Socially Rationalizing Shoddy Psychology Studies

I’ve been trying not to post entire articles (a social etiquette thing) but this one, in the Atlantic, is just TOO blatant an example of “socializing” a practice in psychology that is bad, bad science; that is, rationalizing unscientific behavior as “not all that bad.” Ed Yong is a noted science writer, and I’m a bit shocked at his pandering to the “psychology industry.” Most alarming is the failure to recognize that failed psychological theories, which become institutionalized and form the basis of diagnosis and treatment, have harmed, and continue to harm, REAL LIVE PEOPLE.

How Reliable Are Psychology Studies?

A new study shows that the field suffers from a reproducibility problem, but the extent of the issue is still hard to nail down.

  • Ed Yong
  • Aug 27, 2015, The Atlantic

No one is entirely clear on how Brian Nosek pulled it off, including Nosek himself. Over the last three years, the psychologist from the University of Virginia persuaded some 270 of his peers to channel their free time into repeating 100 published psychological experiments to see if they could get the same results a second time around. There would be no glory, no empirical eurekas, no breaking of fresh ground. Instead, this initiative—the Reproducibility Project—would be the first big systematic attempt to answer questions that have been vexing psychologists for years, if not decades. What proportion of results in their field are reliable? (If psychologists are so concerned, why have they been defending sloppy methods and “religious” premises for decades?)

A few signs hinted that the reliable proportion might be unnervingly small. Psychology has been recently rocked by several high-profile controversies, including: the publication of studies that documented impossible effects like precognition, failures to replicate the results of classic textbook experiments, and some prominent cases of outright fraud.

The causes of such problems have been well-documented. Like many sciences, psychology suffers from publication bias, where journals tend to only publish positive results (that is, those that confirm the researchers’ hypothesis), and negative results are left to linger in file drawers. On top of that, several questionable practices have become common, even accepted. A researcher might, for example, check to see if they had a statistically significant result before deciding whether to collect more data. Or they might only report the results of “successful” experiments. These acts, known colloquially as p-hacking, are attempts to torture positive results out of ambiguous data. They may be done innocuously, but they flood the literature with snazzy but ultimately false “discoveries.” (Innocuously? How does one cook the books without be aware?)

In the last few years, psychologists have become increasingly aware of, and unsettled by, these problems. Some have created an informal movement to draw attention to the “reproducibility crisis” that threatens the credibility of their field. Others have argued that no such crisis exists, and accused critics of being second-stringers and bullies, (here come the social excuses) and of favoring joyless grousing over important science. In the midst of this often acrimonious debate, Nosek has always been a level-headed figure, who gained the respect of both sides. As such, the results of the Reproducibility Project, published today in Science, have been hotly anticipated. (We cannot assume that Nosek is unbiased)

They make for grim reading. Although 97 percent of the 100 studies originally reported statistically significant results, just 36 percent of the replications did.

Does this mean that only a third of psychology results are “true”? Not quite. A result is typically said to be statistically significant if its p-value is less than 0.05—briefly, this means that if you did the study again, your odds of fluking your way to the same results (or better) would be less than 1 in 20. This creates a sharp cut-off at an arbitrary (some would say meaningless) threshold, in which an experiment that skirts over the 0.05 benchmark is somehow magically more “successful” than one that just fails to meet it. (Apply math to garbage – you get organized garbage.)

So Nosek’s team looked beyond statistical significance. They also considered the effect sizes of the studies. These measure the strength of a phenomenon; if your experiment shows that red lights make people angry, the effect size tells you how much angrier they get. And again, the results were worrisome. On average, the effect sizes of the replications were half those of the originals.

“The success rate is lower than I would have thought,” says John Ioannidis from Stanford University, whose classic theoretical paper Why Most Published Research Findings are False has been a lightning rod for the reproducibility movement. “I feel bad to see that some of my predictions have been validated. I wish they’d been proven wrong.” This is a social statement; a “white lie.” 

Nosek, a self-described “congenital optimist,” is less upset. The results aren’t great, but he takes them as a sign that psychologists are leading the way in tackling these problems. “It has been a fantastic experience, all this common energy around a very specific goal,” he says. “The collaborators all contributed their time to the project knowing that they wouldn’t get any credit for being 253rd author.” Another social statement; not about the problem, but “how fun” it was – and how “socially tuned to reward” the participants are.

There are many reasons why two attempts to run the same experiment might produce different results. (Let’s rationalize – soften, undo, explain away- appalling institutional behavior)

Jason Mitchell from Harvard University, who has written critically about the replication movement, agrees. “The work is heroic,” he says. “The sheer number of people involved and the care with which it was carried out is just astonishing. This is an example of science working as it should in being very self-critical and questioning everything, especially its own assumptions, methods, and findings.” (Says nothing concrete: another social statement -ass-kissing)

But even though the project is historic in scope, its results are still hard to interpret. (REALLY? ) Let’s say that only a third of studies are replicable. What does that mean? It seems low, but is it? “Science needs to involve taking risks and pushing frontiers, so even an optimal science will generate false positives,” says Sanjay Srivastava, an associate professor of psychology at the University of Oregon. “If 36 percent of replications are getting statistically significant results, it is not at all clear what that number should be.” (That is – IT’S ARBITRARY)

It is similarly hard to interpret failed replications. Consider the paper’s most controversial finding: that studies from cognitive psychology (which looks at attention, memory, learning, and the like) were twice as likely to replicate as those from social psychology (which looks at how people influence each other). “It was, for me, inconvenient,” says Nosek. “It encourages squabbling. Now you’ll get cognitive people saying ‘Social’s a problem’ and social psychologists saying, ‘You jerks!’” (That is, the results must be “socially acceptable” to the “psychology community” – no hurt feelings! Do proper science, and a lot of people are going to be unhappy.)

Nosek explains that the effect sizes from both disciplines declined with replication; it’s just that cognitive experiments find larger effects than social ones to begin with, because social psychologists wrestle with problems that are more sensitive to context.  (Especially when the “context” is imaginary, as we see in autism / Asperger studies) “How the eye works is probably very consistent across people but how people react to self-esteem threat will vary a lot,” says Nosek. Cognitive experiments also tend to test the same people under different conditions (a within-subject design) while social experiments tend to compare different people under different conditions (a between-subject design). Again, people vary so much that social-psychology experiments can struggle to find signals amid the noise. (No problem: Just make them up!)

