<img loading="lazy" decoding="async" class="alignright size-full wp-image-2154" title="tallshort" src="https://blog-api.23andme.com/wp-content/uploads/2008/12/tallshort.jpg" alt="" width="400" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/12/tallshort.jpg 400w, https://blogcms.23andme.com/wp-content/uploads/2008/12/tallshort-300x225.jpg 300w" sizes="auto, (max-width: 400px) 100vw, 400px" />
The genetics of height is incredibly complex. Though height is strongly determined by genetics, no single gene appears to have much influence over how tall a person will be. Instead, there appear to be dozens of genetic variants involved, none of which account for more than a few millimeters&#8217; height difference.
It will be no small feat for geneticists to identify all of the genetic contributors to height and out how they work together. But by analyzing growth data for a group of 3,538 people who were born in northern Finland in 1966, an international group of researchers has taken a step in that direction by figuring out when a few height-related genes exert their effects. They describe their research in the March issue of <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000409" target="_blank" rel="noopener">PLoS Genetics</a>.

Humans tend to do most of their growing in two spurts, once during infancy and then again around the onset of puberty. Growth during infancy tends to be associated with how much nutrition a child absorbs, whereas the second growth spurt is governed more by hormonal signals. So it would not be surprising to find that different sets of genes are associated with growth during the two periods.
The researchers tested that theory by selecting 48 SNPs that have been associated with adult height in previous studies. Then they looked at growth data for each subject from birth to age 20 to determine whether any of those SNPs was associated with growth during infancy, around puberty or both.
Five SNPs were significantly associated with growth during infancy, and seven with the puberty-associated growth spurt. Only one was associated with growth during both periods.
The researchers were especially interested in two SNPs. One was in the gene SOCS2, which influences growth hormone signaling, and was associated with growth during puberty. The other was in the gene HHIP, which is involved in embryogenesis and development, and was associated with growth during infancy.
(23andMe customers can check their genotype for both of these SNPs using the Genome Browser. Each T version of the SOCS2 SNP was associated with faster growth during infancy, and 4.7 mm of adult height. Each A version of the HHIP SNP was associated with faster growth around the time of puberty, but was not significantly related to adult height.)
This research illustrates the value of collecting data over time in genetic association studies. Knowing not just whether, but when, a particular genetic variation exerts its effects can provide vital clues to how it works.

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New Study Shows When Some Height-Associated Genes Influence Growth

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3000" title="kingtut" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/kingtut.jpg" alt="" width="350" height="278" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/03/kingtut.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/03/kingtut-300x238.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Diagnostic imaging of King Tut&#8217;s mummy suggests the pharaoh may have had a slightly cleft palate.
Last year researchers reported in <a href="https://blog.23andme.com/2008/10/06/snpwatch-genetic-variant-linked-to-cleft-lip/" target="_blank" rel="noopener">Nature Genetics</a> their discovery that a SNP in the gene IRF6, on chromosome 1, is associated with clefting of the lip and/or palate. About one child in 700 is born with clefting, which results from improper fusing during fetal development of the different elements that will make up the lower part of the face. Though some rare conditions are associated with clefting, most cases do not have any identifiable cause.
Now an international team led by German researchers has discovered a second genetic marker that increases the odds of cleft lip and/or palate six-fold among people who inherit the high-risk version of the marker from both parents.
Birnbaum et al. genotyped 224 people who had been born with cleft lips and/or palates and compared them to 383 controls. In the most recent issue of <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.333.html" target="_blank" rel="noopener">Nature Genetics</a> they report finding an association between clefting and a cluster of SNPs on chromosome 8.

