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.
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