<img loading="lazy" decoding="async" class="alignright wp-image-4667 size-medium" title="prostatemri" src="http://35.88.189.111/wp-content/uploads/2009/09/prostatemri-300x223.jpg" alt="" width="300" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/09/prostatemri-300x223.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/09/prostatemri.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />This MRI of a man&#8217;s pelvis shows that his prostate is enlarged to almost three times the regular size, which may be a sign of cancer. The prostate is marked by a cross.
Prostate cancer, the most common cancer to affect men, kills 30,000 men of all ethnicities each year.
The disease is known to have a strong genetic component, and several common DNA variations have been found to affect a man&#8217;s risk of prostate cancer. However, previous research has analyzed men of only European and African ancestry, leaving the effects of these genetic variants in Asian men undetermined.
<h2>New Research</h2>
Recently, researchers analyzed Japanese men for several genetic variants previously linked to prostate cancer in European and African American populations. The study found that some of these variants also affect the risk of developing prostate cancer in Asian men.
A team from Boston and Japan led by Matthew Freedman searched for risk variants by scanning the genomes of nearly 1,350 Japanese men, including more than 300 prostate cancer patients. The results, published online last week in the Journal of the National Cancer Institute, provide evidence that five out of 23 SNPs previously associated with prostate cancer among Europeans and African Americans also impact risk in this Asian population.

Although not every one of the five SNPs had a statistically significant association on its own, the group of SNPs had an association with prostate cancer. Men who carry six or more of the 10 possible risk copies at any of the five associated SNPs (people have two copies of each SNP) had 6.22 times increased odds of developing prostate cancer than men with two or fewer risk copies. The SNPs were not linked to the progression of prostate cancer, but SNPs were associated with a younger age at diagnosis.
<h2>More Research Needed</h2>
Further research with a larger number of patients will be needed to determine how several of these SNPs may have differing effects between populations of different ancestry, suggests John Ioannidis in an accompanying editorial published in the Journal of the National Cancer Institute.
&#8220;When each SNP is analyzed separately, there are clear signs of divergent risks in Asian versus European populations,&#8221; Ioannidis wrote. Several other SNPs may also have considerably different effects in these and African American populations, so more research is needed to accurately determine an individual&#8217;s risk for prostate cancer.

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23andMe Blog Team

Genetic Variations May Increase Risk Of Prostate Cancer In Japanese Men

Scientists are narrowing in on two regions of the human genome that could be responsible for ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig&#8217;s disease.
ALS is a neurodegenerative disorder that weakens muscles and paralyzes patients within three years of onset, and has no known cure. The available drug treatment delays progression by only three to five months.
Despite several attempts to find genetic variations associated with the sporadic form of the disease (which accounts for 95% of ALS cases), no association has been found.
A team of researchers from Netherlands, Van Es et al., analyzed the genes of nearly 20,000 people of European descent, including 5,000 ALS patients. Their results, published online this week in <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.442.html" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, identified several genetic variations on two chromosomes suspected to affect ALS and other neurological functions.

The study revealed that each copy of the C version of &nbsp; a SNP on chromosome 19, is associated with a 1.2 times increased odds of ALS compared to having two copies of A. This SNP is found near UNC13A, a gene that may be involved in the function of motor neurons, which degenerate and die in ALS patients.
Another SNP ,located on chromosome 9, is associated with a 1.16 times increased odds of ALS. This SNP was found in a region of the genome previously associated with the rare familial (non-sporadic) version of ALS. Researchers also found an association between the disease and a third SNP located very close to .
There is increasing evidence that ALS belongs to a broader spectrum of neurodegenerative disorders, including Parkinson’s disease, so researchers speculate that genetic associations with ALS may also lead to clues about other disorders of the nervous system.

