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Genetics has long been a focus and a growing field for the global scientific community, but looking at disease from a genetic perspective isn’t necessarily an old concept. Even so, it’s already being revamped as more and more experts challenge the notion of looking for answers with regard to disease in DNA so that they can, instead, focus more on searching for the answers in mitochondrial DNA specifically. A lot is at stake, though. Already this year, a study’s been released that focuses on the eating habits of Americans and finds that those with eating disorders carry a genetic mutation variant that makes them particularly susceptible to cultural manipulation.
We ended the year, in fact, with the fairly new understanding that one’s genetic background actually informs how many mitochondrial disease-causing mutations manifest in any population. This genetic background refers to the age of the population as well as the ethnic background of the individual. These disease-causing mutations were found by the late 2017 study to be less common among European populations, and its significant findings were published in PLoS Genetics.
Genetic diseases are, in general, believed to result from mutations in mitochondrial DNA; the genome of which comes solely from the mother with no consideration or inclusion of paternal DNA. Different populations typically qualify as what experts call mitochondrial DNA haplogroups, which are just ethnic groups that share a common ancestor. The study focused on one haplogroup in particular and found it to carry all three of the variations for Leber Hereditary Optic Neuropathy (LHON), which is a hereditary disease that causes blindness. In the case of LHON, mutations hinder mitochondrial function and thereby snuff out retinal ganglion cells, which are supposed to relay what the eyes see to the brain.
This led the research team to study 30,506 mitochondrial DNA mutation sequences, and they ultimately confirmed that mutations correlate to certain haplogroups. “The frequent recurrence of the same mutations on a population clade [or haplogroup], and the reduced frequency of European [mitochondrial DNAs] harboring two or more disease-causing mutation [sic], both suggest that the population [mitochondrial DNA] background influences the risk of developing [mitochondrial DNA] mutagenesis,” the study read.
This speaks volumes for the overweight population in the U.S., a so-called melting pot wherein ethnic groups (to varying extents) assimilate with one another under the auspices of a dominant, Eurocentric culture. A nation of 300 million people with sizable quantities of non-White ethnic groups and one dominant collective of White ethnicities is a rather unique target of study in light of this new understanding of how genetic backgrounds influence what diseases pop up and how. In particular, it suggests that there are new factors to consider with regard to eating disorders.
Well established research already illustrates the hereditary nature of eating disorders, and studies indicate that some are more susceptible to inheriting these problems than others. The new study released on Wednesday, though, shows that the genetic correlation may be stronger than was even hypothesized. “The risk of developing an eating disorder is largely inherited, meaning that people with a family history of eating disorders are more likely to have one, but the identity of which genetic variation increases that risk is unknown,” according to Michael Lutter. He’s an attending psychiatrist at the Eating Recovery Center, which is the institution that put this research project together.
Lutter and his team have been looking for a specific genomic mutation for a long time, and finding it is expected to be a major breakthrough for treating eating disorders. In the meantime, though, they draw insightful connections like that of the target mutation and susceptibility to breast cancer. Breast cancer and eating disorders are analogous based on data from the U.S. Centers for Disease Control and Prevention citing two mutations that, if carried, greatly increase the statistical likelihood of one getting breast cancer. The caveat is that only three percent of breast cancers actually result from those, so Lutter is looking for something similar for eating disorders.
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“We are trying to find something similar in the eating disorder population. If we can find the rare mutation, then it gives a better understanding of the underlying neurobiology of eating disorders,” Lutter explains. This doesn’t pertain to mitochondrial DNA necessarily (or even likely), but it furthers the idea that experts are trying to use conventional understanding of DNA in more progressive ways. Some are even trying to harness the immense power of mitochondria to fight disease directly with it.
Mitochondria, mind you, “generate more than 90% of cellular energy,” according to the Children’s Hospital of Philadelphia Research Institute’s Doug Wallace, director of the Center for Mitochondrial and Epigenomic Medicine. “Anything that generates that much energy can’t be trivial.” In the grand scheme of things, the scientific community has only just started paying anywhere near this much attention to mitochondria, and Wallace has been leading scientists toward the new paradigm shift of looking to the body’s energy for answers on a plethora of concerns rather than focusing on its organs.