics here:

http://jamanetwork.com/journals/jama/article-abstract/1028649

http://www.carlapulliam.com/web_documents/bjp_long-term.pdf

So in other words, more human help does tend to make a difference, regardless of the approach.

And in Barry Duncan's analysis of various kinds of therapy, about 80% of clients were better off with therapy than without, and this effect usually increased over longer periods of time. Interestingly, most therapy approaches did similarly well, suggesting that it's the quality of the relationship as perceived by the client that matters most. Supportive human relationships also provides benefits that can last without adverse side effects, so common in drug treatment:

https://www.amazon.com/Heart-Soul-Change-Delivering-Therapy/dp/1433807092/

So giving someone a handful of sessions of “general support”, “CBT”, or “psychoanalytic therapy” (the latter may be a misnomer for a short-term approach) may be about equally supportive over a few months, but it doesn't say much about the value of forming a longer-term helping relationship with an understanding professional or peer. Building a trusting relationship and making significant life changes that lead one to feel less depressed take time, as common sense should tell us.

Lastly, here is another study demonstrating that long-term intensive psychoanalytic therapy (over about 18 months) can make a dramatic difference for very disturbed depressed individuals:

http://www.riksforeningenpsykoterapicentrum.se/psykoterapi/forskning/Fonagy_et_al_2015_Tavistock_Adult_Depression_RCT.pdf

Maybe this type of approach should be tried with adolescents also?

The Ideology of Depression and Suicide

12/25/2016        In the News 1 Comment

despair-513529_960_720by Al Galves, Ph.D.


In Medscape’s article on Depression and Suicidality, the section entitled “Etiology of Depression and Suicidality” contains statements that are not supported by scientific evidence. This section is based on ideology, not on science. It is based on the ideology of the Biopsychiatric Belief System.

The section places unsupported emphasis on the physiological factors associated with depression and greatly underplays the psychosocial factors associated with depression. It contains this statement: “A decrease in the functional balance of (serotonin and norepinephrine) causes certain types of depression”. This statement is not supported by scientific evidence. There may be evidence that depression is associated with changes in neurochemicals, but that is not evidence that the changing neurochemicals caused depression. This is an important distinction. Correlation is not causation.

Furthermore, if we have a research finding an association between depression and a change in neurotransmitters, proper scientific practice would be to be careful about making a determination of the meaning of such an association. There are at least three possible interpretations. One is that the change in neurotransmitters is causing the depression. A second is that the depression is causing change in neurotransmitters. A third is that the relationship between the neurotransmitter dynamics and the depression is so intertwined that it is virtually impossible to determine which causes which. Proper scientific practice would be to use parsimony in choosing an interpretation. In other words, we would base our interpretation on what is clearly known about other mind-body dynamics.

The most widely and deeply studied of such dynamics is the stress response. The stress response is a profound physiological dynamic that affects the entire body. That physiological dynamic is clearly caused by a psychosocial event – a perception of threat and a cognition that the threat is real and needs to be addressed. Thus, through the use of parsimony, we would choose the interpretation that the depression is causing the neurotransmitter changes.

This section of the Medscape article is also inappropriately certain about the current state of knowledge about neurotransmitter dynamics and depression. Many people with neurotransmitter changes do not experience depression. There is more serotonin in the stomach than in the brain, which throws a large monkey wrench into the relationship between serotonin and depression. There is no evidence of depression ever being reliably diagnosed through measurements of neurotransmitter levels in the brain.

The Medscape article erroneously downplays the association between psychosocial factors and depression. The following is evidence of such association: Persons who derive their sense of self-worth from social relationships are more vulnerable to depression after interpersonal loss than those who obtain self-esteem from other domains (Johnson and Roberts, 1995); women who use a ruminating style of thinking suffer more severely from depression than those who don’t (Lehmicke and Hicks, 1995); people who score low on self-esteem and high on stress are more likely to be depressed (Kreger, 1995); nursing home residents who had a bird in their room were significantly less depressed after being moved to a skilled rehabilitation facility than those who didn’t (Jensen, Cardello and Baun, 1996); persons who score high on a Self-Defeating Personality Scale are more likely to be depressed than others (McCutcheon, 1995); chronic pain sufferers are more likely to be depressed (Banks and Kerns, 1996); persons with more emotional strength and resiliency and a higher level of ego control are less likely to be depressed (Hirschfelt et.al., 1989); recovery from depression is facilitated by events that lessen ongoing difficulty or deprivation (Brown, Lemyre and Bifulco, 1992), and; psychotic depressed patients had significantly poorer pre-morbid functioning - particularly adolescent social functioning - than non-psychotic depressed patients (Sands and Harrow, 1995).