Genetic Variations May Increase Risk for ALS

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About 10,000 years ago, the prehistoric hunter-gatherers of Europe began meeting some new neighbors.
These farmers spread gradually at first, expanding from the Near East through Anatolia and the Balkans. Then agriculture exploded, reaching present-day Britain within a few thousand years. The farmers settled into houses, which soon evolved into villages, towns and eventually cities.
The archaeological record tells us that much. But what it doesn&#8217;t reveal is how agriculture spread. Did it spread like a fad, as hunter-gatherer groups saw what their neighbors were doing and imitated their ways? Or was it more of an invasion, with subsequent generations of farmers advancing across the continent and overwhelming indigenous hunter-gatherer populations as they went?
Some genetic studies suggest the former. But in the September 3 issue of <a id="rbdr" title="Science" href="http://www.sciencemag.org/cgi/content/abstract/1176869" target="_blank" rel="noopener">Science</a>, the first study to directly compare ancient DNA (aDNA) from prehistoric burials of hunter-gatherers to that their agricultural neighbors suggests migrants spread farming through Europe.
The research team, led by Barbara Bramanti of Mainz University, sequenced the mitochondrial DNA (mtDNA) of just under 50 individuals unearthed from various prehistoric burial sites across central and eastern Europe. Half the individuals came from hunter-gatherer societies, and the other half from communities based around farming. As a comparison, they also sequenced the mtDNA of nearly 500 modern Europeans from the same parts of Europe.
The authors&#8217; first task was to compare the hunter-gatherer mtDNA to that of the farmers. Upon doing so, they found both groups to be so different from each other that there is no way the two could be closely related. There was absolutely no overlap in the kinds of mtDNA lineages &#8211; known as haplogroups &#8211; between the hunter-gatherers and the farmers. This stark difference suggests the earliest farmers were not related to the hunter-gatherers, and most likely came to the region by migration.
And how do these two groups compare to the modern-day Europeans? The hunter-gatherers had little in common with modern people. Haplogroup U, the most common lineage among the hunter-gatherers, is one of the least common haplogroups among modern Europeans.
But the authors also found little to connect the farmers to modern Europeans. Other studies have pointed to a substantial genetic component from the Near East among Europeans, but the authors found many genetic differences between the two groups.
Based on these results, the authors have proposed an alternative theory. The unexplained component to the genetic make-up of modern Europeans may be explained by later migrations that post-date the skeletal remains examined here. It could have been a later expansion of farmers from the Near East, or perhaps an influx of hunter-gatherers from the west. The exact details remain unclear, but the authors are confident that, with additional DNA analysis, they can hope to unravel the increasingly complex story of the peopling of Europe.

New Clues Shed Light on Genetic Ancestry of Modern Europeans

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3449" title="istock_000004417726xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/istock_000004417726xsmall.jpg" alt="istock_000004417726xsmall" width="334" height="250" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000004417726xsmall.jpg 400w, https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000004417726xsmall-300x225.jpg 300w" sizes="auto, (max-width: 334px) 100vw, 334px" />
Despite years of effort and millions of dollars in research funding, only one gene, APOE, has been conclusively associated with Alzheimer&#8217;s disease risk so far.   But now the results of two of the largest Alzheimer&#8217;s studies ever provide convincing evidence that three more genes affect risk for the disease.
&#8220;These findings are a leap forward for dementia research.   At a time when we are yet to find ways of halting this devastating condition, this development is likely to spark off numerous new ideas, collaborations and more in the race for a cure,&#8221; said a statement from Rebecca Wood, Chief Executive of the Alzheimer&#8217;s Research Trust in the UK.
<a href="https://dx.doi.org/10.1038/ng.440" target="_blank" rel="noopener">A British team</a>, led by Julie Williams, found strong evidence that in the clusterin gene and in the PICALM gene are both associated with risk for Alzheimer&#8217;s. <a href="https://dx.doi.org/10.1038/ng.439" target="_blank" rel="noopener">A French team</a>, lead by Philippe Amouyel, also found strong evidence for an association between and Alzheimer&#8217;s risk, and suggestive evidence for an association with .
In addition, Amouyel&#8217;s research revealed that the A version of in the CR1 gene increases the odds of Alzheimer&#8217;s by 1.21 times. Suggestive evidence for this association was also seen in the work of Williams&#8217; group.
The results from both teams were published online this week in the journal Nature Genetics. 

