Exploring the medical and scientific background of blood drinking
Investigation and Research Into Sanguinarians
Investigation and Research Into Sanguinarians
When we look to the tiny part that defines how each portion of us work, our genes, we are looking at not only function and repair, but mutation, heredity and protein synthesis. We are looking at the introns and the coding genes. We are look at the way they replicate and combine as well as any outside influances on mutations such as viral effects and enviromental changes. So much can change exactly how our Genetics works that there is a wide area of searching Not to mention, each change at this level may define how something changes at a different level. Code the wrong protien and the enzyme doesn't work (biochemistry, gastroenterology). Point mutation may prevent proper hormone conduction (neurology, endocrinology, cytology). A mutation in our grandmother may have led to the issues we are seeing now (embryology, pathology). Genetics is the base science that effects so many other conditions, however the study of point mutations is a tedious process at best. We can, however, look at familial relations and chomosomal changes to see is sanguinarianism is hereditary or not.
Copyright © 2005
by Sarah Mediv
· All Rights reserved
· E-Mail: s_faolchu@yahoo.com
by Sarah Mediv
· All Rights reserved
· E-Mail: s_faolchu@yahoo.com
Genetics
HEREDITY
When we talk about genetic mutations resulting in a change to the child there is a difference in which parent provided the mutation, and if the mutation is recessive or dominant. We know that each parent provides half of the genetic material to make the child. However, the male parent is constatly creating new germ cells (sperm) while the female parent is born with their full compliment of germ cells (eggs). This means mutation in the male can be a point event at any time. Mutations on the female side, however, must have taken place in utero or inherited as a result of mutation of maternal ova chromasomes during development in the grandmother. This is how some conditions seem to skip a generation "The sins of the grandmother", so to speak.
Anectdotally, we see both linear heredity in sanguins (where there seems to be more than one in a family line) and point occurance (where there is no prior mention of sanguins in the family line.) However, this is difficult to interpret due to the nature of the symptom. blood drinking is considered taboo and thus many families either don't mention "the black sheep" or the "black sheep" themselves never mention it to the rest of the family. Familial lines may be more noted simply because of the psychology of sharing between people with similar problems.
It would require a closer look at the family trees of both the familial and point occurance sanguins to narrow down this effect.
CODONS and INTRONS
There are two main portions to our genetic code, codons and introns. Codons are the portions of our DNA that actually make protiens or code for signals of start/stop to a protien. Introns... well, we don't quite know what Introns do. These are pieces of DNA in between codons that don't seem to make a useful protien. some theorize these are portions of DNA that were mutations and now non-viable, but unimportant, some theorize these are portions of viral DNA that because incorporated somewhere in our past and again, don't code for anything useful now. when we look at these two types of DNA, however, the question becomes what if Introns did something? Or what if a mutation to an intron caused it to create an active protien? Is a mix-up in this system the cause of our issues?
VECTOR VIRAL MUTATION
As mentioned above, and will also be discussed more thoroughly in Microbiology, viral DNA occassionally gets incorporated into our genetic structure. The proteins that read the DNA and create the proteins don't differentiate between "self" and "non-self" DNA (which is how virii replicate using the hosts replication system). When this happens, typically the body is able to pluck out and destroy the "non-self" protien, but not always. When a "non-self" protein slips through, what does it do? If it has no purpose it will eventually degrade and get recyled into other proteins, but if it is close enough in structure to a usable protein to bind an enzyme or other protein, but not close enough to actually do the work the "self" protein would do it can cause harm by binding up the enzyme and not allowing it to do the job it is supposed to.
similar to introns in this manner, it is transcribed DNA that shouldn't be part of the normal body. to get passed on, as mentioned above, it would have to have initially become intigrated into the DNA of the grandmother, pass into the testicular germ layer, or crossed the placenta during very early development. Possible events.
WHAT IT MEANS TO THE SANGUIN
This would be the most basic level to look at and see if there are consistant mutations amongst sanguins. However, even that approach has flaws due to genetic redundancy. Many different codons code for the same proteins so if one is damaged another can do the work. Chromosomal changes (large scale mutations) would be more likely than single base pair changes. In addition, at this time, we can map the genome, but we are still not sure what each piece does. As such, looking to this level would currently be highly time consuming but not very fruitful.
