Administrator

Here We Go Again: Pseudo-Science and Autism

2/22/2017        In the News 0 Comments

by Randy Cima, Ph.D.


In a February 17th story on NBC Nightly News entitled, Brain Scans Detect Signs of Autism in High-Risk Babies Before Age 1, Brian Williams reported the results of research on predicting autism. He characterized the research as “something surprising” and he said it might lead to better treatment for children “who haven’t even shown symptoms yet.” He summed up autism as a “neurological disorder that affects the ability to communicate and socialize.” Those terms “symptoms” and “neurological disorder” gnaw at me when the subject is autism.

The headline alerted me. I’ve seen headlines like this before. Here are a few of them:

These were found after only a ten-minute Google search. There are more. As an exercise, I Googled “brain scan bi-polar.” I did the same for ADHD. You can see the results at the end of this article.

More than two decades ago, Dr. Peter Breggin, a nationally recognized psychiatrist, and critic of modern psychiatry, referred to brain scans as “brain scams.” They have not improved any since then. The science is primitive, and when used to predict or find ways to “treat” human behavior, it is useless.

Incidentally, this study about autism and a most recent study about ADHD were announced within days of each other (the ADHD study was also critiqued by ISEPP). The brain scans for autistic infants showed: “The brain volume of infants . . . grew faster in infants later diagnosed with autism, compared with those who did not receive a diagnosis. The ADHD brain scan study begins with this: People diagnosed with attention deficit hyperactivity disorder have smaller brain volume than those without the disorder. Too much brain volume, autism. Two little, ADHD. Within 24 hours of each other.

Funded by the NIH and Autism Speaks, the study was conducted by the Infant Brain Imaging Study Network (IBID). IBID is a consortium of 8 universities in the U.S. and Canada. Dr. Joseph Piven is the director. On February 15, 2017, IBID posted a press release touting “researchers from around the country were able to correctly predict 80 percent of those infants who would later meet criteria for autism at two years of age.” It is an impressive number. It was part of every reporter’s story.

But let’s look at the numbers to understand this claim better. The infants were “high risk” or “low risk.” “High risk” infants have an older sibling with autism, “low risk” do not. They scanned infants, while they slept (sedated), at 6 months, 12 months, and 24 months.

One group consisted of 117 infants with no family autism history. The second group consisted of 248 undiagnosed infants, who also had an autistic sibling. The third group included 70 infants already diagnosed with autism, who also had an autistic sibling. It’s the third group of 70 infants this study highlights.

Looking a little closer, “The brain growth analysis included only 15 of the 70 high-risk children diagnosed with autism,” noted Emily Willingham* in her review, because they were the only participants who had MRI at all three time points (ages 6, 12 and 24 months).” She also noted. “the study population was not large, especially considering the reductions in numbers for some analyses.”

“We now have this finding in these high familial risk infants that we can predict 8 out of 10 that we think will get autism,” says Dr. Piven, IBID’s Director, noted. He agrees the results need to be confirmed with a larger follow-up study. Thus, Dr. Piven’s IBID team has applied for funding from the NIH to do the study. So, Dr. Piven is accurate. The 80% number is for the 15 children used for the brain growth analysis.

This is modern psychiatric science practice. Replicant science means the same team of scientists is allowed to replicate and confirm their own findings, so numbers can be both accurate and misleading at the same time.

I became interested in autism in the late 1960’s. By 1982, as a working professional at the time, my Master’s thesis was Autism and Self-Defiling Phenomena. For a year, I researched everything known at the time about autism. During the same year, I was an intern therapist for 6 families with one of these unique children.

None of the theoretical explanations at the time of my research had anything to do with medicine. The rate of incidence was 4.3 per 10,000. Since psychiatry has intervened, the rate of incidence has increased to 1 in 68. If you already have one autistic child, psychiatry tells us, chances are 1 in 5 you will have another. These numbers are absurd on the face of it.

Reading studies is routine for me. Like the hundreds of brain scans that made headlines, nothing will come of this. The IBID team will be refunded, no new tools will be developed, no new scans that will be embraced by their colleagues, more “evidence” will be presented, more “possibilities” will be exposed, and, as always, “more study will be needed.”

Mostly though, nothing will come of this because autism isn’t a disease, disorder, disability, defect, dysfunction or anything else that can be “detected” by medicine.

