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Great apes really do giggle when tickled, new research says &#8211; just like you and me.
<h6>What&#8217;s So Funny</h6>
Researchers from the University of Hannover in Germany recorded the tickle-induced vocalizations from three human infants and 21 infant and juvenile orangutans, gorillas, chimpanzees and bonobos and analyzed this acoustic data to find similarities and differences among the five species.
Their results, published online today in the journal <a href="http://www.cell.com/current-biology/abstract/S0960-9822(09)01129-4" target="_blank" rel="noopener">Current Biology</a>, show that not only are the hoots, hollers and snorts of the great apes really laughter, but the evolutionary relationships between the sounds match up with the known evolutionary relationships between the species based on genetics.
&#8220;At a minimum, one can conclude that it is appropriate to consider &#8216;laughter&#8217; to be a cross-species phenomenon, and that it is therefore not anthropomorphic to use this term for tickling-induced vocalizations produced by the great apes,&#8221; the authors write.
<h6>Tickling</h6>
But the researchers&#8217; findings also indicate something more profound: rather than being a uniquely human invention, tickle-induced chuckles can be traced back 10 to 16 million years to our last common ancestor with the great apes. Analysis of the chortles of a lesser ape, the siamang, suggests that <a href="https://blog.23andme.com/articles/does-your-dna-make-you-lol">laughter</a> may be even older.
<img loading="lazy" decoding="async" class="alignleft size-medium wp-image-3729" title="slide1" src="https://blog-api.23andme.com/wp-content/uploads/2009/06/slide1-300x225.jpg" alt="" width="318" height="238" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/06/slide1-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/06/slide1.jpg 720w" sizes="auto, (max-width: 318px) 100vw, 318px" />The tree based on laughter matches the genetic tree. 
Despite the all the similarities the researchers found between humans and the great apes, the fact remains that human giggles are distinct — we mostly laugh while exhaling and our vocal chords vibrate to make the &#8220;ha ha ha&#8221; sounds, while ape snickers are more of the in-and-out panting variety.   The question for future research to answer is why particularly human features emerged and what functions they may have served as laughter became a large part of human social interaction.
Insanely cute video of giggling chimps here.

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Evolutionary Link Between Human and Ape Laughter

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It has been known for decades that having the gum disease periodontitis <a href="https://www.medscape.com/viewarticle/501491_9" target="_blank" rel="noopener">increases a person&#8217;s risk for heart attack</a> (free registration required), stroke and other forms of cardiovascular disease. Research suggests that the link is due to inflammation in the gums causing an immune reaction throughout the entire body. That can increase blood pressure and encourage the accumulation of atherosclerotic plaques in the arteries.
Now researchers have drawn a genetic link between periodontitis and heart disease as well. It turns out that variations in a region of chromosome 9 that have already been associated with heart disease also influence a person&#8217;s chances of developing periodontitis.

The specific genetic marker identified by the study is not part of the 23andMe Personal Genome Service. But another marker that has also been linked to heart disease and lies in the same chromosomal neighborhood is described in the Heart Attack research report.
Arne SchÃ¤fer of the Institute for Clinical Molecular Biology in Kiel, Germany presented the research in Vienna, Austria, last week at the annual meeting of the European Society of Human Genetics. He and his colleagues found that people with a marker for increased cardiovascular risk in a stretch of DNA known as 9p21 were more likely to have gum disease as well.
The high-risk version of the marker increased a person&#8217;s chances of having generalized aggressive periodontitis by 1.99 times, and localized aggressive periodontitis 1.72 times. Aggressive periodontitis generally strikes early in life and progresses rapidly, leading to tooth loss as early as age 20.
The 9p21 region of chromosome 9 contains several genes involved in suppressing the proliferation of cells. In a recent <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000378" target="_blank" rel="noopener">PLoS Genetics</a> paper the researchers suggest that the variation they studied somehow affects the function of one of these genes.
Rather than superceding previous findings linking the effects of periodontal inflammation itself on heart disease, the researchers said, their study provides valuable additional information that could help unravel the connection between the two conditions.

