Note: this page was written in 2006. Unfortunately, not much has changed or needs rewriting.
Abbott has built a career on fiddling with the sexual and psychosexual development of common marmosets and rhesus macaques.
Along the way he has dabbled in disrupting the lives of other species.
In the case of marmosets, he has published extensively on the results of disrupting their normal social/sexual milieu. He has invented ways to restrain and manipulate them.
In the case of rhesus macaques, he has continued to induce gross anatomical and physiological deformities by exposing female fetuses to high levels of testosterone.
His work has entailed repeated sampling methods undoubtedly stressful to the animals under his control. Blood draws, injections, biopsies, restraint, electro ejaculations, and various surgeries contribute to the overall diminished well-being of the animals to whom he is given access.
He has claimed that the monkeys subjected to experimental androgenization are good models of polycystic ovary syndrome (PCOS), though he admits that the causes of the naturally occurring human disease are largely unknown.
Pitifully few, if any, of Abbott's experiments on animals have led to advances in the treatment of human disease. His work has done little other than demonstrate that hormones influence development and behavior, a fact known long before he became a vivisector.
Abbott's work is illustrative of the work occurring in primate labs across the country.
Abbott's current studies refer to something he terms:
Briefly, prenatally androgenized females were produced by injecting pregnant rhesus monkeys carrying female fetuses with 10–15 mg TP [testosterone propionate] for 15–35 days. TP was initiated on either Days 40–44 (early-treated, n = 5) or Days 100–115 (late-treated, n = 4) postconception. The physical and psychosexual consequences of prenatal androgen exposure in female rhesus monkeys have been characterized [elsewhere]. Prenatal TP treatment starting before Day 60 postconception induces external genital masculinization and obliteration of the external vaginal orifice. Female offspring exposed to TP beginning after Day 110 postconception show no genital virilization except for clitoromegaly. All prenatally androgenized animals exhibit masculine behavior that occurs independently of genital masculinization in late-treated prenatally androgenized females.
Dumesic DA, Schramm RD, Bird IM, Peterson E, Paprocki AM, Zhou R, Abbott DH. Reduced intrafollicular androstenedione and estradiol levels in early-treated prenatally androgenized female rhesus monkeys receiving follicle-stimulating hormone therapy for in vitro fertilization. Biol Reprod. 2003 Oct;69(4):1213-9. Epub 2003 Jun 11.
Here is what the primate center says about Abbott's work:
The science newsletter of the Wisconsin Regional Primate Research Center
University of Wisconsin-Madison Graduate School and
National Institutes of Health/National Center for Research Resources
Scientists seek origin of "ring of pearls" syndrome
Center scientists are closing in on the origins of polycystic ovarian syndrome (PCOS), a multi- symptom disease that affects as many as one in 15 women in the United States. Despite its prevalence, the syndrome is not well known or understood by the general public and the clinical community alike.
David Abbott, Ph.D., and Mayo Clinic co-principal investigator Daniel Dumesic, M.D., were the first to discover that, even though symptoms do not appear until puberty, PCOS is programmed in the fetus during the second trimester of pregnancy.
In 2005, they made the claim that scientists at the primate center have discovered "the causes of polycystic ovarian syndrome." [ Note: On-line documents have a tendency to change. The link above leads to a saved copy just as it was found on line on December 26, 2005, at: http://www.primate.wisc.edu/wprc/pdfs/05_Discov.pdf ]
But consider what the National Institute of Health says:
What causes Polycystic Ovarian Syndrome (PCOS)?
No one knows the exact cause of PCOS.
Here is what Abbott says:
Polycystic ovary syndrome (PCOS) is a common but complex endocrine disorder and is a major cause of anovulation and consequent subfertility. It is also associated with a metabolic disturbance, characterized by hyperinsulinaemia and insulin resistance that carries an increased risk of type 2 diabetes in later life. Despite its prevalence little is known about its aetiology, but there is increasing evidence for an important genetic involvement. On the basis of experimental observations in the prenatally androgenized sheep and rhesus monkey, and supported by data from human studies, we propose that the clinical and biochemical features of PCOS can arise as a consequence of genetically determined hypersecretion of androgens by the ovary during, or very likely long before, puberty. The resulting hyperandrogenism results in 'programming' of the hypothalamic-pituitary unit to favour excess LH secretion, and encourages preferential abdominal adiposity that predisposes to insulin resistance. The severity of hyperinsulinaemia and insulin resistance (which has a profound influence on the phenotype of PCOS) is further influenced by both genetic factors (such as polymorphism in the insulin gene regulatory region) and environmental factors, notably obesity. This hypothesis therefore suggests a unifying, 'linear' model to explain the aetiology of the heterogeneous phenotype.
Abbott DH, Dumesic DA, Franks S. Developmental origin of polycystic ovary syndrome - a hypothesis. J Endocrinol. 2002 Jul;174(1):1-5.
Notice that the UW spin doctors make a claim about a discovery while two years later, Abbott, et al. state that their ideas are essentially only a proposition, and one that the NIH has yet to endorse.
Nevertheless, the "fact sheet" from the UW proclaiming that the cause of PCOS has been discovered is what is given to news reporters. No wonder that the public remains confused about the research underway since the labs themselves work untiringly to spin the facts and keep the public ignorant.
Amazing. The University of Wisconsin works actively to mislead the public it is charged with educating.