Finally, on the Thinking Person’s Guide to Autism website there is a link "On Autism Orgs". Click on it at you find five tenets they adhere to, almost as a warning to other organizations. The first one is this:

"Support, not cure: autism is a naturally occurring human neurological variation and not a disease process to be cured. Medical or health issues that may accompany autism should be addressed independently."

Please repeat.


*Emily Willingham is a biologist, research scientist, writer, and science editor for Thinking Person’s Guide to Autism, and for the past 20 years, has written dozens about the “science” of autism.

More on purported brain scan "breakthroughs":

The results to follow took 20 minutes to find. You can do the same. Google “brain scan” and nearly anything else. Here’s a few suggestions: anxiety, depression, spouse abusers, sleep deprivation, PTSD, concentration problems, homosexuality, sex addiction, obsession, disorders of dreaming (nightmares), anorexia. You can come up with your own. As you will see, nothing is too ridiculous.

My personal favorite? This one: Location of Sense of Humor Discovered – Medscape, November 2000, here. "A small part of the frontal lobes appears critical to our ability to recognize a joke," said Dean K. Shibata, MD, principal investigator.

BI-POLAR

2015 - Bipolar disorder: New MRI imaging provides new picture, new insight.  https://www.sciencedaily.com/releases/2015/01/150106081217.htm

2014 - Bipolar disorder: brain scans show excitable pleasure response. http://www.medicalnewstoday.com/articles/279338.php

2013 - Is it Bipolar or Depression? New Brain Scan May Have the Answer. https://psychcentral.com/news/2013/09/29/is-it-bipolar-or-depression-new-brain-scan-may-have-the-answer/60060.html

2008 - Cognitive neuroscience and brain imaging in bipolar disorder. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181872/

2006 - Finding Bipolar Disorder with MRI. https://www.technologyreview.com/s/405200/finding-bipolar-disorder-with-mri/

1999 - Brain Magnetic Resonance Imaging of Structural Abnormalities in Bipolar Disorder. http://jamanetwork.com/journals/jamapsychiatry/fullarticle/204822

ADHD

2017 - Brain differences in ADHD. https://www.sciencedaily.com/releases/2017/02/170216105919.htm

2016 - Can a Brain with ADHD Look Different? http://www.healthline.com/health/adhd/brain-scans

2015 - ADHD Patients' Brain Scans Showed This. http://www.webmd.com/add-adhd/childhood-adhd/news/20151215/adhd-patients-show-weaker-connections-in-brain-networks-tied-to-focus-study#1

2014 - Brain scans could save kids from ADHD misdiagnoses. http://www.wired.co.uk/article/adhd-scan-test

2013 - Reading the Brain: FDA Approves First Scan for Diagnosing ADHD. http://healthland.time.com/2013/07/16/reading-the-brain-fda-approves-first-scan-for-diagnosing-adhd/

2012 - ADHD and Stress in Children: Brain Scans. http://newideas.net/adhd-stress-children-brain-scans

2009 - Brain Scans Link ADHD to Biological Flaw Tied to Motivation. http://www.washingtonpost.com/wp-dyn/content/article/2009/09/21/AR2009092103100.html

2007 - Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern. https://www.nimh.nih.gov/news/science-news/2007/brain-matures-a-few-years-late-in-adhd-but-follows-normal-pattern.shtml

2004 - Brain Imaging Data of ADHD. http://www.psychiatrictimes.com/adhd/brain-imaging-data-adhd

Overlooking the Effects of Psychiatric Drugs

2/21/2017        In the News 0 Comments

by Grace Jackson, M.D., Diplomate , American Board of Psychiatry and Neurology


I read with interest the February 18th Washington Post article (“Mental illness and heart disease are often found in the same patients”) by Dr. Nathaniel P. Morris, a physician in training at Stanford University’s psychiatry residency program. The article was correct about the bidirectional relationship between cardiac conditions and the phenomenological entity known as “clinical depression.” However, with the exception of one sentence (“older psychiatric drugs, such as tricyclic antidepressants, came with high-risk side effects on the heart”), the article overlooked the potential for most classes of psychiatric medication to cause or enhance cardiac problems. Equally striking, the article suggested that “newer generations of psychiatric drugs – such as selective serotonin reuptake inhibitors, may protect cardiovascular health.” Such a claim remains contestable, and a fact check is in order.