In short, this section of the article is ideology, not science.

References

Banks, S.R. and Kerns, R.D. (1996). Explaining high rates of depression in chronic pain: A diathesis-stress framework. Psychological Bulletin, 119: 95-110

Brown, G.W., Lemyre, L. and Bifulco, A. (1992). Social factors and recovery from anxiety and depressive disorders: A test of specificity. British Journal of Psychology, 161:44-54

Hirschfeld, R.M.A., Klerman, G.L., Lavori, P. et al. (1989). Pre-morbid personality assessments of first onset of major depression. Archives of General Psychiatry, 46:345-50

Jensen,J., Cardello,F., and Baun,M. (1996). Avian companionship in alleviation of depression, loneliness and low morale in older adults in skilled rehabilitation units. Psychological Reports 78, 339-348

Johnson, S.L. and Roberts, J.E. (1995). Life events and bipolar disorder: Implications from biological theories. Psychological Bulletin, 117(3), 443-449

Kreger, D.W. (1995). Self-esteem, stress and depression among graduate students. Psychological Reports, 76, 345-346

Lehmicke,N. and Hicks,R. (1995). Relationship of Response-set differences in Beck Depression Inventory scores of undergraduate students. Psychology Reports, 76, 15-21

McCutcheon, L.E. (1995). Further validation of the Self-Defeating Personality Scale. Psychological Reports, 76:1135-38

Sand, J.R. and Harrow,M. (1995). Vulnerability to psychosis in unipolar major depression: Is pre-morbid functioning involved? American Journal of Psychiatry, 152, 1009-1015

Treatment Causing the Illness?

12/25/2016        In the News 0 Comments

allergy-18656_960_720by Julie Greene


I cannot help but wonder why those who conducted this study about how Mental Disorders Predict Physical Disease and Vice Versa, reported at Medscape, considered patients who were treated for a particular condition a good base for study. My reasoning is that studying such patients means the researchers will not be able to distinguish which factor, the mental disorder itself (is it even an entity by itself?) or the treatment for mental disorder, caused the physical disorder.

Having taken psychiatric drugs myself in the past, I've noted that one the most universal set of side effects are called anticholinergic effects, also given a variety of nicknames by psychiatric practitioners due to their widespread occurrence. In brief, we patients experienced dry mouth, constipation, decreased sweating, drying out of the entire digestive tract, drying out of tear ducts, and consequences, both long-term and short-term of these effects. These secondary adverse reactions included dental carries and loss of teeth, acid reflux, risk of hyperthermia, overall poor digestion, serious ophthalmic reactions, worsening depression and malaise due to sluggish digestion and decreased desire to participate in vigorous exercise activities.

Antidepressants as well as other psychiatric drugs often given to depression sufferers cross the blood-brain barrier and go inside the nerve cells. This is the intent when giving a patient such a drug, to alter how nerve cells work. Does science even know if these drugs enter nerve cells outside the brain and wreak havoc, possibly causing chronic nerve pain such as Fibromyalgia? This would explain why almost all Fibromyalgia patients were previously or currently take antidepressant drugs or similar acting pharmaceuticals.

As for the relationship between eating disorders and seizures, likewise, eating disorders (or what appear to be such) can be brought on by pharmaceuticals. I myself suffered from an eating disorder for several decades. I noted that some pharmaceuticals cause unnatural and radical changes in weight and appetite, causing a patient to feel completely out of control of his body. Depakote, given for seizures, can cause rapid and extreme weight gain, and Topamax, also an anticonvulsant, can cause some patients to lose too much weight. Patients also reported to me changes in how food tasted, often an “odd metallic taste” to some foods, or suddenly losing their liking to foods they once enjoyed. Other times a drug could cause spontaneous vomiting upon exposure to certain sensual stimuli. I experienced this myself for about a week in reaction to a drug I was given many years ago. Most patients reported to me that prior to taking pharmaceuticals they did not have any issues with weight or food, or that their eating problems that they already had were compounded by the drugs they were given.

