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Neurobiology: A case study of the imminent militarization of biology

Published online by Cambridge University Press:  27 April 2010

Mark Wheelis  and
Malcolm Dando
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Abstract

The revolution in biology, including advances in genomics, will lead to rapid progress in the treatment of mental illness by advancing the discovery of highly specific ligands that affect specific neurological pathways. The status of brain science and its potential for military application to enhance soldier performance, to develop new weapons and to facilitate interrogation are discussed. If such applications are pursued, they will also expand the options available to torturers, dictators and terrorists. Several generic approaches to containing the malign applications of biology are shown, and it is concluded that success or failure in doing so will be significantly dependent on the active involvement of the scientific and medical communities.

Type
Means of Warfare
Information
International Review of the Red Cross , Volume 87 , Issue 859: Means of warfare , September 2005 , pp. 553 - 571
Copyright
Copyright © International Committee of the Red Cross 2005

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References

1 Meselson, Matthew, “Averting the hostile exploitation of biotechnology,” Chemical and Biological Conventions Bulletin, Vol. 48, June 2000, pp. 16–19.Google Scholar

2 Cohen, William, Proliferation: Threat and Response, Department of Defense, Washington DC, 1997.Google Scholar

3 Block, Steven M., “Living Nightmares: Biological Threats Enabled by Molecular Biology,” The New Terror: Facing the Threat of Biological and Chemical Weapons, Drell, Sidney D., Sofaer, Abraham D., Wilson, George D. (eds.), Hoover Institution Press, Stanford, 1999, pp. 39–75.Google Scholar

4 George Poste, “Advances in biotechnology: Promise or peril,” 2002, available at <www.upmc-biosecurity. org/pages/events/2nd_symposia/transcripts/trans_post.html> (visited 24 August 2005).

5 Fraser, Claire and Dando, Malcolm, “Genomics and future bioweapons: The need for preventive action by the biomedical community,” Nature Genetics, Vol. 29, 2001, pp. 253–255.CrossRefGoogle Scholar

6 Petro, James B., Plasse, Theodore R. and McNulty, Jack A., “Biotechnology: Impact on biological warfare and biodefense,” Biosecurity and Bioterrorism, Vol. 1, 2003, pp. 161–168.CrossRefGoogle Scholar

7 Wheelis, Mark, “Does the ‘new biology’ mean new weapons?” Arms Control Today, July/August 2004, p. 6.Google Scholar

8 Office of Transnational Issues, The Darker Bioweapons Future, Central Intelligence Agency, Washington, DC, 3 November 2003, p. 1.Google Scholar

9 Ibid.

10 Dando, Malcolm, The New Biological Weapons: Threat, Proliferation and Control, Lynne Rienner, Boulder, 2001.Google Scholar

11 A form of what are generally termed ligands — small molecules that bind to proteins.

12 Andreasen, Nancy C., Brave New Brain: Conquering Mental Illness in the Era of the Genome, Oxford University Press, Oxford, 2001.Google Scholar

13 Poste, op. cit, (note 4).

14 Ibid.

15 Finger, Stanley, Minds behind the Brain: A History of the Pioneers and their Discoveries, Oxford University Press, Oxford, 2000.Google Scholar

16 Rees, Dai and Rose, Steven, (eds.), The New Brain Sciences: Perils and Prospects, Cambridge University Press, Cambridge, 2004.CrossRefGoogle Scholar

17 World Health Organization, Mental Health: New Understanding, New Hope, World Health Report 2001, WHO, Geneva.

18 Cummings, Jeffrey L. and Maga, Michael S., Neuropsychiatry and Behavioural Neuroscience, Oxford University Press, Oxford, 2003. Some thirty such regularities are discussed, and it is clear that what is being described is a mechanistic science. For example, the first several principles state: “Brain-behaviour relationships underlying neuropsychiatric syndromes are rule-governed and reproducible across individuals (…) All mental processes derive from brain processes (…) Neuro-psychiatric symptoms are manifestations of brain dysfunction (…) [which] reflect abnormalities of underlying brain function, whether produced by genetic, structural or environmental influence…”Google Scholar

19 Working in the nineteenth century, Broca showed that damage to what is now called Broca's area of the cerebral cortex leads to loss of the ability to generate speech, and Wernicke demonstrated that damage to a neighbouring area, now named after him, leads to a loss of ability to understand language.

20 The frontal lobes occupy about a third of the total cortical volume, are amongst the latest of our phylogenetic gains and are one of the last of the brain regions to develop in each individual. As with language, it is reasonable to suggest that they mediate characteristic human behaviours. Damage to this part of the cortex produces three behavioural syndromes. Which is manifest depends on the site of damage: an orbitofrontal syndrome, characterized by disinhibition and impulsiveness; a dorsolateral prefrontal syndrome, manifested primarily by executive dysfunction, and a medial frontal syndrome featuring apathy and akinesia.