More generally, failed replications don’t discredit the original studies, any more than successful ones enshrine them as truth. There are many reasons why two attempts to run the same experiment might produce different results. There’s random chance. The original might be flawed. So might the replication. There could be subtle differences in the people who volunteered for both experiments, or the way in which those experiments were done. And, to be blunt, the replicating team might simply lack nous or technical skill to pull off the original experiments.

Indeed, Jason Mitchell wonders how good the Reproducibility Project’s consortium would be at replicating well-known phenomena, like the Stroop effect (people take longer to name the color of a word if it is printed in mismatching ink) or the endowment effect (people place more value on things they own). “Would it be better than 36 percent or worse? We don’t know and that’s the problem,” he says. “We can’t interpret whether 36 percent is good, bad, or right on the money.”

(The very notion that there is a “correct” percentage of reproducible studies is so UNSCIENTIFIC that it reveals the lack of science-based activity in psychology: this belief renders the entire field “superstitious.” A study is reproducible or it isn’t: to believe that is some number of “reproducible” studies “justifies” what you are doing, is UTTER NONSENSE.)

Mitchell also worries that the kind of researchers who are drawn to this kind of project may be biased towards “disproving” the original findings. How could you tell if they are “unconsciously sabotaging their own replication efforts to bring about the (negative) result they prefer?” he asks. (Another social statement – )

In several ways, according to Nosek. Most of the replicators worked with the scientists behind the original studies, who provided materials, advice, and support—only 3 out of 100 refused to help. (This proves nothing) The teams pre-registered their plans—that is, they decided on every detail of their methods and analyses beforehand to remove the possibility of p-hacking. Nosek also stopped the teams from following vendettas (Wow! There’s a revealing statement of personality and character) by offering them a limited buffet of studies to pick from: only those published in the first issue of three major psychology journals in 2008. Finally, he says that most of the teams that failed to replicate their assigned studies were surprised—even disappointed. “Anecdotally, I observed that as they were assigned to a task, they got invested in their particular effect,” says Nosek. “They got excited. Most of them expected theirs to work out.” Again – a social statement meant to support the results, but having nothing to do with the actual quality of work. What are these people, 5 year-olds?)

“Journals, funders, and scientists are paying a lot more attention to replication, to statistical power, to p-hacking, all of it.”

And yet, they largely didn’t. “This was surprising to most people,” says Nosek. “This doesn’t mean the originals are wrong or false positives. There may be other reasons why they didn’t replicate, but this does mean that we don’t understand those reasons as well as we think we do. We can’t ignore that. We have data that says: We can do better.” (Are you kidding? Denial, denial, denial.)

What does doing better look like? To Dorothy Bishop, a professor of developmental neuropsychology at the University of Oxford, it begins with public pre-registration of research plans. “Simply put, if you are required to specify in advance what your hypothesis is and how you plan to test it, then there is no wiggle room for cherry-picking the most eye-catching results after you have done the study,” she says. (And what if “cheaters” are caught? Do they get sent to time-out?) Psychologists should also make more efforts to run larger studies, which are less likely to throw up spurious results by chance. Geneticists, Bishop says, learned this lesson after many early genetic variants that were linked to human diseases and traits turned out to be phantoms; their solution was to join forces to do large collaborative studies, involving many institutes and huge numbers of volunteers. These steps would reduce the number of false positives that marble the literature.

To help detect the ones that slip through, researchers could describe their methods in more detail, and upload any materials or code to open databases, making it trivially easy for others to check their work. “We also need to be better at amassing the information we already have,” adds Bobbie Spellman from the University of Virginia. Scientists already check each other’s work as part of their daily practice, she says. But that much of that effort is invisible to the wider world because journals have been loath to publish the results of replications. (You cuddle my data, I’ll cuddle yours.)

Change is already in the air. “Journals, funders, and scientists are paying a lot more attention to replication, to statistical power, to p-hacking, all of it,” says Srivastava. He notes that the studies that were targeted in the Reproducibility Project all come from a time before these changes. “Has psychology learned and gotten better?” he wonders.

One would hope so. After all, several journals have started to publish the results of pre-registered studies. In a few cases, scientists from many labs have worked together to jointly replicate controversial earlier studies. Meanwhile, Nosek’s own brainchild, the Center for Open Science established in 2013, has been busy developing standards for transparency and openness. It is also channelling $1 million of funding into a pre-registration challenge, where the first 1,000 teams who pre-register and publish their studies will receive $1,000 awards. “It’s to stimulate people to try pre-registration for the first time,” he says. (This is like High School for drop outs – get extra credit for behavior that you ought to have displayed from the start.)

The Center is also working with scientists from other fields, including ecology and computer science, to address their own concerns about reproducibility. Nosek’s colleague Tim Errington, for example, is leading an effort to replicate the results of 50 high-profile cancer biology studies. “I really hope that this isn’t a one-off but a maturing area of research in its own right,” Nosek says.

$$$$$$$$$$$$$$$$

That’s all in the future, though. For now?I will be having a drink,” he says. (Stat quo.)

 

Saturday in Wyoming / Perfection and Discontent

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It started yesterday: the season of perfection in Wyoming. It’s always a surprise, because we never know from year to year when it will begin or end. I usually just say, “September is my favorite month.” It’s as if the earth inhales the chaos of wind and holds it; sleeps for awhile. The land is silent; so silent that we stop to listen: are we still alive, is the land alive?

The stillness is catching, like a benevolent virus has taken over town. Even the dogs have caught it, gliding through the house to stand outdoors as if lost and waiting for…something; for me of course to grab the keys, the leashes, the water bottles, my walking shoes. The “weeds” are so thick and tall this year; a wet summer array of types not seen formerly. Thick with spikey seed and thorn and perhaps hiding a pygmy rattlesnake. But evening is the time to go, the “yellow world” red and rusty and changing moment to moment.

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The foxtail blizzard was canceled this year; spring water floods the valley where it commonly grows – still flooded and drying slowly, I visit a couple of days a week, waiting and watching for a spectacular mud event that will take its place, and which may overlap with a first freeze.

