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As the director of Britain&#8217;s <a href="http://www.well.ox.ac.uk/" target="_blank" rel="noopener noreferrer">Wellcome Trust Center for Human Genetics</a>, Peter Donnelly oversees research that provides vital raw material for the 23andMe Personal Genome Serviceâ„¢ – specifically, correlations between one-letter DNA variations, known as SNPs, and particular diseases.
Those correlations are made by research projects known as genome-wide association studies (GWAS), which scan the genomes of people with a disease and similar individuals who don&#8217;t, then look for statistically significant genetic differences between the two groups. The studies can be enormous – last year the Wellcome Trust <a href="https://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html" target="_blank" rel="noopener noreferrer">published</a> the results of a GWAS that analyzed data from 17,000 participants and found genetic associations with seven different diseases – coronary heart disease, type 1 diabetes, type 2 diabetes, rheumatoid arthritis, Crohn&#8217;s disease, bipolar disorder and hypertension.

In a commentary published this week by <a href="https://www.nature.com/nature/journal/v456/n7223/abs/nature07631.html" target="_blank" rel="noopener noreferrer">Nature</a>, Donnelly assessed what GWAS have been able to achieve so far, and argued that in most cases, people should be able to gain valuable information from having access to their own genomes.
Here&#8217;s Donnelly&#8217;s reasoning in his own words:
<blockquote>For a particular disease, most individuals will have inherited some sequence variants that confer risk and some variants that provide protection, and they will therefore have an overall risk around average. A small proportion of people, however, will have inherited mainly variants that confer risk of developing the disease. Using Crohn&#8217;s disease as an example &#8230; the top 5% of the UK population &#8230; have a 5–8-fold higher risk than average of developing the disease, whereas the top 1% have a 9–15-fold higher risk.</blockquote>
Using statistics from the US, that amounts to a risk increase from the poplation average of less than 0.5% to somewhere in the neighborhood of 4-7%. Performing the same calculations for type 2 diabetes, Donnelly concludes that 1% of the population would end up having a 4-fold risk increase, which amounts to about a 50/50 chance of developing the disease.
&#8220;Across 50 diseases,&#8221; Donnelly continues (23andMe provides complete estimates of lifetime genetic risk due to known SNPs for 10 common diseases),
<blockquote>making the simplifying assumption that susceptibility to each disease is independent of susceptibility to every other disease, almost everyone will be in the top 5% of risk for at least one disease, and nearly half of all people will be in the top 1% for at least one disease. &#8230; Given that it is possible to reduce the risk of developing certain diseases, I can see the value of knowing about the genetic risks now.</blockquote>

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Leading Geneticist Spells Out the Promise of Personal Genomics

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It seems simple enough: if you eat only as many calories as you burn, you won’t pack on the pounds. Yet for many, balancing this equation is anything but easy. Obesity has become one of the most significant public health threats facing the United States and other developed countries. One-third of adults in the United States today can be considered clinically obese.
While lifestyle choices are certainly important, research has shown that genetics plays a significant role in determining a person’s propensity for being overweight or obese. One especially potent variant in the FTO gene has been consistently linked with weight in Europeans.
In a study of Scottish children published online yesterday by the <a href="http://content.nejm.org/cgi/content/short/359/24/2558" target="_blank" rel="noopener">New England Journal of Medicine</a>, researchers suggest that this FTO variant may contribute to obesity by leading kids to chose foods that, pound for pound, pack a more powerful calorie punch. 
Seventy-six kids between the ages of four and 10, selected from a larger study of 2,726 children who were having their height, weight, and FTO genotypes evaluated, also had their energy expenditure and food intake measured.
There was no difference in the number of calories burned while at rest between children who carried the higher weight-associated version of FTO and those who did not. Energy burned due to physical activity was actually higher for carriers than non-carriers. This suggests that the FTO variant isn’t affecting the basal metabolism rate or conferring a proclivity for a sedentary lifestyle.
There was also no difference in the total weight of the food ingested by the kids with the version of FTO linked to obesity. But these children did consume more calories than their non-carrier friends. The foods they chose during the test meals had “higher energy density” &#8212; they contained more calories per unit weight.
The authors note that most obesity disorders caused by defects in single genes (such as MCR4) affect eating behavior. These new results, and those of other studies (a few examples <a href="https://www.ncbi.nlm.nih.gov/pubmed/19053021?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">here</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/18838977?ordinalpos=2&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">here</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/18583465?ordinalpos=3&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">here</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/18842783?ordinalpos=4&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">here</a>), show that the common FTO variant is no different. It is unclear, however, whether FTO affects appetite regulation or the ability to sense how much food has been ingested.
In an accompanying <a href="http://content.nejm.org/cgi/content/full/359/24/2603" target="_blank" rel="noopener">editorial</a> in NEJM, Dr. Rudolph Leibel says that although the proportion of obesity in the general population that can be attributed to variation in the FTO gene region is high, it’s probably still not enough to start using this SNP as a clinical screening tool.
But he goes on to say that in the not-so distant future more variants such as this one will be found and physicians will be able to assess a “score” based on maybe 15 to 20 genes to predict an individual’s risk for obesity.
“The important role that environment plays in enabling or resisting such susceptibility is clear evidence that such risk can be modified,” Leibel concludes.