21 When an electrical impulse reaches the end of the long projection, or axon, of a neuron, it causes the release of neurotransmitter molecules which then cross the small gap, or synaptic cleft, to the next cell and lock on to the relevant receptors on that cell. When they do this, changes take place within the affected second cell which can either enhance the likelihood of an electrical impulse being generated in that neuron (excitation) or make it less likely (inhibition). Various mechanisms clear the transmitter chemical from the synapse so that its effect is transient. Usually it is either destroyed by enzymes in the synaptic cleft, or taken back up into the secreting cell by membrane transporter proteins, and re-used.

22 Anon, , “Breakthrough of the year: The runners-up,” Science, No. 302, 2003, pp. 2039–2040.Google Scholar

23 Caspi, Avshalomet al., “Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene,” Science, No. 301, 2003, pp. 386–389.CrossRefGoogle Scholar

24 Ibid.

25 The researchers also demonstrated a similar impact of childhood maltreatment on those carrying one or two short alleles. An analogous association has been shown in monkeys (see Barr, Christina S.et al. “Sexual dichotomy of an interaction between early adversity and the serotonin transporter gene promoter variant in rhesus monkeys,” Proc. Nat. Acad. Sci., Vol. 101, 2004, pp. 12358–12363)CrossRefGoogle Scholar and in other children (see Kaufman, Joanet al., “Social supports and serotonin transporter gene moderate depression in maltreated children,” Proc. Nat. Acad. Sci., Vol. 101, 2004, pp. 17316–17321).CrossRefGoogle Scholar However, the latter report showed, too, that adequate social support could greatly reduce the risk to such maltreated children. This happy result also tends to confirm another principle that “[t]he beneficial effects of psychotherapy are mediated through changes in brain function” (see Cummings and Maga, op. cit., note 18). Unfortunately, more recent work has again demonstrated the link between the serotonin transporter promoter polymorphism and suicide (see Pao-Yen Lin and Gaochuan Tsai, “Association between serotonin transporter gene promoter polymorphism and suicide: Results of a meta-analysis,” Bio. Psychiatry, Vol. 55, pp. 1023–1030).

26 Hariri, Ahmad R.et ah, “Serotonin transporter genetic variation and the response of the human amygdala,” Science, Vol. 297, 2002, pp. 400–403. These researchers used a form of functional magnetic resonance imaging to assess subjects’ responses to frightening facial images. They divided people into two groups: those with two long alleles of the 5HTT gene and those with one or two copies of the short form of the gene. The subjects were all healthy but nevertheless there was a clear difference in the responses of the two groups. People with the short form showed greater activity in the amygdala in response to frightening stimuli than those with only the long form. The difference was located in the right amygdala, consistent with the right hemisphere's known role in processing facial images.CrossRefGoogle Scholar

27 Hariri, Ahmad R.et al., “A susceptibility gene for affective disorders and the response of the human amygdala,” Arch. Gen. Psychiatry, Vol. 62, 2005, pp. 146–152.CrossRefGoogle Scholar

28 Furmark, Tomaset al, “Serotonin transporter polymorphism related to amygdala excitability and symptom severity in patients with social phobia,” Neuroscience Letters, Vol. 362, 2004, pp. 189–192.CrossRefGoogle Scholar

29 See Barr, Christina S.et al, “Rearing conditions and rh5-HTTLPR interact to influence limbichypothalamic- pituitary-adrenal axis response to stress in infant macaques,” Biol. Psychiatry, Vol. 55, 2004, pp. 733–738.CrossRefGoogle Scholar Moreover, the serotonin transporter is not the only gene for which this new imaging genomics approach is producing such results; see Hariri, Ahmad R., and Weinberger, Daniel R., “Imaging genomics,” British Medical Bulletin, Vol. 65, 2003, pp. 259–270.CrossRefGoogle Scholar

30 Editorial, “New technologies and the loophole in the Convention,” Chemical Weapons Convention Bulletin, Vol. 23, 1990, pp. 1–2.Google Scholar

31 Cooper, Graham and Rice, Paul, (eds.), “Special issue — chemical casualties: Centrally acting incapacitants,” Journal of the Royal Army Medical Corps, Vol. 148 (4), 2001, pp. 388–391.Google Scholar

32 Research and Technology Organization, Non-Lethal Weapons and Future Peace Enforcement Operations, TR-SAS-040, North Atlantic Treaty Organization, November 2004.