I am such a creature of the weather, like a reptile that needs the sun to “boot up” that I sometimes wonder to what degree physical conditions influence mood; very noticeable to me, but how many people are climate-weather driven and don’t know it, blaming the boss, the economy, what they ate for lunch? Humans remain tropical animals, dressed up for blizzards and gloomy skies; dressed up for concrete underfoot and life in claustrophobic cells, psychically damaged by the sheer volume of bodies impressed on their “space.” Humans need boundaries like any other animal.

Where do we begin and end? We are comfortable asking that question of atoms, but not of ourselves.

 

 

Let’s get physical / Lithium – Bipolar

 imageslipt
This site offers More information than I’ve found at any other source. Now to decode it! What’s shocking is that most studies I’ve found purport lithium to have no importance in The human body and brain. What is the basis for this assumption?

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Biochemical and Physiological Effects of Lithium

Cellular Transport and the Inorganic Biochemistry of Lithium (N.J. Birch)

The chemistry of lithium is unusual. Lithium atoms are very small, highly polarized, and have a high charge density. The chemical and biochemical properties of lithium are similar to those of magnesium, with which it shares a “diagonal relationship” in the periodic table. Because magnesium plays a crucial role in the regulation of biochemical systems, it has been theorized that lithium influences magnesium-dependent processes.

Too many Americans rely on bottled or home-filtered water for their drinking needs. Most filtered and bottled waters provide little or no magnesium. Even most tap water is devoid of this critical mineral

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Lithium can be transported across membranes in five different ways. Of these, passive flux is important for the entry of lithium into cells, and sodium-lithium countertransport for the extrusion of lithium from cells. Lithium can presumably replace sodium in the sodium-sodium countertransport system, although the biological significance of the latter process is still unclear.

It appears that the concentration of lithium in cells does not reach the levels predicted by the Nernst equation. Rather, the (inside the  cell) intracellular lithium concentration is considerably lower than its concentration in blood or (outside the cell) extracellular fluid. This is important for the models which have been proposed for its mechanism of action, as these must be able to explain the effects of lithium at intracellular concentrations of 0.1 mmol/l (i.e. similar to those seen in patients on lithium (preventative treatment) prophylaxis).

One hypothesis suggests that the biological effects of lithium are due to the role it plays at the cell periphery, where, for example, it may influence cell recognition, cell signaling mechanisms at the cell membrane, and certain immunological processes.

Lithium as a Trace Element (K. Lehmann)

In humans endogenous serum lithium levels normally range from 0.14-8.6 micromol/l, with a maximum level of 15.8 micromol/l.  These lithium serum levels are 3 orders of magnitude lower than those necessary for therapeutic/prophylactic treatment (of bipolar). Scientists suspect that endogenous lithium in the human body has a physiological function, although sufficient evidence of this is still lacking.
Daily lithium intake in humans is dependent on both diet and the use of medications that contain lithium. With the latter, a total of 15 micromol to 0.66 mmol of lithium may be administered per day.

Effects of Lithium on Neurotransmitters and Second Messenger Systems (D. van Calker)

Studies examining the effect of lithium ions on the synthesis and metabolism of neurotransmitters have, thus far, yielded inconsistent results, failing to shed any light on the mechanism of action of lithium in vivo. Lithium ions prevent the development of functional supersensitivity to dopamine and acetylcholine receptor stimulation, most likely by influencing second messenger systems.

Lithium ions increase basal cAMP levels and inhibit the neurotransmitter-stimulated accumulation of cAMP in the brain and other tissues. Acute administration of lithium inhibits the stimulation of adenylyl cyclase, most likely through direct competition with magnesium, whose hydrated ionic radius is similar to that of lithium. The effects of chronic lithium treatment, however, probably result from (a) the modification of gene expression among components of the adenylyl cyclase system, especially G protein subunits (G_i, G_s), as well as from (b) a stabilization of the inactive trimeric form of the Gi protein. Lithium has been found to increase basal cAMP levels, which is most likely due to attenuation of the Gi protein and an increase – probably resulting from the effects of lithium on gene transcription – in the levels of adenylyl cyclase type I and type II mRNA.

At therapeutically relevant concentrations, lithium ions inhibit the hydrolysis of inositol mono-phosphatase to inositol. This leads to a depletion of inositol and a strong increase in diacylglycerol (DAG) in susceptible cells and tissues, depending on species and tissue type. Susceptibility is determined by the activity of a high-affinity inositol transport system, as well as by the degree to which the inositolphospholipid (IP) second messenger system is hormonally stimulated. Pronounced inositol depletion can lead to an inhibition of the IP system in affected cells, which is probably a result of attenuated IP synthesis and/or the activation of protein kinase C (PKC) through the accumulation of DAG.

Lithium exposure facilitates the activation of certain PKC isozymes, chronic activation of which can result in a downregulation of PKC activity (i.e. a constitutive activation and redistribution in the cell nucleus). This process is probably responsible for the diverse effects of lithium on the release of neurotransmitters, the inhibition of receptor sensitization and certain membrane transport processes. By influencing transcription factors such as c-fos, this process could also be responsible for the lithium-induced changes in gene transcription which have been observed.
The inhibitory effects of chronic lithium treatment on the PI system have also been demonstrated in humans. Peripheral cells from manic-depressive patients show increased hormonal sensitivity in the phosphoinositide (PI) system. Thus, it appears that lithium ions might compensate for the hyperactivity of the PI system which is associated with illness in these patients.

The Effect of Lithium on Serotoninergic Function (B. Müller-Oerlinghausen)

In animal experiments, lithium administration results in a net rise in 5-HT activity, which is probably caused presynaptically by an increase in the release and transformation of 5-HT precursors, an increase in the release of 5-HT, and by the functional antagonism between lithium and inhibitory presynaptic 5-HT1A receptors.
However, there are considerable differences in the amount of time which elapses before each of the different effects occurs.

An increase in 5-HT uptake in the thrombocytes of depressive patients, but not in those of healthy test subjects, has been observed.

In several studies of patients and healthy volunteers on short-term lithium therapy, neuroendocrine stimulation (e.g. with fenfluramine or tryptophan) led to increased prolactine or cortisol responses via serotoninergic transmission.

