<img loading="lazy" decoding="async" class="alignright size-full wp-image-1483" title="medicalscale" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/medicalscale.jpg" alt="" width="320" height="212" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/medicalscale.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/medicalscale-300x199.jpg 300w" sizes="auto, (max-width: 320px) 100vw, 320px" />
The connection between <a href="http://www.cancer.gov/cancertopics/factsheet/risk/obesity" target="_blank" rel="noopener">obesity and cancer</a> is well established. As many as 25 to 30 percent of several major cancers — colon, breast (postmenopausal), endometrial, kidney, and esophagus — may be accounted for by obesity and physical inactivity. Some studies have also found links between obesity and cancers of the gallbladder, ovaries, and pancreas.
It is not yet clear to scientists, however, how obesity increases the risk for certain cancers. Part of the answer may lie in a hormone released by fat cells &#8212; adiponectin. Decreased blood levels of this hormone, which are found in obese people, have been <a href="https://www.ncbi.nlm.nih.gov/pubmed/18265479?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">linked</a> with breast, endometrial, prostate and colon cancer.
A new study published today in the <a href="http://jama.ama-assn.org/cgi/content/full/300/13/1523" target="_blank" rel="noopener">Journal of the American Medical Association</a> provides further evidence for adiponectin being the link between obesity and cancer. Researchers have demonstrated that a variant in the gene that encodes the hormone influences the risk of developing colorectal cancer.
Kaklamani et al examined several SNPs in the adiponectin and adiponectin receptor genes in a total of 629 people with colorectal cancer and 855 people without the disease. All subjects except for 37 cases and 37 controls were of European ancestry. The researchers found that people with one or two Gs at rs266729 in the adiponectin gene had 27% lower odds of developing colorectal cancer compared to those with two Cs.
(23andMe customers can look up their data for rs266729 using the Browse Raw Data feature)
According to the report’s senior author, Dr. Boris Pasche, these research findings could help identify people who would benefit from increased colorectal cancer screening.

“Our hope is that we can significantly improve the screening and early detection for this disease, and open new avenues for better understanding the genetic and lifestyle factors that influence colon cancer risk, “ he said in a statement.
Pasche went on to caution that additional studies are needed to confirm whether those without the adiponectin variant that appears to protect people from colorectal cancer will benefit from cancer-prevention lifestyle changes such as diet and exercise.
A different variant in the adiponectin gene was recently identified as a <a href="https://www.ncbi.nlm.nih.gov/pubmed/18451143?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">modifier of breast cancer</a> risk in a study co-authored by Pasche. Understanding how variants in this gene influence breast and colorectal cancer risk, and whether the variants affect the risk for other cancers, will require more research.
Colorectal cancer is the second-leading cancer killer of Americans. According to estimates from the American Cancer Society, 149,000 people will be diagnosed with the disease and 50,00 will die this year alone.

23andMe Blog

23andMe Blog Team

Genetic Link Between Obesity and Colorectal Cancer

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1447" title="heartpills" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/heartpills.jpg" alt="" width="350" height="231" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/heartpills.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/heartpills-300x198.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Researchers are sometimes frustrated when a prospective drug proves effective in some patients, but not enough to justify giving it to everyone who has the condition it is intended to treat.
The beta-blocker drug bucindolol met that fate in 2001 when it was originally tested as a treatment for heart failure. Though it did help a fraction of the 2,708 patients in the study, it didn&#8217;t improve the condition of enough patients to be approved for the market.
But <a href="https://online.wsj.com/article/SB122212399407465005.html?mod=googlenews_wsj">now</a> researchers have rescued bucindolol from the pharmaceutical dustbin by identifying a genetic variation that increases a person&#8217;s chances of benefiting from the drug. Researchers collected DNA samples from 1,040 patients who were involved in the original study, and found that genetics plays a significant role in determining its effectiveness. In light of the discovery, the company that owns the drug, <a href="http://www.arcabiopharma.com/">ARCA biopharma</a>, has <a href="http://www.fiercebiotech.com/press-releases/bucindolol-significantly-reduces-hospitalization-and-death-heart-failure-patients-v-0">applied to the FDA</a> for approval to sell it.