Study Draws Genetic Link Between Gum, Cardiovascular Disease

Variations in several genes may affect a young man&#8217;s risk of developing testicular cancer, new research says. One of these variations may also explain why the disease is more common in whites than blacks.
Testicular cancer is the most common type of cancer in men age 15 to 35, and it is on the rise.   The incidence of the disease in the United States has doubled since 1975.   The speed of this increase <a href="https://blog.23andme.com/2009/05/28/environment-not-genes-key-to-increasing-disease-rates/" target="_blank" rel="noopener">suggests that environmental factors </a>are at work, but researchers know that genes have a substantial influence on the disease too — testicular cancer is one of the most heritable types of cancer.
Clear genetic risk factors for most cases of testicular cancer, however, have so far not been identified. But now two groups, publishing online this week in the journal Nature Genetics, report finding several common genetic variations that are associated with increased risk for the disease.
In a study of 730 men with testicular cancer and 1,435 controls, <a href="https://dx.doi.org/10.1038/ng.394" target="_blank" rel="noopener">Rapley et al.</a> found that each copy of the more common G version of a SNP in the KITLG gene increased the odds of testicular cancer by 2.55 times compared to two copies of the A version of this SNP. (The second study by <a href="https://dx.doi.org/10.1038/ng.393" target="_blank" rel="noopener">Kanetsky et al.</a> found a similar association with nearby SNPs in a similarly sized study).
Dr. Katherine Nathanson, an author of the Kanetsky et al. study, pointed out in a statement that the G version is very common in Caucasians.   This is noteworthy because it is usually the less common version of a SNP that is associated with increased disease risk.   In Nathanson&#8217;s opinion, men who carry two copies of the less common A version of the SNP are probably at &#8220;incredibly low risk&#8221; for testicular cancer.
In the same statement, lead author Peter Kanetsky suggested that the high prevalence of the riskier version of this SNPs might mean that it makes some men more susceptible to testicular cancer, but that some environmental factor may also be needed to actually cause disease.   He said that knowing which gene to look more closely at will help guide researchers&#8217; efforts at identifying the other factors that are involved.
The KITLG gene has previously been associated with germ cell development and testicular cancer, but it is also involved in pigmentation.   Changes in this gene that are associated with lighter coloring have been strongly selected for in Europeans, and having a G at is one of the variations that is more common in whites than African Americans. The researchers suggest that this may be part of the reason the disease is almost five times more common in whites.
Rapley et al. also found that each copy of the A version of increased the odds of testicular cancer by 1.37 times compared to having two Gs (Kanetsky et al. also identified a similar association with a nearby SNP.) Each copy of a G at this SNP was found to increase the odds of testicular cancer by 1.50 times compared to having two As.
&#8220;These results raise the possibility that, in conjunction with other know risk factors, these variants may be used in the future for risk prediction, particularly given the availability of relatively simple screening approaches such as testicular ultrasound.   Further studies will be required, however, to refine the risk estimates and their interactions before this can be considered in clinical practice,&#8221; the authors of the Rapley et al. study conclude.

Genetic Variations That May Affect Testicular Cancer Risk Identified

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Having a particular immune system marker greatly increases a person&#8217;s risk of developing liver failure in response to a common antibiotic, a new study reports.
Drug-induced liver injury accounts for more than half of the approximately 2,000 cases of acute liver failure in the United States each year.   Most of this is due to acetaminophen (Tylenol ®), but a range of other drugs can also present a danger.   One of these, flucloxacillin (also called floxacillin), an antibiotic commonly used to treat staphylococcal infections, leads to liver failure within the first 45 days of treatment in an estimated 8.5 out of every 100,000 people taking the drug.
So far, it has been unknown what makes someone more or less susceptible to flucloxacillin-induced liver damage.   But now an international team of researchers has shown that an immune system variation may be the key.   Their results, published online yesterday in the journal <a href="https://dx.doi.org/10.1038/ng.379" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, show that having one or two Gs at increases the odds of drug-induced liver injury in response to flucloxacillin by at least 45 times compared to having two Ts at this SNP.
A G at indicates the presence of an immune marker known as HLA-B*5701.   This same marker has been linked to <a href="https://www.ncbi.nlm.nih.gov/pubmed/18303141?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">hypersensitivity to the HIV drug abacavir</a>, although the researchers say that adverse reactions to flucloxacillin and abacavir may be the result of different biological mechanisms.
HLA-B*5701 is usually found only in people with European ancestry. Approximately 5% of people in this group have one or two copies of the marker.   The authors of the study speculate that because people with Asian and African ancestry rarely carry HLA-B*5701, their risk for drug-induced liver injury in response to flucloxacillin might also be lower, although there is not data for this yet.
The authors conclude that testing for HLA-B*5701 in people suspected of having flucloxacillin drug-induced liver injury could be useful.   If prompt testing were available, they say, alternative drugs such as cloxacillin and dicloxacillin could be substituted for flucloxacillin.   According to their data, an estimated 85% of cases would prove to be HLA-B*5701-positivie.
But, they warn, testing for HLA-B*5701 before administering flucloxacillin would probably not be clinically useful or cost-effective because only one out of every 500 to 1,000 people with the HLA-B*5701 marker is predicted to have liver problems when treated with the drug.

