By Alison Chubb
We&#8217;ve all known teenagers who grow several inches in a year, and then start bumping into people and furniture as they figure out what to do with their big feet and long arms.
The growth spurt that happens during adolescence can account for up to 20 percent of one&#8217;s final height, <img loading="lazy" decoding="async" class="size-full wp-image-19114 alignright" src="https://blog-api.23andme.com/wp-content/uploads/2013/08/KidsHeight.jpg" alt="KidsHeight" width="316" height="380" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/08/KidsHeight.jpg 316w, https://blogcms.23andme.com/wp-content/uploads/2013/08/KidsHeight-249x300.jpg 249w" sizes="auto, (max-width: 316px) 100vw, 316px" />and we know that <a href="https://www.ncbi.nlm.nih.gov/pubmed/18203123">genetics</a> is largely responsible for why kids grow less or more, during that time. But until now, we didn&#8217;t know much about the genetic variants involved in this sometimes awkward phase of childhood growth.
<h6>Growth Data</h6>
Recently, <a href="https://www.ncbi.nlm.nih.gov/pubmed/23449627">researchers</a> from the Early Growth Genetics Consortium analyzed growth data from over 10,000 people of European descent looking for genes relevant to childhood growth rates. They found genetic variants linked to height and growth during adolescence and published their results in the journal Human Molecular Genetics.
The single-nucleotide polymorphism (SNP) was associated with late adolescent growth. People with the C version of this SNP tended to grow slightly more between the ages of 14 and 18 compared to people without the C version. This SNP is located near LIN28B, a gene linked to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869010/">height in adulthood</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3140055/">age at menarche</a> (first period).
<h6>Puberty</h6>
Another SNP was associated with overall adolescent growth. People with the A version of this SNP tended to grow slightly more between the ages of eight and 18, while those with the G version tended to grow slightly less.
The researchers also discovered that women with the G version of experienced their <a href="https://www.23andme.com/health/menarche/">first period</a> at a slightly earlier age, on average. This marker is located near ADCY3 and POMC, two genes implicated in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370100/">childhood</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014648/">adult obesity</a>. ADCY3 is an enzyme important for communication between cells throughout the body, and POMC is expressed in the pituitary gland that releases several hormones important for growth.
We know from epidemiological studies that <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008450">obesity during childhood </a>is linked to earlier puberty, and that earlier puberty raises the risk for obesity and possibly other health conditions in adults.
This new study is interesting because it shows that some of the genetic factors underlying obesity and growth patterns in childhood may overlap, and that they may also influence risk for other diseases in adults, but much more research is needed to unravel these complicated genetic connections.

Alison Chubb

The Genetics of Adolescent Growth Spurts

<img loading="lazy" decoding="async" class="aligncenter wp-image-19130 size-full" src="http://35.88.189.111/wp-content/uploads/2013/08/Pregnancy-Belly.jpg" alt="" width="834" height="576" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly.jpg 834w, https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly-300x207.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly-768x530.jpg 768w" sizes="auto, (max-width: 834px) 100vw, 834px" />Stretch marks are enough to send some new moms into a post partum panic.
That might be what fuels the estimated $5 billion to $10 billion spent on salves and oils to rub away the marks, also known as striae distensae. But scientists still don’t really understand why some individuals –men can also get the marks because of big fluctuations in their weight or BMI – end up with stretch marks while others don’t.
23andMe just published <a href="https://www.jidonline.org/article/S0022-202X(15)36019-X/fulltext">the first of its kind study</a> looking at the genetics behind stretch marks. And the first four genetic variants were found to be associated with developing the marks.
“Through this first of its kind study, we’ve identified new genetic associations that can provide deeper insights into the root causes of stretch marks,” said Joyce Tung, Ph.D., author and 23andMe Director of Research.
In turn, the new insights could help in developing better treatments than spending hours rubbing coco butter and vitamin E oil on the marks. The work also helps point the direction for future study. One area our researchers would like to look at further is the potential effects of genes associated with obesity and the development of stretch marks, both independent of weight changes or because of weight loss or gain
The study – <a href="https://www.jidonline.org/article/S0022-202X(15)36019-X/fulltext">“Genome-wide association analysis implicates elastic microfibrils in the development of non-syndromic striae distensae”</a> – appeared in the Journal of Investigative Dermatology, a peer-reviewed scientific journal, published by the Nature Publishing Group.
Our researchers looked at more than 30,000 customers of European descent who responded to a survey, about a third of whom were cases (reported stretchmarks) and the rest were controls (reported no stretchmarks). The analysis identified an association between stretch marks and a variant near the ELN gene that encodes for the protein elastin. Defects in the gene are known to affect the integrity of the skin as well as cause heart defects. This study also identified an association between stretch marks and a variant in the SRPX gene, but more work is needed to understand how this could play a role in this condition.
Our researchers are continuing to work on the study looking at possible associations in non-European populations.
You can read more on this study <a href="https://www.jidonline.org/article/S0022-202X(15)36019-X/fulltext">here</a>.

