Tuesday, August 28, 2007

The New Simian Census

The New Simian Census
(Including prosimians)

The numbers below represent a conservative snapshot of the number of nonhuman primates on hand for experimentation worldwide at any one time. The total number is growing due largely to the ever-increasing support of primate experimentation by the United States and a few other governments

If you have verifiable data on populations not included here, please email info(at)primatefreedom(dot)com.

These figures, unless noted, were web retrieved between August 23 and 26, 2007, from the Primate Info Net (PIN). PIN is supported by grants RR000167 and RR15311, National Primate Centers Program, National Center for Research Resources, the National Institutes of Health, an agency of the United States government. Additional support for PIN is provided by the International Primatological Society and the Primate Society of Great Britain.

The figures on PIN are the result of voluntary self-reporting. These figures are dynamic; the United States imports approximately 20,000 monkeys a year, primarily for terminal toxicity studies in contract laboratories.

Additional details such as the directors' names, the number of staff, and the type of experiments underway at the facilities named below can be found on the PIN site here, here, and here.

Snapshot of nonhuman primates available for experimentation by country

Argentina (90)
Australia (156)
Barbados (2,000)
Brazil (771)
Canada (300)
Chile (100)
China (12,058)
Czech Republic (193)
France (535)
Gabon (363)
Germany (1,970)
Italy (204)
India (853)
Indonesia (2,394)
Japan (2,407)
Kenya (570)
Mauritius (3000 - 7000)
Mexico (38)
The Netherlands (1,250)
Puerto Rico (1,900)
Russia (3,580)
Saudi Arabia (45)
Sweden (70)
Thailand (90)
United Kingdom (330)
United States (43,275)

Approximate World Total (78,542)

The New Simian Census

Thursday, August 23, 2007

Animal Rights Violence

Gary Francione, well known Rutgers University law professor and animal rights philosopher, has written a piece on his blog explaining why violence should not be advocated nor employed in any attempt to advance animals' rights.

Before I criticise his position, let me make it clear: I'm not advocating violence. We have to think our way out of utilizing violence. My current best effort at doing just this is the National Primate Research Exhibition Hall [the link now goes to an archived copy of the project's website's front page.] But no matter how abhorent we might find violence to be, and no matter how kind and gentle we are and would like others to be, it isn't the same as saying that violence wouldn't work.

Franione has three parts to his argument:
1. The animal rights position is the modern expression of ahimsa.

2. There isn't a fair way to determine who violence should be directed against.

3. Violence is counterproductive.
Francione dosen't use the word ahimsa, but he describes it well enough. He writes, "the animal rights position is the ultimate rejection of violence. It is the ultimate affirmation of peace" and goes on to argue that
Anyone who has ever used violence claims to regret having to resort to it, but argues that some desirable goal supposedly justified its use. The problem is that this facilitates an endless cycle of violence where anyone who feels strongly about something can embrace violence toward others as a means to achieving the greater good and those who are the targets of that violence may find a justification for their violent response. So on and on it goes.
To a certain degree, he's right, but not to a sufficient degree. What should the United States do if some brand of Nazism returns with all its hideousness? Suppose that the evening news is filled with images of smoke billowing from modern crematoriums in some distant land. What then?

Do we negotiate? At what point, should negotiations continue to fail and the chimneys continue to belch smoke, should violence be considered?

If we rely on the philosophical position that violence is always wrong and will just make things worse, and is itself the cause of the "cycle of violence," we must apparently stand by and weep and beg that genocide end, but dare not raise a hand to stop it.

Although violence is repugnant, there do seem to be times -- primarily after all else has been tried -- that it might be immoral not to resort to its use. This is why I can't embrace ahimsa.