Genetic Variation In Immune System Marker May Increase Risk of Liver Injury From Common Antibiotic

It is estimated that there are up to 8,000 distinct languages spoken around the world today.   At birth, the human mind is capable of learning and understanding any of these languages; an impressive feat given how uniquely complex they are.   The fact that humans are able to understand and communicate with one another in such a way that even our closest primate relatives cannot has long been supposed to be the result of some sort of genetic distinction separating us from the rest of the animal kingdom.  
In 2002, scientists believed they had found this genetic distinction in the form of a gene called FOXP2.   Their early studies suggested that FOXP2 was linked to the development of language in humans, and in humans&#8217; ability to manipulate the brain, lungs, and vocal chords to make the complicated suite of sounds and movements resulting in speech.
<h6>Origins of Langauge</h6>
However, the expression of FOXP2 in humans &#8211; and its presence in other species &#8211; is anything but simple.  
Research has revealed that FOXP2 isn&#8217;t expressed just in the brain, but in a host of other tissues and organs throughout the body.   Moreover, FOXP2 isn&#8217;t unique to humans, but is found in many species, from chimpanzees to field mice.   It&#8217;s the version of FOXP2 we humans carry that is distinct from those of other species.   So it is the differences in FOXP2 across species that has been at the heart of scientific research into the origins of complex language.
A few years after the FOXP2 gene&#8217;s possible role in promoting complex language skills was announced in 2002, scientists analyzing ancient DNA extracted from Neanderthals, our closest fossil ancestors, found that they had the same version of FOXP2 as humans.   This discovery was revolutionary, as it meant that humans may not have been the first species capable of complex speech and language. It also pushed back the appearance of this version of FOXP2 to at least 350,000 years ago.
<h6>The Role of FOXP2</h6>
Recently, the focus of genetic research into FOXP2 has focused on the specific role FOXP2 plays in our language ability.   Was it involved in enhancing our cognitive abilities?   Our motor skills? Our breathing patterns?   The results of scientists&#8217; most recent effort to uncover the answers to these questions are in the May 29th issue of <a href="http://www.cell.com/fulltext/S0092-8674%2809%2900378-X" target="_blank" rel="noopener noreferrer">Cell</a>, in a paper published by researchers from the Max-Planck Institute of Evolutionary Anthropology.
In order to advance our understanding of FOXP2, the scientists chose to examine its expression in mice, a surprisingly strong model for many human biological systems.   The chief difference in FOXP2 between humans and many other species such as mice boils down to two changes in the gene.   At some point in human prehistory, these changes arose and quickly became universal in the FOXP2 of humans.
To see what effect those changes might have had, the Max Planck scientists altered the copies of FOXP2 in mice to be identical to the copies of FOXP2 in humans.   They then examined any changes that took place surrounding the cognition and vocal skills of the genetically altered mice, to see how they might be affected by the supposedly advanced copy of FOXP2.   And, while the linguistic skills of the mice failed to rival our own, the scientists did see some surprising changes.  
<h6>Squeaking</h6>
First, they found that the altered mice showed changes in their brain circuitry that bore some similarity to that of humans.   And perhaps most intriguing, the altered mice had distinct ultrasonic vocalizations that differed from their unmodified brethren.   Ultrasonic vocalizations, sometimes referred to as chirps or squeaks, are used by mice to communicate to each other, such as to warn of a predator.  
When the young altered mice were separated from their mothers, something that usually elicits many such squeaks, they emitted ultrasonic vocalizations that were distinctly different in intensity and frequency than their counterparts.   The authors argue that the altered FOXP2 in the mice was influencing the type of squeaks that they were making when separated from their mothers.   And the scientists therefore believe there is some kind of connection to language development.
<h6>Being Human</h6>
But what does all this mean to humans?  
The past several years of research into FOXP2 has revealed that human patients who carry at least one non-functional version of the gene (i.e., the version of the gene found in species other than humans) have problems producing the facial movements necessary to form words.   It had been thought that part of the function of FOXP2 in humans was to develop motor control needed to articulate our mouths, vocal chords, and esophagus to produce complex language.   Many experts have also proposed that FOXP2 in humans plays a role in the development of both the lungs and the esophagus &#8211; both of which are vital to speech.   This most recent study shows that by simply tweaking FOXP2 in mice, we see a noticeable change in how they communicate.
Clearly, there is much more work to be done and many more questions to be answered.   In the future, these researchers envision going even further to understand exactly how FOXP2 influences our ability to communicate with each other.  
Their next goal? 
To understand the exact mechanics behind the version of FOXP2 found in humans, so that they can finally piece together its importance in giving us the power of speech.