The most important gene in determining bucindolol&#8217;s effectiveness is ADRB1, which is not surprising – the gene is involved in activating the &#8220;fight or flight&#8221; response to the hormone adrenaline. Beta-blocker drugs such as bucindolol suppress that response, protecting a weak heart from the strain that an adrenaline response produces.
It appears that bucindolol blocks adrenaline&#8217;s effects only if a person has a particular form of the ADRB1 gene. Among those people, bucindolol decreased the risk of death from heart-related causes 48%.
23andMe customers can determine whether they have the form of ADRB1 that responds to bucindolol by checking their genotypes at the SNP rs1801253; the CC genotype is the responsive form of the gene. 23andMe customers and demo account holders can also read more about bucindolol in the Beta-blocker Response section of My Health and Traits.
Until now, the vast majority of drugs prescribed on the basis of genetics have been for cancer – and their effectiveness has mostly depended on the genetics of the tumor rather than the patient. But the bucindolol story illustrates the broader promise of genetic information for drug developers, physicians and patients. The hope is that eventually, understanding how genetic variations influence the effectiveness of drugs and their side effects will usher in a new era of personalized medicine.

Biotech Company Applies for FDA Permission to Market Gene-Targeted Heart Failure Drug

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1439" title="istock_000003087995xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/istock_000003087995xsmall.jpg" alt="" width="366" height="328" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000003087995xsmall.jpg 366w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000003087995xsmall-300x269.jpg 300w" sizes="auto, (max-width: 366px) 100vw, 366px" />
What is it about humans that distinguishes us from the rest of the animal kingdom?   Is it our upright walking?   Our language?   Our love of Reality TV?   Even though we are said to be 99% genetically identical to our closest evolutionary relative, the chimpanzee, we clearly differ vastly from them physically and behaviorally.
For many years, scientists have attempted to understand how our species came to be so different from any other on the planet.   In the October issue of <a id="ikcg" title="Nature Reviews Genetics" href="https://www.nature.com/nrg/journal/v9/n10/abs/nrg2428.html" target="_blank" rel="noopener noreferrer">Nature Reviews Genetics</a>, scientists at the UCLA and the Howard Hughes Medical Institute examine recent research to understand how genetic mutations have set us apart from our nearest relatives. In addition, they discuss how these genetic changes relate to the vast array of physical and behavioral differences that also have to be considered to fully understand what makes our species so unique.
<h6> 
The 1% Difference</h6>
The authors begin their examination of human uniqueness by focusing on the overall genetic differences between our species and chimpanzees.   Many years ago, research revealed that humans and chimpanzees are remarkably similar in terms of both genetic and biochemical structure.   Scientists hypothesized that because the two species are so structurally similar, the differences between humans and chimps would turn out to be primarily in the way that genes — and therefore proteins — are expressed.   Further analysis confirmed that there is only a 1% difference in overall genetic and biochemical structure between the two species – a number many people still cite today.
However, the authors argue that more recent analysis has actually shown that deletions and duplications of DNA in both species bring the genetic difference between the two to about 4% across the entire genome.   These and other findings have, according to the authors, “dashed the hope that it would be simple to determine the key genetic differences between humans and closest evolutionary relatives, that is, the genomic aspects of ‘what makes us human’ ”.
Yet many recent breakthroughs in comparative genomics have identified human genetic features that may be unique.   Below are two examples:
<h6>MYH16</h6>
One key difference between humans and chimpanzees is the difference in brain size.   Humans have an average brain volume of about 1500 cm3, which is roughly three times the size of a chimp&#8217;s.   While having a comparatively large brain was one of the most important factors in the evolution of our species, it has also resulted in an organ that is very expensive to maintain.   In fact, many anthropologists have argued that in order for our large brains to have evolved, there must have been a simultaneous reduction in the size of other organ systems and muscle mass.
In 2004, scientists discovered a gene, MYH16 that may have been involved in that trade-off between increased brain size and decreased muscle mass.   Believed to be related to the growth of muscles in the jaw of chimpanzees and other apes, MYH16 has been mutated in humans so it remains switched off.   Scientists hypothesize that the gene&#8217;s lack of expression in humans causes an eight-fold reduction in the size of muscle fibers in the human jaw.   Interestingly, the timing of this mutation appears to have happened about 2 million years ago, when Homo erectus — the first of our fossil ancestors to exhibit a significant increase in brain size, evolved in Africa.
<h6>FOXP2</h6>
Sometimes referred to as &#8220;the language gene,&#8221; FOXP2 made a splash in the popular media when it was first described in 2002, because a very slight mutation in the human version is believed by some to have led to the evolution of language in humans.
FOXP2 is not unique to humans.   In fact, many species — including songbirds and alligators — have the gene, which is required for proper brain development.   Though the human FOXP2 gene is slightly different, it has been found to be related to vocal learning in birds, and may even be tied to the evolution of echolocation in bats.
In addition, new research has suggested that it may not be the FOXP2 gene itself, but rather a related genetic pathway, and it is that related gene that may be involved in the evolution of speech and language development in humans.   At the moment the exact relationship between FOXP2 and human language remains unresolved – an illustration of the genome&#8217;s complexity.
<h6>Genotype vs. Phenotype</h6>
The authors conclude their review by proposing a method of examining human uniqueness from a genomic perspective in light of the fact that “traditional evolutionary biology approaches have yet to explain most of the unique features of humans.”   They argue that in order to move the field of evolutionary genomics forward, and to truly understand what it means to be ‘human,’ there must be more of an effort to connect changes at the genetic level (our genotype) to changes at the physical level (our phenotype).   Interestingly, questions of the relationship between genotype and phenotype form the cornerstone of 23andMe’s research arm, <a id="t3pm" title="23andWe" href="https://www.23andme.com/research/" target="_blank" rel="noopener noreferrer">23andWe</a>.
Finally, the authors argue that it will take scientists from a variety of disciplines — developmental biology, genetics, anthropology, anatomy, sociology, and many others — to fully examine the myriad of ways in which humans are set apart from our closest relatives.   It is at this point, the authors conclude, that we will fully understand what it means to be ‘human.’