Psychiatry’s Cruelest Invented Diagnoses

12/23/2016        In the News 0 Comments

4bd6f881-a898-4829-8318-65e1b827d1acby Randy Cima, Ph.D.


Medscape online publishes yet another bold headline about the real cause of one of psychiatry’s cruelest invented diagnoses: “ADHD Likely Due to Genes, Not Parenting or Environment”. According to this study, children who don’t pay attention to adults and are always off task are victims of a mutated gene. At least, they conclude, ADHD is likely due to their self-selected mutated gene in one out of five participants in the study. (I added this one to my ever-growing long list of causes and cures I’ve collected over the years for ADHD. You can see 10 at the end*).

When I read a new study in psychiatry, I always begin at the same place:

Funding: Medgenics is the funder of this study. Founded in 2011 and recently added to the NASDAQ, Medgenics is one of many new drug companies formed to create and distribute their chemicals to treat genetic flaws, not brain flaws. Genetic psychiatry is the latest iteration of psychiatry’s failed science**.

Medgenics presented their results to AACAP in late October. Liza Squires, M.D., Vice President of Research & Development, announced the next phase of the study is being prepared. According to Dr. Squires, the company’s goal is “to develop a . . . product for this subpopulation . . . the first targeted therapy in any CNS disease . . .” Further, Dr. Squires proclaimed this study the “emergence of precision medicine."

And there you have it, dear customer. This is the one of the newest formulas drug companies use to make money for their stockholders. Keep an eye out for other “targeted therapy” and “precision medicine” studies.

How To Carve Out a Market in an Already Saturated Market: Maybe you wonder about the fuss this company makes out of a study that shows just 20% have this particular “gene mutation.” What about the other 80% who don’t, you ask? What’s the likely due for them? It doesn’t matter. Fortunately for psychiatry, their invented disorders can have multiple “causes,” to their financial advantage.

So, Medgenics is aggressively pursuing their business plan. The final results will be publicized as a newly discovered “sub-population” of ADHD children, requiring genetic treatment. Like magic, Medgenics financed the creation of new customers (the ”subculture”) for their soon to be created genetic repair chemicals (the medication), in order to fix their self-selected genetic mutation (the “likely due”).

Something is very wrong with this picture.

This Is Not Science: First clue? The headline. A legitimate scientist would never use the term “likely due,” unless you’re talking about earthquakes. That’s a marketing term used at the direction of corporate lawyers to avoid the term cause. That word – cause – has significant implications in court.

Instead, terms like association, correlation, relationship, interrelation, connection, interconnection, link, and others, are used because they are vague and subjective – and defensible in court. This study exposed me to one I hadn't seen before: “likely due.” Lots of wiggle room in “likely due.”

Second Clue? Confirmatory Findings, in bold. This is impossible in science. Any scientist, student or enthusiast understands that under no circumstances can a scientist confirm her own science. In this study, this scientist not only did so, her study found an increase of 100% of this sub-population from her prior study – the same sub-population she invented. That’s a remarkable increase. On the other hand, it sounds like good news for the investment team at Medgenics. Their market size doubled.

This process is an example of a marketing scheme, not science. Still, it begs the question: how is it possible that this type of scientific charade continues to be so successful - over and over and over again?

The Enduring Failure of Treatment: In the last half century, psychiatry has created more than 50 chemicals - just for ADHD. Alternatives include diet supplements and restrictions, hormonal medications, acupuncture, exercise, behavioral plans, talk therapy, and many, many, many more. Fame and fortunes have been made, and continue to be made, providing “treatment” for this lucrative, invented, destructive diagnosis.

Here’s the rub. None of them “work.” That’s why there’s always room for next years new batch of chemicals or procedures. Last years miracle cures failed too.

Then again, how could they work? There is no such disease, or disorder, or dysfunction, or disability, or deficiency, or disturbance. There is nothing medical about behavior, thus, medicine and medics are out of their element. Failure is unavoidable.