A thorough review of the medical literature (see sample abstracts, below) suggests that psychiatric drugs – particularly, antipsychotics and antidepressants -- remain a significant and controllable risk factor for coronary artery disease, sudden cardiac death, myocarditis, cardiomyopathy, arrhythmias (including pulseless electrical association), thromboembolic disease, stroke, transient ischemic attacks, and small vessel ischemia in the brain. Before any psychiatrist can act constructively as a consultant to other specialists, he or she must master the “target organ toxicities” associated with psychiatric and non-psychiatric pharmaceuticals.

While it was reassuring to read the empathic remarks of Dr. Morris, whose writings reflected a commendable sensitivity to the physical and emotional impact of the medical procedures which his patients had endured, I found myself frightened by possible inadequacies and omissions in his current training. I hope his empathy will be bolstered by unbiased instruction which must include the mortality and morbidity associated with all psychiatric drugs.

Sample abstracts:
-Epidemiol Psychiatr Sci. 2017 Feb;26(1):18-21. doi: 10.1017/S204579601600086X. Epub 2016 Nov 22. Antipsychotic drug exposure and risk of myocardial infarction. Barbui C1, Gastaldon C1, Papola D1, Ostuzzi G1.

It found nine studies and calculated that the odds (risk) for developing MI were 1.88-fold higher in antipsychotic users compared with individuals who had not taken antipsychotic drugs.

-Circulation. 2014 Jul 15;130(3):235-43. doi: 10.1161/CIRCULATIONAHA.114.008779. Epub 2014 May 16. Association between antipsychotic use and risk of acute myocardial infarction: a nationwide case-crossover study. Lin ST1, Chen CC2, Tsang HY2, Lee CS2, Yang P2, Cheng KD2, Li DJ2, Wang CJ2, Hsieh YC2, Yang WC2.

The adjusted odds ratio of AMI risk was 2.52 (95% confidence interval, 2.37-2.68) for any antipsychotics, 2.32 (95% confidence interval, 2.17-2.47) for first-generation antipsychotics, and 2.74 (95% confidence interval, 2.49-3.02) for second-generation antipsychotics.

-Arch Intern Med. 2004 Jun 28;164(12):1293-7. Antipsychotics and the risk of sudden cardiac death. Straus SM1, Bleumink GS, Dieleman JP, van der Lei J, 't Jong GW, Kingma JH, Sturkenboom MC, Stricker BH.

Current use of antipsychotics was associated with a 3-fold increase in risk of sudden cardiac death. Current use of antipsychotics in a general population is associated with an increased risk of sudden cardiac death, even at a low dose and for indications other than schizophrenia.

-Eur J Clin Pharmacol. 2017 Jan 9. doi: 10.1007/s00228-016-2187-x. [Epub ahead of print] Use of antidepressants and the risk of cardiovascular and cerebrovascular disease: a meta-analysis of observational studies. Biffi A1, Scotti L2, Corrao G2.

Use of SSRIs was associated with an increased risk of cerebrovascular disease (RRs, 1.24; 95% CI, 1.15 to 1.34), while the use of TCA was associated with an increased risk of acute heart disease (RRs, 1.29; 95% CI, 1.09 to 1.54).

-Neuropsychopharmacology. 2015 Dec;40(13):3027-35. doi: 10.1038/npp.2015.158. Epub 2015 Jun 10. White Matter Hyperintensity Accumulation During Treatment of Late-Life Depression. Khalaf A1, Edelman K1, Tudorascu D1, Andreescu C1, Reynolds CF1, Aizenstein H1.

Among all patients, there was as a significant increase in WMHs over 12 weeks (t(46)=2.36, P=0.02).

-Int J Cardiol. 2016 Jan 15;203:867-73. doi: 10.1016/j.ijcard.2015.11.032. Epub 2015 Nov 6. Antidepressant use and risk for mortality in 121,252 heart failure patients with or without a diagnosis of clinical depression. Brouwers C1, Christensen SB2, Damen NL1, Denollet J1, Torp-Pedersen C2, Gislason GH3, Pedersen SS4.

Patients with HF taking antidepressants had an increased risk for all-cause and CV-mortality, irrespectively of having clinical depression.

-Biomed Sci Instrum. 2015;51:400-6. The Effect Of Selective Serotonin Reuptake Inhibitors and Antidiabetic Drugs on Cardiomyocytes. Nelson SA1, Wilson GA, Tucci M, Benghuzzi H.