What it Means to be Human

Already well-known for expanding technological frontiers, Google co-founder Sergey Brin is now pushing the boundaries of personal genomics with a remarkable post on his new personal blog, <a href="http://too.blogspot.com">TOO</a>.
In the post, Brin shares information from his 23andMe account that indicates he is at substantially increased risk for Parkinson&#8217;s Disease. Brin&#8217;s mother, who has already been diagnosed with the disease, has the same genetic mutation.
The mutation in question is in a gene known as LRRK2 on chromosome 12. The single-letter change in the DNA code dramatically increases a person&#8217;s odds of developing Parkinson&#8217;s from one or two in a hundred to as much as eight in 10.
One recent <a href="http://www.thelancet.com/journals/laneur/article/PIIS1474442208701170/abstract" target="_blank" rel="noopener">study</a> found that a person who inherits the mutation has a 28% chance of developing Parkinson&#8217;s by the age of 59, 51% by the age of 69 and 74% by the age of 79.
It&#8217;s sobering to hear this news about someone so closely affiliated with our company (Sergey is married to Anne Wojcicki, one of our co-founders). But we&#8217;re encouraged too, because Sergey&#8217;s post also illustrates the benefit that comes with having access to your genetic information – and the power of sharing it. As Sergey says: 

<blockquote>&#8220;I now have the opportunity to adjust my life to reduce those odds (e.g. there is evidence that exercise may be protective against Parkinson&#8217;s). I also have the opportunity to perform and support research into this disease long before it may affect me. And, regardless of my own health it can help my family members as well as others.&#8221;</blockquote>
There are a number of LRRK2 mutations that substantially increase Parkinson&#8217;s risk. The one Brin has, which is known as G2019S, is most commonly found among people of Ashkenazi Jewish and North African descent. It has occasionally been found in some non-Jewish European populations, but is virtually unknown in East Asia. Any customers who want to know their LRRK2 G2019S status now can find out by using the 23andMe <a href="https://www.23andme.com/you/explorer/">Genome Browser</a> to search for their genotype at the SNP .
Having one or two copies of the A version of this SNP substantially increases a person&#8217;s chances of developing Parkinson&#8217;s Disease. Our upcoming Parkinson&#8217;s Disease entry will offer much more complete information about the significance of having or not having the G2019S mutation. In the coming weeks and months we plan to provide much more information about Parkinson&#8217;s and many other diseases, conditions and traits that are affected by genetics. We hope that like Sergey, you&#8217;ll want to join us on this exploration of the genetic frontier.

