Exploring the medical and scientific background of blood drinking
Investigation and Research Into Sanguinarians
Investigation and Research Into Sanguinarians
Copyright © 2005
by Sarah Mediv
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Biron, D. G., et al . "Behavioural manipulation in a grasshopper harboring hairworm: a proteomics approach". Proc. R. Soc. B. 272: 2117-2126. 2005. web <http://neurophilosophy.files.wordpress.com/2006/11/biron_etal.pdf>
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Thomas, F., et al. "Biochemical and histological changes in the brain of the cricket Nemobius sylvestris infected by the manipulative parasite Paragordius tricuspidatus (Nematomorpha)". Int. J. Parasitol. 33: 435-443. 2003. Web. <http://neurophilosophy.files.wordpress.com/2006/11/thomas_etal.pdf>
Webster, J and McConkey, G. "Toxoplasma gondii-altered host behaviour: clues as to mechanism of action" Folia Parasitologica 57: 95-104, 2010. Web. <http://folia.paru.cas.cz/pdfs/showpdf.php?pdf=21376>
Microbiology is sort of an interesting subset we are looking at for the questions "Is it infectious?" Can we pass this on to other people? Often, sanguins will not donate blood because of this question. If it something that can be passed on, we would not wish to be responsible for that potential. It seems like an odd set of signs to be related to a "mere" bacterial infection, right? Maybe. Below, we will see how microbiology and "simple" bacteria have been show to cause dramatic changes in our behaviour.
WHEN BACTERIA GO BAD
Schizophrenia and Bi-Polar disorder are the two mental diseases most linked to infection at an early age. It has been found that maternal infection with influenza, Rubella, and Toxoplasmosis. We don't yet know why this occurs. However, it is good to point out that schizophrenia and bi-polar are not contagious in and of themselves which makes it slightly different from the question we are asking here. However, it does beg the question... is there another infection that would pre-dispose a person to being sanguin? Interestingly, the normal period to first showing signs of schizophrenia is the same, around puberty, as that of what sanguins have reported.
The thought of pre-natal infection is an interesting one. As mentioned in genetics, viral DNA can become intigrated with our own and fetal development is a critical time for mutation to occur. We would have to look back at our moths, and perhaps even grandmothers, for possible infection during pregnancy to see if there were any common factors.
LOOKING DEEPER AT EPIDEMIOLOGY
When we look at most contagious diseases, such as influenza ("the flu") or bacterial outbreaks we see the diseases most heavily affecting the young and the old, with the middle population having cases but typically shorter in course and requiring less hospitalization or serious complications. this comes down to the immune system. In the average middle age adult, our immune system is functioning at its best. It has aquired several "memory" cells it can put to work and has the best body reserves for fighting infection. The younger body does not yet have that immune response of "memory" cells, and often the older body they are not functioning as much as they should. This means those populations are most at risk for serious disease.
If being sanguin was the result of a strait forward infection, it has that in reverse. Signs are first noted most frequently at puberty or early 20s, when the body should be functioning at peak and able to fend off most viral or bacterial invaders. So, we can probably safely say it is not the common cold.
FEEDING THE INVADER?
Another interesting line of thought to consider for the sanguin. When a sanguin ingests blood, is it feeding the invader instead of the body? As discussed in Immunology, iron is needed by almost all bacteria for replication. the body has natural systems for "hidding" this iron away and starving the invading bacteria. What if what we are seeing is the result not of our own body saying "I need blood" but of the bacteria? If we go back to toxoplasmosis mentioned above, we see presidence for microorganisms affecting behaviors in a host. Toxoplasma has only one diffinitive host, the cat, in which it can reproduce and be passed on. However, part of it's lifecycle takes place by forming "bradyzoites" in tissue of intermediate hosts. the only way these bradyzoites can reach the diffinitive host is to be eaten by the cat. Interestingly, mice and rats affected by toxoplasma show less predator aversion and fear of novel smells creating an almost "suicidal" mouse or rat more likely to be caught and eaten by the cat diffinative host. This effect only seems to last a few weeks, however. Other examples of invader manipulation of host behaviour occurs in fungi (causing carpenter ants to clime to tops of plants to facilitation sporulation from the fungi) and hairworms (causing insects to commit "suicide" by jumping into bodies of water where the parasite emerges as a free-living aquatic adult).
WHAT WE ARE NOT LOOKING AT
Fiction has also picked up on the "viral blood-sucker" concept and passed it on is several forms. Some of these have even been touted as "true facts" but are complete malarchy and should be ignored. Among these are:
V5 virus: Created for the BBC television show "Ultraviolet" in 1998. Despite many websites that tout it has the "cause" it is a fictional virus.
K17 virus: Created for "Reign in Darkness" a 2001 Australian movie. Again, fake virus created by writers for the film.
WHAT WE COULD BE LOOKING FOR
Prenatal infections or infections as infants would be the best place to look for this hypothesis. Looking for diseases that occured at a higher rate than in the general population would rasie a flag for closer inspection. Possible also would be looking at bacterial culures from sanguins to look for bacteria with unique features or a higher prevalance than the regular population that may lean toward the "feeding the bacteria" hypothesis.