Sunday, September 28, 2014

UW-Madison: Playing with statistics

Date: 2014
To: [my redaction]
Cc: Rebecca Blank
Subject: Re: From a Bascom Hill Society member

Mr. [my redaction],

On behalf of Chancellor Blank [who doesn't actually give a shit about your concerns], I wanted to respond to your message with [pretend and misleading] detailed information about research at UW-Madison.

The planned research with young monkeys is aimed at understanding how adversity early in life influences the development of the brain [and making us lots of money for redecorating the Chancellor's office]. That knowledge -- coupled with clinical work with human patients -- could provide the basis for new and better treatments [but never has] for people suffering from anxiety, depression, bipolar disorder and other psychological conditions that lead to undue suffering for tens of millions of people in the United States alone.

Critics of this mission draw comparisons between the modern study and the important work done at UW-Madison decades ago by Harry Harlow. It is true that the current study, like Harlow's work, is aimed at better understanding how the brain and behavior change when early infant environments are disrupted [even though Harlow didn't study the brains of the baby monkeys he tortured]. But the current study is also fundamentally different from Harlow's work. The infant monkeys are reared with human contact [as they grab and manhandle them], with other [freaked out and abused] infant monkeys, with toys [?] and environment enrichment [like water and air]. And advances in brain imaging and chemistry allow modern UW-Madison researchers to address basic causes and associations between brain development and mental illness that Harlow would never have been able explore. [So, please ignore the fact that Ned Kalin is taking baby monkeys away from their mothers at birth for the same reason Harry Harlow did.]

A [misleading and not at all] detailed description of the research and its [ridiculous and obviously bullshit] rationale can be found here: [Note: The university's link might not remain active. You can read the unattributed original document here, just in case.]

The way animal research is undertaken on our campus has also changed a great deal in the decades since Harlow was active in Madison. [Now, unlike or PR colleagues from Harlow's day, we know that filming and broadcasting the animals suffering would be a mistake.] This vital anxiety research [though the term 'vital' is completely misleading and false] has been assessed by several university committees [made up of other vivisectors] tasked with making sure that [Kalin has claimed in writing that] potentially beneficial research subjects the fewest animals to the least invasive possible measures. [That sentence needed some more editing.] As with all animal research on campus, specially trained veterinarians [whose livelihood depends on them staying quite about the animals' suffering] will care for the monkeys involved and ensure that all the work is done in accordance with [the meaningless and wildly permissive] federal regulations [nominally] enforced by the National Institutes for Health and the U.S. Department of Agriculture [the two agencies in bed with us.]

We remain committed to [lying about] the humane conduct of important [sounding] biomedical research. We appreciate your willingness [to suspend all critical thought and] to consider all sides of the story before judging our work in light of rhetoric clearly intended to mislead and inflame emotions on the sensitive issue of animal-based research [that we try so hard to keep hidden.]

John Lucas
Executive Director of University Communications

The document linked to in the letter above is something other than the "detailed" description spin-meister John Lucas claims it to be. But then very little about the university's use of animals is what it claims. This is part of the linked document they sent in response to a (now previous) financial donor who wrote with alarm and disgust over psychiatrist Ned Kalin's experiments on infant rhesus monkeys:
Mental illnesses such as anxiety disorders, depression, bipolar disorder, and schizophrenia are extremely common, can be very disabling, and negatively impact physical health. Anxiety disorders are the most common mental illnesses and are frequently accompanied by depression and substance abuse. In addition to creating immeasurable suffering and dysfunction, the worst outcome of mental illness, suicide, is increasing and is among the leading causes of death in adolescents. Each year over 30,000 lives are lost to suicide in the United States, and worldwide suicide is the leading cause of violent deaths. It is estimated that in any 12 months 26% of the population suffers from a diagnosable mental illness. Forty-six percent of the American population will suffer from a mental illness at some point during their life. A study by the World Health Organization shows that of all the medical illnesses, mental illness and substance abuse are the most costly to society and the most disabling. Most mental illnesses have their beginnings during childhood and the earliest presentation of these problems frequently is increased levels of anxiety. Abnormal levels of childhood anxiety can greatly increase the risk for adolescent and adult mental illness.

This is pretty interesting. It makes me wonder how many people at the university reviewed these claims before making the document publicly available. It is a study in propaganda.

The claims in the statement are similar to Kalin's earlier explanations. I wrote about them here. I'm not going to repeat them, very much.

The university argues that Ned Kalin's cruel experiments are justified because mental illness is "extremely common" and "can be very disabling." Mental illness can be disabling. But it usually isn't. Only a tiny percentage of people with a mental illness are disabled and an even smaller number are very disabled.

Kalin's work is funded by the National Institute of Mental Health (NIMH), one of the twenty-seven Institutes and Centers that comprise the National Institutes of Health. NIMH keeps statistics and provides some explanation of the terms it uses in the course of reporting on mental health problems.