The most statistically significant association was with rs987525. Subjects with one A at the SNP had 2.57 times the odds of clefting compared to those with a C at both copies. And subjects with an A at both copies had about six times the odds of clefting.
(23andMe customers can check their data using SNP rs987525 in the Browse Raw Data feature.)
The stretch of chromosome 8 where rs987525 is located is a particularly featureless region of the human genome, so it is difficult to pin down the mechanism behind the association. But whatever that mechanism is, the authors estimate that it accounts for 41% of the clefting cases in the population they studied.
Clefting is most common among Asian populations, with intermediate incidence among Europeans and the lowest rates observed among Africans. Yet the high-risk version of rs987525 shows the opposite distribution; it is almost three times more common among Africans than Europeans, and nearly absent among Asians.
In their Nature Genetics paper, the authors offer several possible explanations for this anomaly. It could be that there are other genetic or environmental factors associated with clefting that remain undiscovered, or that the linkage between rs987525 and the as-yet-unknown genetic mechanism it is pinpointing differs in the various continental populations.

Second Variant Linked to Cleft Lip and Palate

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3045" title="skeleton" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/skeleton.gif" alt="" width="300" height="219">
Throughout the course of human evolution, there have been plenty of <a href="https://blog.23andme.com/2008/09/24/what-it-means-to-be-human/" target="_blank" rel="noopener">firsts</a>. Small changes in our genetic code have laid the groundwork for our bipedal gait, our large brains, and our ability to speak complex languages.
There are countless genes throughout the human genome that distinguish us from our evolutionary relatives; now scientists have found yet another example. However, unlike novel and uniquely human mutations like <a href="https://en.wikipedia.org/wiki/FOXP2" target="_blank" rel="noopener">FOXP2</a> and <a href="https://en.wikipedia.org/wiki/MYH16" target="_blank" rel="noopener">MYH16</a>, this gene has been nestled in suspended animation within our genomes for tens of millions of years: it just needed a wake-up call. In this week&#8217;s issue of <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000403" target="_blank" rel="noopener">PLoS Genetics</a> , an international team of scientists investigates this gene&#8217;s unique history.

Their analysis centers on a family of genes known as Immunity Related GTPases (or, IRG). Most mammals have many copies of these types of genes, which play a vital role in helping the immune system resist pathogens like bacteria. But humans and our closest relatives &#8211; the Great Apes &#8211; have one IRG gene, IRGM. Yet our slightly more distant relatives, such as the monkeys, have no working copies of IRGM, or any other members of the IRG gene family.
How could it come to pass that we and the apes share more in common with mice &#8211; at least in terms of IRG &#8211; as opposed to other primates? That apparent discrepancy turned out to be central to understanding the genetic history of IRGM.
The answer, according to the geneticists, was relatively simple: When looking at the evolution of our species, going back tens of millions of years, it is clear that IRGM was never &#8216;erased&#8217; from our genomes. Instead, it simply laid dormant, and it was not until the common ancestor of apes and humans split off from monkeys that IRGM awoke from its long slumber.
The exact reason that IRGM was reborn in species such as humans and apes, but not monkeys, is not yet completely understood. We do know, however, that the fact that most humans have a working copy of IRGM is quite fortuitous. As mentioned above, the IRG genes are essential to controlling bacteria, specifically by maintaining the delicate balance of bacterial growth and immune control in our intestines. Recent research has shown that those without a working copy of IRGM have a greater risk of developing Crohn&#8217;s Disease, in which an individual&#8217;s immune system begins attacking the friendly bacteria living in our guts. The results are chronic &#8211; and painful &#8211; digestive problems. Without a doubt, IRGM is beneficial to the health and well-being of our digestive system, and its role in decreasing the risks of Crohn&#8217;s Disease cannot be underestimated.
Beyond shedding light on the practical value of IRGM, this study has revealed the first instance of a gene being &#8216;reborn&#8217; after lying dormant for millions of years. As the study&#8217;s team leader, University of Washington professor of Genomic Sciences Evan Eichler put it, &#8220;These findings tell us we shouldn&#8217;t count a gene out until it has been completely deleted.&#8221;
How many other resurrected genes are sprinkled throughout the human genome? As the field of genetics explores the hidden depths of our genomes, we can only begin to wonder how many similar discoveries await.