The presumably adaptive mechanisms which tend to emerge after chronic lithium administration (e.g. a decrease in the number and sensitivity of postsynaptic 5-HT receptors) probably result in a stabilization of serotoninergic neurotransmission rather than a unidirectional increase in 5-HT activity.

The Effects of Lithium on the Hematopoietic System (V.S. Gallicchio)

Lithium increases the number of neutrophil and eosinophil granulocytes, but probably not that of monocytes, basophil granulocytes, thrombocytes or erythrocytes / reticulocytes in peripheral blood. Whereas lithium increases the number of pluripotent stem cells in bone marrow, as well as of granulocyte-macrophage and megakaryocyte precursors, it probably reduces the number of erythrocyte progenitor cells.
Researchers suspect that these phenomena result from both the direct and indirect effects of lithium on cells, including an increase in the number of macrophages that produce growth factors and cytokines. A lithium-induced increase in bone marrow activity also appears to play a role in this context. A decline in erythropoiesis during lithium therapy may be due to inhibition of cAMP which, in turn, inhibits prostaglandin E production.

Thus, lithium can be used to treat toxic impairment of the hematopoietic system, whether this damage be caused by chemotherapy, radiation, antiviral medication, or granulocytopenia induced by carbamazepine or neuroleptics. To date there has been no scientific evidence that lithium can cause leukemia.

The Effects of Lithium on the Immune System (V.S. Gallicchio)

In humans lithium therapy may lead to an increase in immunoglobulin synthesis by B-lymphocytes. However, the results of in vitro experiments and animal testing are contradictory.

Lithium stimulates the proliferation of T-lymphocytes and appears to increase the phagocytic activity of macrophages, but only at doses higher than those prescribed for medical treatment.

Experimental evidence suggests that lithium can increase cytokine production. This has been confirmed in the case of interleukin-2. Moreover, lithium potentiates tumor necrosis factor-mediated cytotoxicity. In high doses, lithium inhibits cyclic AMP (cAMP), which leads to an increase in the synthesis of interferon products.
It appears that lithium influences the immune system in part by reducing intracellular concentrations of cAMP and inositol phosphate.

Because of the high doses involved, the potential usefulness of lithium in the treatment of inflammatory and auto-immune diseases is still unclear. However, because it can increase interleukin-2 production, as well as potentiate killer cell activity, high-dose lithium has been used in the treatment of various cancers. Recent evidence also indicates that, by inhibiting T-suppressor cells lithium can reduce the severity of graft-versus-host reactions following transplants.

Of great importance is the potential use of lithium in the treatment of immune deficiency syndromes such as AIDS. In vitro experiments have shown that lithium can lead to a more robust immune response in patients with AIDS. The direct antiviral effects of lithium, e.g. in herpes virus infections, are already being utilized in clinical practice.

Chronobiological Aspects of Lithium Prophylaxis (B. Pflug)

Repetitive variations with a periodicity of approximately 24 hours are part of the circadian system. This system can be found among single-celled organisms, plants, animals, and humans. In humans the circadian system is based on a number of oscillators of varying strengths which exert mutual influence on one another. The main pacemaker of this multi-oscillatory system is the nucleus suprachiasmaticus.

Lithium ions are chronobiologically active. They influence the circardian system by modifying phase relationships and lengthening the free-running period.
During manic-depressive episodes a variety of circadian rhythm dysfunctions have been observed. The chronobiological effects of lithium salts help explain their efficacy in the treatment of manic-depressive disorders.

The Psychological Approach to the Effects of Lithium Prophylaxis (W. Classen)

The main effect of long-term lithium treatment is based on the modification of behavior and perception. These effects can be explained within psychological models and need not be reduced to other, lower levels of explanation.
Over the last 25 years, animal studies, psychophysiological investigations in humans, and routine clinical observation have led to the development of models which help explain the psychological effects of lithium salts. The phenomenological model developed by Kropf integrates concepts of genetic disease, aspects of the illness described in psychological terms, as well as the acute and chronic effects of lithium.
Among healthy test subjects lithium can cause fatigue, apathy, irritability, alternation between increased and decreased susceptibility to external stimuli, and general feelings of illness along with negative thinking, dysphoria, and lethargy.
Depressive patients exhibit a rigid and non-regulable behavioral repertoire, both during acute episodes and over the long term. This indicates a change in mental functions, such as cognition, perception, emotions, and the ability to structure thoughts and process information. Lithium most likely modulates these processes by raising the perception threshold for various stimuli and improving information processing structures.

The aggression-dampening effect of lithium which has been observed in human and animal studies is probably due to changes in the perception of aggression-inducing stimuli, as well as to improved control over aggressive impulses accompanied by a reduction in the number of aggressive behavioral patterns.

The Pharmacokinetics of Lithium Salts (K. Lehmann)

The kinetics of lithium are determined by the fact that it is a simple, monovalent cation (Positive). The anion and/or the galenic formulation chosen for the final drug product primarily influence the resorption phase. This needs to be taken into account when initiating lithium treatment or changing a patient’s prescription. The primary route of lithium elimination is renal (via glomerular filtration). Between 70-80% is reabsorbed in the proximal tubule. The overall elimination half-life of lithium is approximately 24 hours.

The exogenous clearance of lithium (ca. 19-20%) is approximately equal to the endogenous clearance of the drug in patients with normal renal function.
The renal clearance of lithium is subject to manifold influences, the most significant of which are (a) changes in electrolyte levels and (b) the secretion of aldosterone.
Impaired kidney function and age-related decreases in renal clearance can lead to a dramatic rise in serum lithium levels.

Lithium is distributed slowly and unevenly in the human body. Distribution is usually complete within 12 hours of first ingestion. During lithium therapy, steady state concentrations are generally reached within 4-7 days of repeated oral application in patients with normal renal function.

Exact drug monitoring is absolutely essential not only in all problem cases or when medication(s) are adjusted or switched, but also during routine follow-up exams.

The efficacy of lithium

The main goal of treatment in patients with bipolar disorder is to prevent recurrences and suicidal acts. Of the variety of drugs now available to treat this condition, lithium has been shown to be the most efficacious in the long-term treatment of bipolar disorder. The earliest controlled studies were performed in the 1960s and demonstrated response rates of 70 to 80%. However, later studies were not always able to replicate these findings. This led to a growing critique of lithium treatment, primarily from researchers in the United States. Some US researchers also advanced the hypothesis that long-term lithium treatment would lose its efficacy over time, or after discontinuation and subsequent reinstallation. However, this hypothesis was based on preliminary findings in small patient groups and could not be replicated elsewhere.