23andMe Blog

23andMe Blog Team

Genetics found to influence likelihood of stretch marks

By Nick Furlotte and Shirley Wu
For many of us, the battle of the bulge is more like an all-out war.
We all know people who can eat whatever they want, not work out, and yet not gain a pound. Meanwhile, eating just one burger, or missing just one cardio session, can weigh much more heavily on others (pun intended).  No doubt many of the differences we observe in weight gain and its relation to food intake and exercise are due to genetics.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-19018" src="https://blog-api.23andme.com/wp-content/uploads/2013/08/Scale-300x282.jpg" alt="Scale" width="300" height="282" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/08/Scale-300x282.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/08/Scale.jpg 357w" sizes="auto, (max-width: 300px) 100vw, 300px" />
At 23andMe we are very interested in identifying the genetic components that contribute to these differences between individuals. So we assessed people’s food and exercise habits, their physical characteristics (like whether they are “apple” or “pear” shaped), and we compared these answers to genetic data for tens of thousands of customers with European ancestry.
<h6>How do fast food and exercise affect weight on average?*</h6>
In our customers, a man of average height (5’9), average age (35) and European ancestry weighs about 180 pounds (corresponding to a body mass index (BMI) of 26.5, lower than the<img loading="lazy" decoding="async" class="alignright size-medium wp-image-19022" src="https://blog-api.23andme.com/wp-content/uploads/2013/08/WeightByGRS-female-300x195.jpg" alt="WeightByGRS-female" width="300" height="195" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/08/WeightByGRS-female-300x195.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/08/WeightByGRS-female.jpg 631w" sizes="auto, (max-width: 300px) 100vw, 300px" />
The story is similar for the average height and average aged woman (5’4 and 35 years old) with European ancestry, who weighs about 145 pounds (a BMI of 24.8, much lower than the U.S. average of 29).  She will weigh about eight pounds less if she exercises once or twice a week, but will weigh three pounds more if she also eats fast food once or twice a week.
<h6>Why you should care if you’re apple or pear</h6>
None of this is surprising — exercise leads to lower weight on average while eating fast food leads to higher weight on average.  But it turns out that body type makes a difference.
In our customers, men with pear and apple body types weighed more if they ate fast food occasionally while men with a neutral body type weighed less with the same fast food intake. For women, having an apple shape is associated with a higher average weight (around 155 pounds) but there is very little difference in weight due to occasional fast food intake between the different body types.
Just don’t go overboard: women who ate fast food nearly every day tended to weigh about 20 pounds more than the average, and this went up by an additional six pounds for women with apple or pear shapes.
<h6>More reason to exercise</h6>
We all burn calories while we’re just sitting around, but wouldn’t it be great if you could burn more? It all depends on your “metabolic rate”, or how much energy (calories) your body uses while resting, and you can actually increase your metabolic rate by exercising regularly.
In 23andMe customers, we see this play out in the fact that physical activity level affects the degree to which fast food consumption impacts weight.  For example, an average man who eats fast food once or twice a week who also works out five to seven times a week weighs five pounds less than a man eating the same amount of fast food who does not work out at all. The story is similar for women: eating fast food and not exercising is associated with weighing 10 pounds more than average, while those who ate the same amount of fast food but also exercised frequently weighed only seven pounds more.
Of course, the difference in weight might not be due just to exercise frequency. People who exercise might also be doing other things that lead to lower weight, including eating a healthier diet overall. But the fact that exercise raises the metabolic rate makes it a plausible explanation.
<h6>Adding genetics to the picture</h6>
So how do our genetics influence all of this?    We know that certain genetic factors predispose to obesity while others may protect against it. But a recent study published in<a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1003607"> PLOS Genetics</a> adds a twist. The researchers showed that a set of 12 genetic factors known to be associated with obesity had less of an effect in people who exercised more and a larger effect in people who did not exercise as often.
We examined the same idea using the data from our customers and found similar results.  In women who do not exercise, the genetic risk factors were associated with weighing 1.4 pounds more than average, while women who exercised weighed only 0.75 pounds more for each risk factor.  In other words, lifestyle may actually influence the effect our DNA has on our weight.
As the size of the weight loss industry attests, weight and obesity are very challenging problems. But with more data, we’ll be able to unravel the relationship between food intake, exercise, genetics, and weight gain even more, hopefully leading to more personalized and effective healthy weight strategies.
* Analyses of average weight controlled for age, exercise frequency, fast food intake, and ancestry substructure.