Don’t Call it a Comeback:  The Life, Death, and Rebirth of the Human IRGM Gene

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3026" title="africanpygmiesmap" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/africanpygmiesmap.png" alt="" width="350" height="247" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/03/africanpygmiesmap.png 350w, https://blogcms.23andme.com/wp-content/uploads/2009/03/africanpygmiesmap-300x212.png 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Once distributed throughout tropical Africa, Pygmies now live in pockets of the continent&#8217;s rainforest.
Africa is home to a number of dwindling hunter-gatherer populations, most of them living deep in the rainforests that stretch from western Africa&#8217;s Atlantic coast to the eastern edge of the Democratic Republic of Congo. Known as &#8220;Pygmies&#8221; because of their short stature, previous studies (including <a href="http://www.sciencemag.org/cgi/content/abstract/319/5866/1100" target="_blank" rel="noopener">one</a> funded by 23andMe) have shown that these forest-dwelling groups are descended from populations that arose 20,000 to 50,000 years ago.
But today populations such as the Mbuti, who live in the eastern forest, speak radically different languages from those spoken by the Biaka and other groups who live in the west. In fact, the Biaka speak a language belonging to the Niger-Congo linguistic family, which is associated with the expansion of agriculture throughout sub-Saharan Africa less than 5,000 years ago.
How did a hunter-gatherers in the African rainforest end up speaking less like their distant cousins and more like their farming neighbors? A paper published last month in <a href="http://www.cell.com/current-biology/abstract/S0960-9822(09)00542-9" target="_blank" rel="noopener">Current Biology</a> offers an explanation by genetically modeling the population history of the western African Pygmies and their farming neighbors using autosomal DNA, which is inherited from both parents.

Verdu and colleagues suggest that for most of the last 50,000 years western Pygmy groups were a single population, exchanging marriage partners and migrating through large tracts of the western forest. They also suggest that, contrary to earlier studies, the western African Pygmies were isolated from non-Pygmy populations until about 2,800 years ago, when they began exchanging marriage partners with neighboring farming populations.
Today, social taboos discourage Pygmy men from taking wives belonging to neighboring farming groups. But farming men and Pygmy women can marry, and sometimes the children of these unions sometimes return to their mother’s natal group in the forest. These cultural taboos and the resulting sex-biased gene flow probably began after western Africans invented farming techniques and began expanding through the rainforests about 5,000 years ago.
The research by Verdu and colleagues is the first to put a date on the breakdown of western Pygmy migration patterns due to the expansion of farmers – about 2,800 years ago. The integration of western Pygmy groups and farmers is also reflected in the linguistic similarity between the groups; both speak Niger-Congo languages. It is generally assumed that this linguistic shift occurred as farmers and hunter-gatherers intermarried.
The original languages of these western Pygmies have now been lost. But because Pygmy women have been marrying into farming groups for millennia, their genetic signature is well preserved in both populations. Using mitochondrial DNA, which is passed down from mother to child, genetic researchers discovered that over 80% of western Pygmies carried lineages derived from haplogroup L1c1a. About 20% of farmers from neighboring villages in western Africa carry the same haplogroup as evidence of their Pygmy maternal ancestry.
Could you have Pygmy ancestors? That&#8217;s difficult to say. About 12% of African Americans carry mitochondrial DNA lineages belonging to haplogroup L1c, which indicates maternal ancestry somewhere in the Congo basin and surrounding areas, but not Pygmy ancestry per se. Absent a confirmed assignment to L1c1a, the odds are that the maternal ancestry of an African American individual in haplogroup L1c traces back to farming rather than Pygmy populations.