New Research on FOXP2 Gene in Mice Reveals Insights to Origins of Language in Humans

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Type 1 diabetes is on the rise in European children, says a new report.
Researchers studied type 1 diabetes data collected between 1989 and 2003 at 20 centers in 17 European countries. Their results, published online yesterday in the <a href="https://dx.doi.org/10.1016/s0140-6736(09)60568-7" target="_blank" rel="noopener">Lancet</a>, show that more children, especially younger children, are being diagnosed with the disease each year.   Based on the trends they saw, the scientists calculate that there were 94,000 kids under the age of 15 with type 1 diabetes in Europe in 2005, and that by 2020 that number will soar to 160,000.
While researchers aren&#8217;t exactly sure why this is, they do know that it&#8217;s not due to changes in the prevalence of susceptibility genes.   Genes just don&#8217;t change that quickly.
An almost 70% increase in disease prevalence in one generation must be due to changes in non-genetic factors. Most random genetic changes in a population come and go pretty quickly, especially mutations that reduce fitness.   And if a new mutation does manage to stick, it would take millions of years, not tens of years, to see its effects.   Even for mutations that provide a benefit, like the one that led to the lactose tolerance seen in many people with European ancestry today, it takes a few hundred years to build-up to high enough levels in the population to cause an observable change in a trait.
An increase in disease incidence due to changes in non-genetic factors, whether they are environmental or cultural, has been seen for many diseases.   It&#8217;s especially apparent when groups migrate from low- to high-risk countries for a particular condition.   Just this month a <a href="https://www.ncbi.nlm.nih.gov/pubmed/19451499?log$=activity" target="_blank" rel="noopener">study</a> showed that Asian Americans who are <a href="http://www.physorg.com/news161883101.html" target="_blank" rel="noopener">more &#8220;westernized&#8221; have adopted the sunbathing ways</a> of their families&#8217; new homes, which the authors suggest may be the cause of increasing rates of skin cancer in this group.
But the effects of lifestyle changes can also be seen in shifts in disease rates within a population. The prevalence of obesity in United States adults, for example, jumped from 15% in the late 1970&#8217;s to nearly 35% today thanks to the trend toward eating more and exercising less.   And because of the increase in obesity, rates of type 2 diabetes are also up.
Many scientists attribute the increase in incidence of several immune system-related disease to what on the surface seems like a good thing about modern lifestyles: fewer infections.   The so-called &#8220;<a href="https://en.wikipedia.org/wiki/Hygiene_hypothesis" target="_blank" rel="noopener">hygiene hypothesis</a>&#8221; suggests that without the types of infections our species evolved to deal with (many of which are still prevalent in developing nations), our immune systems don&#8217;t get the right training.   The lack of challenges to the immune system has been linked to increased rates of allergic diseases like asthma and eczema and autoimmune diseases like Crohn&#8217;s and multiple sclerosis.
For some diseases, the reason behind their apparent increases has more to do with increased detection than changes in environment. Up until a few years ago, for example, it was thought that only about one in every 3,000 people in the United States had celiac disease.   But now, thanks to better guidelines on how to diagnose the disease, physicians are finding that about one in every 133 is affected.
On the other hand, some conditions may appear to be increasing because disease awareness is a hammer that makes a lot of people feel like nails.   It has been put forward that restless legs syndrome, for example, is far less prevalent than some estimates suggest and that increases in diagnoses can be traced to &#8220;<a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030170" target="_blank" rel="noopener">disease mongering</a>&#8221; by pharmaceutical companies.
The authors of the Lancet study suggest that the changes in type 1 diabetes rates they are seeing are due to something about modernization.   They point to the fact that the biggest increases were seen in eastern European countries, which have seen the most rapid changes in lifestyle in the last few decades.   But whatever the culprit is, it is obviously not affecting all children.   And that&#8217;s where genetic susceptibility comes in.   DNA variations that increase risk may not be changing in prevalence, but type 1 diabetes, like almost every other common disease, is the result of a complex interplay of genes and environment.
(23andMe customers can see how their genes influence their risk of type 1 diabetes in Clinical Reports.)