Williams said in a statement that the number of people who fall victim to Alzheimer&#8217;s could be reduced by 20% if treatments addressing the effects of the three newly identified genes could be found.
The proteins made by the clusterin and CR1 genes are known to play a part in clearing out amyloid beta, the protein that forms plaques in the brains of people with Alzheimer&#8217;s.   PICALM encodes a protein important for proper communication between brain cells, a process that is known to be disturbed in Alzheimer&#8217;s patients.
In total, the DNA of more than 10,000 people with Alzheimer&#8217;s disease and more than 18,000 controls from ten countries was analyzed by the two teams of researchers.   But both groups agree that there is still much more to find.   Williams&#8217; team is already planning an even larger study involving 60,000 people that she believes can be completed within the next year.
&#8212;&#8212;&#8212;&#8211; 
<a href="http://www.alz.org/index.asp" target="_blank" rel="noopener">Alzheimer&#8217;s</a>, the most common cause of dementia in people 65 years and older, currently affects about five million people in the United States. As the population ages, many more people are expected to be afflicted; some estimate 14 million Americans will have Alzheimer&#8217;s by the year 2050.

Largest Alzheimer’s Genetic Studies To Date Identify Three New Susceptibility Genes

<img loading="lazy" decoding="async" class="alignright wp-image-5500 size-medium" title="800px-ÐœÑ‹ÑˆÑŒ_2" src="http://35.88.189.111/wp-content/uploads/2009/12/iStock_000003710874XSmall-300x211.jpg" alt="" width="300" height="211" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/iStock_000003710874XSmall-300x211.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/12/iStock_000003710874XSmall.jpg 413w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Scientists who are studying mice with a mutation that makes them resistant to obesity even in the face of a high-fat diet may have identified a new way to treat both obesity and diabetes.
Carrying extra weight is known to trigger a state of chronic, low-grade inflammation in the body, which can lead to insulin resistance and, in turn, diabetes.   When scientists at the University of Michigan discovered that an inflammatory protein called IKKÎµ seemed to be a key step in this pathway, they theorized that they could protect mice fed a high-fat diet from developing signs of diabetes by genetically engineering them to lack the protein.
Much to the researchers&#8217; surprise, IKKÎµ knockout mice were spared from not only from chronic inflammation and insulin resistanceâŽ¯they also stayed relatively slim even when fed a lard-like chow with 45% of its calories from fat. After three months on this diet, normal mice gained 20 grams, while the IKKÎµ-deficient mice gained only 12 grams.
&#8220;We&#8217;ve studied other genes associated with obesity … but this is the first one we&#8217;ve found that, when deleted, stops the animal from gaining weight.   The fact that you can disrupt all the effects of a high-fat diet by deleting this one gene in mice is pretty interesting and surprising,&#8221; said the study&#8217;s senior author, Alan Saltiel, in a statement.
The results were published this week in the journal <a href="https://dx.doi.org/10.1016/j.cell.2009.06.046" target="_blank" rel="noopener">Cell</a>.
Saltiel&#8217;s lab is already working to find drugs that inhibit IKKÎµ and could someday be used to prevent obesity and diabetes in humans.   He estimates that new treatments could be available in about a decade, once successful candidate compounds are identified.
But finding a compound that inhibits IKKÎµ isn&#8217;t the only obstacle on the road from the lab to the pharmacy.   Researchers will also need to confirm that IKKe works in humans the same way it does in mice.
Then there&#8217;s the issue of safety.   Mice lacking the IKKe gene were protected from obesity and related complications, but they were more susceptible to lethal viral infections than their normal littermatesâŽ¯a complication that would need to be carefully evaluated before any attempt to reduce IKKÎµ activity is undertaken in humans.
Image: <a href="https://en.wikipedia.org/wiki/File:%D0%9C%D1%8B%D1%88%D1%8C_2.jpg" target="_blank" rel="noopener">George Shuklin</a>

Surprisingly Skinny Mice Could Point the Way to Obesity and Diabetes Treatments

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-4589" title="chimp" src="https://blog-api.23andme.com/wp-content/uploads/2009/09/chimp-300x200.jpg" alt="chimp" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/09/chimp-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/09/chimp.jpg 600w" sizes="auto, (max-width: 300px) 100vw, 300px" />
We may be another step closer to discovering what makes us human.
A new study published online this week in <a href="https://genome.cshlp.org/content/early/2009/08/31/gr.095026.109.abstract" target="_blank" rel="noopener noreferrer">Genome Research</a> has pinpointed three genes in humans that may genetically differentiate us from chimps and other primates.
<h6>Shared DNA</h6>
Genetically we are very similar to chimps, so most of the differences researchers have observed to date regard physical appearance and <a href="http://www.archive.org/details/comparative_tests_on_human_chimp_infants" target="_blank" rel="noopener noreferrer">behaviors</a>.
The new study found several genes that were once silent and nonfunctional in our primate ancestors. They seem to have awakened around the time that humans formed a new evolutionary branch.
Researchers at the University of Dublin compared sections of the human genome with those of chimps and other primates. They found active genes that are absent from the chimp genome.
<h6>Human Genes</h6>
They found three human genes, CLLU1, C22orf45 and DNAHI0OS, that were present but inactive in non-human primates.