In a large sample of 163 bipolar patients on long-term lithium treatment, the IGSLI demonstrated that it was indeed possible for patients who had shown an excellent primary response to remain stable for decades, regardless of discontinuations (Grof 1999). During the 1990s, it became evident that the decrease in response rates observed previously had been due to the widespread use of lithium in naturalistic, and therefore less controlled, settings. The introduction of modern diagnostic systems (DSM III R, ICD 10) had also broadened the criteria of bipolar disorder, thus leading to a more heterogeneous group of patients.

Different subtypes of bipolar disorder

The IGSLI is currently working on the hypothesis that the diagnosis of bipolar subtypes may help achieve maximal response in patients on long-term treatment. When used to treat the classical type of bipolar illness (i.e. without psychiatric comorbidity and without mood-incongruent psychotic features), lithium is superior to other treatment options. However, lithium is less effective in patients with atypical bipolar disorder, which is characterised by mood-incongruent psychotic features, substance abuse, anxiety disorders or other psychiatric comorbidity, and frequently by residual non-affective symptoms between episodes. Results from several other European research groups support this hypothesis.

Distinguishing between subtypes may also be useful for evaluating the prognosis of bipolar women during pregnancy. In a retrospective study, the IGSLI demonstrated that in women with typical, or type I bipolar disorder, the risk of recurrence during pregnancy was markedly lower than had been expected in light of the normal clinical course of the disease. Exploring the underlying protective mechanisms in such cases may help lead to a new understanding of the pathophysiology of affective disorders and to new approaches to treatment and prevention.

The spectrum of therapeutic options has broadened since the emergence of anticonvulsants as a means of treating affective disorders. Applying lithium and anticonvulsants in a more differential manner might bring considerable benefits, especially to the large number of patients whose illness differs significantly from the classical type of bipolar disorder and who belong to the bipolar spectrum.

This site Nevertheless, recently released, high-quality guidelines and overviews underscore the fact that lithium is still the first-line treatment in the prophylaxis of bipolar affective disorder.

High-dose thyroxine research

The problem of refractory recurrent affective illness deserves special attention, since a relatively high percentage of patients have a less than adequate response to standard prophylactic agents. For one decade now, the IGSLI has been engaged in research on high-dose thyroxine as an add-on therapy in refractory patients, especially in lithium-nonresponders. The “Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of Levothyroxine as Add-on Therapy in Bipolar Depression” (Sponsor: The Stanley Medical Research Institute of the Stanley Foundation, Bethesda, MD, USA; Grant ID #02T-238) started recently as a cooperation of several IGSLI members and other European and US research centers:

Investigators and participating study sites are:
Charité University Medical Center Berlin, Germany: Michael Bauer (P.I.), Martin Schäfer, Mazda Adli, Johanna Sasse, Igor Sutej
Ludwig-Maximilians-Universität Munich, Germany: Heinz Grunze; Emanuel Severus
Technische Universität Dresden, Germany: Tom Bschor
University Medical Center Utrecht, The Netherlands: Ralph Kupka, Willem A. Nolen
University of California Los Angeles (UCLA), USA: Mark Frye, Lori Altshuler
Stanford University School of Medicine, Stanford, USA: Natalie Rasgon
Statistical Consultant: Michael Smolka, Central Institute of Mental Health, University Heidelberg, Germany.

New Technologies to Improve Longitudinal Research in Bipolar Disorder

Longitudinal studies are an optimal approach to understand the variable course and outcome of mood disorders. However, longitudinal studies have been limited by missing and unbalanced data values collected at unequal time intervals and by reliance on paper-based forms for data collection. To overcome methodological limitations, several IGSLI centers collect data for longitudinal studies using a validated computer-based system (ChronoRecord). Using software available in English, German and Spanish and being translated into Czech and Polish, patients record mood, medications, sleep, life events, and menstrual data onto a home computer every day. Weight is entered weekly. This technology facilitates compilation of data from multiple IGSLI centers into a large database for analysis. Automation of data collection can reduce missing data, eliminate errors associated with data entry and allows the use of familiar statistical techniques for analysis. Additionally, ongoing feedback is provided for patients and researchers in the form of graphical mood charts and statistical analyses. For more information on ChronoRecord visit www.chronorecord.org.

Neuroprotective Effects of Lithium

Some affective disorders appear to be accompanied by persistent neurocognitive impairment, an increased risk for mild cognitive impairment and morphological changes in the brain. Imaging, neuropsychological and postmortem brain studies suggest that there are abnormalities in specific brain regions in bipolar disorders.

There is accumulating literature on neuroprotective effects of lithium which mainly stems from studies with cell cultures and animal research. Chronic but not acute lithium treatment appears to have robust neuroprotective effects against a variety of insults including glutamatergic damage, ischemia, neurodegeneration and oxidative stress. The effects of lithium include prevention of cellular damage and loss as well as in some instances, reversal of damage after subsequent treatment with lithium. The mechanisms for the neuroprotective effects of lithium appear to be diverse.

At present little is known about the potential neuroprotective effects of lithium treatment in bipolar patients. A number of studies indicate that chronic lithium treatment may correct some of the previously reported neurocognitive abnormalities in these patients.

IGSLI currently conducts a multi-center cross-sectional study which aims at evaluating the potential of lithium in the prevention of neurocognitive impairment and volume changes of specific brain areas in patients with bipolar disorders.

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There are suggestions flying about that Lithium may have similar positive affects in the brain in numerous “disorders” –

Autism Expert / Isabelle Rapin

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published on Simons Foundation Autism Research Institute SFARI website, 24 May 2011 
Full physical: Clinicians should test children for hearing impairments before they diagnose them with autism, cautions Isabelle Rapin.

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Why is the clear-cut, yes-or-no diagnosis of an autism spectrum disorder so difficult?

There is much disagreement among experts about borderline cases of autism, precisely because it is behaviorally defined and lacks — and will continue to lack — a test that provides a definitive answer.