The full embrace of this attractive idea means that I wouldn't defend you from a mugger if significant force was needed. In regard to my person, I am willing to use nonviolence as a foil to violence. I have been hurt intensely and repeatedly by police officers who have physically forced me into custody during nonviolent protests. I have never resisted and have paid the consequences willingly. And, when others have borne the same abuse, willingly, I have not interfered. But if the same thing were being done to someone on the street by a mugger and I did nothing to intervene physically, even if it meant hitting them in the head with a brick (after yelling and calling for help failed), I would be acting immorally.

Francione's second argument is that because essentially everyone is complicit to a degree in our societal abuse of animals, that no one can be singled out fairly as a possible target of violence.

This seems to get everyone off the hook for everything, always. Personal responsibility is eliminated. You can't hold me personally responsible for slapping my children around and stealing my neighbor's barbeque grill because society is structured in such a way that I matured into a cruel and dishonest SOB. Everyone is responsible for the things I do, so, hey, you can't blame me.

This doesn't make any sense to me whatsoever. There is compelling evidence that we are all personally responsible for our own actions and that even though the milieu in which we find ourselves can control us to a degree, it isn't an absolute. For more on this, I recommend a review of Ordinary Men: Reserve Police Battalion 101 and the Final Solution in Poland by Christopher R. Browning and Obedience to Authority: An Experimental View by Stanley Milgram.

Francione's third argument seems incompatable with, or to undercut his first two claims (although, maybe he sees each of them as independently sufficient.) He argues that violence is or would be counterproductive. If he thought it could be productive would he then dismiss his first two claims, or is he arguing that even if violence worked, he'd still be against it and would, in effect, be content to weep and beg? It isn't clear to me.

So, would violence be counterproductive?

I confess to being completely baffled by this question, not on its face, but because of its hidden assumption, an assumption I find absurd.

As Francione accurately observes, we live "in a world in which eating animal products is considered by most people as 'natural' or 'normal' as drinking water or breathing air." So, how could things get any worse?

Would we go from killing 8.9 billion "broiler" chickens a year in the U.S. to 9 billion?

Would we dock puppies' tails a little shorter?

Would we start televising dog, cock, and bull fights? Could the animals suffer any more than they already are?

One possible result might be a loss of revenue for the large mainstream animal welfare organizations if the animal exploitation industry could successfully brand them as terrorists.

But other than that, how could it be any worse than it is now? The University of Wisconsin sanctioned a two-decades long series of experiments that kept monkeys strapped into chairs for four days at a time while any of fifty different chemicals were pumped into and sucked from deep in their brains.

How could things have gotten any worse for those animals?

It seems a matter of fact that violence and the fear it engenders is a productive method of control. This isn't to say that it should be used, or that it's a good thing, or that we shouldn't try as hard as we can to find alternatives; but denying that violence can be effective seems more an exercise in absolving people from even considering it than explaining why it shouldn't be used.

It's up to activists to think creatively, to invent new ways to get our message out, to inform people of the extent and details of the ubiquitous horror occuring to the animals, and to motivate them to change their behaviour and to get involved. If we can't come up with successful nonviolent means to significantly diminish the harm we do, we can't really fault those who decide to use other means, given the gravity of the situation. Our work is made all the harder because of the self interest of those with economic interests in maintaining and expanding animal exploitation. We do seem to be headed toward violence, and the industry seems intent on keeping us herded onto that path.

Unlike Francione, I understand why people might be attracted to violence and believe that it could have positive effect; to some degree, I think that the absence of violence acts as a subtle signal to the collective societal perception that the animal question isn't very serious; if it were really serious, like political or religious freedom, or national autonomy, wouldn't we be seeing the same sort of violence?

The animal rights movement attracts nonviolent people. It is this single fact, I think, that explains why the movement hasn't yet seen any significant amount of violence. I worry though that this reticence is unlikely to continue. Everything changes with time.

