Parsing Out the Effects of Genetics, Environment, and Exercise on Overall Health

Physicians, nutritionists, athletes, and everyday citizens all share a vested interest in understanding the effects of diet and exercise, as well as ways to maximize lifelong health. While studies show that simply eating an apple a day may not keep the doctor away, there exists a wealth of research showing that the foods that we eat and the ways that we use our bodies do in fact change our bodies in profound ways. A team of researchers from the University of Jyvaskyla, particularly interested in the effects of exercise, conducted a recent study in an attempt to prove that exercise or the lack thereof differentially and directly impacts health, even in individuals who share similar genetic and environmental backgrounds. Using previous research from identical twin studies stored in Finland’s FinnTwin16 Database, this team of researchers identified 10 pairs of identical male twins, where one twin regularly exercised, while the other did not. In studying endurance, body composition, insulin sensitivity, overall fitness and metabolic health as well as indicators of brain functioning, the researchers found greater risks of poor health in the more sedentary twins including higher body fat, signs of insulin resistance, early signs of metabolic problems, as well as greater amounts of grey brain matter in the areas of the brain that control motor functioning and coordination in the more active twins. In isolating the effects of genetics and environment via identical twin studies, these researchers show that “genetics and environment don’t have to be destiny when it comes to exercise habits,” even despite the fact that our genes affect our “innate athletic capacity” and childhood environment shapes interests and behaviors. The evidence is quite compelling—our bodies are constantly changing, via nature and nurture, via habits of the past and present.

 

 

New York Times Article: http://nyti.ms/1AZWFoa

Original Study in the Journal of Medicine & Science in Sports & Exercise: http://www.ncbi.nlm.nih.gov/pubmed/25003773

DOI: 10.1249/MSS.0000000000000437 

 

Post by: Vera-Jo Kiefer

Disclosure of Genetic Information After Death

The article “You can’t take your genes with you: Strategies to share genetic information after death” discusses a research article published in the March 2 issue of Trends in Molecular Medicine. This paper asks if it is ethically acceptable for medical professionals to disclose the genetic information of deceased individuals to their family members, particularly if there is risk of a heritable disease. The authors distinguish between the ideas of active disclosure, when healthcare professionals offer unsolicited information to the deceased’s family, and passive disclosure, when they only provide information after a specific request. They also recommend policies and propose topics for further research, such as different cultural norms that might impact institutions’ individual policies.

Meredith Katz

http://www.eurekalert.org/pub_releases/2015-03/cp-yct022315.php

Original article: http://www.ncbi.nlm.nih.gov/pubmed/25743261

Bacterial Diversity Within the Human Body

            A recently published article entitled The Microbiome of Uncontacted Amerindians explores the ecology of bacteria within the human body. As the title suggests, the microbiomes of people from an uncontacted South American village were evaluated which allowed researchers to shed light on the effects that a “Western” lifestyle might have on microbial diversity. Moreover, it was found that these specific people, the Yanomami, had the highest diversity of bacteria ever observed in any human group. Perhaps even more significant, was the discovery of AR genes in the characterized microbes that would protect the organisms from antibiotics of which these people had presumably had zero exposure to. This study represents a unique opportunity for both microbiologists and evolutionary anthropologists as the microbiome provides insights into host physiology, immune response, and even metabolism. Moreover it may be said that microbes found within the human body have had the potential for antibiotic resistance against synthetic compounds before industrialized societies even began to treat disease with drugs.

 (Xavier Holmes)

Clemente, Jose C. "Microbiome of Uncontacted Amerindians." Science Advances 1.3 (2015): 1-12. Web. 

Oldest Neanderthal DNA Confirmed

In the March 2015 issue of the Journal of Human Evolution, a group of researchers based in Italy confirmed that the Altamura Man, a hominin skeleton found in a limestone cave in Altamura Italy, belonged to Homo Neanderthalensis. Species confirmation was previously complicated by the limestone encasing the skeleton, which made extraction without damage to the specimen impossible, and by it's unusual morphology. Specifically, it's brow ridges were much thicker than the typical Neanderthal, though it's other features seemed to fit within the normal variation found in Neanderthals. Using the articular portion of the scapula, researchers were able to extract and sequence the whole HVR-1 of the specimen's mtDNA using PCR. After comparing to known Neanderthal and Denisovian genomes, they were able to conclude that the Altamura man was a Neanderthal. Given that dating has placed the Altamura man to be around 130k to 172k years old, this is the oldest Neanderthal DNA confirmed to date. This find will be able to provide some insight into the early Neanderthal evolution, given the DNA and morhpological data the Altamura man is able to provide.

- Justine Tamesis

Is our evolution progressing faster?