A image of double helix showing a variant

Google Co-Founder Blogs About 23andMe Data, Parkinson’s Risk

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1414" title="istock_000001804366xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall.jpg" alt="" width="266" height="265" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-271x271.jpg 271w" sizes="auto, (max-width: 266px) 100vw, 266px" />
A special supplement to Nature Reviews Genetics, published online today, details how four countries with emerging economies are building capacity for human genomic variation.  
The study looks at Mexico, India, Thailand, and South Africa and steps scientists there are taking to build capacity for genomics and its applications to healthcare.
Following the completion of the HapMap Project, several consortiums in the developed world have undertaken large-scale genotyping projects. The hope is that these efforts will lead to advances in personalized diagnostics and therapeutics that could one day improve health outcomes.
The authors of the six-part series, all from the McLaughlin-Rotman Centre for Global Health (MRC) in Toronto, conclude that similar initiatives in genomic medicine have great potential to help developing countries by strengthening local research infrastructure and local intellectual property regimes, addressing local health needs and reducing health-care costs.

(The reports are <a href="https://www.nature.com/nrg/journal/v9/n10_supp/index.html" target="_blank" rel="noopener noreferrer">available</a> free of charge from Nature Genetics with registration)

The highlighted initiatives:
<ul>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2442" target="_blank" rel="noopener noreferrer">Mexico</a></h6>

Mexico has formed the National Institute of Genomic Medicine (INMEGEN), the first Mexican institute to systematically describe the genomic diversity of the Mexican population. INMEGEN will allow Mexico to focus on the link between genomic variation in the Mexican population, disease susceptibility and drug-response variability.</li>
<li>
<h6><a href="https://dx.doi.org/doi:10.1038/nrg2440" target="_blank" rel="noopener noreferrer">India</a></h6>

The Indian Genome Variation (IGV) database is a collaborative network that will capture essential data about disease predisposition, adverse drug reactions (ADRs) and population migration within India.</li>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2443" target="_blank" rel="noopener noreferrer">Thailand</a></h6>

The Thai SNP Discovery Project and the Thai Centre for Excellence in Life Sciences Pharmacogenomics Project will help Thailand understand the genomic diversity of its population and explore the role that this diversity has in drug response and disease susceptibility.</li>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2441" target="_blank" rel="noopener noreferrer">South Africa</a></h6>

The South African government is in the early stages of planning a national genomic medicine research program. Public engagement in genomic issues is spear-headed by The Africa Genome Education Institute.</li>
</ul>
“The world has reached a historic moment on the path to genomic medicine — the point where theory is about to be translated into practice,” said the project’s principal investigator, Professor Abdallah Daar, in a statement.
“Benefits of this emerging science cannot be an exclusive luxury reserved for wealthier industrialized countries. Instead, it must be universally advanced by developed and developing countries alike to prevent an increased widening of an already huge difference in global health care quality,” said the project leader.

New Study Looks at Progress and Potential for Genomic Medicine in Developing Nations