Nick Furlotte

The Genetics of Bellies and Burgers

<img loading="lazy" decoding="async" class="aligncenter wp-image-18480 size-full" src="http://35.88.189.111/wp-content/uploads/2013/06/AA-Menarche--scaled.jpg" alt="" width="2560" height="1978" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--scaled.jpg 2560w, https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--300x232.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--768x593.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--1024x791.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--880x680.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2013/06/AA-Menarche--1180x912.jpg 1180w" sizes="auto, (max-width: 2560px) 100vw, 2560px" />By Anne Pinckard
The high rates of <a href="https://blog.23andme.com/ancestry/african-ancestry-and-risk-for-type-2-diabetes/">type 2 diabetes</a> in some minority communities as well as the rates for <a href="https://blog.23andme.com/23andme-research/ethnicity-matters-in-research-a-case-study-in-prostate-cancer/">prostate cancer</a> among African American men are a good illustration of how a person’s risk for a disease can depend on ancestry.
The problem is scientists haven’t done enough research in minority communities to be able to learn just how much of a role ancestry plays in the development of those and other diseases. While some of the differences in risk may be due to environment and lifestyle, it’s a good bet that genetics also plays a role.
A recent study highlights why it’s so important to conduct ancestry-specific research, and why research findings are difficult to apply across different ethnicities. In this case, scientists were investigating the genetic influences of breast cancer in African-American women.
Most of the genetic factors linked to breast cancer were discovered among women of European and Asian ancestry. But African American women not only have higher rates of breast cancer, but they are 40 percent more likely to die from the disease than women of European ancestry. African-American women also tend to be diagnosed at a younger age and are more likely to experience the more aggressive types of the disease. While there may be many factors involved in these differences, including access to early screening and quality care, understanding the role genetics may play in these differences is also important.
The study, titled <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0058350">“Evaluating Genome-Wide Association Study-Identified Breast Cancer Risk Variants in African-American Women” </a>  and published by the peer-reviewed journal <a href="http://www.plosone.org/">PLOS One</a>, claims to be the first to examine all the known breast cancer genetic markers in African-American women. The international team of scientists looked at 67 genetic variants associated with breast cancer in women of Asian and European ancestry. This is the first study to investigate how relevant these variants are in African-American women, say the researchers. To find out, they tested the DNA of about 1200 African-American women diagnosed with breast cancer and 2,000 African-American women who served as a control group.
What researchers found was that only about 10 percent of the genetic markers associated with breast cancer in women of Asian and European ancestry were found to have significant associations with breast cancer in African American women. In that group of genetic markers associated with breast cancer among African American women, researchers found one that is linked to one of the more aggressive types of breast cancer – known as estrogen receptor (ER)-negative breast cancer. This type of breast cancer is also much more prevalent among African American women.
The findings also mean, of course, that 90 percent of the markers associated with breast cancer in European-and Asian-American women aren’t necessarily linked to the disease in African-American women. This conclusion is consistent with results from previous studies.
But the new study underscores the complexity of applying previous research to a specific population, and the need for more large-scale studies on African-American women.