Autism is diagnosed based on the severity and variety of its symptoms — in other words, its symptoms mimic height, weight, blood pressure or blood sugar, which are dimensional. In each, the cut-off between yes and no, or affected and normal, is based on agreement among experts and not a specific test — such as an X-ray that shows a fractured bone. You or I would be diagnosed as giant, dwarfed, obese, hypertensive or diabetic depending on how far from average we are on these measures.

No one disagrees with or doubts the diagnosis if the measure is very far from average, but there is a wide gray area at the edges of both normality and disease. This is also the case for many other developmental disorders, such as language delay, attention deficit hyperactivity disorder and intellectual disability. This makes diagnosing autism very difficult and easy to confuse with these and other disorders.

Especially in the days before autism was all over the Internet and print media, parents who came for advice were most likely to report problems with language: Either their preschooler’s language was delayed, or it had ceased to progress, had deteriorated, or even disappeared. Parents told us that it was usually between the ages of 15 to 30 months — occasionally even earlier — that they had become aware of the delayed language, plateau or regression.

Awareness of this problem was rarely sudden, but had occurred over several weeks, so that it often escaped attention — sometimes for months. To make matters worse, pediatricians frequently reassured parents, telling them that development can progress in leaps and starts or that little boys are likely to speak later and not as clearly and eagerly as little girls do.

Often it was a nursery school teacher, a speech pathologist friend, a grandmother or the worried parents themselves who pushed for an investigation that brought them to my office. At the time, parents’ main worries were intellectual deficiency or a developmental disorder limited to language. I would bring up two additional concerns: hearing loss or an autism spectrum disorder (ASD).

A glaring example: Quite recently, I saw a lovely 3-year-old girl whose language was clearly deficient. Her nursery school teacher brought up the question of an ASD (this suspicion indicates how much better teachers are educated about autism than they were in the past). The child was very cute, intelligent and did not respond reliably when called by name, a frequent feature of children with autism. She related well to her parents and I was able to engage her in playing ball, neither of which is sufficient to rule out a diagnosis of ASD.

I spent a lot of time discussing diagnostic dilemmas, until I realized that I hadn’t asked whether the parents had an audiogram, or formal hearing test, to show me. The child had passed the newborn screen and the test had not yet been performed. The next phone call from this family reported that she had a significant hearing loss, especially for the high-pitched sounds critical for differentiating one consonant from another, and thus for language development.

As you can imagine, this cute little girl was promptly fitted with hearing aids, which she readily accepted, and the diagnosis of ASD flew out the window — her hearing loss is caused by an inner ear problem; it not currently severe enough to contemplate a cochlear implant, although we do not yet know whether it is progressive or not. The lesson is that prompt and competent hearing testing must be number one on the agenda for any child in whom there is a concern about language development, and must never be neglected. It must be performed even if the child appears to be hearing and needs to be repeated if language deteriorates.

Diagnostic difficulty: These days, Internet-savvy parents worry about autism but do not always tell me their concerns when they visit my office, because they want to hear my independent diagnosis. Let me emphasize that autism is a behavioral diagnosis for which there is no biological test.

The importance of genetics has come to the forefront. Well over 100 different genetic mutations and other chromosomal abnormalities are known. But the key diagnostic dilemma is that, with some exceptions, virtually all these same gene variants or conditions can be found in healthy people.

There is also no prenatal diagnosis for behaviorally-defined autism, only for some neurological conditions that may be associated with autism — such as fragile X syndrome and Rett syndrome, and a small number of severe metabolic illnesses such as phenylketonuria, and malformations such as Joubert syndrome.

In the majority of individuals with an ASD for whom there is no obvious physical or neurological abnormality, multiple different genes probably contribute to the clinical picture. Knowing about these genes is useful to scientists trying to understand some of the biochemical or metabolic differences in the cells of people with autism, and may enable them to develop effective, scientifically-based medications.

But these differences will not determine whether the diagnosis of autism is correct. They will not be able to predict whether individuals with these genes will definitely have the group of symptoms we call autism. Differences in cellular metabolism may indicate that a person is at higher risk for autism, but not necessarily that a behavioral difference will be severe enough for a diagnosis of ASD.

What to do: Most schools cannot deal with fuzzy dimensional diagnoses.

In order to assign Paul to an enclosed classroom with only eight children, a specialized teacher and aides, he needs to be categorically diagnosed as unequivocally having autism and being severely affected — regardless of the biological cause of his ASD. Another child on the spectrum with adequate language and IQ may be assigned to a class for typical children, yet be provided an aide if his behaviors are sufficiently handicapping. But he could also ‘lose his diagnosis’ and the extra help if his social skills are adequate. Such changing diagnostic labels and services are the result of being forced to assign categorical labels for what are dimensional deficits of variable severity.

This last sentence is so important! Subjective judgments are being used to make diagnosis instead of fact-based evidence in individual children. Why? It’s easier, cheaper and – expands the number of children who will be diagnosed by people without experience and credentials. Never forget that diagnosis and treatment produces immense profits. Below: We prefer to drug our children into submission instead of utilizing treatment. This is inhumane and morally reprehensible.

Parents and teachers — and especially financially-strapped school districts — often ask for medication to minimize the expenditures associated with coping with such children’s behaviors. A review of medications widely prescribed for children with ASD concludes that only two fulfill research criteria for efficacy. And those two help only with aggressive behaviors, and have troublesome side effects1. A companion review indicates that the most effective intervention is intensive individualized intervention starting at the earliest possible age2.

These findings agree with my longstanding clinical experience. Knowing that no medical treatment is curative, as a neurologist I worry about potential long-term consequences of psychotropic medications and advocate for behavioral management, which, although more expensive, may help the child learn and permanently alter his brain development.

Lessons learned: Autism has come a long way since I entered this field half a century ago. We have done away with the theory of refrigerator mothers. We know that autism spectrum disorders are disorders of the developing brain and have learned that genetics plays a major — but by no means exclusive — role in their cause. We are aware that epilepsy is linked to autism in ways we do not yet understand fully, but that it needs to be treated vigorously, especially if it occurs in infants and toddlers.

We need much more neurological, and genetic information, even though at present it rarely leads to a change in management of the child or provides firm genetic counseling for the family.