NIMH notes: "While mental disorders are common in the United States, their burden of illness is particularly concentrated among those who experience disability due to serious mental illness (SMI)." This suggests that not all people with serious mental illnesses experience disability as a result.

According to NIMH, about 4.1 percent of all U.S. adults have a serious mental illness and some of those will be disabled as a result. But the university says: "Forty-six percent of the American population will suffer from a mental illness at some point during their life." The university's claim is off by more than 131 million people.

The university says: "A study by the World Health Organization shows that of all the medical illnesses, mental illness and substance abuse are the most costly to society and the most disabling." I wrote to Mr. Lucas and asked for the title of that WHO report, but alas, he never replied. Why didn't they supply the title of the report in the letter? And Kalin doesn't claim to be studying substance abuse, so why would the university have appealed to substance abuse in its defense of Kalin's cruelty?

The university says that over 30,000 people kill themselves in the United States each year and that worldwide, suicide is the leading cause of violent deaths." That's sad, but torturing baby monkeys won't change those statistics. World Health Organization statistics help put the university's numbers in perspective: WHO, in its "The top 10 causes of death" reports that:
Ischaemic heart disease, stroke, lower respiratory infections and chronic obstructive lung disease have remained the top major killers during the past decade.

HIV deaths decreased slightly from 1.7 million (3.2%) deaths in 2000 to 1.5 million (2.7%) deaths in 2012. Diarrhoea is no longer among the 5 leading causes of death, but is still among the top 10, killing 1.5 million people in 2012.

Chronic diseases cause increasing numbers of deaths worldwide. Lung cancers (along with trachea and bronchus cancers) caused 1.6 million (2.9%) deaths in 2012, up from 1.2 million (2.2%) deaths in 2000. Similarly, diabetes caused 1.5 million (2.7%) deaths in 2012, up from 1.0 million (2.0%) deaths in 2000.

WHO makes no mention of mental illness in that report,

Quite simply, the claims made by the university, while not outright lies, are misleading and are probably knowingly misleading. After all, misleading people about the use of animals on campus is part of the PR department's job. Their claims are doubly bad because the university has a much greater than normal duty than most to verify that its claims are accurate and not misleading when communicating with the public. The university has an overwhelming responsibility to the citizens of Wisconsin to be honest, forthcoming, and to make the facts plain. The university is violating its public trust.

The university writes: "Based on work performed at the University of Wisconsin with young rhesus monkeys born into UW-Madison’s primate research colonies, we now know that brain alterations are at the root of early abnormal anxiety." But like the misleadingly reported statistics cited by the university, this is also misleading.

Much of Ned Kalin's NIH-funded work has been based largely on his discovery that it is possible to identify some rhesus monkeys who are more anxious and fearful than others by injecting them with them diazapam (Valium) and then scanning their brains. (See Lateralized response to diazepam predicts temperamental style in rhesus monkeys. Davidson RJ, Kalin NH, Shelton SE. Behav Neurosci. 1993.) But they did not and have not demonstrated that the monkeys without the lateralized response to Valium don't develop abnormal anxiety.

One confounding factor among a symphony of confounding factors in his experiments, is that anxiety is epidemic in the monkey labs. (See: Stereotypic and self-injurious behavior in rhesus macaques: a survey and retrospective analysis of environment and early experience. Lutz C, Well A, Novak M. Am J Primatol. 2003; and Risk factors and remediation of self-injurious and self-abuse behavior in rhesus macaques. Rommeck I, Anderson K, Heagerty A, Cameron A, McCowan B. J Appl Anim Welf Sci. 2009.) In Lutz. et al., the researchers found that essentially all the monkeys -- 321 out of the 362 animals surveyed -- had at least one abnormal behavior.

And who wouldn't be anxious in that setting? You are powerless; confined to a small space, occasionally, sometimes regularly hurt, hear others screaming, are socially isolated, and have no support group. Exactly what is the university referring to when it mentions "abnormal anxiety"? Was any of the anxiety experienced by the people in the Nazi camps abnormal? Do Kalin and the university believe that monkeys in its labs ought not be worried?

The university asserts that Kalin's prior work on young fearful monkeys not only: "demonstrates the specific parts of the brain that have altered function, but also shows that this altered brain function that is important for anxiety can be inherited &"

Kalin has always claimed prudently that the fearfulness he has been studying is a "trait-like" phenomena. The university tries to support its claim by pointing to two press releases linked above. The first starts out with an important qualifying remark:
A new study focused on anxiety and brain activity pinpoints the brain regions that are relevant to developing childhood anxiety. The findings, published in the August 12 edition of the journal Nature, may lead to new strategies for early detection and treatment of at-risk children.

And I might purchase the winning lottery ticket. And while it might be understandable that people working in the public relations office are somewhat ignorant about many things scientific, even they should know that a press release hyping a newly published paper isn't evidence of genuine merit. I suspect that at least some of them know that, but their actual goal isn't public education, its all about muddying the water and keeping the details and ethical implications as murky as possible.