A note to my faithful pro-vivisection audience:
I'm not arguing for violence here. I am simply saying that violence can have a strong positive effect and that arguments to the contrary are inaccurate. One of two things are going to happen: Significant and meaningful change is going to occur in the short term (do you think that's likely?), or young activists' frustraton is going to boil over. As much as it is activists' responsibility to think our way out of this seeming impasse, so too is it the industry's. I recommend that you work diligently toward an increase in open and participatory public dialog about human society's relationship with animals.

Thursday, August 16, 2007

Cruel Buddhist Sick Shrink

Out at the Buddhist monastery he’s known as Richie. The Buddhists there think the world of him. Dr. Richard Davidson is a well-known neuroscientist at the University of Wisconsin, Madison. Time magazine named him one of the world’s 100 most influential people in 2006. His good friend, the living embodiment of compassion, His Holiness the Dalai Lama, was a 2005 recipient.

Ned Kalin, MD, is the Chair of the Department of Psychiatry and a member of the Faculty at the University of Wisconsin School of Medicine and Public Health.

The Sunday Wisconsin State Journal filled its front page with the announcement that the university has just opened a new building with 43,000 sq.ft. for new brain labs and a new MRI scanner. The new building greatly expanded the HealthEmotions Research Institute, co-directed by Davidson and Kalin. (Scanning The Brain: Uw Madison's Noted Mental Health Research Program Is Expanding With A New Building, More Faculty On The Way And Big Plans. Wisconsin State Journal :: FRONT ::Sunday, August 12, 2007
By DAVID WAHLBERG dwahlberg@madison.com 608-252-6125.)

The story began with the line, “A low-profile building opening in Madison this month comes with high expectatons in one of medicine's most dynamic fields: brain research.” (It's a short building? Is the Sunday front page low profile?)

Some, maybe even most, of the publications by labs associated with the HealthEmotions Research Institute seem to be of the highest caliber and focused on important medical and scientific questions. But the co-directors collaborate on studies using monkeys that are cruel and controversial.

The newspaper didn’t mention Kalin’s and Davidson’s most recent scientific discoveries:

Administration of IFN-alpha can evoke depressive-like, huddling behavior in rhesus monkeys.

And, experimental lesions of the orbitofrontal cortex can significantly decrease adolescent rhesus monkeys threat-induced freezing and can marginally decrease fearful responses to a snake.

August 1, 2007, Kalin, in collaboration with researchers from Emory University:
Interferon (IFN)-alpha is an innate immune cytokine that causes high rates of depression in humans and therefore has been used to study the impact of cytokines on the brain and behavior. To establish a nonhuman primate model of cytokine-induced depression, we examined the effects of IFN-alpha on rhesus monkeys. METHODS: Eight rhesus monkeys were administered recombinant human (rHu)-IFN-alpha (20 MIU/m(2)) or saline for 4 weeks in counterbalanced fashion, and videotaped behavior, as well as plasma and cerebrospinal fluid (CSF), were obtained at regular intervals to assess behavioral, neuroendocrine, immune, and neurotransmitter parameters. (Felger JC, Alagbe O, Hu F, Mook D, Freeman AA, Sanchez MM, Kalin NH, Ratti E, Nemeroff CB, Miller AH. Effects of Interferon-Alpha on Rhesus Monkeys: A Nonhuman Primate Model of Cytokine-Induced Depression. Biol Psychiatry. 2007 Aug 1.)
Cytokines are chemicals secreted by cells that signal other cells. Cytokines make up a sort of cell-to-cell communication system. They are part of the cell-mediated immune response.