Environment, Not Genes, Key To Increasing Disease Rates

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Malaria is one of the leading causes of death in the developing world, claiming nearly a million victims each year. The great majority of them are African children below the age of five. The illness is caused by a single-celled parasite called Plasmodium that is transmitted by mosquito bites to humans. In a paper published today in <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.388.html" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, a group of African and British doctors and scientists report on their study of the genetic roots of malaria susceptibility. They found no new smoking gun with this effort, but learned much about how to improve African genetic studies in the future.

The researchers gathered the SNP genotypes of 2,500 children, with the consent of their parents, from a small region in The Gambia. About 1,000 of the children had been admitted to the hospital with a case of severe malaria – the other 1,500 were newborns. In a <a href="https://www.genome.gov/20019523" target="_blank" rel="noopener noreferrer">genomewide association study</a>, the researchers checked each of a half-million SNPs (single nucleotide polymorphisms) for sharp differences in genetic composition between the group of children suffering from malaria and the group of newborns, who served as an approximation of a malaria-free group. If one version of an individual SNP was seen at high frequency among the malaria victims, but at low frequency in the newborns, then the difference might be because the SNP tends to cause malaria or is nearby one that does.
Upon scanning their data, the researchers came up more or less empty-handed: by the usual standards of the field, none of the 500,000 SNPs would pass muster.
This deflating result stands at odds with what is known already about the genetics of malaria susceptibility. Most people who have taken a biology class learn that human populations in malarial regions have developed a natural immunity to malaria infection, not through their immune systems, but through a genetic modification of hemoglobin. Hemoglobin is a molecule charged with ferrying oxygen from your lungs (and the lungs of most life forms that have them) to all your cells, an essential task. Biologists have traced hemoglobin-based malaria resistance to a change at a single DNA base pair on chromosome 11 – wouldn&#8217;t we expect at least this SNP to light up as significant?
In truth, the failure wasn&#8217;t so surprising; it arises from the interplay of genetics with our species&#8217; history. Humans first arose in Africa, so that&#8217;s where genetic variation has had the longest time to build up. Modern-day Asian, European, and Native American people descend from people who emigrated from Africa about 50,000 years ago. These migrants carried just a subset of the African gene pool with them, so non-African populations today have much less &#8220;well-mixed&#8221; genomes than African populations. The present study uses genotyping chips developed for use in European populations, and its failure to find the known hemoglobin SNP (which isn&#8217;t even genotyped by the chip) and other known genetic contributors to malaria resistance is essentially due to the fact that you&#8217;d need more like two million SNPs than half a million to do the job right.
The solution, you&#8217;d think, is just to make a chip with a lot of markers for specific use in Africa, and be done with it. But the authors show that African genomes appear to be mixed so well that no single such chip could be designed. Instead, they propose an alternative approach: use a good but inevitably suboptimal African SNP chip in your full study sample, then obtain full genome sequences from a small number of the members of that sample. Then, using a powerful statistical method called imputation, you use the full sequences of the smaller group to fill in the full genomes of the entire study sample based on their SNP genotypes. This approach, as the authors demonstrate convincingly in the case of hemoglobin-based malaria resistance, would provide a statistically powerful and economically viable means of tracking down the causes of some of the most challenging health problems of our time.