At the location of each of the three human genes, a disabling sequence of DNA was found in the genomes of the chimp, macaque, gorilla, gibbon and partially in the orangutan.
The study suggests that the awakened human genes shed their disabling components. But these awakened genes gained &#8220;enabling&#8221; sequences that helped them do the work of forming proteins in the body.
<h6>Awakened Genes</h6>
Previous research found that genes arising from inactive DNA were present in flies and yeast. The study suggests there may be a total of 18 awakened genes in humans. Yet researchers were limited to analyzing only a part of the 24,000-gene human genome.
The functions of these novel genes are not yet known. However, it is tempting to infer that these genes, specific to humans, are responsible for the attributes that differentiate us from other primates.

What Makes Us Human? Study Finds Hints By Comparing Chimp and Human DNA

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Editor&#8217;s note: This post has been edited slightly since publication.
Many examples worldwide of two distinct ethnic groups living side by side.
Sometimes, these groups co-exist peacefully. Other times, they do not.
Differences
Often, the differences between two groups &#8211; along with circumstantial factors &#8211; lead to tension between them and sometimes violence. The Hutus and Tutsis of Rwanda, the Sunnis and Shiites of Iraq, and the Croats and Serbs of former Yugoslavia all illustrate how cultural distinctions &#8211; like language and religion &#8211; can contribute to tensions and conflict around the globe.
But do these cultural and ethnic distinctions translate to biological distinctions as well?
<h6>A Study of Differences and Similarities</h6>
Exactly how biologically distinct are two ethnic groups living side by side? Anthropologist Evelyn Heyer and an international team of researchers set out to answer these and many other questions by studying the adjacent &#8211; and culturally very different &#8211; Tajik and Turkic speakers along the Silk Road of Central Asia. Their results are published in this week&#8217;s <a href="http://www.biomedcentral.com/1471-2156/10/49/abstract" target="_blank" rel="noopener">BMC Genetics</a>.

The authors focused on the Tajik and Turkic speakers because those groups offered a unique perspective on how two groups living in such close proximity can be so different from each other.
<h6>Language and Cultural Differences</h6>
The Turks are largely nomadic herders. They speak Indo-Iranian languages like Azerbaijani, Turkish, and Altay. Their society is organized into clans, or &#8220;descent groups,&#8221; whose membership is passed down from father to children.
The Tajiks are, conversely, agriculturalists. They speak various dialects of the the Tajik, or Tajik Persian, language that may have arrived with Muslim invaders 1,000 years ago. Their society is largely patrilocal &#8211; meaning that when couples marry they put up residence near the husband&#8217;s family; and first cousin marriages are encouraged.
The two societies are supposedly closed, and members of both groups are said to rarely leave their clan or village. This cultural isolation made them perfect candidates for Heyer and her team to study.
The researchers collected maternally inherited mitochondrial DNA and paternally inherited Y chromosome DNA from more than 1,000 individuals spanning 24 Turkic and Tajik populations.
<h6>Shared Genetics</h6>
They found that, genetically, the Tajiks and the Turks were virtually indistinguishable.
Genetically, the Tajiks and the Turks were virtually indistinguishable. The authors found the overall level of genetic diversity between the two groups to be less than 1 percent—so small that there was greater diversity within each group than between the two.
Their analysis also sheds some light on the origins of these two ethnic groups. The modern-day people of Central Asia maintain their own origin stories unique to their particular group. These unique origin stories, in part, distinguish them from one another.
But Heyer&#8217;s analysis proves that these groups share the same roots; they are simply a hodgepodge of the clans, tribes, and villages that have called Central Asia their home for thousands of years. Over many generations, they banded together to form larger groups until they consolidated into just two major divisions: the Tajiks and the Turks.