Kalin’s monkey experiments weren’t much of a discovery:
Immune-mediated and infectious diseases -- such as systemic lupus erythematosis (SLE) and neurosyphyllis, respectively -- provided the first evidence that the immune system may be involved in the pathophysiology of depression because these diseases are often associated with psychiatric symptoms. Strong evidence supporting the role of cytokines in depression was originally derived from the clinical observation of patients who received immune therapy, mainly IFN (interferons), for the treatment of viral infection (eg, hepatitis) and cancer. IFN administration was associated with affective and behavioral changes, referred to as "sickness behavior." This syndrome includes fatigue, anorexia, depressed mood, hopelessness, malaise, anhedonia, poor concentration, social isolation, and suicidal ideation. A recent prospective study of 85 patients on IFN showed that 37% developed depression. (MedScape Today.(You must be registered to access the article, but registration is free.) The Role of the Immune System in Depression)
Kalin goes on to say:
Compared with saline treatment, IFN-alpha administration was associated with persistent increases in anxiety-like behaviors and decreases in environmental exploration.... Interestingly, in three animals, depressive-like, huddling behavior was observed. ...CONCLUSIONS: IFN-alpha evoked behavioral, neuroendocrine, and immune responses in rhesus monkeys that are similar to humans. Moreover, alterations in hypothalamic-pituitary-adrenal axis responses and dopamine metabolism may contribute to IFN-alpha-induced depressive-like huddling behavior.
And, just prior to that paper, in July, 2007, Davison and Kalin published “Role of the Primate Orbitofrontal Cortex in Mediating Anxious Temperament.”
METHODS: Twelve adolescent rhesus monkeys were studied (six lesion and six control monkeys). Lesions were targeted at regions of the OFC that are most interconnected with the amygdala. Behavior and physiological parameters were assessed before and after the lesions. RESULTS: The OFC lesions significantly decreased threat-induced freezing and marginally decreased fearful responses to a snake. … CONCLUSIONS: These findings demonstrate a role for the OFC in mediating anxious temperament and fear-related responses in adolescent primates. (Kalin NH, Shelton SE, Davidson RJ. Role of the Primate Orbitofrontal Cortex in Mediating Anxious Temperament. Biol Psychiatry. 2007 Jul 20.)
And not only are this Buddhist and Shrink cruel and sick, but they are also anti-science when it serves their purposes. Kalin lists on one of his many university-related webpages that his 1993 article in Scientific American, “The Neurobiology of Fear,” is representative of his publications. In that paper, he makes note of the fact that many of his conclusions are based on his analysis of his videotapes of monkeys under a variety of stressful conditions.

Requests for copies of these and other videotapes made by Kalin, Davidson, and their colleagues resulted in the university's absolute refusals and subsequent shredding of 628 videos of monkeys being used in various brain research projects. Silence in the face of the destruction of nearly two decades of their own irreplaceable data is a complete denial of the public’s right to be informed. It is anti-knowledge; anti-science.

The Wisconsin State Journal’s zestful coverage of basic biomedical science at the university is oddly biased. For some reason, vivisectors are showcased (even if no mention is made of their cruel pastimes,) even as other scientists at the university win awards to develop non-animal research methods. The paper chooses not to write very much about the real scientists there doing the yeoman’s work of improving human health. These many scientists are dealing with the real world of human patients, large human populations, and the real very heterogeneous species of interest.

Monday, August 13, 2007


I'm in the middle of reading Science and Ethics: Can Science Help Us Make Wise Moral Judgements. (David Koepsell (Collaborator), Paul Kurtz (Editor) Promethias, 2007.) The Amazon editorial review says that it:
presents a unique collection of authors who generally maintain that science can help us make wise choices and that an increase in scientific knowledge can help modify our ethical values and bring new ethical principles into social awareness.
This isn't a review of the book.

In one of the essays, "From Human-Racism to Personhood: Humanism After Human Nature," author James Hughes, explains what he means by human-racism.
The use of the concept of human nature today is, we see, inescapably racist, human-racist, with the same consequences for tyranny, violence, and suppression of human diversity, as the ideology of European racism before it. The human-racists are more inclusive racists than their forebears, but racists nonetheless in their effort to ground solidarity in biological characteristics instead of shared recognition that another being has self-awareness, feelings, and thoughts like our own.
Hughes is a proponent of enhancement of human capabilites by means of genetic engineering, surgical implants and other enhancements which is what he alludes to above in the comment about human diversity.