Science is for Sale in Psychiatry: I usually stop reading a new psychiatric study after learning a drug company supplies the cash – and they almost always supply the cash. Corporations rightly expect something in return for their often very large investments – or they won’t be using your “science” the next time they need a study to create some business.

In summary, as a long time mental health practitioner, I found nothing of interest and nothing of value from this psychiatric study. I must admit - I wasn’t surprised. I never am.

* I collect causes and cures of all of psychiatry’s false diseases (I call them Faults and Fixes). Here are ten for ADHD. There are many more: • Acetaminophen while pregnant: here • Dietary Factors (too much/too little: sugar, gluten, omega-3, food additives, GMO, etc): here • Abnormal brain iron levels: here • Pesticide: here • Smoking while pregnant: here • Pregnant women taking antidepressants: here • Smog: here • Marketing: here • Energy Drinks: here • Single Mothers: here

** Regarding the science of genetics, from the National Institutes of Health, 2012: “. . . In human behavior genetics, however, powerful new methods have failed to reveal even one bona fide, replicable gene effect pertinent to the normal range of variation in intelligence and personality. There is no explanatory or predictive value in that genetic information . . . The promises of the molecular genetic revolution have not been fulfilled in behavioral domains of most interest to human psychology.”

Hiding in Plain Sight: The Charade of Depression

12/20/2016        In the News 0 Comments

scanby Chuck Ruby, Ph.D.


A recent Medscape article reported the results of a study that concluded "...patients with depression can be subdivided into four biotypes defined by distinct patterns of dysfunctional connectivity in limbic and frontostriatal networks...." The study is complete with a litany of technical language and statistical analyses, along with very colorful charts and graphs, to once and for all prove that depression has biomarkers that can be used to diagnose and treat it.

But, all this fanfare obscures one important thing hiding in plain sight: Depression is not a real brain disease! Neither are any of the other 300 or so mental disorder categories. Depression is a natural and expected human reaction to emotional pain and at best is a metaphorical disease. It shouldn’t be treated as if it were a clinical or medical problem, and the people experiencing it shouldn’t be treated like patients. Yet this study is an example of how a curtain of complex technical and clinical jargon hides a reality that the devotees of this disease model of mental illness don’t want revealed. Let’s pull the curtain back and see what’s hiding behind it.

First, these kinds of studies come on the heels of the 2013 pronouncement by the Director of the National Institute of Mental Health (NIMH) that the still-in-use-today Diagnostic and Statistical Manual of Mental Disorders (DSM) is invalid and that a new diagnostic system needed to be developed from the ground up using brain scans to identify valid mental disorders rather than using symptom pictures. This study is an attempt to do just that. Yet the invalidity of the DSM is not the only problem here.

The bigger problem is that, as I said earlier, depression is not a real brain disease. The claim of disease is an a priori assumption, based on nothing. In this case “depression” is anointed as a disease at the outset (just because) and then it is discussed as if we all agree and that “biomarkers” can be used to diagnose it. But a “biomarker” is not the same as evidence of disease. The brain is “plastic”, in that it changes with use, and chronic use will result in more permanent change in both structure and activity levels. The fact that certain human experiences are accompanied by signature brain patterns merely reflects this fact. Such brain correlates of human behavior are not evidence of disease. Still, this concept of “biomarker” is used in order to give the impression of disease.

So given this, is it really that surprising to find different brain patterns in people who are having different types of depressive experiences? How is this a justification for describing those brain patterns as “abnormal connectivity”? The article also uses the phrases “reduced connectivity” and “hyperconnectivity” to give the same impression of dysfunction (disease). Similar to how the term “biomarker” implies disease when it really has nothing to do with disease, using the phrase “reduced connectivity” merely mean less activity, not some kind of defect in the connection between brain cells or circuits. And “hyperconnectivity” just means the particular brain areas are more active. This is linguistic sleight of hand, making it appear the brain activity in question is abnormal (diseased), when in fact, there is no such evidence of abnormality, dysfunction, or disease.

These kinds of studies will continue. But unless they come up with evidence (remember, we’re supposed to be scientific) of actual disease in the brain, the only thing they’ll demonstrate is that human activity affects brain patterns. But that is something we’ve known already for a long time. Of course, if they do find evidence of brain disease, we already have a medial specialty for that. It is called neurology.