When we talk about genetic mutations resulting in a change to the child there is a difference in which parent provided the mutation, and if the mutation is recessive or dominant. We know that each parent provides half of the genetic material to make the child. However, the male parent is constatly creating new germ cells (sperm) while the female parent is born with their full compliment of germ cells (eggs). This means mutation in the male can be a point event at any time. Mutations on the female side, however, must have taken place in utero or inherited as a result of mutation of maternal ova chromasomes during development in the grandmother. This is how some conditions seem to skip a generation "The sins of the grandmother", so to speak.
Anectdotally, we see both linear heredity in sanguins (where there seems to be more than one in a family line) and point occurance (where there is no prior mention of sanguins in the family line.) However, this is difficult to interpret due to the nature of the symptom. blood drinking is considered taboo and thus many families either don't mention "the black sheep" or the "black sheep" themselves never mention it to the rest of the family. Familial lines may be more noted simply because of the psychology of sharing between people with similar problems.
It would require a closer look at the family trees of both the familial and point occurance sanguins to narrow down this effect.
CODONS and INTRONS
There are two main portions to our genetic code, codons and introns. Codons are the portions of our DNA that actually make protiens or code for signals of start/stop to a protien. Introns... well, we don't quite know what Introns do. These are pieces of DNA in between codons that don't seem to make a useful protien. some theorize these are portions of DNA that were mutations and now non-viable, but unimportant, some theorize these are portions of viral DNA that because incorporated somewhere in our past and again, don't code for anything useful now. when we look at these two types of DNA, however, the question becomes what if Introns did something? Or what if a mutation to an intron caused it to create an active protien? Is a mix-up in this system the cause of our issues?
VECTOR VIRAL MUTATION
As mentioned above, and will also be discussed more thoroughly in Microbiology, viral DNA occassionally gets incorporated into our genetic structure. The proteins that read the DNA and create the proteins don't differentiate between "self" and "non-self" DNA (which is how virii replicate using the hosts replication system). When this happens, typically the body is able to pluck out and destroy the "non-self" protien, but not always. When a "non-self" protein slips through, what does it do? If it has no purpose it will eventually degrade and get recyled into other proteins, but if it is close enough in structure to a usable protein to bind an enzyme or other protein, but not close enough to actually do the work the "self" protein would do it can cause harm by binding up the enzyme and not allowing it to do the job it is supposed to.
similar to introns in this manner, it is transcribed DNA that shouldn't be part of the normal body. to get passed on, as mentioned above, it would have to have initially become intigrated into the DNA of the grandmother, pass into the testicular germ layer, or crossed the placenta during very early development. Possible events.
WHAT IT MEANS TO THE SANGUIN
This would be the most basic level to look at and see if there are consistant mutations amongst sanguins. However, even that approach has flaws due to genetic redundancy. Many different codons code for the same proteins so if one is damaged another can do the work. Chromosomal changes (large scale mutations) would be more likely than single base pair changes. In addition, at this time, we can map the genome, but we are still not sure what each piece does. As such, looking to this level would currently be highly time consuming but not very fruitful.
References:
Hesman, Tina. "Human genome is Part Bornavirus" Science News. January, 2010. Web.<http://www.wired.com/wiredscience/2010/01/bornavirus-in-human-dna/>
Mattick, John. "Introns: Evolution and function" Current Opinion in Genetics and Development. Vol. 4. 1994. Pg 823-831. <http://imb.uq.edu.au/download/large/Introns_1994.pdf>
Nagaya, T , T Nakamura, T Tokino, et al. "The mode of hepatitis B virus DNA integration in chromosomes in human hepatocellular carcinoma" Genes Dev. vol.1 1987. p 773-782. <http://genesdev.cshlp.org/content/1/8/773.full.pdf>
Hesman, Tina. "Human genome is Part Bornavirus" Science News. January, 2010. Web.<http://www.wired.com/wiredscience/2010/01/bornavirus-in-human-dna/>
Mattick, John. "Introns: Evolution and function" Current Opinion in Genetics and Development. Vol. 4. 1994. Pg 823-831. <http://imb.uq.edu.au/download/large/Introns_1994.pdf>
Nagaya, T , T Nakamura, T Tokino, et al. "The mode of hepatitis B virus DNA integration in chromosomes in human hepatocellular carcinoma" Genes Dev. vol.1 1987. p 773-782. <http://genesdev.cshlp.org/content/1/8/773.full.pdf>