Human-racists ground solidarity in biological characteristics instead of shared recognition that another being has self-awareness, feelings, and thoughts like our own.

Human-racist. This may be more easily understood than speciesist.

Friday, August 10, 2007

Arthur L. Rosenbaum

Arthur L. Rosenbaum, a pediatric ophthalmologist and researcher at UCLA's Jules Stein Eye Institute, has embarked on a series of experiments using rhesus monkeys that will cause severe and extensive suffering. He has come under increasing pressure to abandon these experiments. According the L.A. Weekly, some of Dr. Rosenbaum's experiments have been gruesome.
Most notably, Rosenbaum’s have involved shooting Botox into the eyes of fully conscious rhesus monkeys. In another case, when a vervet monkey was strapped in a metal cage, the terrified animal reacted by biting its tongue, banging its head, and chipping its teeth. The monkey wounded itself so badly that it had to be euthanized. On the less tragic end, mice were given shots of Accutane, a drug used to treat acne, which helped advance gene therapies for blind Stargardt’s patients.
The L.A. Weekly article, "Monkey Madness at UCLA" is subtitled "Violent radicals aim to kill Jules Stein Eye Institute researchers who test on animals." You should read the article for yourself. The quote above is the only hint that readers are given concerning Rosenbaum's experiments on animals.

Oddly, he seems to have returned to animal experimentation after a 20 year hiatus. His currently funded study, "Lateral Rectus Reanimation following Sixth Nerve Palsy," -- using macaques -- has funding for four years, 2004 through 2008. There seems to be no record of Rosenbaum using animals since 1987, in spite of the L.A. Weekly comments about the injections of Botox, Accutane, or the vervet that was killed. (A vervet is an African monkey species. Although, given the fact that UCLA has a large vervet colony, this makes some sense.) He seems never to have published anything related to rhesus monkeys, vervets, or mice. Between 1977 and 1987, he published at least five papers detailing his experiments on kittens:

Phelps DL, Rosenbaum AL.
Effects of variable oxygenation and gradual withdrawal of oxygen during the recovery phase in oxygen-induced retinopathy: kitten model.
Pediatr Res. 1987 Sep;22(3):297-301.
The effects of two types of prolonged oxygen supplementation were tested in the kitten model of oxygen induced retinopathy. Thirty-one litters were placed in 80% oxygen for 65 h starting the 3rd day after birth to initiate a moderately severe retinopathy. One-half of each litter thereafter served as controls, remaining in room air during the development of the retinopathy. In the remaining half, the retinopathy was allowed to develop in either a variably hyperoxic/hypoxic environment (one-half of each of 16 litters) or in an oxygen environment that was gradually reduced to room air by 4 wk (one-half of each of 15 litters). The retinopathy scores in the controls were comparable in both studies and the same as in previous experience with this model. Kittens exposed to the variable oxygen recovery environment had significantly less severe retinopathy than their room air recovery littermates (p less than 0.05). The retinopathy scores in the group with gradually withdrawn oxygen did not differ from the littermate controls (power greater than 80%). These data support the hypothesis that conditions of oxygenation during the recovery process from an acute oxygen-induced vascular injury have a significant effect on the healing process.
Phelps DL, Rosenbaum AL.
Effects of marginal hypoxemia on recovery from oxygen-induced retinopathy in the kitten model.
Pediatrics. 1984 Jan;73(1):1-6.

Phelps DL, Rosenbaum AL.
Observations of vitamin E in experimental oxygen-induced retinopathy.
Ophthalmology. 1979 Oct;86(10):1741-8.

Phelps DL, Rosenbaum AL.
Vitamin E in kitten oxygen-induced retinopathy. II. Blockage of vitreal neovascularization.
Arch Ophthalmol. 1979 Aug;97(8):1522-6.

