In collaboration with The Milken Institute and Lundbeck, 23andMe is launching a groundbreaking<a href="https://www.23andme.com/depression-bipolar/"> new study</a> leveraging 23andMe’s unique research model to look at the <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-300x157.png" alt="" class="alignright size-medium wp-image-25590" width="300" height="157" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-300x157.png 300w, https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-768x402.png 768w, https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-1024x536.png 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-880x461.png 880w, https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628-1180x618.png 1180w, https://blogcms.23andme.com/wp-content/uploads/2017/07/BiPolar_metadata_1200x628.png 1200w" sizes="auto, (max-width: 300px) 100vw, 300px" />genetics underlying depression and bipolar disorder.
In the United States alone, depression and bipolar disorders impact more than <a href="http://www.adaa.org/about-adaa/press-room/facts-statistics">16 million people</a>, and fewer than half ever receive effective treatment. According to the World Health Organization, depression alone accounts for the most<a href="https://www.nature.com/news/mental-health-a-world-of-depression-1.16318"> ‘years lost’</a> in disability than any other health condition worldwide.
Although scientists have spent decades studying the conditions, our understanding of the underlying biology remains rudimentary. Recent studies have offered some intriguing clues for future inquiry, but there’s still so much left to discover. This study will combine genetic information with cognitive assessments and behavioral data that researchers hope will glean new insights that could inform new treatments.
“We need a wider, more varied data set to make additional discoveries,” said Emily Drabant Conley, PhD., vice president of Business Development at 23andMe. “By studying intermediate phenotypes such as cognitive function alongside genetics and other environmental variables on a massive scale, we hope to take a significant step forward in the study of depression and bipolar.” 
   
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The goal is to enroll 15,000 people with depression and 10,000 individuals with bipolar disorder and then incorporate their data to assess better how genes influence brain processes such as attention, decision-making and visual perception.
It’s a unique approach that leverages 23andMe’s research model, which can rapidly gather vast amounts of genetic, cognitive and behavioral data for the study.
Already considered a pioneer in genetic research, 23andMe has successfully established research communities to study Parkinson’s disease, lupus, IBD, and fertility, adding to the more than 75 studies the company has already published in scientific journals to date. Additionally, this research builds on the largest study of its kind on the genetics of major depressive disorder conducted by 23andMe.
Last summer 23andMe, along with Massachusetts General Hospital and Pfizer, published findings in what was by far the<a href="http://nature.com/articles/doi:10.1038/ng.3623"> largest study</a> of its kind focused on major depressive disorder. In that study, researchers identified 15 new genetic regions linked to depression. The study was instructive not just in what it found, but in how it drew on the massive amount of data from 23andMe customers who had consented to research.
And that is the hope here &#8211; that 23andMe’s unique research model, and its ability to quickly recruit individuals with depression and bipolar disorder will help lead to new breakthroughs in research into these conditions.
Go<a href="https://www.23andme.com/depression-bipolar/"> here</a> to find out more about this study.

23andMe Blog

23andMe Blog Team

23andMe Now Enrolling For A New Genetic Study on Depression and Bipolar Disorder

In the article <a href="https://www.nytimes.com/2017/01/11/magazine/neanderthals-were-people-too.html?_r=0">Neanderthals Were People Too</a>, Jon Mooallem describes an electric moment where he felt a visceral connection to our long lost human cousins.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-25260" src="https://blog-api.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-212x300.jpg" alt="" width="212" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-212x300.jpg 212w, https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-768x1084.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-725x1024.jpg 725w, https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-623x880.jpg 623w, https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-836x1180.jpg 836w, https://blogcms.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-scaled.jpg 1813w" sizes="auto, (max-width: 212px) 100vw, 212px" />
Watching a group of archeologist painstakingly excavate a small hearth in a cave in Gibraltar, Mooallen is suddenly struck by what he’s seeing. The bits of charcoal, the fire stained ground where embers are scattered and the smoke stained walls where the cinders from the fire had pushed up against the rock wall.


“Suddenly, it struck me — though it should have earlier — that what we were looking at were the remnants of a single event: a specific fire, on a specific night, made by specific Neanderthals. Maybe this won’t sound that profound, but it snapped that prehistoric abstraction into focus. This wasn’t just a “hearth,” I realized; it was a campfire.”