The Origins of the Forest-Dwelling African Pygmies

<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="153" height="268" />
Autism, a neurological disorder that impairs a person’s ability to communicate with and relate to others, affects one in every 150 American children. Genetics is thought to be at least partly to blame for this condition, but research aimed at finding the genes involved has been frustratingly slow.
This is due at least in part to the fact that it’s unlikely that there is one or even a small number of “autism genes.” Autism is a &#8220;spectrum disorder&#8221; that affects individuals differently and to varying degrees.   There are probably different genetic and environmental factors at work in different types of autism.
New research, published online this week by the journal <a href="https://dx.doi.org/10.1542/peds.2008-0819" target="_blank" rel="noopener">Pediatrics</a>, may shed light on the genetic underpinnings of at least one subtype of autism. Research has shown that gastrointestinal (GI) problems are more common in people with autism than the general population.   The new work shows that variation in a signaling protein involved in both brain development and gastrointestinal repair may contribute to an increased risk for the types of autism that include gastrointestinal dysfunction.
“Our study is the first to bring together genetic risk for autism and co-occurring GI disorders in a way that provides a biologically plausible explanation for why they are seen together so often,” said Pat Levitt, director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of USC and senior author of the study, in a statement.
<a href="https://dx.doi.org/10.1073/pnas.0605296103" target="_blank" rel="noopener">Previous research</a> by Levitt’s group showed that a SNP in the Met gene increases the risk of autism. People with one copy of the variation have 1.67 times the risk of autism and people with two copies have 2.27 times the risk.
The current study looked at 918 people from 214 families with at least one child affected by autism and found that the association between the condition and the SNP holds only in those patients with GI disorders such as chronic constipation or diarrhea, irritable bowel syndrome, gastroesophogeal reflux or peptic ulcer disease.
The researchers suggest that types of autism that include GI disorders may be a distinct class of the condition, with the Met gene playing an important part.     Their previous work demonstrated that the version of the variation that increases the risk of autism reduces the amount of protein made from the Met gene.   People with autism were also shown to have less Met protein in their brains than age and gender matched controls.
The authors warn that their study was small and the association of the variation they focused on does not completely explain the high prevalence of GI disorders in people with autism.   They say their results should be considered “exploratory.” Nevertheless, the findings may bring researchers closer to understanding the complex genetics of autism.

Researchers Identify Genetic Variant Linking Autism And Gastrointestinal Disorders

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2907" title="kitonly" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/kitonly.jpg" alt="" width="388" height="259" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/kitonly.jpg 388w, https://blogcms.23andme.com/wp-content/uploads/2009/02/kitonly-300x200.jpg 300w" sizes="auto, (max-width: 388px) 100vw, 388px" />
The way our Personal Genome Serviceâ„¢ works is pretty straightforward, at least from a customer&#8217;s point of view. We send you a saliva collection kit, which is at its heart a plastic tube. You spit in the tube and send it to our laboratory, which extracts DNA from your saliva, analyzes it and deposits the resulting genetic data in your account.
Though the process usually goes off without a hitch, each sample has to clear a number of quality control hurdles in order to be processed. If it doesn&#8217;t, a customer&#8217;s data may take a little longer than expected.
Sample problems can almost always be corrected one way or another. It is only in very rare cases that a person&#8217;s saliva contains so little DNA that repeated efforts to analyze it fail (In those situations, we do provide a refund!).
For those of you who really want to know all the messy details, below is a detailed account of what can go wrong with a sample, and what we do if it does:

<h6>Step One: The Visual Exam</h6>
Samples arrive at our lab every day. The first thing technicians do with each new sample is scan the barcode on it, because that&#8217;s the only identifying information the laboratory has. For privacy reasons, the customer&#8217;s name and other account information never passes beyond the 23andMe firewall.
As soon as the samples have been scanned, they undergo their first test – a visual inspection to make sure they contain fluid up to the &#8220;fill line&#8221; on the side of the tube. Occasionally samples do not pass, either because they leaked in transit or the preservative solution (buffer) isn&#8217;t released into the tube when the customer snaps the oblong cap onto the collection funnel. Either way, if a sample tube doesn&#8217;t contain enough liquid we immediately contact the customer and ship a free replacement kit so he or she can spit again.
<h6>Step Two: DNA Extraction</h6>
If a sample passes visual inspection, it&#8217;s time for DNA extraction. The process our laboratory uses to isolate and purify the DNA in your saliva is simply an automated version of the same one you can do at home that allows technicians to process batches of 96 samples. Technicians remove a portion of the saliva from each tube, then put the rest of the sample aside so they can try again in case their first attempt fails. If a second attempt to extract DNA from a particular sample fails as well, we send a second kit to the customer who provided it (free of charge) so that person can provide a fresh (and hopefully DNA-rich) one.
A sample may lack enough DNA for extraction if the preservative solution is not released when the customer snaps the cap onto the funnel during the collection process. A sample could also contain an insufficient amount of DNA simply because there are not enough cells floating around in it. Some people seem to have less DNA in their spit, though almost everyone has enough for the purposes of our analysis.
<h6>Step Three: Genotyping</h6>
Samples that yield sufficient quantities of DNA are submitted for genotyping,   which scans the genetic material at the approximately 580,000 markers (SNPs) included in our service. This process is also performed in batches of 96 samples. And once again, we monitor the process to make sure it is going as expected. If it isn&#8217;t, we try again. In this case a sample is re-run if the analysis process cannot determine its genotype at a minimum of 98.5% of the locations we probe (roughly 570,000 out of the 580,000). If the second attempt fails as well &#8230; we ship the customer another sample collection kit for free.
Once a sample has been successfully analyzed, the laboratory sends the resulting data to 23andMe along with the barcode that came with the sample. That allows our database to deposit the information in the proper account and send an automated email notification to the customer who holds it.
With all the things that can go wrong, the sample analysis process may seem a little precarious. But it&#8217;s actually quite robust – the vast majority of samples sail right through without a hitch. If things do go smoothly, we can generally return data within eight to 10 weeks of the date a sample is sent to the lab.
My name is Varsha Baichwal and I work here at 23andMe as Director of Operations. You can share your genome with me if you wish — my 23andMe ID is “varsha”.

What Happens After I Spit? A Saliva Sample’s Saga

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2958" title="cocainelabel" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/cocainelabel.jpg" alt="" width="350" height="215" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/03/cocainelabel.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/03/cocainelabel-300x184.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Cocaine use, and its attendant dangers, cut across all regional, age, ethnic and socioeconomic lines. A 2002 survey revealed that almost six million Americans 12 and older used cocaine during the preceding year, with more than one million compulsively taking the drug and meeting the criteria for being deemed “dependent”.
Several studies have suggested that genes play a part in determining how a person will react to cocaine.   Identifying these genetic factors could help scientists understand why some people become dependent on the drug and might provide clues as how to best treat addiction. In a study published online this week in the <a href="http://archpsyc.ama-assn.org/cgi/content/short/66/3/267" target="_blank" rel="noopener">Archives of General Psychiatry</a>, researchers show that one piece of the genetic puzzle might be an unlikely candidate — a gene involved in quality control of proteins within cells.
“This finding…suggests that drug dependence and associated behaviors may involve biological pathways not typically associated with brain metabolism and opens a new pathway to understanding these highly prevalent disorders and their psychopathologic manifestations,” the author write.
Based on evidence from a <a href="https://www.ncbi.nlm.nih.gov/pubmed/18438686?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">previous study</a> of substance abuse disorders that suggested that the MANEA gene plays a part in cocaine dependence, the researchers studied 11 genetic variations scattered throughout the gene in approximately 4,000 Americans of either European or African ancestry. The protein encoded by MANEA is involved in regulating how sugar molecules are attached to certain proteins, a process important for the proper function of many proteins.
Although the results varied somewhat between the study groups examined, and the evidence was stronger for a link between MANEA and cocaine-induced paranoia than it was for cocaine dependence in general, the researchers conclude that the gene is a good candidate for further research.   The strongest association across all groups studied was between cocaine-induced paranoia and the SNP .   Having the A version of this SNP increased odds of paranoia.
The authors say that additional studies, in both cocaine dependent people and perhaps in people with other disorders involving paranoia, will be necessary to determine whether the variations in the MANEA gene are specifically associated with cocaine-induced paranoia.
Even if variations in MANEA are confirmed to be associated with cocaine dependence and/or cocaine-induced paranoia, the question of why will still remain. The authors suggest that one possibility is that changes in the protein encoded by the MANEA gene could interfere with the sugar modifications on another protein, dopamine Î²-hydroxylase, which is involved in the conversion of dopamine to norepinephrine in the brain.   The dopamine pathway is a key target of cocaine, and abnormally low levels of dopamine Î²-hydroxylase have been associated with psychotic symptoms in several psychiatric disorders, including cocaine dependence.   Changes in the MANEA protein could also affect how cocaine is processed in the liver.

