Society

Animal Models and Ethnicities

| by Dr Ray Greek
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The reasons individual humans differ in their response to drugs and disease are essentially the same as why animals and humans differ. Even if two individuals share 100% of the same genes, the way those genes are regulated and expressed can vary hence drug and disease response can vary. For example, scientists in the UK discovered that ethnic background influences the immune response to tuberculosis (TB).

Apparently people of African descent react to TB differently that people of European and Asian descent. The scientists measured 57 inflammation "markers" in 128 people living in London. In the two groups, only 4 markers moved in the same direction. Another study had shown that most TB infections in Europeans manifest in the lungs but Asians and Africans are affected in other organs. Studies like this are important since these difference probably mean different ethnic groups need different medication for TB. (Coussens et al.)

Different ethnicities also regulate insulin differently. (Kodama et al. 2013) Damon Tojjar  states: “Africans tend to have lower insulin sensitivity. However, they appear to compensate for this by releasing larger quantities of insulin. Among those of East Asian origin, the reverse appears to be the case. They have very good insulin sensitivity, but appear to have a poorer ability to release more insulin if it is needed. Caucasians fall somewhere between the two extremes. Both insulin release and insulin sensitivity are affected.” Groop stated: “The findings are consistent with what we see in clinical settings – East Asians are more sensitive to developing diabetes and they do so at a lower BMI. Because a lack of insulin is a condition for developing diabetes, it is not surprising that East Asians show lower insulin release and generally need to start insulin treatment at an earlier stage. The situation in Africa is still so complicated and heterogeneous that new studies are needed.”

A related study was also recently published. Seventy-five scientists and conservationists from around the world studied the genetic make-up of nine humans, chimpanzees, bonobos, Sumatran orangutans, Bornean orangutans, eastern gorillas, and western lowland gorillas, and seven subspecies. The study reported a great amount of diversity, which will aid in delineating divergence of populations. The data will also be a boon for comparative research (research that compares and contrasts species). Interestingly, it appears that the evolutionary history of the great ape populations is more complex than the history of humans. (Prado-Martinez et al. 2013, Sudmant et al. 2013)

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Compare the above to the following heralding breakthroughs due to animal models.

Scientists state they have data that indicates that zebrafish have “strong comparisons with the human genome.” Apparently 70% of protein-coding human genes have counter parts in the zebrafish as do 84% of genes associated with disease. A press release states: “Their study highlights the importance of zebrafish as a model organism for human disease research.” Lest there be any doubt what the scientists think of their animal model or how they intend to use it: “Our aim with this project, like with all biomedical research, is to improve human health. This genome will allow researchers to understand how our genes work and how genetic variants can cause disease in ways that cannot be easily studied in humans or other organisms. This genome will help to uncover the biological processes responsible for common and rare disease and opens up exciting new avenues for disease screening and drug development.” No modesty there! Another scientist involved in the research stated: “By modeling these human disease genes in zebrafish, we hope that resources worldwide will produce important biological information regarding the function of these genes and possibly find new targets for drug development.” (Howe et al. 2013) I hope so too, but there is no scientific basis for this hope.

Another headline from a press release states: “Strikingly Similar Brains of Human and Fly May Aid Mental Health Research.” The press release continues: “A new study by scientists at King's College London and the University of Arizona (UA) published in Science reveals the deep similarities in how the brain regulates behaviour in arthropods (such as flies and crabs) and vertebrates (such as fish, mice and humans). The findings shed new light on the evolution of the brain and behaviour and may aid understanding of disease mechanisms underlying mental health problems.” The authors conclude that “despite the major differences between species, their respective constitutions and specifications derive from similar genetic programmes.” They continue: “Flies, crabs, mice, humans: all experience hunger, need sleep and have a preference for a comfortable temperature so we speculated there must be a similar mechanism regulating these behaviours. We were amazed to find just how deep the similarities go, despite the differences in size and appearance of these species and their brains.” This study

(Strausfeld and Hirth 2013), while offering little hope to those suffering from neuropathology, actually is important for animal protection as there is continuing debate regarding: “Where do you draw the line?” In other words what animals are sentient and which one are not. While this study does prove anything one way or the other, it does show that “their brains work, at least superficially, like our brains.” The superficial is the key. The brains of men and women are superficially alike but we differ in disease incidence and response to drugs.

If scientists want to understand the details of human response to drugs and disease, they must study humans. As I have stated many times, animals can be used to study basic physiology and many other facets of life, but they cannot be used to predict human response to drugs and disease. Vivisection activists want to gloss over this distinction and this means they want to ignore established science from evo devo, evolutionary biology, complexity theory, genetics, and philosophy of science along with other areas. That’s not science. Its religion.

Just FYI

Three new publications.

Greek, R. and Hansen, L.A., 2013. Questions regarding the predictive value of one evolved complex adaptive system for a second: exemplified by the SOD1 mouse Progress in Biophysics and Molecular Biology. http://dx.doi.org/10.1016/j.pbiomolbio.2013.06.002.

http://www.sciencedirect.com/science/article/pii/S0079610713000539

Greek, R. and Hansen, L., 2013. The Strengths and Limits of Animal Models as Illustrated by the Discovery and Development of Antibacterials, Biological Systems: Open Access. 2, 109. doi: 10.4172/BSO.1000109 http://www.omicsgroup.org/journals/BSO/BSO-2-109.php?aid=14441

Jones, R.C. and Greek, R., 2013. A Review of the Institute of Medicine's Analysis of using Chimpanzees in Biomedical Research, Sci Eng Ethics. http://www.ncbi.nlm.nih.gov/pubmed/23616243

References

Coussens et al. "Ethnic Variation in Inflammatory Profile in Tuberculosis. ." PLoS Pathog no. 9 (7):e1003468. doi:10.1371/journal.ppat.1003468.

Howe et al. 2013. "The zebrafish reference genome sequence and its relationship to the human genome." Nature no. 496 (7446):498-503. doi: 10.1038/nature12111.

Kodama, Keiichi, Damon Tojjar, Satoru Yamada, Kyoko Toda, Chirag J. Patel, and Atul J. Butte. 2013. "Ethnic Differences in the Relationship Between Insulin Sensitivity and Insulin Response: A systematic review and meta-analysis." Diabetes Care no. 36 (6):1789-1796. doi: 10.2337/dc12-1235.

Prado-Martinez et al. 2013. "Great ape genetic diversity and population history." Nature no. advance online publication. doi: 10.1038/nature12228

http://www.nature.com/nature/journal/vaop/ncurrent/abs/nature12228.html - supplementary-information.

Strausfeld, N. J., and F. Hirth. 2013. "Deep homology of arthropod central complex and vertebrate basal ganglia." Science no. 340 (6129):157-61. doi: 10.1126/science.1231828.

Sudmant et al. 2013. "Evolution and diversity of copy number variation in the great ape lineage." Genome Research. doi: 10.1101/gr.158543.113.