Gene Variant Linked to Obesity Affects Food Choices in Children

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Archaeologists rarely agree on anything.   So it&#8217;s no surprise that for years two groups of scholars have drawn completely opposite conclusions about the relationship between the ancient people of Thailand and China.
Some experts argue that, thousands of years ago, people from Thailand migrated into East Asia, becoming the ancestors of present-day Chinese peoples.   Others argue the exact opposite: that it was people from East Asia who migrated south into Thailand.   Unfortunately, the sheer complexity of languages and cultures in the region, combined with conflicting archaeological reports, makes it next to impossible to draw concrete conclusions.

In situations like this one researchers increasingly turn to the field of genetics to help fill in the gaps and piece together the history of various populations – and that is just what a team from Thailand has done.   In this month’s issue of the <a id="ruzb" title="American Journal of Physical Anthropology" href="https://www.ncbi.nlm.nih.gov/pubmed/18615504?ordinalpos=2&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">American Journal of Physical Anthropology</a>, a bipartisan team of archaeologists and geneticists from across Thailand describes how the mitochondrial DNA (mtDNA) of both ancient and modern Thai populations can help us understand the peopling of the country.
Because the demographics of Thailand are so complex, the authors felt that just sampling modern Thai populations would not give a clear picture into the peopling of the region.   So, the researchers dug deeper by sampling archaeological remains as well.   They extracted DNA from 43 skeletons excavated at two sites in northeastern Thailand that date to about 3,500 years ago.   The authors chose these particular sites, called Noen U-loke and Ban Lum-Khao, because they represented typical ancient farming communities &#8211; some of the earliest settlements in existence.
Right away, the authors noticed the ancient and modern samples were very similar genetically – an indication that within the last 3,500 years, people haven’t moved around very much in northeastern Thailand.   Some of the modern people tested may in fact be descendants of these early Thai farmers — a very exciting prospect.
More importantly, however, the authors believe they have worked out the peopling of Thailand from the genetic information they gathered.   Their data support the hypothesis that many present-day Thai populations are actually descended from people who migrated from southern China only a few thousand years ago — an idea that has gained prominence in recent years among many archaeologists.
These results are compelling for a number of reasons – most notably the fact that the authors were able to use genetic data to resolve uncertainties about the peopling of Thailand when other types of data could not.   It also shows how useful it can be to compare ancient and modern DNA when tracing prehistoric migrations.   Many studies use only one or the other.   Finally, these authors were able to utilize genetics in a region – Southeast Asia – that has not seen much genetics research compared to other regions.   Hopefully future research on the genetic history of this region will continue down the path laid out by these researchers, following their lead of taking evidence from all disciplines in reshaping theories on ancient civilizations.   Perhaps we will even see more agreement from archaeologists.