33 Furmanski, Martin and Dando, Malcolm R., “Midspectrum incapacitant programs,” in Wheelis, M., Rosza, L. and Dando, M., Deadly Cultures: Biological Weapons from 1945 to the Present. Harvard University Press, Cambridge, 2006, pp. 236–251.Google Scholar

34 Coupland, Robin, “Incapacitating chemical weapons: A year after the Moscow theatre siege,” The Lancet, Vol. 362, 2003, p. 1346.CrossRefGoogle Scholar

35 Lakoski, Joan M.et al., The Advantages and Limitations of Calmatives for Use as a Non-Lethal Technique, Applied Research Laboratory, College of Medicine, Pennsylvania State University, 2000. According to the report, the researchers identified several drug classes (e.g. alpha2-adrenoreceptor agonists) and individual drugs (…dexmedetomidine) found appropriate for immediate consideration as non-lethal [agents] involving e.g. unconsciousness or calming.Google Scholar

36 Dando, Malcolm R., The Danger to the Chemical Weapons Convention from Incapacitating Chemicals, First CWC Review Conference, Paper No. 4, University of Bradford, March 2003.Google Scholar

37 A Survey of Biological and Biochemical Weapons Related Research Activities in France, Country Study No. 2, Sunshine Project, November 2004.

38 Williams, Michael et al., “Same brain, new decade: Challenges in CNS drug discovery in the postgenomic, postproteomic era,” Annual Reports in Medicinal Chemistry, Vol. 36, 2001 pp. 1–10.CrossRefGoogle Scholar

39 Broad Area Announcement, Non-Lethal Weapons Science and Technology: Applied Research and Technology Development Efforts, M67854–05-R-5009, 2004, Contracts Home Page, US Marine Corps.

40 National Research Council, Opportunities in Biotechnology for Future Army Operations, National Academies Press, Washington, DC, 2001.Google Scholar

41 Fidler, David P., “Non-lethal’ weapons and international law: Three perspectives on the future,” Medicine, Conflict and Survival Vol. 17, 2000, pp. 194–200.CrossRefGoogle Scholar

42 Paul L. Howard, Technical Report: Operational Aspects of Agent CS, Deseret Test Center, Fort Douglas, Utah, April 1973, DTC-FR-S700M. The principal use of CS was for terrain denial (persistent CS was applied in enormous amounts on the Ho Chi Minh Trail, and around the perimeter of isolated US firebases). The most common combat use was to drive enemy troops from cover to increase their vulnerability to lethal fire, and to break combat when US troops were ambushed.

43 Bender, Bryan, “US testing nonlethal weapons arsenal for use in Iraq,” Boston Globe, 5 August 2005.Google Scholar

44 Hart, John, Kuhlau, Frida and Simon, Jacqueline, “Chemical and biological weapons developments and arms control,” Chapter 16, in SIPRI Yearbook 2003: Armaments, Disarmament and International Security, Oxford University Press, Oxford, 2003, pp. 645–682.Google Scholar

45 Bowden, Mark, “The dark art of interrogation,” Atlantic Monthly, Vol. 292, October 2003, pp. 51–76.Google Scholar

46 Perry-Robinson, Julian P., Disabling Chemical Weapons: A Documented Chronology of Events, 1945–2003, Harvard Sussex Program, University of Sussex, 2003, pp. 8–9.Google Scholar

47 James Meek, “People the law forgot,” The Guardian, 3 December 2003, available at <http://www.guardian. co.uk/g2/story/0,3604,1098391,00.html> (visited 24 August 2005).

48 Slevin, P. and Stephens, J., “Detainees’ medical files shared: Guantanamo interrogators’ access criticized,” Washington Post, 10 June 2004, A01Google Scholar

49 Anderson, Michael C.et. al., “Neural systems underlying the suppression of unwanted memories,” Science, Vol. 303, 2004, pp. 232–235.CrossRefGoogle Scholar

50 The Pain Merchants: Security Equipment and Its Use in Torture and Other Ill-Treatment. Amnesty International, London, 2 December 2003.

51 Carmena, Jose M.et al, “Learning to control a brain-machine interface for reaching and grasping by primates,” PLoS Biology, Vol. 1, No. 2, 2003, pp. 1–16.CrossRefGoogle Scholar

52 Harder, Ben, “Scientists ‘drive’ rats by remote control,” National Geographic News, 1 May 2002.Google Scholar

53 Carlson, Robert, “The pace and proliferation of biological technologies,” Biosecurity and Bioterrorism, Vol. 1, 2003, pp. 203–214.CrossRefGoogle Scholar

54 Wheelis, Mark, and Dando, Malcolm R., “Back to bioweapons?”, Bulletin of the Atomic Scientists, January/February 2003, pp. 40–46.Google Scholar

55 National Research Council, Biotechnology Research in an Age of Terrorism, National Academies Press, Washington DC, 2004.Google Scholar

56 See <http://www.biosecurityboard.gov> (visited 24 August 2005).

57 Harris, Elisa D. and Steinbrunner, John D, “Controlling dangerous pathogens,” Issues in Science and Technology Online, spring 2003, pp. 74–78.Google Scholar

58 For relevant developments related to codes of conduct see: http://www.ex.ac.uk/codesofconduct/ (visited 24 August 2005).

59 Coupland, Robin, and Leins, Kobi-Renee, “Science and prohibited weapons”, Science, Vol. 308, 2005, p. 1841.CrossRefGoogle Scholar