Cardiomyocytes were grown in a tissue culture environment and challenged with therapeutic concentrations of SSRIs alone or a combination of SSRIs and antidiabetic drugs. Intracellular markers for stress and cytomorphometric analysis indicated SSRIs and SSRIs in combination with antidiabetic drugs negatively impact the health of the cardiomyocytes with time in culture.

-Int J Cardiol. 2011 Jan 7;146(1):64-7. doi: 10.1016/j.ijcard.2010.01.006. Epub 2010 Feb 26. High mortality among heart failure patients treated with antidepressants. Veien KT1, Videbæk L, Schou M, Gustafsson F, Hald-Steffensen F, Hildebrandt PR; Danish Heart Failure Clinics Network.

In a Cox Proportional Hazard Model, pharmacologically treated depression was associated with a 49% increased mortality risk (Hazard ratio: 1.49, 95% confidence interval: 1.03-2.16) after adjustment for traditional confounders.

-Circ Heart Fail. 2009 Nov;2(6):582-90. doi: 10.1161/CIRCHEARTFAILURE.109.851246. Epub 2009 Sep 22. Prognosis in heart failure and the value of {beta}-blockers are altered by the use of antidepressants and depend on the type of antidepressants used. Fosbøl EL1, Gislason GH, Poulsen HE, Hansen ML, Folke F, Schramm TK, Olesen JB, Bretler DM, Abildstrøm SZ, Sørensen R, Hvelplund A, Køber L, Torp-Pedersen C.

Antidepressants were prescribed to 19,411 patients, and both TCA and SSRI were associated with increased risk of overall and cardiovascular death (TCA: HR, 1.33; CI, 1.26 to 1.40; and HR, 1.25; CI, 1.17 to 1.32; SSRI: HR, 1.37; CI, 1.34 to 1.40; and HR, 1.34; CI, 1.30 to 1.38, respectively). Coadministration of SSRI and beta-blockers was associated with a higher risk of overall and cardiovascular death compared with coadministration of beta-blockers and TCA (P for interaction <0.01). Coadministration of SSRIs and beta-blockers was associated with increased risk of overall death and cardiovascular death compared with coadministration of TCAs and beta-blockers.

-J Biochem Mol Toxicol. 2016 Sep 2. doi: 10.1002/jbt.21836. [Epub ahead of print]. Toxicity of lithium on isolated heart mitochondria and cardiomyocyte: A justification for its cardiotoxic adverse effect. Salimi A1,2,3, Gholamifar E1, Naserzadeh P1,3, Hosseini MJ4,5, Pourahmad J6.

Results revealed that Li+ induced a concentration- and time-dependent rise in mitochondrial ROS formation, inhibition of respiratory complexes (II), mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release in rat heart mitochondria and also induced Caspase 3 activation through mitochondrial pathway, decline of ATP and lipid peroxidation in rat cardiomyocytes. These results indicate that the cardiotoxic effects of Li+ were initiated from mitochondrial dysfunction and oxidative stress, which finally ends in cytochrome c release and cell death signaling heart cardiomyocytes.

-Am J Emerg Med. 2015 Sep;33(9):1330.e1-5. doi: 10.1016/j.ajem.2015.03.023. Epub 2015 May 18. Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? Anantha Narayanan M1, Mahfood Haddad T2, Bansal O3, Baskaran J4, Azzouz MS3, Akinapelli A3, Esterbrooks DJ3.

A patient with typical features of lithium toxicity including sinus bradycardia and junctional rhythm, who, in addition, presented atypical features with diffuse T-wave inversions, QT prolongation, and acute left ventricular systolic dysfunction with serum cardiac marker elevation.

-Drug Saf Case Rep. 2016 Dec;3(1):10. STEMI Secondary to Coronary Vasospasm: Possible Adverse Event of Methylphenidate in a 21-Year-Old Man with ADHD. Baumeister TB1, Wickenbrock I2, Perings CA2.

The case of a 21-year-old man diagnosed with ADHD who recently started therapy with Ritalin® Adult 20 mg for at least 3 days. Afterwards he presented with chest pain, elevated troponin and creatine kinase, and posterolateral ST elevations. A myocarditis was initially supposed. In the coronary angiography, signs of coronary artery spasm could be found. The echocardiography showed mild left ventricular dysfunction; no acute myocarditis could be found in the cardiac MRI and myocardial biopsy. The medication with methylphenidate was stopped, and after 12 days the asymptomatic patient was discharged from hospital.