The university's announcement from 08/11/2010 about the "new study" doesn't provide a citation or a link to the actual paper. Maybe they didn't want people reading it, or just knew that few reporters would take to the time to review it or care what it said. It's all about sound bites. The unidentified paper was Amygdalar and hippocampal substrates of anxious temperament differ in their heritability. Oler JA, Fox AS, Shelton SE, Rogers J, Dyer TD, Davidson RJ, Shelledy W, Oakes TR, Blangero J, Kalin NH. Nature. 2010 Aug 12.

Like most of Kalin's work with monkeys and rats, there doesn't seem to be much insight into what it might be like to be one of the animals he uses. The paper starts out by implying that the things they did to the monkeys used in the study were mild: "Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli."

Given that the paper's few readers are most likely other vivisectors, his characterization might make some sense given the spectrum of terrible things they do to animals. But from the animals' perspective, mild is probably just a sick joke.

Here's the gist:
... monkey AT was assessed using measures of threat-induced freezing behaviour and inhibited vocalizations, as well as plasma cortisol concentrations.... AT and brain metabolism were assessed when monkeys freely behaved in a test cage by themselves for 30 minutes in a potentially threatening situation in which a human “intruder” entered the room and stood 2.5 meters from the cage. During this time the intruder presented his profile to the monkey ensuring that he avoided eye contact with the animal (No Eye Contact; NEC). Animals with the greatest AT froze longer, vocalized less, and had elevated plasma cortisol levels. ....

The authors also explain it this way:
Each monkey was injected with FDG immediately preceding the No Eye Contact (NEC) challenge. During the experimental paradigm, FDG-uptake occurred and behaviors were monitored non-invasively. During NEC the animals were placed in a test-cage and a male human (the “intruder”) entered the room and stood still at a distance of 2.5 meters presenting his profile to the animal. Following 30-minutes of exposure to the experimental condition, animals were anesthetized and blood samples were taken.

From the monkey's vantage, the entire episode was probably something other than mildly threatening. Consider who the monkeys were. This is the description from Kalin et al:
All animals were mother-reared, and pair-housed at the Harlow Primate Laboratory and the Wisconsin National Primate Research Center. At the time of behavioural testing/brain scans, the mean age was 2.4 years (range = 0.74 – 4.2 years), the median age was 2.34 years, there were only four animals that had reached the age of 4 years, and there were only nine animals less than 1 year of age. The typical life span of a rhesus macaque is approximately 25 years. Females reach puberty around three years old, and males reach puberty between three and 3.5 years of age (cf. Wisconsin Primate Research Center). This would correspond to a human sample of mostly prepubescent children with some peri-adolescents.

The youngest monkeys were the victims of recent trauma. It appears to be the standard practice at the university to take babies from their mothers at 6 months of age and place them with a similarly aged monkey. This is a dramatic departure from the millennia-old normal course of a rhesus macaque's life. Behavior is largely gene-mediated, a foundational claim in all of Kalin's experiments on animals. Millions of years of evolution have molded the behavior of rhesus macaques. These animals are adapted to live in large multi-generational family groups in complex environments and societies. Mothers and a single infant in a small barren metal box are profound deviations from the norm. It is a near certainty that the normal course of development, particularly emotional reactivity is profoundly altered by the near complete absence of normal social stimuli. Mothers and their daughters typically remain together for their entire lives. Mothers and their sons sometimes do as well. In the lab, the isolated mother-child pair are torn apart; the infant is put with a similarly traumatized infant. The cause of their misery is clear; giants in white coats and face masks who have them cornered and who must be recognized and reacted to by every other monkeys in the room as a threat, in fact, the only threat most of them will face.

I wonder if the Jews in the camps felt that a guard looking them was merely a mild threat?

Kalin et al claim that the "anxious temperament" they have identified is trait-like. That is, they can't identify the genes responsible for the monkeys' anxiety, but because the offspring of highly anxious monkeys are also anxious, ergo it must be genetic.

But another possibility exists. Perhaps it is simply a matter of modeling. If my mother was frightened by the approach of one of the white-clad monsters, why wouldn't I learn to be frightened too?

Our ward, Mickey, is a designer dog bred at a puppy mill in a nearby town. We adopted him from the local shelter. Once, when we had two other dogs staying over for a weekend, there was an electrical storm with lots of thunder, something fairly common in our area of the country. Prior to that weekend, Mickey had seemed relatively unconcerned by the thunder claps. But the two visiting dogs were visibly frightened. Their behavior and fear resulted in Mickey adopting a similar opinion. Now, he too is frightened by thunder. After one night of seeing other dogs being afraid. I'm not surprised that a young monkey would quickly learn from their mother to be very worried about visits from lab workers. That's not trait-like, it's simply learned and warranted wariness.

The second press release is from 10/18/2012. It starts out like this:
Decreased activity of a group of genes may explain why in young children the “fear center” of the anxious brain can’t learn to distinguish real threats from the imaginary, according to a new University of Wisconsin study.