New Approach Studying Genetic History of Southeast Asia

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As anyone who indulges in both smoking and drinking can tell you, the two are a natural – if unhealthy – combination.
Now research suggests that some people possess a single genetic variation that makes them prone to greater indulgence in both vices – and the attendant health risks.
<h6>Nicotine Receptors</h6>
Several research papers published in the last year or so show that a cluster of genes on chromosome 15 encoding nicotinic receptors, which regulate the brain&#8217;s response to nicotine, are related to smoking behavior. We cite <a href="https://www.nature.com/nature/journal/v452/n7187/abs/nature06846.html" target="_blank" rel="noopener noreferrer">one</a> of those papers in the 23andMe Health and Traits entry for Nicotine Dependence – it shows that on average, smokers with an A at both copies of the SNP rs1051730 light up once more per day compared to those with the AG or GG genotype.
The authors of the new study, which appears in the latest issue of the <a href="https://www.pnas.org/content/early/2008/12/08/0810970105" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>, noted that connection between chromosome 15 and nicotine dependence. They also observed the fact that twin studies have established a genetic connection between smoking and alcohol abuse and that experiments show mice consume less alcohol when treated with a drug that blocks nicotinic receptors.
<h6>Test the Hypothesis</h6>
So the researchers, who were from the <a href="http://www.galloresearch.org/" target="_blank" rel="noopener noreferrer">Ernest Gallo Clinic and Research Center</a> in Emeryville, Calif., and the <a href="http://www.ucsd.edu/portal/site/ucsd" target="_blank" rel="noopener noreferrer">University of California, San Diego</a>, reasoned that the very same genetic variations recently associated with smoking behavior could influence drinking as well. To test that hypothesis, they genotyped 367 participants aged 18 to 29 and tested them on various measures of alcohol response.
Those with an A at both copies of rs1051730 were better able to maintain their coordination after drinking a given amount of alcohol and reported feeling less drunk compared to those with either the AG or GG genotypes. The researchers also found a second SNP nearby on chromosome 15 – rs8034191. That SNPwas also linked to alcohol sensitivity. In that case, having a C at both copies of the SNP decreased a person&#8217;s response to alcohol.
23andMe customers can check their own genotypes at both SNPs using the <a href="https://www.23andme.com/you/explorer/" target="_self" rel="noopener noreferrer">Browse Raw Data</a> feature.
Some people might consider it good news to learn that they have a genetically enhanced ability to hold their drink. But a reduced response to alcohol increases a person&#8217;s risk of alcohol abuse. This particular genetic signature also appears to threaten health by increasing a drinker&#8217;s chances of developing problems with alcohol.

Drinking and Smoking and Genes

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The online publication of three papers by Nature Genetics this week has roughly doubled the number of genetic locations associated with levels of cholesterol and triglycerides in the blood.
With the addition of so many new SNPs, researchers have a wealth of opportunities to better understand how the body regulates cholesterol and triglyceride levels, find new targets for drugs to control them, and identify people who are at increased risk of cardiovascular disease.