For years we have known about mitochondrial Eve, the so called last common ancestor that all women share traced through their mitochondrial DNA, but what is not often discussed in the mainstream media is 'Genetic Adam'. Unlike Mitochondrial Eve, Genetic Adam stems from the Y-chromosome DNA of living men. While some researchers used to think that genetic Adam lived around 350KYA, a recent study done by deCODE Genetics points to a date of about 250KYA, about 100,000 years earlier than previously thought. Using a population of 753 Icelandic men who were grouped in 274 paternal lines they used the molecular clock method of analysis to attempt to discover when this Adam possibly lived. While the terms Adam and Eve are slightly deceitful, (Adam and Eve were not the only humans living, nor are they likely the only one who contributed to future generations), the discovery of a date that puts Adam and Eve at a date that is closer together is a great discovery.
The article goes on to further discuss that a University of Wisconsin study shows that humans are likely to have split from our most recent ancestor about 6MYA which is more recent then expected as well which means that our evolution is progressing much faster than previously anticipated.

Work Cited

• Devlin, Hannah. "Study Shows Humans Are Evolving Faster than Previously Thought."Science. Science, 25 Mar. 2015. Web.
• "HOME - DeCODE Genetics." DeCODE Genetics. N.p., n.d. Web. 12 Apr. 2015.
• Poznik, G. David. "Sequencing Y Chromosomes Resolves Discrepancy in Time to Common Ancestor of Males Versus Females." Science 341.6145 (2013): 562-65. JSTOR. Web. 12 Apr. 2015.

By Kathryn Leonard

Sorry it's late, totally blanked. 

Why Don't Animals get Schizophrenia?

We see evidence of all sorts of traits associated with abnormal psychology in non-humans species, including separation anxiety in dogs, obsessive behavior in birds, and self-mutilating behavior in dolphins kept captive. One thing that we never seem to see in non-human species is psychosis and the big question here is: why is that?  Researchers know that humans have sections in our DNA called human accelerated regions (HARs) that were conserved in most species but underwent rapid evolution in human beings. HARs are regulatory regions and do not code for protein.The new question that came out of this was if HARs and Schizophrenia are both human specific, are they at all related? To answer this question team of researchers used the Psychiatric Genomic Consortium to look at the genomes of persons with Schizophrenia. What they found was the HARs and genes associated with schizophrenia were close by on DNA (closer than would be random chance) and that the HAR related genes associated with schizophrenia were under more positive selection than other genes related to schizophrenia. This lead the researchers to believe that these HAR genes are beneficial to us in some way, when they are not causing schizophrenia. To look further, the researchers looked at gene expression profiles and found that these HAR genes were regulating genes that were expressed in the prefrontal cortex were we do our higher level thinking and some were involved with the transmission of GABA, an inhibitory neurotransmitter highly linked to schizophrenia. The end conclusion is that as humans developed more complex neural pathways, we developed more complex things that can go wrong. As Bret Stetka said in his article "complex function begets complex malfunction".

The main article:
 —Stetka, Bret. "Why Don't Animals Get Schizophrenia (and How Come We Do)?" Scientific American Global RSS. N.p., 24 Mar. 2015. Web. 20 Apr. 2015. <http://www.scientificamerican.com/article/why-don-t-animals-get-schizophrenia-and-how-come-we-do/>.

The study about Schizophrenia:—
Ke Xu, Eric E. Schadt, Katherine S. Pollard, Panos Roussos, and Joel T. Dudley “Genomic and network patterns of schizophrenia genetic variation in human evolutionary accelerated regions” Mol. Biol. Evol. 2015 : msv031v1-msv031. 3 Feb. 2015. Web. 20 Apr. 2015.


Another similar study about Autism:—
Clarke, T. K., M. K. Lupton, A. M. Fernandez-Pujals, J. Starr, G. Davies, and S. Cox. "Common Polygenic Risk for Autism Spectrum Disorder (ASD) Is Associated with Cognitive Ability in the General Population." Molecular Psychiatry. Nature, 10 Mar. 2015. Web. 20 Apr. 2015.

By Sadina Videlock-Prentice

In Iceland’s DNA, New Clues to Disease-Causing Genes

On March 25^th, an article was published describing the studies and data that a genetics firm in Iceland called Decode was able to collect. Researchers sequenced 2, 636 genomes in an attempt to discover unknown gene mutations that could potentially play an impact in terms of increasing likeability to contract an illness. Through the study, they were able to identify mutations on certain genes that are associated with both rare and common illnesses by observing which people suffering from what illness had what specific gene mutation in common. This study is important in finding effective drugs for diseases and being able to generate reports for genetic disease on individuals who haven’t even participated in the testing themselves.

Sources:

—  http://www.nytimes.com/2015/03/26/science/in-icelands-dna-clues-to-what-genes-may-cause-disease.html

—  http://www.decode.com/publications/
Nadia Khan 

In Big Shift, 23andMe Will Invent Drugs Using Customer Data

Personal genomics and biotech company 23andMe recently announced that it will begin using its customer genetic database to develop medicines itself. The rationale behind this move is that "it will allow it to capture a much greater proportion of the economic value its genetic database could create". In other words, instead of selling information from their database to companies that will use the information to make and sell medicines, they will just do all of that themselves, and make a lot more money.