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1400" title="bloodclot" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/bloodclot.jpg" alt="" width="303" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/bloodclot.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/bloodclot-300x223.jpg 300w" sizes="auto, (max-width: 303px) 100vw, 303px" />
This Monday acting Surgeon General Steven K. Galson issued a Call to Action to reduce the number of people in the United States affected by two serious blood clotting conditions: deep vein thrombosis and pulmonary embolism.
<h6>DVTs &amp; PEs</h6>
Deep vein thrombosis (DVT), sometimes called “<a href="https://www.ncbi.nlm.nih.gov/pubmed/2900413?dopt=Abstract" target="_blank" rel="noopener noreferrer">economy class syndrome</a>” is the formation of a blood clot in a vein deep within the body, usually in the legs. Pulmonary embolism (PE) occurs if the clot breaks free and travels through the circulatory system to the lungs. Together these two conditions affect an estimated 350,000 to 600,000 Americans each year and contribute to at least 100,000 deaths.
&#8220;Deep vein thrombosis and pulmonary embolisms are often &#8216;silent&#8217; conditions – they can occur suddenly and without symptoms,&#8221; Galson said in a statement. &#8220;But we have made a lot of progress in understanding how these disorders develop and how to prevent, diagnose, and treat them. It&#8217;s time to put this knowledge into action.&#8221;
<h6>Factor V Leiden</h6>
Researchers have found that DVT and PE usually develop in response to a triggering event — being hospitalized or confined to bed rest, having major surgery, suffering a trauma, or traveling for several hours &#8212; in people who either have an inherited predisposition to blood clotting disorders or another risk factor.
Having the riskier version of one or both of the SNPs 23andMe reports data for (<a href="http://circ.ahajournals.org/cgi/content/full/107/15/e94" target="_blank" rel="noopener noreferrer">Factor V Leiden</a> and Prothrombin 20210) significantly increases the risk of developing DVT or PE. An estimated 15 to 20 percent of DVT/PE patients have the Factor V Leiden mutation, while 6 percent have the Prothrombin 20210 mutation.
<h6>Risk</h6>
The average risk of DVT/PE in people between the ages of 40 and 59 (anyone can be afflicted, but the risk does increase with age) is 2.5%. But in those people in this age group who inherit a copy of the Factor V Leiden mutation, the risk jumps to 11%. Having one copy of the Prothrombin 20210 mutation raises the risk to 8.8%. In the unlucky few who have one copy of each of these mutations, the risk is a 32%. And in the extremely rare case that someone inherits two copies of both mutations, the risk of DVT/PE is 69%.
(This information applies only to those with European ancestry. Average risk numbers are different for other groups, and the genetic risk factors discussed here are not usually found in people with African or Asian ancestry.)
Other risk factors for DVT and PE include being overweight or obese, cancer and its treatment, pregnancy, and childbirth, use of hormones for birth control or menopause, and smoking.
“We want to increase the awareness and knowledge of these potentially deadly conditions and encourage patients and health care providers to take the steps to prevent them,” Galson said.
For more information:
<ul>
<li>Surgeon General’s Fact Sheet on Deep Vein Thrombosis and Pulmonary Embolism</li>
<li>The Coalition to Prevent Deep-Vein Thrombosis</li>
<li><a href="http://www.ahrq.gov/consumer/bloodclots.htm" target="_blank" rel="noopener noreferrer">Patient</a> and <a href="http://www.ahrq.gov/qual/vtguide/" target="_blank" rel="noopener noreferrer">Provider</a> Guides from the Agency for Healthcare Research and Quality (also available in <a href="http://www.ahrq.gov/consumer/spblclots.htm" target="_blank" rel="noopener noreferrer">Spanish</a>)</li>
</ul>

Surgeon General Issues Call to Action on VTE: 23andMe Assesses Genetic Risk for Customers

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This is Fashion Week in New York City, a twice-yearly spectacle where designers, models, celebrities, and the merely style-obsessed meet to consider next season&#8217;s top looks. 23andMe managed to lure a few hundred people away from the catwalks Tuesday night to consider the beauty that lies within – DNA.
Our Fashion Week spit party was sort of like a Tupperware party, except instead of buying plastic containers the guests were invited to deposit a saliva sample into one. And instead of taking place at a suburban ranch house designed by Richard Neutra, our spit party went down at the spectacular Manhattan headquarters of IAC/InterActiveCorporation, designed by architect Frank Gehry. The building resembles white curtains billowing in a fresh breeze off the Hudson River. Two gigantic high-resolution video walls line the lobby; the larger one is 118 feet long and 11 feet high.
23andMe team members were on hand to explain the features of our new v2 chip, our new community features. Guests also had the opportunity to purchase our Personal Genome Serviceâ„¢ and produce their saliva samples on the spot (but only if they&#8217;d waited the requisite 30 minutes after consuming an hors d&#8217;oeuvre).
You can see some photos <a href="http://www.zimbio.com/pictures/O2GXwQoazL6/23andMe+Spit+Party" target="_blank" rel="noopener noreferrer">here</a>, or click <a href="https://blog.23andme.com/2008/09/11/23andme-struts-its-stuff-in-nyc-during-fashion-week/#more-1316" target="_self" rel="noopener noreferrer">here</a> for a slide show with more party pics.