Phelps DL, Rosenbaum AL.
The role of tocopherol in oxygen-induced retinopathy: kitten model.
Pediatrics. 1977 Jun;59 Suppl(6 Pt 2):998-1005.
The effect of tocopherol (vitamin E) on oxygen-induced retinopathy was studied in 75 kittens following the development of a 12-point scoring system to quantitate the degree of retinopathy seen at three weeks. The tocopherol was found to be beneficial when given daily from the day of birth (P less than .0001) with oxygen exposures of two to three days (79% FiO2) beginning on day 3. Caution is urged in applying these data to humans because (1) hepatosplenomegaly was noted in the treated animals, and (2) the kitten model for oxygen-induced retinopathy is not entirely satisfactory.
One of the claims in the L.A. Weekly article, is that "UCLA is credited with a breakthrough for curing visual loss in patients with the eye disease known as Stargardt’s," and that Rosenbaum injected mice with Accutane, a drug used to treat acne, "which helped advance gene therapies for blind Stargardt’s patients." If any of this is true, it ought to be publicized more widely because currently there are no clinical trials of gene therapy for Stargardt's taking place, and moreover, Rosenbaum is not named as an author in any published rsearch on Stargardt's.

One website has this to say about the condition:
The Good News: Stargardt’s never causes total vision loss. Peripheral vision is left intact. Central vision is usually in the range of 20/100 to 20/400 with younger patients usually showing less loss. Low vision care can help Stargardt’s patients lead very normal lives. Following diagnosis every Stargardt’s patient should have a low vision examination by a doctor skilled in low vision rehabilitation.

Low Vision Care: Stargardt’s patients respond well to magnification. Simple bifocals may be used in the early stages. In later stages, CCTV systems are helpful. It is important to maintain good cosmetic appearance for young patients. Mobility is usually minimally affected. Some Stargardt’s patients can become bioptic drivers, but it may be for a limited time.
Hum, they don't seem to be talking about a cure. The American Macular Degeneration Foundation says:
At present there is no cure for Stargardt’s disease and there is very little that can be done to slow its progression. Wearing sunglasses to protect the eyes from ultra-violet (UV) and bright light may be of some benefit.
Hum, people at UCLA are known for their cool sunglasses.

Monday, August 6, 2007


This post adds supporting information from recent news that is related to previous posts:

Experts fear escape of 1918 flu from lab
Millions dead within weeks
NBAF Fiasco Reveals Idiocy of UW Decision-Makers
When Spin Turns Deadly
Madison Chambers
Courting Cash-Tajima-ushi Risks Deadly Return to 1918

In 2001, the British government killed 7 million cows to halt a fast moving outbreak of hoof and mouth disease. It was covered by the world press and heaps of burning carcasses were featured for a while on the evening news. The govenment's response was highly criticized. It seems reasonable to assume that there were lessons learned from the event. The risk of another outbreak and the potential consequences must have been well understood when the current 2007 outbreak occured. Scientists working in the Merial Animal Health and the Institute for Animal Health labs at Pirbright must have been very aware of the inherent dangers in the virus and an accidental release.

In spite of this, the worse seems to have happened.

Brown cancels family holiday to lead foot and mouth fightback

From the article:
Experts pointed the finger at the lab's air-filtration system, saying poor maintenance could have led to the virus being expelled outside.

Department of Environment officials will examine whether a Pirbright worker could have poured away unsterilised vaccine, which could then have been washed up from the sewers by rising floodwaters.

According to a 2002 report by the government-funded Biotechnology and Biological Sciences Research Council, the Pirbright complex is in urgent need of investment. "Some of the laboratories and other areas of the Pirbright estate are not close to the standard expected of a modern biomedical facility and are well below that expected of a facility of such importance," the report said.
Human error may have led to outbreak
Patrick Wintour and John Vidal
Monday August 6, 2007
The Guardian

Merial researches and manufactures animal vaccines, andshares the Pirbright site with the government's Institute for Animal Health (IAH). It has been established that the strain of the highly contagious virus found in the infected cattle was held by both organisations and was used in a vaccine batch manufactured by Merial on July 16.