<h6>The Connection</h6>

He was looking at the remains of a fire that warmed these human cousins of ours on a night 50,000 years ago, and he felt connected.
Whether we feel it or not, most humans living today are connected to Neanderthals.
All non-Africans have between one and three percent Neanderthal DNA, a remnant of interbreeding as modern humans migrated out of Africa and met Neanderthals for the first time. And we likely carry remnants of other hominids in our DNA, such as the Denisovans.
Perhaps it’s that genetic connection that fuels our fascination with Neanderthal, or maybe it’s that what we learn is informing us all more about what it means to be human.
We know that we owe much to the Neanderthals. It’s likely that interbreeding with Neanderthals helped give humans an evolutionary advantage to adapt — beneficial immune response and blood clotting for instance — but it also left us with a subtle risk for certain diseases, according to <a href="http://www.sciencemag.org/news/2016/02/our-hidden-neandertal-dna-may-increase-risk-allergies-depression">research published early last year</a>.

<h6>The Neanderthal Advantage</h6>

Vanderbilt University&#8217;s John Anthony Capra, was the lead author of that study, which we previously wrote about in the <a href="https://blog.23andme.com/news/the-lasting-legacy-of-neanderthals/">blog</a>. Capra recently spoke with <a href="https://www.nytimes.com/2017/01/20/science/john-anthony-capra-neanderthals-dna-humans.html">The New York Times</a> about that research.
Over time humans <a href="https://blog.23andme.com/23andme-research/new-neanderthal-research/">purged</a> all but the last vestiges of Neanderthal DNA — but some of what remains, even some of what previously could have been beneficial, is deleterious, according to Capra.


“What we’ve been finding is that Neanderthal DNA has a subtle influence on risk for disease,” Capra said.


For the research, Capra and his team looked at electronic health records from 50,000 individuals and found associations with Neanderthal DNA and immune response, blood clotting, and depression.
These findings and others indicate that Neanderthals were much more like us than we previously thought.


“We tend to think of them as dumb and brutish,” Capra said. “There’s no reason to believe that. Maybe those of us of European heritage should be thinking, “Let’s improve their standing in the popular imagination. They’re our ancestors, too.’”

The Neanderthal Within

A lot of people bite their nails. It’s not that unusual, but researchers looking at the underlying biology for individuals who do it often are learning that frequent nail-biting may point to more serious conditions.<img loading="lazy" decoding="async" class="size-full wp-image-21024 alignright" src="https://blog-api.23andme.com/wp-content/uploads/2014/05/@PITER-23andMe-ChaoTian-25.jpg" alt="@PITER-23andMe-ChaoTian-25" width="199" height="287" />


For people who frequently bite their nails, the habit is associated with higher chances of having some psychiatric disorders or compulsive behaviors, according to new research by 23andMe senior statistical geneticist Chao Tian. In a short talk at the annual American Society of Human Genetics meeting in Vancouver, Chao presented findings showing   genetic associations with frequent nail-biting as well as other associations with the habit.
Before diving into her findings, it’s important to note again that in most cases nail-biting is not out of the ordinary. In children and teens, it <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556753/">isn’t associated</a> with any psychiatric disorder. It is more a reflection of boredom, stress or even behavior modeled from parents, according to psychiatrists who study the condition.
The habit is fairly common. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556753/">Estimates</a> are that about 30 percent of children and 45 percent of teens bite their nails, and as people move into adulthood the percent of people who bite their nails diminishes.
But where there are interesting associations are among those who report that they frequently bite their nails. For those individuals the habit is associated with higher chances of having some psychiatric disorders or compulsive behavior, according to new research by 23andMe senior statistical geneticist Chao Tian.
In her talk at the annual American Society of Human Genetics meeting in Vancouver this week, Chao presented findings showing both genetic associations with frequent nail-biting as well as associations between the habit and certain psychiatric disorders.