We are convinced that massive and expensive tests such as imaging, electrophysiology and genetics are almost always uninformative clinically, unless there are features that raise the suspicion of a diagnosable condition.

Families deserve the credit for major steps forward, because they banded together to insist that the results of such tests be collected and stored in large data banks accessible to researchers. Parents got the ball rolling by raising money and persuading the National Institutes of Health and the research community that autism spectrum disorders were crying out for investigation and for novel educational and medical treatments.

I salute them and anticipate that we can make much more progress if we can find the means to sustain the momentum of the past decade.

Isabelle Rapin was professor of neurology and pediatrics at the Albert Einstein College of Medicine in New York.

 

Phrenology / Brain Scans: Tools of Psychology

We’re sure lucky that brain scans came along to put an end to this nonsense!

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From Frontiers of Psychology: Fifty psychological and psychiatric terms to avoid: 

(4) Brain region X lights up. Many authors in the popular and academic literatures use such phrases as “brain area X lit up following manipulation Y” (e.g., Morin, 2011). This phrase is unfortunate for several reasons. First, the bright red and orange colors seen on functional brain imaging scans are superimposed by researchers to reflect regions of higher brain activation. Nevertheless, they may engender a perception of “illumination” in viewers. Second, the activations represented by these colors do not reflect neural activity per se; they reflect oxygen uptake by neurons and are at best indirect proxies of brain activity. Even then, this linkage may sometimes be unclear or perhaps absent (Ekstrom, 2010). Third, in almost all cases, the activations observed on brain scans are the products of subtraction of one experimental condition from another. Hence, they typically do not reflect the raw levels of neural activation in response to an experimental manipulation. For this reason, referring to a brain region that displays little or no activation in response to an experimental manipulation as a “dead zone” (e.g., Lamont, 2008) is similarly misleading. Fourth, depending on the neurotransmitters released and the brain areas in which they are released, the regions that are “activated” in a brain scan may actually be being inhibited rather than excited (Satel and Lilienfeld, 2013). Hence, from a functional perspective, these areas may be being “lit down” rather than “lit up.”

Phrenology: Examining The Bumps of Your Brain

PSYCHCENTRAL Website, By Associate Editor 

The next time you say, “so and so should have her head examined,” remember that this was literally done in the 19th century.

Phrenology, as it became known, is the study of brain function. Specifically, phrenologists believed that different parts of the brain were responsible for different emotional and intellectual functions. Furthermore, they felt that these functions could be ascertained by measuring the bumps and indentations in your skull. That is, the shape of your skull revealed your character and talents.

Viennese doctor and anatomist Franz Josef Gall originated phrenology, though he called it cranioscopy. He was correct in saying that brain function was localized (this was a novel idea at the time), but unfortunately, he got everything else wrong.

When Gall was young, he noticed a relationship between people’s attributes and behaviors and the shape of their heads. For instance, he observed that his classmates who had better memories had protruding eyes.  This inspired him to start forming his theories and collecting anecdotal evidence. It’s this type of evidence that is the foundation of phrenology.

The problem? Phrenologists would simply dismiss cases that didn’t support their principles, or just revise their explanation to fit any example.

It was also thought that criminals could be identified by the shape of their brains.

It was also thought that criminals could be identified by the shape of their brains.

Phrenology’s Principles

Johann Spurzheim collaborated with Gall on his brain research, and he is the one who actually coined the term phrenology. He eventually went out on his own. He believed that there were 21 emotional faculties (the term for abilities or attributes) and 14 intellectual faculties.

Phrenology had five main principles, which Spurzheim laid out in Outlines of Phrenology (Goodwin, 1999):

  1. “The brain is the organ of the mind.”
  2. The mind consists of about three dozen faculties, which are either intellectual or emotional.
  3. Each faculty has its own brain location.
  4. People have different amounts of these faculties. A person that has more of a certain faculty will have more brain tissue at that location.
  5. Because the shape of the skull is similar to the shape of your brain, it’s possible to measure the skull to assess these faculties (known as the “doctrine of the skull”).

In this text, Spurzheim featured highly detailed descriptions of the faculties and their locations. Spurzheim popularized phrenology in the U.S. While he was on a lecture tour in America, he passed away. Former attorney turned phrenologist George Combe took over Spurzheim’s work and kept his categories.

Phrenology’s Popularity

Phrenology was particularly popular in the U.S. because it fit so well with the idea of the American dream–the notion that we can accomplish our goals despite a humble heritage. Spurzheim believed that the brain was like a muscle that could be exercised. Like weights for your biceps, a good education could strengthen your intellectual faculties. Plus, phrenology promised to improve the public’s everyday lives with simple solutions.

Soon, phrenology became big business and spread to various areas of life. Phrenologists would test couples for compatibility, potential suitors for marriage, and job applicants for different positions.

Brothers Lorenzo and Orson Fowler (who, as an Amherst college student, actually charged students two cents a head) became phrenology marketing gurus. They opened up phrenology clinics, sold supplies to other phrenologists and even started the American Phrenological Journal in 1838. (Its last issue was published in 1911.) Sound familiar?

The Fowler brothers sold pamphlets on a variety of subjects. A few of the titles: The Indications of Character, Wedlock and Choice of Pursuits. They also gave lectures and offered classes to phrenologists and the public.

They even created a faculties manual that a person would take home after being examined by a phrenologist. The phrenologist would indicate the strength of a faculty from two to seven and then check either the box that said “cultivate” or “restrain.” Then, the person would refer to the necessary sections of the 175-paged book.

While much of the public was fascinated by phrenology, the scientific community wasn’t impressed. By the 1830s, it was already considered pseudoscience. Pierre Flourens, a French physiologist and surgeon, questioned the movement and discredited it by performing experimental studies. He experimented on a variety of animals by observing what happened when he’d remove specific sections of their brains.

But science didn’t cause phrenology to fall out of favor. Psychology professionals offering new methods did.

Phrenology’s Influence on Psychology

If you’ve ever read an introductory psychology book, you might remember that phrenology was depicted as basically a fraud.  It was viewed “as a bizarre scientific dead end in which charlatans read character by looking at the bumps on someone’s head,” wrote C. James Goodwin in A History of Modern Psychology.