[minislides]
Photos by Monica De Armond

23andMe Struts its Stuff in NYC During Fashion Week

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1326" title="beer" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/beer.jpg" alt="" width="279" height="207" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/beer.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/beer-300x223.jpg 300w" sizes="auto, (max-width: 279px) 100vw, 279px" />
Just four simple ingredients &#8212; water, malt, hops, and yeast — go into making beer, a delicious and intoxicating brew that has been enjoyed for the past 6000 years.
The yeast not only ferments sugars into alcohol, but also affects the appearance, aroma and taste of a beer. It’s not surprising then that each brewery maintains it own unique yeast strains. These strains, however, can be broken down into two main types: ale yeasts and lager yeasts.
It’s been known for some time that lager yeast is a genetic mix of yeast species S. cerevisiae (the same species ale yeasts hail from) and another species, S. bayanus. But the results of a new Stanford study that will be published online Thursday in <a href="http://www.genome.org/cgi/doi/10.1101/gr.076075.108" target="_blank" rel="noopener noreferrer">Genome Research</a> are the first to show that this mixing of DNA actually happened twice during the history of lager, and that the strain of S. cerevisiae involved was an ale yeast both times.
“We were excited to find this connection, because it makes so much sense,” said Gavin Sherlock,one of the study&#8217;s authors, in a statement. “The same breweries were used for both ale and lager, so it was really gratifying.”
Lager beers are brewed at much cooler temperatures than ales (52-58 ° F vs. 64-70 ° F), a tradition that dates back to Bavarian brewers who stored their beer in icy caves in the Alps during the summer months.
“It’s possible that the ale strain provides a certain flavor profile, while the second strain conferred the ability to ferment at cooler temperatures,” said Barbara Dunn, the other study author, referring to the hybridization events that created lager yeasts.

“Mixing them together is a nice way for the yeast to double its genetic options.”
When the researchers looked at yeast descended from the two groups of lager yeast, they saw further variation between strains.
“The fact that lager yeasts isolated from different breweries each seem to have a unique genomic make-up may indicate that the yeasts are adapting to the conditions specific to each brewery,” explained Dunn.
“Our discovery that unique genomic structures may be characteristic of each brewery and/or beer type could lead to insights on how to directly control flavor and aroma in beer.”
That’s the kind of science we can all raise a glass to.

BEER! Now that we have your attention, a little science…

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1282" title="amish" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/amish.jpg" alt="" width="276" height="205" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/amish.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/amish-300x223.jpg 300w" sizes="auto, (max-width: 276px) 100vw, 276px" />
A good diet and plenty of exercise are important for maintaining a healthy weight, but they’re not the whole story. Studies have shown that there’s a substantial genetic component to body mass index. Research published today in <a href="http://archinte.ama-assn.org/cgi/content/short/168/16/1791" target="_blank" rel="noopener noreferrer">Archives of Internal Medicine </a>demonstrates, however, that in people with a genetic predisposition for obesity, DNA is not necessarily destiny.
Scientists studying about 700 Old Order Amish men and women in Pennsylvania found that SNPs in a gene called FTO were associated with being obese or overweight. These associations, however, applied only to people with low physical activity levels. In people categorized as highly active for their age and sex, their FTO variants didn’t make a difference.
The high and low activity groups differed by about 900 kcal/day in their energy expenditures &#8212; the equivalent of three or four extra hours of moderately intensive physical activity like brisk walking, house cleaning, or gardening. While this might seem like a lot of activity, the authors point out that it’s typical for the lifestyle of the Old Order Amish, who farm without the aid of modern machinery.
Additional research is needed to determine the lower bound of how much exercise is really needed to negate the effect of an FTO-related genetic predisposition to weight gain. And then comes the hard part — figuring out exactly how the FTO gene influences weight and why physical activity seems to modulate its effect.

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