1 : The Blood Warfare !FREE!
Objective: The research agenda for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) has emphasized the need for a more etiologically-based classification system, especially for stress-induced and fear-circuitry disorders. Testable hypotheses based on threats to survival during particular segments of the human era of evolutionary adaptedness (EEA) may be useful in developing a brain-evolution-based classification for the wide spectrum of disorders ranging from disorders which are mostly overconsolidationally such as PTSD, to fear-circuitry disorders which are mostly innate such as specific phobias. The recently presented Paleolithic-human-warfare hypothesis posits that blood-injection phobia can be traced to a "survival (fitness) enhancing" trait, which evolved in some females of reproductive-age during the millennia of intergroup warfare in the Paleolithic EEA. The study presented here tests the key a priori prediction of this hypothesis-that current blood-injection phobia will have higher prevalence in reproductive-age women than in post-menopausal women.
1 : The Blood Warfare
Results: Data on BII phobia was available on 1724 subjects (1078 women and 646 males). The prevalence of current blood-injection phobia was 3.3% in women aged 27-49 and 1.1% in women over age 50 (OR 3.05, 95% CI 1.20-7.73). [The corresponding figures for males were 0.8% and 0.7% (OR 1.19, 95% CI 0.20-7.14)].
Conclusions: This epidemiological study provides one source of support for the Paleolithic-human-warfare (Paleolithic-threat) hypothesis regarding the evolutionary (distal) etiology of bloodletting-related phobia, and may contribute to a more brain-evolution-based re-conceptualization and classification of this fear circuitry-related trait for the DSM-V. In addition, the finding reported here may also stimulate new research directions on more proximal mechanisms which can lead to the development of evidence-based psychopharmacological preventive interventions for this common and sometimes disabling fear-circuitry disorder.
An overview is given of biological markers of exposure to chemical warfare agents. Metabolites, protein, and/or DNA adducts have been identified for most nerve agents and vesicants and validated in experimental animals or in a small number of human exposures. For several agents, metabolites derived from hydrolysis are unsatisfactory biomarkers of exposure because of background levels in the human population. These are assumed to result from environmental exposure to commercial products that contain these hydrolysis products or chemicals that are metabolized to them. In these cases, metabolites derived from glutathione pathways, or covalent adducts with proteins or DNA, provide more definitive biomarkers. Biomarkers for cyanide and phosgene are unsatisfactory as indicators of chemical warfare exposure because of other sources of these chemicals or their metabolites.
The effects of nerve agents are the result of the action on the muscurinic and nicotinic receptors on the receptors within the central nervous system. They include constriction of the pupil (meiosis), increased production of saliva, running nose, increased perspiration, urination, defecation, bronchosecretion, bronchoconstriction, decreased heart rate and blood pressure, muscular twitches and cramps, cardiac arrhythmias, tremors and convulsions. The most critical effects are paralysis of the respiratory muscles and inhibition of the respiratory center. Ultimately, death results due to respiratory paralysis. If the concentration of the nerve agent is high, death is immediate.
Sulfur mustard is the vesicant with the highest military significance since its use in WWI. The nitrogen mustards were synthesized in the 1930s but were not produced in large amounts for warfare. Mechlorethamine (HN2, Mustargen) has found more peaceful applications as a cancer chemotherapeutic agent and has remained the standard compound for this purpose for many years. Lewisite (L) was synthesized in 1918 for military purpose due to its non-flammable property and toxicity similar to mustard, but has probably not been used on a battlefield.
The mechanism by which LSD causes such profound effects on the human perception still has not been established.[66,67] LSD stimulates centers of the sympathetic nervous system in the midbrain, which leads to pupillary dilation, increase in body temperature and rise in the blood sugar level. LSD also has a serotonin-blocking effect. Serotonin is a hormone-like substance occurring naturally in various organs of warm-blooded animals. Concentrated in the midbrain, it plays an important role in the propagation of impulses in certain nerves and, therefore, in the biochemistry of psychic functions. LSD also influences neurophysiologic functions that are connected with dopamine, which is another naturally occurring hormone-like substance. Most of the brain centers receptive to dopamine become activated by LSD, while the others are depressed. The structure of LSD is very similar to other hallucinogenic drugs such as mescaline and psilocybin, all of which contain a substituted indole ring (or a related structure).