For this study, Chao looked at data from 180,000 23andMe customers of European ancestry who consented to research. About 37 percent of whom reported that they bite their nails, with about seven percent of the total saying they did so frequently.<img loading="lazy" decoding="async" class="alignright size-full wp-image-24474" src="https://blog-api.23andme.com/wp-content/uploads/2016/10/Nail-biter-1.jpg" alt="nail-biter" width="147" height="193" />
Chao and other researchers at 23andMe found two dozen genetic associations with nail-biting, known by the medical term onychophagy.
While nibbling on nails during times of stress doesn’t mean one has a psychiatric disorder, among those who report that they frequently bite their nails the picture changes a bit.
Data shows that frequent nail biters are more likely to have certain disorders and habits such as depression, anxiety, and trichotillomania, the scientific name for the urge to pull out one’s own hair.
What’s also interesting is that the function of some of the genes in which nail biting associations were found point to links with things like nail structure, BMI, taste perception and neuronal regulation in the brain, Chao said.


What’s important to note here is that most cases of nail biting among children and teens isn’t associated with any psychiatric disorder, but rather a sign of boredom, stress or even behavior modeled from parents. About 30 percent of children and 45 percent of teens bite their nails. Nail-biting tends to diminish as people move into adulthood.
In this study, Chao also looked other characteristics like conscientiousness, openness, neuroticism, agreeableness and perceived stress, and found that those people who reported biting their nails often were also more likely to be neurotic and stressed. On the other hand, her research showed that people who didn’t bite their nails were more likely to be conscientious.


In and of itself this study is interesting, but it also illustrates the power of collecting large amounts of phenotypic data with genotypic data to study the underlying biology of many different kinds of conditions.

A Real Nail Biter

A new study has found a genetic variant associated with whether a commonly prescribed antidepressant is effective.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-7843" src="https://blog-api.23andme.com/wp-content/uploads/2010/11/cartoon-pills-300x284.png" alt="cartoon-pills" width="300" height="284" />
In a recently published <a href="https://www.nature.com/tp/journal/v6/n9/full/tp2016171a.html">paper</a>, scientists from <a href="http://www.janssen.com/research-and-development">Janssen Research &amp; Development</a> and 23andMe report finding a genetic association for the efficacy of the drug bupropion – marketed for treatment of depression under the name Wellbutrin®.
The biological significance of the genetic variant identified in the study is not yet known, and, according to the researchers, will still have to be replicated. But this finding offers intriguing possibilities for future research.

<h5>
</h5>
<h4>Different Response to Treatments</h4>
Major depressive disorder is one of the leading causes of disability and is estimated to affect more than <a href="https://www.nature.com/news/mental-health-a-world-of-depression-1.16318">350 million</a> people worldwide. In the past efforts to understanding the role genetics plays in the condition and its treatment – particularly among patients who do not respond well to current medication – have been hindered by the heterogeneity of the disorder and by studies that <a href="http://nature.com/articles/doi:10.1038/ng.3623">until recently</a> have been undersized.
“Genetic predisposition may contribute to the differences in drug-specific, class-specific, or antidepressant-wide treatment resistance,”   the authors said. “Clinical studies with genetic data are often limited in sample sizes. Drug response obtained from self-reports may offer an alternative approach to conduct a study with much larger sample size.”<img loading="lazy" decoding="async" class="alignright size-medium wp-image-24308" src="https://blog-api.23andme.com/wp-content/uploads/2016/09/computer-survey-300x243.jpg" alt="computer-survey" width="300" height="243" />
In this study published in the journal <a href="https://www.nature.com/tp/journal/v6/n9/full/tp2016171a.html">Translational Psychiatry</a>, researchers were able to use data from more than 48,000 23andMe customers of European ancestry who completed a survey on antidepressant efficacy and side effects and another 190,000 healthy controls self-reported to be free of any major psychiatric disorders, all of those included in the study consented to participate in research.
The survey that was used to ask customers about the efficacy of treatments for their depression was developed with the assistance of Dr. Steven Hamilton of Kaiser Permanente and Carol Schaffner, from the University of California San Francisco.
The scientists working on this study analyzed the self-reported data from customers to study the effectiveness of three different types of drugs used to treat major depressive disorder. The researchers also included customers who did not report having depression and used them as controls in the study. In each case the study looked at “responders” and “nonresponders” to different treatment and compared them with the healthy individuals who were used as controls.
Currently there are about 30 different prescription antidepressants, many of which affect neurotransmitters in the brain associated with depression.
Although there have been studies that have attempted to look at the role genetics may play in the effectiveness of different treatments, this study is by far the largest effort in that regard.
The three types of medications included in this study were selective serotonin reuptake inhibitors also known as SSRIs; norepinephrine-dopamine reuptake inhibitors, known as NDRIs, which include the drug bupropion (Wellbutrinâ„¢); and citalopram/escitalopram responders.
All of these drugs work by suppressing certain kinds of chemicals in the brain that are associated with depression and are known as neurotransmitters – these include serotonin, norepinephrine and dopamine.
The only association found that met genome-wide significance was for a variant in a region between two genes – GPRIN3 and SNCA. People with the variant had higher odds that treatment with bupropion (Wellbutrin®) would be ineffective. While the function of that gene region is not fully known, the researchers noted that when looking at what is called a “gene set enrichment analysis of buproprion GWAS&#8221; they noticed that many of the suggestive associated genes play roles in circadian rhythm and long-term depression pathways. Sleep disturbances are common features of depression, the researchers noted.
The study can be found in the journal <a href="https://www.nature.com/tp/journal/v6/n9/full/tp2016171a.html" target="_blank" rel="noopener noreferrer">Transitional Psychiatry</a>.