Merial also insisted that it was innocent of any wrongdoing. "Our centre operates to the very highest international standards, and we insist on stringent adherence to processes and procedures for health, safety and environmental protection, quality control, quality assurance and regulatory compliance," it said.

Last night, the company's managing director, David Biland, said: "We have been operating from this site for 15 years and during that time have produced hundreds of millions of vaccine doses. In all that time we have never had a breach in our biosecurity."


The possibilities of the unwitting escape of a virus were also raised by a former government microbiologist, Harash Narang, who wrote twice to Tony Blair in 2001 expressing concern that Pirbright was using "live" viruses to make vaccines for foot and mouth. He said all future vaccination programmes there should only use the dead form of the virus. "It is easy for a virus to escape," he wrote. Dr Narang, who worked in the government's public health laboratory for 30 years, established the link between BSE disease and its human form, CJD, several years before government scientists admitted the connection.

Merial's official statement about the matter.

Saturday, August 4, 2007

Induced Mental Illness in Mice

First Mouse Model Of Schizophrenia Developed” announced the headline at ScienceDaily.

A handful of headlines joined in to herald this “breakthrough”:

US researchers create schizophrenic mice

Scientists Engineer World's First Schizophrenic Mice

Most of the articles qualified their headline’s claims and explained that this was the “first” genetically engineered schizophrenic mouse and that other mouse models of schizophrenia were chemically (or behaviorally) induced.

In fact, there have been very many (always unfruitful) claims that mice and rats dosed with amphetamine, amphetamine-like drugs, LSD, DMT, mescaline, PCP, or exposed to startling stimuli or raised in social isolation are useful models of schizophrenia. (see “Animal Models of Psychiatric Disorders.” Mark A. Geyer and Athina Markou in Psychopharmacology - The Fourth Generation of Progress. American College of Neuropsychopharmacology.)

It is a near certainty that each and every one of the scientists involved in those studies made claims about the implications of their research that uniformly proved to be false. Not one of those studies resulted in benefit to human sufferers of schizophrenia – not one. Not one. Weigh zero, nada, none, against the suffering of the mice and rats. There was benefit of course, it can be measured in the dollars and cents that went into the vivisectors’ bank accounts.

The report that led to the headlines was “Dominant-negative DISC1 transgenic mice display schizophrenia-associated phenotypes detected by measures translatable to humans.” (Hikida et al. PNAS. 2007.) The senior author was Akira Sawa.

DISC1 (“Disrupted-In-Schizophrenia 1”) is a gene that was discovered and named in 2000.

DISC1 was discovered by Scottish geneticists studying a Scottish family with a high incidence of schizophrenia. DISC1 was subsequently shown to be associated with a variety of major mental illnesses.

In 2005, Sawa autopsied 60 brains from humans with major mental disorders. “Human postmortem orbital cortices … from normal controls as well as patients with [schizophrenia], bipolar disorder, and [major depression] were obtained … Each group had 15 subjects.” The researchers found an association between these conditions and DISC1 in these human brains.

It wasn’t long after the discovery and naming of DISC1 that Sawa and others began inserting the gene into mice and rats. There was, apparently, a sort of race to do this and claim credit for creating a new model. While reading about this “breakthrough,” I happened upon an article on about.com, written by a high-functioning idiot, that led me to read about Dr. Jacqueline Crawley.

According to an NIMH web page, “Dr. Crawley is chief of the Laboratory of Behavioral Neuroscience of the Intramural Research Program, National Institute of Mental Health (NIMH), National Institutes of Health (NIH) in Bethesda, Maryland.”