More Diversity Needed in Genetic Research

New rules issued by the US Food and Drug Administration earlier this month mean we may finally know what it means when a label on food we buy says “Gluten-Free.”<img loading="lazy" decoding="async" class="alignright size-medium wp-image-8468" src="https://blog-api.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall-300x199.jpg" alt="Flour wheat celiac" width="300" height="199" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall-300x199.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />
The new standards are hugely important for the more than 3 million Americans with celiac disease as well as many others who for other reasons may need to avoid gluten.
Gluten, a protein found in wheat, triggers a mistaken immune response in those with <a href="http://www.celiacdiseasecenter.org/">Celiac</a>. This in turn can damage the lining of the small intestines and undermine the absorption of nutrients, ultimately causing symptoms that range from stomachaches to diarrhea and iron deficiency.
For those without Celiac who are also trying to avoid gluten – namely people who have allergies to wheat or simply a gluten intolerance – <a href="https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm">the new standards</a> are also important.
Now anyone buying food with a “gluten-free” label, knows that means that to get that label the food must contain less than 20 parts per million of gluten.

New Standards Regulating Gluten Labeling

<img loading="lazy" decoding="async" class="alignnone size-large wp-image-18943" src="https://blog-api.23andme.com/wp-content/uploads/2013/08/psoriasis-graphic-700x440.jpg" alt="psoriasis graphic" width="700" height="440" />For the live-updated, fully-labelled, interactive version of this infographic, <a href="http://curetogether.com/psoriasis/ig/treatment-effectiveness-vs-popularity">click here</a>.
By Alexandra Carmichael, Co-Founder of CureTogether
People living with Psoriasis have reported that some of the most effective treatments for their skin include simple interventions like sunlight, salt water, and avoiding stresses. 
<img loading="lazy" decoding="async" class="alignright size-full wp-image-3290" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/itchy.jpg" alt="itchy" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/itchy.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/04/itchy-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" /> 
This is according to a new study by CureTogether, a free resource owned by 23andMe that allows people to share information about their health and treatments.
Psoriasis is one of the most prevalent autoimmune disorders in the United States, affecting an estimated seven million Americans and 125 million worldwide. The condition is characterized by patches of itchy, scaly skin. In its mild form, psoriasis may be just a nuisance, but severe cases can be both painful,   disfiguring and debilitating.
Finding the right treatment can be difficult, so CureTogether asked people living with Psoriasis to rate the effectiveness of 34 different patient-reported treatments.
Participants in the study said they found that phototherapy, cortisone injections, swimming in the ocean, and sunlight were among the most effective, in addition to avoiding stress and triggers and the medications Dovonex and T-Gel. Conversely some common treatments such as oatmeal baths, Epsom salts, and Vitamin D, were among the least effective, according to the study.
<div style="float: right; text-align: justified; width: 200px; background-color: #eee; padding: 15px; margin-left: 10px;">
Most Effective Rated Treatments for Psoriasis 
1. UVB Phototherapy 
2. Cortisone injection 
3. Salt water/ocean 
4. Sunlight 
5. Topical corticosteroids 
6. Avoid triggers 
7. Avoid stress 
8. Dovonex 
9. UVA Phototherapy 
10. T-Gel
</div>
Where did this data come from? This is the result of a four-year CureTogether study on <a href="http://curetogether.com/psoriasis/symptoms/">Psoriasis</a>, in which 275 people living with the condition shared information about their symptoms and what treatments worked best for them. We’d like to thank those who participated. And just as they shared their experience with treatments, we’re freely and openly sharing the results of the Psoriasis study.
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.
Please tweet, blog, or pass this along to anyone who can benefit or is interested in Psoriasis. Thank you!
<div style="background-color: #ffc; padding: 10px; margin-top: 5px; margin-bottom: 15px; border: 1px solid #ccc;"><img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="small_23andMe_logo" width="24" height="40" />Your Genetic Risk for Psoriasis 
23andMe Customers can view their results for three gene variants that affect their risk for psoriasis here. Not yet a member? <a href="https://www.23andme.com/store/cart/http://" target="_blank" rel="noopener noreferrer">Visit our store</a>!</div>