The paper referred in the press release is Central amygdala nucleus (Ce) gene expression linked to increased trait-like Ce metabolism and anxious temperament in young primates. Fox AS, Oler JA, Shelton SE, Nanda SA, Davidson RJ, Roseboom PH, Kalin NH. Proc Natl Acad Sci U S A. 2012, Oct 30.

I'm always amazed at the gibberish that is passed off as science among vivisectors. Kalin et al: "The rhesus monkey is ideal for studying the origin of human AT because these species share the genetic, neural, and phenotypic underpinnings of complex social and emotional functioning (5–10)."

First, we actually have only the most sparse understanding of the genetics underpinning complexities like social and emotional functioning. Complexity and complicated are not synonyms. Complex systems are not good models of each other. But, as I mentioned above, the realities of laboratory incarceration negate the expression of the complex social and emotional functioning in humans that Kalin mistakenly claims are modeled by profoundly deprived rhesus monkeys.

In the six citations provided by Kalin et al as supporting evidence for their claims, not one of them supports their claim of some shared genetic underpinning of social or emotional functioning. None. Not one. Kalin makes claims apparently, and then points to 'evidence' that he must assume no one will review.

--- Let me pause here for a moment to mention that this phenomena is apparently widespread and fully understood and accepted by insiders. One of the times I debated primate vivisector Paul Kaufman, UW-Madison's Ophthalmology department head, I called attention to his wild claims about the need and importance for finding better treatments for near-sightedness. Reading glasses do a pretty good job already, I said, and experimenting on the eyes of monkeys was needlessly cruel. Kaufman replied that his claims, which I had quoted from his grant, should not be taken seriously; they were mere grantsmanship. When I pushed the point, moderator Robert Streiffer, "bio-ethicist" and critic of the Kalin project, stopped further discussion. He and the rest of the panel of "experts" asking us questions seemed to fully understand that the rhetoric used in grants (and publications?) is just so much blather. ---

Equally silly is their next claim: Importantly, the rhesus developmental model bridges the critical gap between human psychopathology and rodent models, allowing for translation to humans by using in vivo imaging measures and translation to rodents by using ex vivo molecular methods. Thus, the unique hypotheses that can be generated from the rhesus model are invaluable in guiding both imaging studies in children and mechanistic efforts in rodents.

You can be excused for not noticing the spin and absurdity in that statement.

After a scathing 2003 editorial in the Journal of the American Medical Association titled "Translating Biomedical Research to the Bedside: A National Crisis and a Call to Action," the term "translation" quickly became a buzz word among those tying to justify the use of animals. Numerous "Centers" and "Institutes" for the translation of basic science -- a euphemism for animal experimentation -- have been started around the country, as if doing so could improve the translation rate. The UW Institute for Clinical and Translational Research, created in 2007 apparently, is a local example. "Translation" has become a sort of talisman; if it is chanted long enough, maybe it will come to pass. See too: Evolution and translation of research findings: from bench to where? Ioannidis JP. PLoS Clin Trials. 2006.

The primary purported justification of Kalin's experiments on monkeys, written by him, one of his collaborating students, or a university PR hack, is based on statistics regarding the incidence of mental illnesses. Their purported justifications rest on claims about the incidence of mental illness that do not withstand even cursory inspection. They are not being honest. It appears to me that they are knowingly dishonest. Money has a well known corrupting influence on people's behavior. In this case, the millions of dollars of other people's given to Kalin and the university by the other vivisectors who comprise the NIH committee that sanctions his projects is a mere data point in the flood of taxpayer dollars pouring into the university coffers from NIH. The university defends every funded project because they fear that even one admission of error could be the hole in the dam that leads to a financial catastrophe for them.

The simple fact that they have written a PR piece to foist off on donors who contact them about Kalin et al's cruelty is an indication that many people are writing in alarm and disgust. But the university can't back down. NIH can't back down. It would be like the Nazis having said that they had made a mistake about trying to achieve racial purity.

Friday, September 19, 2014

Young Monkeys and Children

UW-Madison vivisector Ned Kalin, and by extension every supporter of his use of infant rhesus monkeys to model early adversity in children, have terminally muddled notions about monkeys and humans.

If you read the public relations rhetoric from the university you'll see all sorts of silly and (probably) knowingly misleading claims. One of the silliest is that putting an infant monkey in an incubator is no different than putting an infant human in an incubator. Imagine putting a young goldfish in an incubator; the poor thing wouldn't last very long.

This might come as news to the university egg-heads, but, like fish, infant humans have different needs than infant rhesus macaques. Infant humans can be set down without causing them serious trauma. This isn't true for infant macaques and most other infant primates.

Infant monkeys either hang on to their mother or die. The psychological need to cling to their mother is a deep and genetically driven response to their natural history. It isn't shared with humans. At any moment, a mother monkey might leap through the forest canopy or rush up a tree. If the infant releases his or her grip, their life is likely over.