Genetics found to influence antidepressant efficacy

Your genetics, whether your partner suffers from chronic pain and the environment you share with your partner, all contribute to your <img loading="lazy" decoding="async" class="alignright size-medium wp-image-24219" src="https://blog-api.23andme.com/wp-content/uploads/2016/08/DNA-strand-129x300.jpg" alt="10192015_Icons_Set1_Working.ai" width="129" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/08/DNA-strand-129x300.jpg 129w, https://blogcms.23andme.com/wp-content/uploads/2016/08/DNA-strand-442x1024.jpg 442w, https://blogcms.23andme.com/wp-content/uploads/2016/08/DNA-strand-380x880.jpg 380w, https://blogcms.23andme.com/wp-content/uploads/2016/08/DNA-strand.jpg 500w" sizes="auto, (max-width: 129px) 100vw, 129px" />own risk for having the condition, according to a new study into the complex mix of environmental and genetic factors that influence both the risk for chronic pain and for depression.


Scientists at the University of Edinburgh also <a href="http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002090">found</a> that the two conditions share some of the same environmental and genetic associations.


&#8220;We hope our research will encourage people to think about the relationship between chronic pain and depression and whether physical and mental illnesses are as separate as some believe,&#8221; study author Andrew McIntosh said in a University of Edinburgh news release.

<h6>Separate Studies</h6>

Published in PLOS Medicine, the study relied on data from Generation Scotland, a Scottish Family Health History study, as well as data from the <a href="http://www.ukbiobank.ac.uk/about-biobank-uk/">UK Biobank</a>.
In a separate study, researchers from 23andMe, Massachusetts General Hospital and Pfizer conducted genome wide association studies using data from 23andMe customers, who consented to participate in research.
They found that chronic pain could arise through the combined effect of many genetic factors. They also found that the risk for chronic pain is heightened if there is also a genetic risk for depression.


All of this is of interest because health researchers have seen that chronic pain and depression often go hand-in-hand.
<h6>A Link With Depression</h6>
While some of the links between the two conditions are quite evident – for example, dealing with a painful and debilitating injury can take a toll on even the most resilient individuals and their partners. But independent of those issues this study found that other factors are also at play.


“Chronic pain is caused by an accumulation of many small genetic effects and is associated with some of the same genetic and environmental risk factors that confer risk of depression,” according to the researchers, adding that “both genetic factors and chronic pain in a partner or spouse contribute to the risk of chronic pain for an individual.”


By identifying those shared contributions, researchers said they hoped it would help in the search for new approaches for treating depression and chronic pain.
The study can be found in the <a href="http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002090" target="_blank" rel="noopener noreferrer">PLoS Genetics.</a>

Genetics found to influence risk of chronic pain and depression

Editor&#8217;s note: 23andMe is now enrolling for a new genetic study on depression and biopolar disorder. Check out the <a href="https://blog.23andme.com/23andme-research/23andme-launches-new-genetic-study-depression-bipolar-disorder/">blog post</a> about the study or see more about the study <a href="https://www.23andme.com/depression-bipolar/">here</a>. 
In a new study, scientists have found genetic markers associated with depression in people of European descent.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22305" src="https://blog-api.23andme.com/wp-content/uploads/2015/03/teardrop-300x234.jpg" alt="Pencil drawing eye" width="300" height="234" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/03/teardrop-300x234.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/03/teardrop-768x600.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/03/teardrop-1024x800.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2015/03/teardrop-880x687.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2015/03/teardrop-1180x921.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />


In what is by far the <a href="https://www.nature.com/articles/ng.3623.epdf?shared_access_token=2L701P0aoTugcpIZV_UxDtRgN0jAjWel9jnR3ZoTv0PP-e6MaKfwdoFYRj8g9D1xDb6bJ1uGA1UjyIKokNVDLTnRuKcWMhh79nIxx72yX9SVmCk7BF6wsPtOYEwU_jusesdKi0iT9c3E5z3SwC0sXWsNXiGGmHdldHOLvCJ7EvE%3D">largest study</a> of its kind focused on major depressive disorder, researchers from Pfizer, Massachusetts General Hospital and 23andMe identified 17 single nucleotide polymorphisms in 15 genetic loci significantly associated with depression among people of European ancestry.
The study may lead to better understanding of the biology of the condition. Major depressive disorder is characterized by mood changes, sleep disruption, fatigue and loss of appetite, and is one of the leading causes of disability and is estimated to affect more than<a href="https://www.nature.com/news/mental-health-a-world-of-depression-1.16318"> 350 million</a> people worldwide.
The study drew on massive amounts of data from 23andMe customers who’ve consented to research and completed online surveys about depression.


“These studies provide evidence for large-scale consumer genomic data as a powerful and efficient alternative  complement to data from traditional means of ascertainment for neuropsychiatric disease genomics,” according to the study. “If one reasonable strategy adopted by that study is to develop more precise or refined phenotypes, another is to efficiently identify much larger cohorts for study despite less intensive phenotyping.”


Although researchers have long known that genetics plays an important role in the development of depression, attempts in the past to study the genetics behind the disorder have failed to produce results. One<a href="https://www.ncbi.nlm.nih.gov/pubmed/22472876"> study</a> in 2013 by the Psychiatric Genomics Consortium (PGC) looked at data from more than 17,000 people with depression but couldn’t detect any genetic hits. For a time researchers thought the studies were being confounded by how major depressive disorders were being diagnosed – by basically lumping different forms of depression together – or that the studies were undersized.
Depression is a heterogeneous disease, with many genes contributing to the condition. Environmental influences also play a role in its development.
Jonathan Flint, a geneticist at the University of Oxford and a key researcher in the PGC study, concluded that he either needed more data from more individuals to find a signal or a more select group of individuals to study, according to an <a href="https://www.nature.com/news/first-robust-genetic-links-to-depression-emerge-1.17979">article</a> in the journal Nature. Flint took the latter strategy studying data from about 10,000 individuals in China, a cohort that was relatively homogenous and had the most severe depression. Last year he and other researchers published their findings, <a href="https://www.nature.com/nature/journal/v523/n7562/full/nature14659.html">uncovering two variants</a> associated with the condition among people of Han Chinese ancestry, but those variants do not appear to influence the condition in people of European descent.


Another approach would be to find a much larger cohort of individuals and that’s what this latest study has done by tapping into 23andMe’s data from customers. The study includes more than 450,000 customers, who consented to participate in research, about 120,000 of whom reported being diagnosed with depression.


By using 23andMe’s online method and collecting data from a very large group of individuals, the researchers were able to gather enough data to power their study. The sheer volume of data – the number of people, the amount of both phenotypic and genotypic data – allowed the scientists to see signals that they may not have seen otherwise.
The variant most strongly associated with depression was found in a gene region involved with brain function.
The most statistically significant variant is located between two genes that are expressed in the brain, MEF2C and TMEM161B. MEF2C is involved in the regulation of synapses and studies have associated variants in this gene with epilepsy and intellectual disability.