I almost titled this essay, “The Miracle Worker,” because Crawley’s lab has solved just about every medical problem facing society today. According to NIMH, her lab has characterized mutant mouse models for “behavioral phenotypes with conceptual analogies to human symptoms” of: autism, Alzheimer's, cognitive decline, anxiety, depression, schizophrenia, attention deficit hyperactivity disorder, Tay-Sachs, Sandhoff’s, Lowe syndrome, Smith-Lemli-Opitz syndrome, Fragile X syndrome, ataxia telangiectasia, epilepsy, and obesity. Wow. Wow!!! I wonder what’s holding up all the cures? Maybe those “conceptual analogies” are a little too conceptual?
To discover genes underlying autism, mouse behavioral assays with face validity to the diagnostic symptoms of autism are being developed, including social approach, reciprocal social interaction, juvenile play, auditory and olfactory communication, motor stereotypies, repetitive and perseverative behaviors, and resistance to change in routine. Applying this approach, an obscure inbred strain of mice, BTBR T+tf/J, was discovered to display social deficits, communication abnormalities, and repetitive self-grooming, relevant to the three core symptoms of autism.

Mark A. Geyer and Athina Markou (in “Animal Models of Psychiatric Disorders”) have this to say about “face validity”:
Face validity refers to the phenomenological similarity between the behavior (i.e., dependent variable) exhibited by the animal model and the specific symptoms of the human condition. Although face validity appears to be a desirable and is certainly an intuitively appealing criterion with which to validate models, such a criterion is actually not necessary, can be misleading, and is difficult to defend rigorously. Because the majority of models involve a species other than the one whose condition one tries to mimic, it is unrealistic to expect the two species to exhibit similar symptoms or phenomenology, even in cases where the etiology of the condition is known. In contrast, finding similarities between certain aspects of the behavior or physiology of animals and humans does not necessarily implicate similar etiology. Moreover, establishing the face validity of a model objectively is impossible, because claims for face validity of a model almost invariably involve subjective arbitrary arguments that are not necessarily accepted by all investigators in the field. While face validity can provide a heuristic starting point for the development of an animal model, it cannot be used to establish the validity of the model. In summary, the face validity of most models of human psychopathology is difficult to establish objectively and is irrelevant to the potential usefulness of the model in understanding the disease. It should be understood that face validity refers to the superficial similarity in symptomatology between the model and the disorder (e.g. changes in appetite or activity levels which are dependent variables) and can be distinguished from construct validity, which relies on similarities in underlying processes or mechanisms (e.g. hypothetical constructs specifying the mechanisms that lead to changes in appetite or activity levels). Thus, while face validity does not detract from an animal model, it simply does not provide scientific support for a model.
This new trend -- inserting genes associated with disease in humans into animals -- is burdened with insurmountable problems. No gene operates in isolation from other genes. Genes associated with mental illness in humans exist naturally in a milieu of human genes that respond to and interact with those genes. When such a gene is inserted into a different organism, it interacts with and influences the action of a new constellation of genes. Expectations that drugs that block the expression or influence of such a gene in a mouse will act similarly in a different species are based on a false understanding of the dynamics of complex systems.

Meanwhile, we should be counseling persons who are carriers of DISC1 of the risks of procreating.

Thursday, August 2, 2007

Lessons from the Khmer Rouge

Between 1975 and 1979, Cambodian government employees, following orders from their government, killed an estimated 1.7 million of their fellow citizens. Now, three decades later, they are beginning to be being held accountable.

They are being held accountable because people refused to forget. They are being held accountable because following orders and participating in government sanctioned activities is not a justification for one's behaviour. Government edicts do not supercede morality.

There will be a day in the future when animal abusers and murderers will be held accountable. People will look back and ask how such attrocities were allowed, paid for by taxpayers, the actors hired by government. The best that the abusers can hope for is to expire before the list of their crimes is read.

They will defend themselves with the claim that what they were doing was legal and government sponsored. But that, of course, is what previous members of the Khmer Rouge are saying; it is what the Nazi's said.