But as Goodwin said in his book, that’s a simplistic explanation. In fact, phrenology helped move American psychology forward in various ways. (And while there were charlatans, there were phrenologists who truly wanted to help.)

For instance, the basis of phrenology was individual faculties, and thereby individual differences. Phrenologists were interested in analyzing and measuring individual differences, like psychologists do today.

As mentioned above, phrenology also proposed that one’s DNA didn’t predetermine their life. The environment, including education, played a big role, too. You could improve upon your skills and talents. You — not your genes — had control over your future, and that was a hopeful and exciting notion. It still is!

 

 

Anxiety / Worse for Visual Thinkers?

Animals in the wild must deal with anxiety, but observations suggest that they are able to quickly recover, let go of the triggering incident, and go on with their activities. No animal could survive long if it didn’t recover from trauma and had to function in a permanent state of panic and anxiety – and yet humans do just that. Unlike wild animals, humans think about their trauma and hold on to it, causing chronic anxiety and fear. Americans live in a culture that promotes fear from low-level and non-existent threats.

Animals may be truly lucky not to have higher order brain functions: Humans create long lasting memories of traumas, large and small, by making up stories that run like never ending soap operas. Those memories become part of our physical state: chronic elevation of stress hormones take a toll and can lead to serious illnesses. Short of amnesia, the ongoing creation of stories is difficult to stop or reverse.

Wild animals retreat to safety for a period and then go their way. Some scientists think that because the animal experiences the anxiety only in its body, when the physical effects dissipate, the trauma is finished. However, this is not the case when animals, both domestic and wild, are subjected to chronic maltreatment by humans.

In humans, whenever we replay past trauma in our minds, the trauma becomes more entrenched in our bodies through reactivating the fear and anxiety we felt. If the experience was extreme, we may experience the symptoms of PTSD –  flashbacks, nightmares, unwanted memories and terrifying physical sensations. Avoidance of anything that may trigger such episodes becomes paramount and restricts behavior.

As an Asperger individual my “worst” symptom has always been severe anxiety, not everyday anxiety that we all experience, but anxiety that is off the charts. The example that closely resembles how I feel is seeing how a wild animal reacts to being cornered, captured, caged or otherwise trapped. When I watch a “nature” show, I actually envy an  animal that is shot with a tranquilizer – no lie!

I am aware that my anxiety is out of scale with whatever caused the anxiety, but this knowledge does nothing to keep the anxiety from escalating. Something has reached deep into my memory and resurrected old anxieties. I have thought about this a great deal, and have come up with a possible explanation. I am one of those Asperger individuals who is a visual thinker; my memories are visual. Visual memories are not time bound; they exist always as part of the present and resurface whenever a visual stimulus “matches” –  If I see a blue shoe in a store, pictures of blue footwear I have seen will “join the party” and if a fear-provoking event involved that blue shoe, well – it joins the party. This can be a very rich resource for an artist, if painful. Some art appears to me as the manifestation of this process. The artist is drawing or painting unconscious pictures.

The bad news is that when a traumatic picture is “called up” by a present situation, the picture is not buried by time or relegated to the past through language, stories, denial or defense: it is experienced just as it happened. Which leads me to wonder: are visual people more susceptible to PTSD, and are highly visual experiences (carnage in war or natural disasters) more likely to result in PTSD?

An Asperger Lifestyle / Find Yours

I haven’t done much the past week with this blog, having taken time out to create a new blog from my book on “being a nomad.” The content is likely not what people would expect from a nomadic “travel journal.” Keywords can hit the mark exactly or be poor approximations; generalized to the point where, once again, language is a barrier to knowledge. “Nomad” conjures pictures of young persons with backpacks, hiking third world trails, or trains of people and camels enduring unendurable hardship, neither of which appeal to me.

But we live now in a world of keywords, which cause us to skim the top of the Internet, skipping like a stone across a pond until our search sinks in the dead end of superficial and generic nonsense. A tool that promises a new and magical human “connectivity” is instead a noxious resurrection and proliferation of old time hucksters, snake oil salesman, card sharks and fortune tellers: hustlers.

“Search” is a dull knife that cannot cut to the heart of being human.

Being a nomad has been a life-long consequence of being me. Why? Because curiosity makes one a natural traveler and the social insufficiency of the Asperger-type instigates a search for Where do I belong?  In other words, I’m an observer and wanderer by temperament, seeking and searching whether I’m on the road or cooking dinner at home.

The period described in my book is one of the rare times when the physical and existential journeys coincided, and although I didn’t know about Asperger’s then, looking back I can see an Asperger “lifestyle” emerging; values realized, a way of being in the world that allowed me to discover a genuine self as the encrusted rust of social mythology fell away.

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To understand another human being, or the environment, requires sensory information. I know that as a writer and photographer this is difficult to do: How does one write a “cloud” of movement, odor, texture and choice of personal presentation to the world that envelopes a person? We each are composed of a “self” that walks and talks and moves through space; an unconscious being that arises out of the mists of time, just like all other animals. But our clever brains wait, hoping to speak and to be heard, to be recognized for a moment, for someone to hear our story. Being heard is what matters to human beings, but that requires a listener. Communication of that sort is very intimate, and not found on Google, Bing or Firefox, which detour the searcher  into a universe of lies and clichés, shopping carts, and desperately lonely faces who “like you.”

http://somepeoplearelost.wordpress.com

 

 

A ‘Normal’ Human does not Exist

These individuals are all Homo sapiens – “Humans”

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White EuroAmerican males DO NOT REPRESENT humankind, they simply seek to dominate other humans by defining what it is to be human as “themselves” and excluding everyone else. There is no generic, normal, average human being. There are only individuals who are obligate bipeds, with a large brain to body ratio; we all communicate using visual and verbal languages. Each of us varies in talents and preferences, with a few being avid tool-makers and inventors. Others are artists, thinkers and parents. We all contribute to H. sapiens. So stop pretending that EuroAmerican white males represent anything other than a tiny (and highly predatory)percentage of human beings.

NEW! PODCAST / Listen as I ramble on….

http://auticulture.com/liminalist-26/

Auticulture interviewed me last week (it’s more like we just talk). Check it out! I’m very pleased. A big – Well Done – to Jasun. Lots more interesting material on his site. Love the music.