Gloom but not Doom, Concludes Study in Malaria Area

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Congenital general hypertrichosis (CGH) is one of humans&#8217; most unusual genetic conditions. Sometimes known as &#8220;bearded lady syndrome,&#8221; it leads to excessive hair across the body and faces at levels much higher than the normal range for humans.   The condition has been of interest for centuries, becoming more well-known during the 19th century as P.T. Barnum&#8217;s traveling circuses began exhibiting those suffering from it.   Most famously,   <a href="https://en.wikipedia.org/wiki/Julia_Pastrana" target="_blank" rel="noopener">Julia Pastrana</a> (pictured, right), a Mexican-born woman afflicted with CGH, was exhibited in circuses across the United States and Europe during the mid-19th century.   She was often described as not only being excessively hairy all over her body and face, but of having a wide nose, enlarged gums, and overall &#8216;ape-like&#8217; features.
Since the Middle Ages, when this condition was first reported, there has been much speculation over the root causes of CGH. Some have argued that CGH is an example of atavism or an evolutionary &#8216;throwback&#8217; to a more primitive ancestor.   Others have reasoned (incorrectly) that individuals suffering from CGH represented the missing link between apes and humans, and thus, further evidence to support Darwin&#8217;s theory of evolution.
Because CGH tends to run in families, many believed there was a genetic component to the condition.   A team of geneticists led by Xue Zhang of the Chinese Academy of Medical Scientists have uncovered the genetic basis for this condition after examining several families with a history of CGH.   Their results are described in the June 12 issue of the <a href="http://www.cell.com/AJHG/abstract/S0002-9297(09)00160-8" target="_blank" rel="noopener">American Journal of Human Genetics</a>.

One of the researchers&#8217; major challenges was simply finding subjects to study; there have been only a handful of confirmed cases over the past few hundred years.   Zhang and his team, however, were able to isolate several examples of CGH for study.   They examined three Han Chinese families whose members exhibited various degrees of a form of CGH known as congenital general hypertrichosis terminalis (CGHT).   This type of CGH usually causes overgrowth of very thick, dark hair on the face and body, enlarged gums and otherwise distorted facial features.   It is believed that Julia Pastrana suffered from CGHT.
The researchers also examined an unrelated Chinese individual with a severe case of the condition.   For the three Chinese families, the authors created a detailed pedigree in order to determine how CGH was passed down from generation to generation.   Then, they performed a high-resolution genetic analysis of each individual.   They found at least four distinct genes that were likely related to this condition, all on Chromosome 17.   The authors believe that mutations in these genes, specifically either insertions or deletions of strands of DNA within them, may be at the root of the condition.   In fact, there have been reports of CGH (or at least CGH-related symptoms) among individuals suffering from trisomy 17; when someone inherits three copies of chromosome 17 from his or her parents, rather than the standard two copies.
However, there are several different levels of severity of CGHT, as well as other types of CGH, so it is also clear that much more work must be done to tease out the precise molecular mechanisms for why these four genes on a particular stretch of chromosome 17 should be so central to the prevalence of this rare condition.

Genetics Behind “Bearded Lady Syndrome”

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2970" title="autismawareness" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/autismawareness.jpg" alt="" width="141" height="247" />
Researchers have identified <a href="https://blog.23andme.com/articles/snpwatch-connections-between-brain-cells-may-be-key-to-autism-puzzle/" target="_blank" rel="noopener">yet another</a> common genetic variation that appears to be associated with autism.   The results, published this week in the journal <a href="https://dx.doi.org/10.1038/mp.2009.41" target="_blank" rel="noopener">Molecular Psychiatry</a>, show that each copy of an G at in the CACNA1G gene increase the odds of autism in boys (but not girls) by about 2.2 times.
But Stanley Nelson, senior author of the study and a 23adMe scientific advisor, points out that the G version of this SNP is actually fairly common.
&#8220;Most people with the risk genotype will not develop autism.&#8221;
For more on this story:
<ul>
<li><a href="https://www.bloomberg.com/apps/news?pid=20601124&amp;sid=aLhQfJuxV8.s&amp;refer=home" target="_blank" rel="noopener">Gene May Offer Clue Why Autism Risk Is Fourfold Higher in Boys</a></li>
<li>A Genetic Clue to Why Autism Affects Boys More</li>
<li><a href="http://newsroom.ucla.edu/portal/ucla/ucla-scientists-identify-new-gene-92513.aspx" target="_blank" rel="noopener">UCLA scientists identify new gene linked to autism risk</a></li>
</ul>

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