The remainder of the single nucleotide polymorphisms found to reach genome-wide significance for association with depression were in 13 other genes or gene regions. Many of these are expressed in the central nervous system for neurodevelopment or have been identified in other genome-wide association studies to be related to different psychiatric traits.
All of these variants are different than the two variants associated with depression in people of Han Chinese ancestry, but the variants found in both studies may help in the ongoing effort to understand the underlying biology of depression.
Researchers hope these new findings will offer a better understanding of the biology of the disease and could help in the search for the right treatments for depression.
This study can be found in the journal <a href="https://www.nature.com/ng/journal/v48/n9/full/ng.3623.html" target="_blank" rel="noopener noreferrer">Nature Genetics.</a>

New genetic variants linked to depression

<div id="attachment_23819" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-23819" class="wp-image-23819 size-medium" src="https://blog-api.23andme.com/wp-content/uploads/2016/04/picture-40-1425534389-1-200x300.jpg" alt="picture-40-1425534389" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/04/picture-40-1425534389-1-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2016/04/picture-40-1425534389-1.jpg 350w" sizes="auto, (max-width: 200px) 100vw, 200px" />Dan Benjamin, an Associate Professor of Economics at USC and one of the principal investigators with the Social Science Genetic Association Consortium. </div>
In one of the largest-ever genome wide association studies for behavioral traits, researchers have found three genetic variants associated with a person’s sense of well-being.
The study <a href="https://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3552.html" target="_blank" rel="noopener noreferrer">published this week</a> in the journal Nature Genetics also looked at genetic associations with depression and what is called &#8220;neuroticism&#8221; – personality traits that are characterized by feelings of anxiety, fear and negativity. The study found two variants associated with depression and 11 with neuroticism. Most of the variants associated with depression and neuroticism were also associated with well-being, according to the study.
&#8220;We found that most of the genetic variants associated with depressive symptoms and or neuroticism also were linked to subjective well-being, and vice-versa,” said Daniel Benjamin, corresponding author and an associate professor at USC’s Center for Economic and Social Research at USC. “When examined individually, each genetic variant explains very little about these traits. But when taken together, these findings imply that the genetic influences on depression, neuroticism and subjective well-being result from the cumulative effects of at least thousands, if not millions, of different variants.”


The study was spearheaded by the<a href="http://www.ssgac.org/Home.php">  Social Science Genetic Association Consortium</a>, an international group of more than 190 scientists that was co-founded by<a href="https://cesr.usc.edu/people/staff/djbenjam"> Benjamin</a>, along with<a href="http://econ.as.nyu.edu/object/DavidCesarini.html"> David Cesarini</a>, at New York University and<a href="http://www.erim.eur.nl/people/philipp-koellinger/"> Philipp Koellinger</a>, at Erasmus University in Rotterdam. The consortium investigates the influence of genetics on human behavior, well-being and social science-related outcomes through large-scale studies of human genomes.


In this work, the researchers also found a strong link between the variants associated with these traits and those associated with anxiety disorders. The variants also had some moderate overlap with variants associated with schizophrenia and bipolar disorder.
Benjamin and the other study authors noted that the findings were driven in part by the size of the their genome wide association study, which included analysis of data from 298,420 individuals who were part of 59 different study cohorts that looked at subjective well-being.
The researchers also included data on depressive symptoms and neuroticism from other study cohorts that together included data from more than 300,000 individuals.

The role of genetics in well-being

Like all good photographers Alan Babbitt sees what’s invisible to most of us.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22262" src="https://blog-api.23andme.com/wp-content/uploads/2015/02/Alan-B-300x300.jpeg" alt="Alan B" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-300x300.jpeg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-150x150.jpeg 150w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-768x768.jpeg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-271x271.jpeg 271w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-372x372.jpeg 372w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B-574x574.jpeg 574w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Alan-B.jpeg 800w" sizes="auto, (max-width: 300px) 100vw, 300px" />
With a steady hand and a willingness to go almost anywhere for a good shot, Alan spent decades turning his lens on people and places to create images he thought would draw the viewer in and tell a story.
“I’d call it street photography,” he said. “I wanted to document what’s around me.”
But when his steady hand began to fail him in 2003, he thought he’d lost what defined him as a photographer.
“First my thumb started twitching,” he said.
<h6>Parkinson&#8217;s Photographer</h6>
Then the tremors became more pronounced. After seeing a neurologist, he got a diagnosis that shook him to his core – Alan learned he had Parkinson’s disease.
“It was devastating,” he said.
He was a still photographer, he liked to say, but he couldn’t keep his camera from shaking. Alan drifted into depression, and for a time stopped taking photos all together.