Alexandra Carmichael

What Patients Say Works for Psoriasis

The New Yorker recently described the artist Laurel Nakadate as an “unpredictable, sometimes infuriating young photographer.”
Perhaps. But whatever description you use, the images she creates are singularly arresting.
In her latest series of portraits – called “Strangers and Relations”  – she turned to her 23andMe DNA relative matches for inspiration.
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2013/07/LN_Suki_Dhanda_Portrait_LR-225x300.jpg" alt="Laurel Nakadate. Photo: © Suki Dhanda, 2011, Courtesy Leslie Tonkonow Artworks + Projects, New York" class="size-medium wp-image-18738" width="225" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Suki_Dhanda_Portrait_LR-225x300.jpg 225w, https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Suki_Dhanda_Portrait_LR-660x880.jpg 660w, https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Suki_Dhanda_Portrait_LR.jpg 768w" sizes="auto, (max-width: 225px) 100vw, 225px" /> Laurel Nakadate. Photo: © Suki Dhanda, 2011, Courtesy Leslie Tonkonow Artworks + Projects, New York
Laurel, who was born in Texas but raised in Iowa, is of primarily Japanese and European ancestry. But what that meant didn’t really come to life for her until she opened her  23andMe results and saw  the melange of ancestry among her relatives not only on her mother&#8217;s side, but with all the distant relations she found through 23andMe.
“It did surprise me,” she said. &#8220;My mom&#8217;s family always said we were primarily English, Irish and Scottish, but I was delighted to learn that we are also part African.&#8221;
Laurel was struck by the idea that these people who were strangers to her were also connected to her by a common distant relative. And it was that incongruous mix of the familiar and foreign that spurred Laurel on her project to document these people to whom she was related. It turned into a 37,000-mile journey in which she crisscrossed the United States to photograph those distant cousins.
<div style="float: right; text-align: justified; width: 275px; background-color: #eee; padding: 10px; margin-left: 10px;">An Upcoming solo exhibit of Laurel Nakadate work: &#8211; Laurel Nakadate: Strangers and Relations University Art Gallery, Sewanee: The University of the South, Sewanee, TN February &#8211; April 2014 Upcoming group exhibits that include Laurel’s work: &#8211; Damage Control: Art and Destruction Since 1950 Hirshhorn Museum and Sculpture Garden, Washington, D.C. October 24, 2013 — February 9, 2014 &#8211; Dis-semblance: Perceiving and Projecting Identity Today 21c Museum, Cincinnati, OH July &#8211; December, 2013</div>
These were all relatives she found on her maternal line. In each case she connected with them through 23andMe, which allows you to connect to your relative “matches” if both parties wish to make that connection. In Laurel’s case she made contact and sent messages explaining what she was doing and asked the people who were matched with her if they would be interested in participating. Quite a few welcomed the opportunity. As she fanned out across the United States, Laurel not only got to take photographs she also learned a little bit about their shared family history.
The portraits – all outdoors, all at night with people standing alone and lit-up by a flashlight – are all taken from a distance. The photos feel both distant and intimate – with the subjects wearing everything from what looks like a fake fur coat, to camouflage hunting gear, to a doctor’s white coat. One reviewer described the mix of photos as &#8220;a collected portrait of America.&#8221;
If you have the chance, you should check out the exhibit.
23andMe provides genetic testing services for informational purposes; your results may or may not help you to search for or identify relatives or family members.

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			</dt>
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				Kalispell, Montana #1, 2013 © Laurel Nakadate, Courtesy Leslie Tonkonow Artworks + Projects, New York
				</dd></dl><dl class='gallery-item'>
			<dt class='gallery-icon landscape'>
				<img loading="lazy" decoding="async" width="150" height="150" src="https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Relations_Cleveland_MG_9246_LR-150x150.jpg" class="attachment-thumbnail size-thumbnail" alt="" aria-describedby="gallery-1-18731" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Relations_Cleveland_MG_9246_LR-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Relations_Cleveland_MG_9246_LR-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Relations_Cleveland_MG_9246_LR-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2013/07/LN_Relations_Cleveland_MG_9246_LR-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
			</dt>
				<dd class='wp-caption-text gallery-caption' id='gallery-1-18731'>
				Cleveland, Ohio #1, 2012 © Laurel Nakadate, Courtesy Leslie Tonkonow Artworks + Projects, New York
				</dd></dl> 
		</div>