Monkeys are active semi-arboreal animals while humans are plodding fully terrestrial animals. There probably isn't a more stressful experience for an infant rhesus monkey than being pulled from his or her mother. Taking a human infant from his or her mother is not at all similar.

The physical pulling of an infant monkey from his or her mother may be the most distressing thing anyone can do to an infant rhesus monkey. After the separation, any other cruelty is just salt in the wound.

Because this particular psychological need and experience isn't shared by humans it is improbable that the resulting changes in a baby monkey's brain chemistry are meaningfully similar to what happens in a child's brain when he or she experiences a completely different kind of adverse event. Claims that there are meaningful similarities are little more than appeals to alchemy. It's just BS.

Kalin's cruelty exacerbates the already profound differences in the neurobiology of human's and rhesus monkeys' brains. After being socially isolated for a month or so, the infants are paired with other infants who were also taken from their mothers and isolated. All the monkeys are males. It is well established that male rhesus monkeys are much more negatively impacted by laboratory conditions and isolation than are females. Infant monkeys need to cling, and when they have only each other, they cling tightly together. Periodically, Kalin pulls them apart and separates them, re-wounding them in a way similar to their initial removal from their mother. While isolated, he frightens them in various ways, none of which would bother a human child of the same age, because humans aren't repetitively traumatized monkeys.

Kalin claims that a human child who is abused and a traumatized infant monkey have similar brain chemistry as a result of their different experiences. I doubt that he believes his own claims. He must chuckle to himself over that absurdity and the willingness of others to look like fools or ignoramuses by defending it. Although he nominally claims to be looking for some new molecular pathway that might be modified in some unknown way by some future drug that will cure or vaccinate children from the occasional bad effects of poor, or neglectful, or abusive parenting, I suspect that he is actually hoping only to find yet another patentable molecular pathway that he can add to his and university's portfolio of similar patents. It really is all about money. His decades of hurting, frightening, and killing young monkeys has never resulted in anything of benefit to human patients. Nothing. Nada. Zilch. Zippo. It won't this time either.

Sunday, September 14, 2014

Doctor Says Maternal Deprivation Research is Unethical Promotion of Mind-Altering Drug Use for All At-Risk Children.

Dr. Francis Collins, Director
National Institutes of Health

Michael Gottesman, M.D.
Deputy Director for Intramural Research

Dear Doctors:

It has recently come to my attention that researchers at the National Institutes of Health (NIH) Intramural Research Program are using maternal deprivation to study anxiety and depression in infant macaques. As a pediatric psychiatrist who has treated abused and neglected children, and who is concerned about the welfare of primates used in research as well as the welfare of my patients, I am particularly interested in this issue. Dr. Stephen J. Suomi, leader of the project, offered this explanation to CBS News:

"These findings assist researchers in identifying humans most likely to suffer negative effects in at-risk situations and develop behavioral and drug therapies to improve negative outcomes early in development."

Perhaps more than any other medical specialty, pediatric psychiatry is an art as much as it is a science. As children are constantly growing and developing, their symptoms require frequent reassessment, and their treatment plans must continually be revised and updated. Clinical psychiatrists already know that children respond to psychotropic medications with great variability and unpredictability, and that the side effects of these medications can be debilitating. For these reasons, I believe that it is unethical and inappropriate for any physician to recommend the use of psychotropic medications in children who are "at risk" but have not yet been medically diagnosed with a DSM-5 psychiatric disorder. In his 2002 research paper on childhood predictors of anxiety, Dr. Jerome Kagan concluded with a note of caution:

"It is also important to note that a high-reactive temperament protects the child from engaging in risky behavior -whether drugs, driving at high speeds, or temptation for delinquent, behavior. Thus, the child with a high-reactive temperament has some advantages in our society and parents of such infants might decide not to change their child's behavior when the next set of pharmacological advances permits them that choice."

Identifying children who are at risk for the development of mood and anxiety disorders is a great idea, as is the use of family support and individual counseling as preventive medicine. However, there are many researchers successfully working on these issues with human subjects, utilizing low-risk and non-invasive functional brain scans which make the use of animal models obsolete. And unlike monkey researchers, who have yet to propose a single new treatment for psychiatric patients despite decades of experiments and promises, researchers who study humans can often give us useful information immediately. For example, from a 2011 study of human beings with inhibited temperament:

"Thus, a sustained amygdala response to newly familiar people may be one cause of social anxiety in inhibited individuals. This finding may also have implications for prevention or intervention. For individuals with temperament-based risk for social anxiety, increased exposure to human faces through traditional exposure therapy or through computer-based training may enhance amygdala habituation and reduce social anxiety."

I urge NIH to put an end to all maternal deprivation psychiatric research in primates, as an unnecessary use of animal models as well as an unethical promotion of the use of psychotropic medications in asymptomatic children. I have additionally contacted my representatives in the United States Congress and asked them to investigate why our public tax dollars continue to fund these studies when they do nothing to help human patients.


Sujatha Ramakrishna, M.D

Wednesday, September 10, 2014

I just can't resist... war is peace.