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				<img loading="lazy" decoding="async" width="150" height="150" src="https://blogcms.23andme.com/wp-content/uploads/2015/02/Moving-Landscape-Example-150x150.jpg" class="attachment-thumbnail size-thumbnail" alt="" aria-describedby="gallery-1-22260" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/02/Moving-Landscape-Example-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Moving-Landscape-Example-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Moving-Landscape-Example-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Moving-Landscape-Example-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
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				Copyright Alan Babbitt
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				<img loading="lazy" decoding="async" width="150" height="150" src="https://blogcms.23andme.com/wp-content/uploads/2015/02/las-vegas-150x150.jpg" class="attachment-thumbnail size-thumbnail" alt="" aria-describedby="gallery-1-22256" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/02/las-vegas-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2015/02/las-vegas-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2015/02/las-vegas-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2015/02/las-vegas-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
			</dt>
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				Copyright Alan Babbitt
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				<img loading="lazy" decoding="async" width="150" height="150" src="https://blogcms.23andme.com/wp-content/uploads/2015/02/Vegas-example-III-150x150.jpg" class="attachment-thumbnail size-thumbnail" alt="" aria-describedby="gallery-1-22258" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/02/Vegas-example-III-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Vegas-example-III-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Vegas-example-III-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Vegas-example-III-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
			</dt>
				<dd class='wp-caption-text gallery-caption' id='gallery-1-22258'>
				Copyright Alan Babbitt
				</dd></dl><dl class='gallery-item'>
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				<img loading="lazy" decoding="async" width="150" height="150" src="https://blogcms.23andme.com/wp-content/uploads/2015/02/Ferris-Wheel-150x150.jpg" class="attachment-thumbnail size-thumbnail" alt="" aria-describedby="gallery-1-22259" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/02/Ferris-Wheel-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Ferris-Wheel-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Ferris-Wheel-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2015/02/Ferris-Wheel-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
			</dt>
				<dd class='wp-caption-text gallery-caption' id='gallery-1-22259'>
				Copyright Alan Babbitt
				</dd></dl> 
		</div>

The difficult news was compounded by a side effect of the disease. Parkinson’s causes chemical changes in the brain that can lead to depression. Ironically when Alan began taking an anti-depressant, it compounded his problem, one of the drug’s side effects included tremors.
“It was hard,” he said.
It felt like the passion of his life – the thing Alan had been doing since he was a kid with his first camera, a Kodak Brownie Hawkeye – was slipping away.
<h6>Seeing Anew</h6>
And then Alan saw something that no one else could see.
“It was almost by accident,” he said.
In Las Vegas, he went out one evening with his camera. He was taking photos in the low light, frustrated by every image being out-of-focus.
“But you know the beauty of digital cameras is you can see things instantly,” Alan said.
As he looked at the photos on the camera, he was suddenly struck by the blurry images his shaky hands were taking. It was one of those a-ha moments.
<h6>Unstill Photography</h6>
He decided to push it one step further, clicking off the flash, slowing the shutter speed down, and turning his small point-and-shoot digital camera back at the neon lit streets of Las Vegas. Instead of trying to deny what was happening to him, Alan made his Parkinson’s part of how he made his images.
“After a couple years of fighting my tremor and trying to work around it, I had the notion to just let go and let it do its thing,” Alan said. “The camera quickly showed me I was onto something.”
Just as he’d always done as a good photographer, Alan captured what was invisible to most of us. And thus the creation of what he now calls his “Un-Still Photography.” Instead of trying to steady his hand, the tremors were part of his creative process, generating the swirls and whirls of light that offered unique and arresting images of the world around him.
<h6>New Possibilities</h6>
His epiphany in Las Vegas energized him and he folded that feeling into how the diagnosis itself had changed him. His priorities changed, so did his goals and his notion of what he wanted out of life.
“The world and everything in it became new and fresh and the possibilities were endless,” Alan said.
From that moment in <a href="http://www.abproductions.com/las_vegas/las_vegas.html" target="_blank" rel="noopener noreferrer">Las Vegas</a>, Alan has begun to push his <a href="http://www.abproductions.com/moving_landscapes/moving_landscapes.html" target="_blank" rel="noopener noreferrer">“Un-Still Photography”</a> into other unexpected arenas including sports photography, particularly <a href="http://www.abproductions.com/ballpark/ballpark_ss.html" target="_blank" rel="noopener noreferrer">baseball</a>. The images he captures including the swirl of a batter’s swing, or the buzzing color of the crowds in the stadium, you can’t see in most sports images.
For Alan, who joined 23andMe’s Parkinson’s research community almost six years ago, his condition has become something that he is embracing.
“It’s turning a negative into a positive,” he said.
That’s what also motivated him to join 23andMe and contribute to research.
“If they can learn something from me about this disease that can help someone else then I’m all for it,” he said.
Check out some of Alan’s images on <a href="http://abproductions.com/" target="_blank" rel="noopener noreferrer">his website</a>.