The father of the Japanese biological weapons programme, the radical nationalist Shiro Ishii, thought that such weapons would constitute formidable tools to further Japan's imperialistic plans. He started his research in 1930 at the Tokyo Army Medical School and later became head of Japan's bioweapon programme during the Second World War (Harris, 1992, 1999, 2002). At its height, the programme employed more than 5,000 people, and killed as many as 600 prisoners a year in human experiments in just one of its 26 centres. The Japanese tested at least 25 different disease-causing agents on prisoners and unsuspecting civilians. During the war, the Japanese army poisoned more than 1,000 water wells in Chinese villages to study cholera and typhus outbreaks. Japanese planes dropped plague-infested fleas over Chinese cities or distributed them by means of saboteurs in rice fields and along roads. Some of the epidemics they caused persisted for years and continued to kill more than 30,000 people in 1947, long after the Japanese had surrendered (Harris, 1992, 2002). Ishii's troops also used some of their agents against the Soviet army, but it is unclear as to whether the casualties on both sides were caused by this deliberate spread of disease or by natural infections (Harris, 1999). After the war, the Soviets convicted some of the Japanese biowarfare researchers for war crimes, but the USA granted freedom to all researchers in exchange for information on their human experiments. In this way, war criminals once more became respected citizens, and some went on to found pharmaceutical companies. Ishii's successor, Masaji Kitano, even published postwar research articles on human experiments, replacing 'human' with 'monkey' when referring to the experiments in wartime China (Harris, 1992, 2002).
Although some US scientists thought the Japanese information insightful, it is now largely assumed that it was of no real help to the US biological warfare programme projects. These started in 1941 on a small scale, but increased during the war to include more than 5,000 people by 1945. The main effort focused on developing capabilities to counter a Japanese attack with biological weapons, but documents indicate that the US government also discussed the offensive use of anti-crop weapons (Bernstein, 1987). Soon after the war, the US military started open-air tests, exposing test animals, human volunteers and unsuspecting civilians to both pathogenic and non-pathogenic microbes (Cole, 1988; Regis, 1999). A release of bacteria from naval vessels off
Even though they had just signed the BTWC, the Soviet Union established Biopreparat, a gigantic biowarfare project that, at its height, employed more than 50,000 people in various research and production centres (Alibek & Handelman, 1999). The size and scope of the Soviet Union's efforts were truly staggering: they produced and stockpiled tons of anthrax bacilli and smallpox virus, some for use in intercontinental ballistic missiles, and engineered multidrug-resistant bacteria, including plague. They worked on haemorrhagic fever viruses, some of the deadliest pathogens that humankind has encountered. When virologist Nikolai Ustinov died after injecting himself with the deadly Marburg virus, his colleagues, with the mad logic and enthusiasm of bioweapon developers, re-isolated the virus from his body and found that it had mutated into a more virulent form than the one that Ustinov had used. And few took any notice, even when accidents happened. In 1971, smallpox broke out in the Kazakh city of Aralsk and killed three of the ten people that were infected. It is speculated that they were infected from a bioweapons research centre on a small island in the Aral Sea (Enserink, 2002). In the same area, on other occasions, several fishermen and a researcher died from plague and glanders, respectively (Miller et al., 2002). In 1979, the Soviet secret police orchestrated a large cover-up to explain an outbreak of anthrax in Sverdlovsk, now Ekaterinburg, Russia, with poisoned meat from anthrax-contaminated animals sold on the black market. It was eventually revealed to have been due to an accident in a bioweapons factory, where a clogged air filter was removed but not replaced between shifts (Fig. 1) (Meselson et al., 1994; Alibek & Handelman, 1999).
Detecting biological warfare research. A comparison of the number of publications from two Russian scientists. L. Sandakchiev (black bars) was involved, as the head of the Vector Institute for viral research, in the Soviet project to produce smallpox as an offensive biological weapon. V. Krylov (white bars) was not. Note the decrease in publications by Sandakchiev compared with those by Krylov. The data were compiled from citations from a PubMed search for the researchers on 15 August 2002. 041b061a72