The Dane County Board executive committee's decision to indefinitely postpone any decision on the matter of Resolution 275 was covered as a news item in the Isthmus, the paper that finally published an article on Ned Kalin's revival of maternal deprivation and emotional torment as a means to create infant monkey "models" of human depression. You can read the front page article here: Motherless monkeys: UW-Madison to revive controversial primate experiments. Noah Phillips. 07/31/2014.

Doublethink is alive and well in the exalted towers of academia. The executive committee, four present, two absent,was presented with nearly two hours of comment from seventeen people; three people with a financial interest in the use of animals at the university were the only ones who spoke in opposition. The committee then deliberated. Note: indefinitely postponing a decision on an agenda item is intended to kill it. A vote against an item allows it to move out of committee and then be considered by another committee, just as a vote in favor would do. Indefinitely postponing a decision is a way to circumvent further discussion and undermines our democratic system of governance. This is a transcript of the executive committee's entire public deliberation. As one observer noted afterwards, "How very embarrassing for the board."

Chair, Sharon Corrigan: We just have a few minutes, but before we can continue, could we, to discuss it, is there a motion on the resolution? Is there a motion?

Supervisor Mary Kolar: Move to table, based on, uh, we've only heard, so...

Corrigan: The motion would be to postpone indefinitely?

Kolar: [Nods in agreement.] I move to postpone indefinitely.

Corrigan: Is there a second to postpone indefinitely?

Supervisor Dave Ripp: Second.

Corrigan: Is there discussion?

Supervisor Carousel Bayrd who represents the UW Research Park and lives a couple of streets away from Eric Sandgren: [Mumbles something unclear]

Corrigan: If there's no motion it would be the same impact. [Looks around, then back at Supervisor Kolar] Do you want to...

Kolar: Postpone indefinitely.

Corrigan: All those in favor?

All: Aye.

Corrigan: Opposed?

Corrigan: The motion is approved and it is postponed.

Afterwards, speaking to the Isthmus reporter, chief UW vivisection spin-doctor Eric Sandgren said: "Tonight was a victory for public discussion."

They spew this crap with a straight face and utter disdain for the truth. Unbelievable but true. War is peace.

Monday, September 8, 2014

Robert Golden: "... the opinion of the top leaders..."

I am writing here mostly about one claim that was made in various forms by Dr. Robert Golden, dean of the University of Wisconsin-Madison's School of Medicine and Public Health in his comments to the Dane County Executive Committee (which you can watch in its entirety in the video above) regarding Supervisor Al Matano's Resolution calling for the condemnation of the university's renewed use of maternal deprivation to create monkey-models of early adversity-induced depression.

His talk is pretty much a load of crap throughout that seems intended only to soothe and delude his listeners, or else he really is as dull as he appears, but that seems unlikely. See some previous observations of mine regarding some of his previous ridiculous claims here and here. Or, maybe he believes everything he said during the committee's meeting and has simply lost touch with reality.

Dr. Golden said: [Beginning at about 58:22] "More important than my opinion quite frankly though is the opinion of the top leaders, his competitors in the field [which field is that?], who get together and decide that his work is so promising, that they will take money from the limited pot that's available to fund their resource [research] and recommend that it be given to his. His grants have received the very top ratings in the outstanding category from neuroscientists who are competing with him to get their work funded."

"His papers are reviewed by his competitors who feel that they are worthy of publication, because of the progress already being made in the very top journals in the world."

Wow! Kalin's work must be really something!

[Kalin's experiments on monkeys have not led to one single improvement in the care and treatment of people suffering with a mental illness. Golden should point to the improvement(s?) if I'm wrong. He won't. He can't. There is nothing to point to. Golden's talk of "progress" is hyperbole and has no foundation in fact, none whatsoever. Maybe Golden is hoping for a Chancellor's position somewhere and he feels a need to demonstrate his facts-be-damned allegiance to his current institution. Institutions like the UW carefully vet the people they hire as spokespersons, and no quibbling over cruelty and suffering is wanted. But all this isn't what I am writing about here.]

Ned Kalin's longest running grant is DEVELOPMENT AND REGULATION OF EMOTION IN PRIMATES. [Grant: 5 R01MH046729 20.] It's been continuously funded for 20 years. In 2014 it was allotted another $629,176. [Direct Costs: $425,588. Indirect Costs: $203,588. Indirect costs are the part of the grant that the scientist's institution is able to deposit into its general fund. Legal skimming.]

Most NIH-funded research projects, like the this one, are approved by committees sponsored and organized by the Center for Scientific Review, a part of the NIH. The CSR creates peer review groups or study sections charged with evaluating grant applications and deciding which should be funded. Kalin's project was approved by the PMDA study section.

Robert Golden says that Ned Kalin's research must be important because the people who approved it are the "top leaders," the cream-of-the-crop of the scientists around the country.