Two of the Nature Genetics papers combined data from a number of previous studies to increase their statistical power to detect SNPs associated with cholesterol and triglyceride levels. <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.269.html" target="_blank" rel="noopener noreferrer">One</a> looked at between 17,798 and 22,562 European subjects (depending on the specific measurement being examined) and found six genes or locations on five chromosomes that were significantly associated with total cholesterol, HDL, LDL, or triglycerides. The <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.291.html" target="_blank" rel="noopener noreferrer">other</a> studied 20,623 people from Europe and the United States, and identified 11 genetic regions that were not previously known to be associated with cholesterol or triglyceride levels.
The third <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.271.html" target="_blank" rel="noopener noreferrer">paper</a> found five genetic regions associated with cholesterol or triglycerides in a cohort of 4,763 people born in northern Finland in 1966.
A number of the new associations were located near places in the genome where rare mutations are already known to completely disable cholesterol-regulating genes, causing serious disruptions in cholesterol metabolism. The newly discovered SNPs apparently cause much subtler effects, however; in most cases, they appear to modulate the activity of the genes they affect.
The authors of one study (Kathiresan et al.) also provided evidence that seven of their new SNPs modulate the expression of genes in the liver, where cholesterol is produced.
In spite of their success in both discovering new genetic locations associated with cholesterol and triglyceride levels – the papers also replicated virtually all previously known associations as well – the value of all this information for personal genomics is somewhat limited. After all, blood levels of cholesterol and trigylcerides are themselves indicators of cardiovascular disease risk. Knowing a person&#8217;s genetic risk on top of their actual cholesterol levels provides only an &#8220;incremental&#8221; amount of additional information, Kathiresan et al. wrote.
Even so, Kathiresan et al. developed an &#8220;allelic dosage score&#8221; that consisted of a person&#8217;s number of elevated-risk genotypes out of 32 previously known and newly discovered SNPs. Study subjects with scores in the top tenth of the distribution were more than twice as likely to have LDL cholesterol about 160 mg/dl, HDL cholesterol below 40 mg/dl and trigylcerides above 200 mg/dl.
Researchers still have captured only a small fraction of the gene variation that explains why one person&#8217;s cholesterol level is higher or lower than the next person&#8217;s. The authors of the Finnish study, who found one cholesterol-increasing version of the AR gene that was present in less than 2% of subjects, suggest that much of that unknown risk may lie in similarly rare variants.
&nbsp;

New Papers from Nature Genetics Yield a Bounty of Cholesterol SNPs

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With the return of Christian rule to Spain in 1492 after nearly 800 years of Muslim rule, hundreds of thousands of people – both Muslim and Jewish – were faced with the choice of exile, conversion or occasionally even death.
Exile or Conversion
Historical accounts estimate that nearly 400,000 Jews and Muslims were expelled from Spain or Portugal within only 100 years.
But what about those who didn&#8217;t leave?
Many Muslims and Jews converted to Christianity, only to face the scrutiny of the Spanish Inquisition.   Can the descendants of those converts still be found among modern Spanish and Portuguese peoples today?   These very questions were at the heart of the <a id="h60k" title="new study" href="http://www.cell.com/AJHG/abstract/S0002-9297%2808%2900592-2" target="_blank" rel="noopener">new study</a> by geneticist Mark Jobling and his colleagues at Leicester University.
In order to answer these questions, Jobling and his colleagues performed genetic analyses on 1,140 males from the Iberian Peninsula.   They focused on the Y-chromosome DNA, which is passed down from father to son and can be used to trace paternal ancestry.   Jobling and his team found a surprisingly large percentage of DNA types that can be traced back to either Jewish (19.8%) or North African Muslim (10.6%) populations.
These levels stand in contrast to historical accounts, which emphasize the expulsion of these two minority groups from Spain and Portugal.   According to Jobling, “These findings attest to a high level of religious conversion (whether voluntary or enforced) driven by historical episodes of religious intolerance.”
The genetic evidence lends support to the idea that most Jews and Muslims preferred conversion to Christianity, as opposed to expulsion from the region.   Ultimately, the descendants of those who converted began to integrate into the Christian population.   Today, most of these descendants remain unaware of their ancestors’ religious conversion.
The conclusions reached by Jobling and his colleagues illustrate how useful genetic analysis can be in assessing the historical record. Since researchers began using genetics to understand the past about two decades ago, they have focused their attention on prehistoric events such as the origin of the human species in Africa, the migration of people into new territories and the expansion of innovations such as agriculture and pottery.
But the gradual accumulation of data now allows scientists to tackle more recent and localized events. Just last month, researchers with the National Genographic Project used the genetic diversity of modern populations around the Mediterranean to piece together <a id="h_id" title="Phoenician" href="https://blog.23andme.com/articles/ripples-in-the-mediterranean-tracing-the-genetic-origins-of-the-phoenicians" target="_blank" rel="noopener">Phoenician</a> trade routes from nearly 3,500 years ago.
This latest study shows that genetic data can actually be used to test historical claims and assumptions, and even to overturn conventional wisdom. In fact, the results of this research actually contradict some historians&#8217; beliefs about the fate of the majority of Jews and Muslims living in the Iberian Peninsula during the Inquisition.   Clearly, using genetic data to test hypotheses based on historical or archaeological evidence promises to be surprisingly informative in the future.
Photograph of &#8220;Auto de Fe&#8221; by Francisco Ricci from Wikimedia Commons.