Steady On

<img loading="lazy" decoding="async" class="alignnone size-full wp-image-20269" alt="Depression infographic" src="https://blog-api.23andme.com/wp-content/uploads/2014/01/Depression-infographic.jpg" width="690" height="447" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/01/Depression-infographic.jpg 690w, https://blogcms.23andme.com/wp-content/uploads/2014/01/Depression-infographic-300x194.jpg 300w" sizes="auto, (max-width: 690px) 100vw, 690px" />
For the live-updated, fully-labeled, interactive version of this infographic, <a href="http://curetogether.com/depression/ig/treatment-effectiveness-vs-popularity">click here</a>.
By Alex Carmichael, Co-Founder of CureTogether
The top treatments for depression are simple lifestyle changes, according to patients who contributed to a new study by CureTogether, a free resource owned by 23andMe that allows people to share information about their health and treatments.

Participants in the study said they found that interventions like exercise, spending time with pets, and listening to music were the most effective for them in treating their depression. Conversely, some popular treatments such as alcohol, Paxil, and caffeine were among the least effective, according to the participants in the CureTogether survey.

Depression is the number one condition among participants in CureTogether, with 11,443 members contributing data on what works and doesn’t work for them. While many people feel sad from time to time, depression is a serious mood disorder that causes a persistent feeling of sadness and loss of interest. It often goes untreated, according to the National Institutes for Health. The participants in the CureTogether survey may not be diagnosed with clinical depression. They are self-reporting that they have depression and the associated symptoms. There are a number of causes and treatments for the condition. In this survey, participants pointed to stress and social isolation as the most common <a href="http://curetogether.com/depression/ig/treatment-effectiveness-vs-popularity" target="_blank" rel="noopener noreferrer">causes of their depression</a>. 
study.

<div style="float: right; text-align: justified; width: 200px; background-color: #eee; padding: 15px; margin-left: 10px;">Top-Rated Treatments for Depression in Survey
1. Exercise
2. Spend time with a pet
3. Play outside
4. Music with exercise
5. Music therapy
6. Daily aerobic exercise
7. Daily sunlight exposure
8. Art therapy
9. Psychotherapy
10. Psychotherapy
*For a list of all the treatments listed in the survey go <a href="http://curetogether.com/depression/treatments/ae/" target="_blank" rel="noopener noreferrer">here</a>.</div>

Participants in this survey also did not rank some of the most commonly used drugs for treating depression in their list of the top 25 effective treatments. But among the medication that many participants listed as effective were SSRIs, Xanax and  Low Dose Naltrexone.
Where did this data come from? This is the result of a five-year CureTogether study on <a href="http://curetogether.com/depression/treatments/" target="_blank" rel="noopener noreferrer">depression,</a> in which people suffering from the condition shared information about their symptoms and treatment effectiveness.
We’d like to thank those who participated. And just as they shared their experience with depression treatments, we’re freely and openly sharing the results of the Depression 
This is part of a regular series of CureTogether <a href="http://curetogether.com/blog/category/research-findings/">research findings</a>. CureTogether’s research findings are different than <a href="https://www.23andme.com/about/factoids/">those made by 23andMe</a>, which look at genetic associations with illness, traits and drug response. But as we continue our work with the CureTogether community, 23andMe hopes to incorporate more of this kind of self-reported information into our own research. CureTogether present its findings just as they are — patient-reported data — to stimulate discussion and generate new insights for further research.


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