But the system doesn't work. It is inbred and circular. The members of the committees that evaluate experiments using animals are by and large made up of scientists who also use animals in stupid, cruel, dead-end experiments like Kalin's. These committees aren't made up of the "top leaders" working on human health and basic human biology, they are made up of vivisectors doing work that has little merit. Of course they endorse research methods like their own; and as long as the system is as it is, self-interest will continue to maintain the status quo.

Let's look at the members of the PMDA study section, the committee that has decided to keep giving Dr. Kalin lavish handouts of the public's tax dollars. Dr. Golden's characterization of these scientists and their work is dead wrong. Only two of these fourteen scientists are studying human biology, the work of the twelve vivisectors has next to no chance of leading to better patient care or the prevention of disease. Dr. Golden's estimation of what is and isn't good science seems to be colored by the money flowing into his institution and sustaining ridiculous and terribly cruel experiments on animals.

Here's the roster of the "top leaders" in Kalin's "field." Golden must mean dead-end and horribly cruel when he claims Kalin's work is part of a particular field of study.

Center For Scientific Review

(Terms end 6/30 of the designated year)


NEW YORK, NY 10029

One of Dr. Hurd's currently funded projects is titled NEURODEVELOPMENTAL EFFECTS OF CANNABIS AND ITS EPIGENETIC REGULATION. [Project Number: 5R01DA030359-04. $409,073. Direct Costs: $241,916. Indirect Costs: $167,157.]

She writes: "Importantly, PENK and D2 gene expression impairments persisted into adulthood following either prenatal or adolescent THC exposure and the animals [rats] exhibited increased heroin self-administration and inhibitory control deficit, phenotypes predictive of drug addiction vulnerability.... In this project, we propose to study chromatin modification at specific regulatory regions of the PENK and D2 genes in the ventral striatum of adult rats with developmental THC exposure."

Dr. Robert Golden says this is the best of the best publicly funded research going on right now. Wow.

NEW YORK, NY 10065

This is from Dr. Angulo's lab's webpage "... We study the mechanism by which neuropeptides restore homeostasis in the neostriatum after exposure to psychostimulants at behavioral, neurochemical, and molecular levels. In addition, histological methods are used to study the damaging effects of the pscyhostimulant methamphetamine and to demonstrate that some neuropeptides protect neurons from the damaging impact of this commonly abused drug. We utilize both Sprague-Dawley rats and mice as model systems....".

Top notch.


As she describes it here, Dr. Berretta's description of her work seems to be the real McCoy. This looks like the sort of research that may be getting bumped by projects like Kalin's.


Dr. Dwivedi is also studying humans.

IRVINE, CA 92697

One of Dr. Gall's currently funded projects is BDNF AND THE RESTORATION OF SYNAPTIC PLASTICITY IN FRAGILE X AND AUTISM. [Total Funding: $453,289. Direct Costs: $377,278. Indirect Costs: $76,011.]

Dr. Gall writes: "... Finally, Aim 5 will test if TBS-induced LTP, and steps in actin signaling that are perturbed in the Fmr1-KO mice, are disturbed in other animal models of autistic phenotype and corrected by BDNF: this work will evaluate effects in the BTBR T[+] tf/J mice and Tuberous Sclerosis complex model mice. Together these studies will identify mechanisms underlying deficits in LTP stabilization in FXS model mice, determine if the same processes are disturbed in other mouse strains with features of autism, and test if increasing endogenous BDNF is an effective therapeutic strategy for correcting impairments in the cellular mechanisms of learning and memory in models of cognitive conditions associated with autism."

I wonder whether she has heard the idea that limiting the number variables is a good idea in the conduct of most experimental science? Top notch.


Dr. Jentsch is a central element in this video. He's the odd, very loud fellow who appears to be pregnant. I've written a bit about his cruelties in the past. Just stick his last name in the little search window above. I suspect that Dr. Golden got this right. Jentsch (rhymes with Grinch) is definitely one of the leaders od this so-called field. Yes sir, cream-of-the-crop, top notch all the way.


Dr. June's most recent grant, funded last in 2013, is titled: EFFICACY OF NOVEL TRIPLE UPTAKE INHIBITORS IN TREATING ALCOHOLISM AND DEPRESSION. [Total Funding: $311,069. Direct Costs: $210,182. Indirect Costs: $100,887.]

Dr. June writes: "The first aim will test the hypothesis that orally-administered TUIs can effectively attenuate excessive alcohol drinking in the binge and prolonged repeated alcohol deprivation [PRAD] models using the alcohol-preferring [P] rat. Initial studies will employ DOV 102,677 [our lead compound], recently shown to reduce limited alcohol responding for six days after a single administration. It is hypothesized that acute treatment for binge drinking, and chronic treatment for PRAD drinking, will selectively reduce intake in both models." (Brackets in original.)

Binge drinking in rats... I'm sure he's on the cusp of a major breakthrough.