-Case Rep Pediatr. 2015;2015:905097. doi: 10.1155/2015/905097. Epub 2015 Jun 28. Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Munk K1, Gormsen L2, Kim WY1, Andersen NH1.

A case with an 11-year-old child, treated with methylphenidate, who suffered cardiac arrest and was diagnosed with a remote myocardial infarction. This demonstrates that myocardial infarction can happen due to methylphenidate exposure in a cardiac healthy child, without cardiovascular risk factors.

But see:

-Atherosclerosis. 2014 Aug;235(2):496-502. doi: 10.1016/j.atherosclerosis.2014.05.918. Epub 2014 Jun 5. Anti-anxiety drugs use and cardiovascular outcomes in patients with myocardial infarction: a national wide assessment. Wu CK1, Huang YT2, Lee JK3, Jimmy Juang JM4, Tsai CT4, Lai LP4, Hwang JJ4, Chiang FT4, Lin JL4, Chen PC5, Lin LY6.

Anti-anxiety medications are independent associated with a decreased risk of cardiac mortality and heart failure hospitalization in patients after a new MI.

-J Cardiovasc Pharmacol. 1994 Jul;24(1):55-8. Antiischemic effects of intravenous diazepam in patients with coronary artery disease. Rossetti E1, Fragasso G, Xuereb RG, Xuereb M, Margonato A, Chierchia SL.

DZP significantly delays onset of exercise-induced myocardial ischemia in patients with coronary artery disease.

 

Another False Claim About ADHD

2/21/2017        In the News 1 Comment

by Al Galves, Ph.D.


A careful reading of this CNN article about brain differences related to ADHD tells me that nothing in it will be very useful to human beings. The article reports on a study that finds that persons diagnosed with ADHD have smaller parts of the brain, which are related to the processing of emotions. How, pray tell, is this going to be useful to human beings?

We don’t have any psychotropic drugs or any forms of psychosurgery that can be used to improve the emotional processing of human beings. We have drugs and psychosurgery that can dull emotions or artificially enervate emotions but we don’t have any drugs or psychosurgery that can help people do a better job of learning from their emotions or using them in beneficial ways.

On the other hand, psychotherapy can and regularly does help people learn how to use their emotions in beneficial ways. And psychotherapy does this without causing the kind of harmful “side effects” that are associated with psychotropic drugs and psychosurgery.

Although it isn’t explicit in saying so, this article implies that ADHD is a result of smaller brain structures in areas that process emotions. There is no evidence of that being the case. All we have is a finding of correlation between smaller brain structures and ADHD. That is not evidence that such brain anomalies cause ADHD. It is merely a correlation, and a small one at that. Knowing what we know about the stress response in humans it is more likely that the behavior and state of being related to diagnoses of ADHD is causing the brain anomalies than the other way around.

Plus, as is typical of the claims in these studies, the claim is not supported by the data. The largest brain region difference reported in the study was with the amygdala. The difference between the ADHD and non-ADHD groups’ was a Cohen’s d of .19. But this is such a small difference in the group averages that the groups overlap so much that most people in the ADHD group don’t have the claimed smaller amygdala than those in the non-ADHD group. How can this be if the title reads, “Brains of those with ADHD show smaller structures related to emotion”? See the display below, which shows an even larger Cohen’s d of .20. The ADHD group would be the darker one.

In stating that ADHD is a neurodevelopmental disorder, the article tells an untruth. There is no scientific reason to believe that ADHD is a neurodevelopmental disorder. ADHD is diagnosed through observations of certain behavior, not brain scans. There can be many reasons for such behavior, including concern about being abused or mistreated at home, not being able to do the work being assigned in school, being bored in school, not caring about what is being focused on in school, being frightened by an abusive teacher, etc., etc., etc. Neurodevelopmental anomaly is only one of many explanations for the behavior associated with a diagnosis of ADHD, and it is a poor one. In order to call it a neurodevelopmental disorder, one must first show evidence of a neurodevelopmental defect, and that has not been done.

In closing, although the author of the article and the authors of the study may believe they have a finding which is useful to human beings, such is not the case.

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 0 Comments

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