A photo of people on the street in New York

New Study on Genetics of Ethnic Groups Reveals We May Not Be So Different After All

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Although environment plays a major part in addiction – you can&#8217;t get hooked on something you&#8217;ve never tried – genetics plays a substantial role in determining whether a person who does use a drug will become addicted to it.
A few DNA variations have been identified that seem to increase the odds a person will become addicted to a specific drug. But <a href="https://www.ncbi.nlm.nih.gov/pubmed/10401514" target="_blank" rel="noopener noreferrer">twin studies suggest</a> that there might be genes influencing addiction in general.
Xiang Chen and colleagues at Yale and Princeton set out to find some of these genes by analyzing the genetic data from several cohorts of people previously studied for addictions. &nbsp; The researchers&#8217; approach was to look for variations found more frequently in people addicted to at least two out of six categories of substances: nicotine, alcohol, marijuana, cocaine, opiates and other drugs. &nbsp; Their results, published online this week in the Proceedings of the National Academy of Sciences, reveal a significant association between addiction and variations in a gene, PKNOX2, previously associated with alcohol dependence in mice.
The strongest signal was seen with in white women was found at a SNP inthe PKNOX2 gene and was associated with a higher risk for addition. The association of with addiction did not hold when the researchers looked at individual substances separately.
&#8220;This suggests that substance dependence or addiction as a whole has different risk genes compared to any single addiction outcome,&#8221; the authors write.
The authors admit that there are weaknesses in their study. &nbsp; For example, people addicted to two or more substances might just have more access to drugs – not a biological predisposition to addiction. &nbsp; Moe research in this area will definitely be needed.
SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting because they offer a glimpse into how genetics may affect our bodies and health; but in most cases, more work is needed before this research can provide information of value to individuals. For that reason it is important to remember that like all information we provide, the studies we describe in SNPwatch are for research and educational purposes only. SNPwatch is not intended to be a substitute for professional medical advice; you should always seek the advice of your physician or other appropriate healthcare professional with any questions you may have regarding diagnosis, cure, treatment or prevention of any disease or other medical condition.
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Genetic Variation Associated With Addiction In Caucasian Women

New genetic research may explain why Fluffy is so fluffy.
A study led by researchers at the National Human Genome Research Institute scanned 1,000 dogs from 80 breeds, looking for genes associated with different hair types: curly, wavy, straight, wiry, long, and any combination of these. Their results, published online last week in <a href="http://www.sciencemag.org/cgi/content/abstract/1177808" target="_blank" rel="noopener noreferrer">Science</a>, show that variations in just three genes account for nearly all types of coats worn by man’s best friend.
<h2>Dog Hair</h2>
The study found that purebred dogs with similar hair types were found to have similar variations in three particular genes, RSPO2, FGF5, and KRT71.
A particular variation in the RSPO2 gene was linked to wiry hair in a pattern that gives dogs a mustache and eyebrows, such as in a schnauzer.

A variation in the FGF5 gene was associated with long hair, whether silky or fluffy, like that in a Pomeranian. Variations in the KRT71 gene seem to affect the extent of hair curl in dogs like Irish water spaniels.
Previous studies have shown that the FGF5 and KRT71 genes also affect hair type in cats and mice, suggesting that their effects may be relevant to all mammals, including humans.
<h2>Short Hair, Long Hair, and In Between</h2>
Some dogs have all three variations identified by the researchers, including Portuguese water dogs, a breed you may have seen taking walks on the White House lawn.
Short-haired dogs like beagles, who don’t exhibit any different types of hair studied by the researchers, all seem to have the ancestral versions of the FGF5, RSPO2, and KRT71 genes. The study also found that wolves carry the non-mutated forms of these genes, suggesting that the different hair types evolved after the evolutionary split between the two canine subspecies.
Despite what we know about the genetics of hair type in dogs, little is known about what makes <a href="https://blog.23andme.com/articles/snpwatch-researchers-find-link-between-red-hair-and-avoiding-the-dentist/" target="_blank" rel="noopener noreferrer">human hair</a> straight, wavy, curly, frizzy, kinky, woolly, or helical. While hair type in dogs is easily classified, studying human hair is not as simple. Some scientists have suggested characterizing hair by curl ratios and other measurements, but our diverse biological background poses a challenge in classifying human hair types for research.
This study could help researchers better understand the genetics of hair type in humans. It has also unleashed new possibilities for human disease research because these three genes that affect dogs&#8217; coats also regulate many other processes in living organisms, allowing researchers to study how powerful genes interact.

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