Genetics Sheds Light on the Spanish Inquisition

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A new genome-wide association study has yielded two more genes associated with height. But just like the amount of height difference the new genes explain, their discovery amounts to no more than an inch of progress in understanding the genetics of the trait.
Height is one of the most genetically complex traits scientists face. There are probably hundreds of different genes that influence stature, with each one accounting for only a tiny fraction of the difference in height from one person to the next. And though genes are by far the most important determinant of height, all other things being equal, all other things are by no means equal. Differences in childhood nutrition, prenatal care and infection history can cause even identical twins can to reach very different heights (more on that <a href="http://www.sciam.com/article.cfm?id=how-much-of-human-height" target="_blank" rel="noopener">here</a>).

Discerning the effect of a single genetic variation in such a noisy environment requires multiple studies involving large numbers of subjects. The latest study, published online last week by Human Molecular Genetics, looked at 379,319 SNPs in 1,000 people of European descent.
The study found statistically significant associations with height for 134 SNPs. The researchers focused on about two dozen that clustered around two genes that had not previously been associated with height, SBF2 and FLNB.
FLNB is plausible as a height-associated gene, because it is involved in skeletal development. Though SBF2 is not as clearly related to height, mutations in the gene are known to cause <a href="http://www.ninds.nih.gov/disorders/charcot_marie_tooth/detail_charcot_marie_tooth.htm" target="_blank" rel="noopener">Charcot-Marie-Tooth disease</a>, which causes muscle weakness and skeletal deformities in the limbs.
The effect of SBF2 was surprisingly large – subjects with the TT genotype at one SNP in the gene, rs1867138, were about an inch taller on average than those with the CC genotype. Though the effect of FLNB was less impressive, the study found that each G at the the SNP rs9834312 in that gene slightly increased a subject&#8217;s height.
23andMe customers can check their genotypes at two equivalent SNPs using the <a href="https://www.23andme.com/you/explorer/" target="_self" rel="noopener">Browse Raw Data</a> feature. Having a G at rs1867137 is the same as having a T at rs1867138. So the GG genotype at rs1867137 is worth about an inch compared to AA. In FLNB, rs939882 is equivalent to rs9834312. In both cases, having a G is correlated with slightly greater height.
When the researchers attempted to replicate their findings in Chinese subjects, they found that both genes were associated with height in that population as well – but not all of it. The SNP in FLNB was associated with height among 619 northern Chinese subjects, while the SNP in SBF2 was associated with height only in a sample of 2,953 southern Chinese.
But when the researchers tried to replicate previously discovered height associations using their data, their results were mixed. Out of 58 they looked for, only 13 showed up. That doesn&#8217;t necessarily mean the 45 associations that could not be replicated are invalid; but it does illustrate how difficult it will be to work out the genetic basis of height.

Two More Genes Associated with Height

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People sometimes think of ancestry as the &#8220;fun&#8221; part of the 23andMe Personal Genome Serviceâ„¢, an intriguing glimpse at the past that is completely unrelated to our more serious Health and Traits features.
But a new paper shows how ancestry can actually reveal quite a bit about the genetics of disease. In the December issue of <a href="http://cancerres.aacrjournals.org/cgi/content/abstract/68/23/9723" target="_blank" rel="noopener noreferrer">Cancer Research</a>, Laura Fejerman of the University of California San Francisco and several colleagues show that among Latinas, a woman&#8217;s breast cancer risk increases with her proportion of European ancestry.