Strangers and Relations

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-18816" src="https://blog-api.23andme.com/wp-content/uploads/2013/07/Google-Doodle-300x200.jpg" alt="Google Doodle" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/07/Google-Doodle-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/07/Google-Doodle.jpg 600w" sizes="auto, (max-width: 300px) 100vw, 300px" />Francis Crick and James Watson might not have been able to describe the iconic double helix structure of DNA more than 60 years ago, if it hadn’t been for <a href="http://www.csmonitor.com/Innovation/Tech-Culture/2013/0725/Google-Doodle-How-Rosalind-Franklin-photographed-DNA">Rosalind Franklin</a>, who was honored today in a <a href="https://www.google.com/">Google Doodle.</a>
Franklin, who would have turned 93 today, took an x-ray image that helped Watson and Crick as they were working on what became a seminal paper in Nature. She died just five years later. Crick, Watson and a co-worker of Franklin’s, Maurice Wilkins, were awarded the Nobel Prize in 1962.

R-E-S-P-E-C-T

<img loading="lazy" decoding="async" class="aligncenter wp-image-18756 size-full" src="http://35.88.189.111/wp-content/uploads/2013/07/Fibromyalgia-Graphic.jpg" alt="" width="925" height="601" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/07/Fibromyalgia-Graphic.jpg 925w, https://blogcms.23andme.com/wp-content/uploads/2013/07/Fibromyalgia-Graphic-300x195.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/07/Fibromyalgia-Graphic-768x499.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2013/07/Fibromyalgia-Graphic-880x572.jpg 880w" sizes="auto, (max-width: 925px) 100vw, 925px" />For the live-updated, fully-labelled, interactive version of this infographic, <a href="http://curetogether.com/fibromyalgia/ig/treatment-effectiveness-vs-popularity">click here</a>.
By Alexandra Carmichael, Co-Founder of CureTogether 
In a surprising finding, patients who live with the painful disorder fibromyalgia have reported that commonly prescribed drugs for this condition actually make their symptoms worse. This is according to a new study by CureTogether, a free resource owned by 23andMe that allows people to share information about their health and treatments.
People in the study said they found that lifestyle changes like rest, heat, and various ways of reducing stress offered the most effective relief. In addition many of those surveyed said that the drug Naltrexone at a low dose worked well. Conversely, well-known fibromyalgia drugs such as Lyrica, Savella, Cymbalta, and Effexor, were reported to worsen rather than improve patients’ symptoms, according to the study.
<div style="float: right; text-align: justified; width: 200px; background-color: #eee; padding: 15px; margin-left: 10px;">
Most Effective Rated Treatments for People with Fibromyalgia 
1. Low-dose Naltrexone (LDN) 
2. Rest 
3. Hot showers/baths 
4. Heating pads 
5. Getting enough sleep 
6. Hydrotherapy 
7. Vicodin 
8. Reduce stress 
9. Meditation 
10. Gluten-free diet
</div>
Fibromyalgia affects at least 5 million Americans, according to the Centers for Disease Control. The disorder is characterized by musculoskeletal pain, and other symptoms including fatigue, disrupted sleep, as well as depression. Researchers believe that fibromyalgia amplifies painful sensations by affecting the way a patient’s brain processes pain signals. The condition is poorly understood,, so finding accurate recommendations on treatments can be challenging.
In the CureTogether study, researchers asked 1,401 people suffering from <a href="http://curetogether.com/fibromyalgia/symptoms/">fibromyalgia</a>  to rate the effectiveness of 104 different treatments. Participants shared information about their symptoms as well as what treatments worked best for them. We’d like to thank those who participated. And just as they shared their experience with treatments, we’re freely and openly sharing the results of the Fibromyalgia study.
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.
Please tweet, blog, or pass this along to anyone who can benefit or is interested in Fibromyalgia. Thank you!

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