NEW YORK, NY 10021

Dr. Lee writes a recent paper: "Relatively little is known about neurobiological changes attributable to early-life stressors (e.g., orphanage rearing), even though they have been associated with a heightened risk for later psychopathology. Human neuroimaging and animal studies provide complementary insights into the neural basis of problem behaviors following stress, but too often are limited by dissimilar experimental designs. The current mouse study manipulates the type and timing of a stressor to parallel the early-life stress experience of orphanage rearing, controlling for genetic and environmental confounds inherent in human studies. The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress."

Top notch. His and Kalin's work are not so different.

One of Dr. Lewis's currently funded projects is titled: CANNABIS AND ADOLESCENT BRAIN DEVELOPMENT [Total Funding: $550,394. Direct Costs: $365,178. Indirect Costs: $185,216.]

Dr. Lewis writes in his grant abstract: "To test this hypothesis we will determine the postnatal developmental changes in the expression of CB1R mRNA and protein (Aim 1), the innervation patterns of CB1R-IR axons (Aim 2), and the electrophysiological consequences of CB1R activation (Aim 3) in the macaque monkey DLFPC, a model system that uniquely recapitulates the circuitry and protracted development of the human DLPFC. We will also assess the impact of chronic cannabis exposure during adolescence on working memory performance in monkeys (Aim 4) and on the maturation of perisomatic inputs to DLPFC pyramidal neurons (Aim 5). Thus, these studies will provide an explicit test of the biological events and mechanisms that make the adolescent brain especially vulnerable to the effects of cannabis."

Monkeys and marijuana. Top notch no doubt. What real medical research was dumped in lieu of this cruel silliness?


One of Dr. Middleton's projects is in its 29th year of continuous funding. It is titled: FETAL ALCOHOL SYNDROME. [Grant: 5R01AA006916-29. Total Funding: $353,190. Direct Costs: $221,436. Indirect Costs: $131,754.]

Dr. Middleton writes: "Fetal alcohol spectrum disorder is common (affects ~2% of all live births) and is a major cause of mental dysfunction.... Three complementary aims will be addressed using p53 deficient mice and cells. ... Vulnerability of cortical neurons to ethanol will be addressed in long- and short-term in vivo studies. Long-term studies will determine the ethanol-induced loss of neurons in cortical layers occurring in the deficient mice."

Top notch all the way.


In a fairly recent paper [Physical activity-associated gene expression signature in nonhuman primate motor cortex. Mitchell AC, Leak RK, Garbett K, Zigmond MJ, Cameron JL, Mirnics K. Obesity (Silver Spring). 2012.] Dr. Mirnics et al write: "The Animal Care and Use Committee of the Oregon National Primate Research Center reviewed and approved all experiments. Fourteen adult female ovariectomized Rhesus monkeys (M. mulatta) with various levels of spontaneous activity were used in this study with care methods previously published (1,2,24). Their activity levels were measured in counts/ day with an accelerometer throughout the study and ranged from 46,378 to 897,948 activity counts per day. These monkeys also participated in a previous weight loss study (1). Monkeys were deeply anesthetized with ketamine/pentobarbital, quickly decapitated, and the entire brain was removed from the skull....".


In one paper reporting on work supported by Dr. Penzes's grant: ROLE OF KALIRIN SIGNALING IN SYNAPTIC PLASTICITY. [5R01MH071316-10. Total Funding: $375,369. Direct Costs: $247,500. Indirect Costs: $127,869.] Dr. Pezes et all write: "Because we have previously shown that complete absence of the KALRN gene leads to significant cortical deficits and behavioral impairments in young mice, we reasoned that analysis of spine densities in different brain regions in both heterozygote and knockout adult mice and their correlation with cognitive phenotypes, might reveal important relationships between spine plasticity and behavior."


One of Dr. Plentnikov's currently funded projects is DISC-1 IN NEURON-ASTROCYTE INTERACTIONS IN NEURODEVELOPMENT. [5R01MH083728-05. Total Funding: $405,000. Direct Costs: $250,000. Indirect Costs: $155,000.]

Dr. Plentnikov is just another mouse vivisector.


"... The purpose of this study, therefore, was to assess the functional effects of re-exposure to cocaine in nonhuman primates after the discontinuation of cocaine self-administration for 30 or 90 days, .... Rhesus monkeys self-administered cocaine (fixed interval 3-min schedule, 30 infusions per session, 0.3 mg/kg/infusion) for 100 sessions followed by 30 (n=4) or 90 days (n=3) during which experimental sessions were not conducted. Food-reinforced control animals (n=5) underwent identical schedules of reinforcement. Animals were then re-exposed to cocaine or food for one final session ... Compared to controls, re-exposure to cocaine after 30 or 90 day drug-free periods resulted in lower rates of glucose utilization in ventral and dorsal striatum, prefrontal and temporal cortex, limbic system, thalamus, and midbrain." Functional consequences of cocaine re-exposure after discontinuation of cocaine availability. Beveridge TJ, Smith HR, Nader SH, Nader MA, Porrino LJ. Neuropharmacology. 2014.

These are the leaders? Just imagine what the average scientists in this field are up to. Dr. Golden needs his head and ethics examined.