Most Latinos are descended from mix of Native American ancestors and European immigrants. In countries such as Brazil, where slavery was practiced until the late 19th century, many people have substantial African ancestry as well.
Fejerman and her colleagues used 106 <a href="https://en.wikipedia.org/wiki/Ancestry-informative_marker" target="_blank" rel="noopener noreferrer">ancestry informative markers</a> (AIMs) to estimate the relative European and Native American ancestry of 440 Latina women from the San Francisco Bay area with breast cancer and 597 control subjects without the disease. With every 25 percent increase in European ancestry, the researchers found, a woman&#8217;s chances of having breast cancer rose 79 percent.
The finding is no surprise – Latinas have lower breast cancer rates compared to European women, as do Native Americans. But the study does demonstrate that ancestry and population history can be valuable tools for understanding the genetics of disease.
And researchers still have a lot more to learn about population differences in rates of breast cancer. Though environmental factors are known to play a role, the new study strongly suggests that genetics is worth investigating as well.
There&#8217;s also an intriguing puzzle in breast cancer mortality differences among different populations. Though Latinas, Native Americans and African Americans are less likely to develop the disease, when they do their chances of dying from it are greater. Researchers would like to know whether those differences are due to genetics, differences in access to health care, or other factors.
Image: Peruvian &#8220;<a href="http://www.artnet.com/magazine_pre2000/features/ramirez/ramirez12-02-96.asp" target="_blank" rel="noopener noreferrer">casta</a>&#8221; painting, late 18th c.

Study of Breast Cancer among Latinas

This is a repeat of a post we ran back in September. While you&#8217;re sitting around the table with your loved ones, don&#8217;t forget that it&#8217;s National Family History Day!
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I’m a bad patient.
Every time I go to a doctor she asks, “Do you have a family history of any diseases?”
I’m ashamed to say that my answer is always “I don’t think so.”
Your family health history is a powerful tool for your doctor; it can help him or her make vital screening and treatment decisions. Yet a recent survey (Porter Novelli Healthstyles 2004) found that although 96% of Americans recognize the importance of their family history, only 33% have ever tried to gather and organize this data for themselves.
23andMe helps people see what their DNA might have to say about a host of common and not-so common diseases and conditions; but we don’t want anyone to think that purchasing our Personal Genome Serviceâ„¢ is a substitute for a detailed family health history.

For example, the effect of the SNPs 23andMe reports on for breast cancer pales in comparison to that of mutations in the well-known BRCA1 and BRCA2 genes, which run in families and can increase a woman’s breast cancer risk three- to seven-fold (23andMe does not report data on these mutations). So even if your 23andMe data says that you have average or even below-average risk for breast cancer, a strong family history of the disease indicates the strong possibility of a genetic mutation that trumps the information we have gleaned from your SNPs.
In other cases, your family health history might dovetail with your 23andMe data, giving a fuller picture of, and perhaps increasing, your predicted risk for a certain disease. For example, a report published just last week in the <a href="https://www.ncbi.nlm.nih.gov/pubmed/18780872?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">Journal of the National Cancer Institute</a> showed that a SNP recently associated with lung cancer (customers can see their data in Health and Traits) has a significantly larger effect in people where three or more first-degree relatives have been diagnosed than in people who develop a sporadic case of the disease.
The bottom line: It is very helpful to be aware of your family health history and share it with your medical provider. Here are a few resources to help you get you started:
<ul>
<li>The U.S. Surgeon General’s Family History Initiative 
For the past four years the Surgeon General has designated Thanksgiving, a time when families naturally gather together, as National Family History Day. You can use the online tool “My Health Portrait” to help guide you in collecting your own family’s health history. (Also available in Chinese, Polish, Spanish, French and Portuguese from the Brigham and Women’s Hospital National Family Health Initiative Website.)</li>
</ul>
<ul>
<li>The Genetic Alliance 
Links to sites that can help with collecting a family health history, including resources for family reunion organizers who want to incorporate this into their next gathering.</li>
</ul>
Mom, get ready for some questions.

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