Unlikely Gene May Contribute To Cocaine Dependence and Paranoia

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2950" title="cutemouse" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/cutemouse.jpg" alt="" width="350" height="184" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/03/cutemouse.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/03/cutemouse-300x158.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Our bodies need iron: to form the oxygen-carrying hemoglobin for our red blood cells, maintain our immune systems and keep our muscles and brains functioning properly.
But not too much.
<h6>Iron Build Up</h6>
Excess iron can build up in tissues like the liver, heart and pancreas, causing damage and possibly organ failure.
Other than blood loss, there’s no way for the human body to rid itself of excess iron.   The only way to regulate iron levels is by adjusting how much is taken in from food. Low iron levels in the body lead to more absorption in the gut, high iron leads to less.
There are several known genetic mutations that interrupt this iron absorption control mechanism, leading to a condition called hereditary hemochromatosis.   But there are some forms of this disease for which the causative mutation isn’t known, and not everyone with one of the known mutations actually ends up having hemochromatosis.   These observations suggest there are genetic factors affecting iron level control that have yet to be identified.
<h6>Iron Overload</h6>
Two reports published online yesterday by the journal <a href="https://dx.doi.org/10.1038/ng.335" target="_blank" rel="noopener noreferrer">Nature</a> <a href="https://dx.doi.org/10.1038/ng.320" target="_blank" rel="noopener noreferrer">Genetics</a> may have identified one of these additional genetic factors.   Researchers working with mice have found that disrupting the function of the BMP6 gene can lead to iron overload much like that seen in the severe childhood-onset forms of human hemochromatosis.
“Although no human patients with BMP6 mutations have yet been described, our data …suggests that BMP6 mutations or BMP6 gene variants may function as another cause of hereditary hemochromatosis or a modifier of disease penetrance,” write the authors of <a href="https://dx.doi.org/10.1038/ng.335" target="_blank" rel="noopener noreferrer">one of the studies</a>.
23andMe customers can learn whether they are carriers of the mutations that cause adult-onset hemochromatosis using the Health and Traits feature.

Mouse Research May Shed Light On Human Iron Disorder

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2941" title="istock_000005831286xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/istock_000005831286xsmall.jpg" alt="" width="301" height="309" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/istock_000005831286xsmall.jpg 342w, https://blogcms.23andme.com/wp-content/uploads/2009/02/istock_000005831286xsmall-292x300.jpg 292w" sizes="auto, (max-width: 301px) 100vw, 301px" />
Each of us is made up of about 50 trillion cells, which is pretty mind-blowing until you consider the number of microbial cells living on or in each of us.   It’s estimated that a healthy adult is lugging around 10 times more bugs. Most of them are bacteria rather than human cells.
Just as the tiny differences we each harbor in our DNA can reveal information about our health and our ancestry. It might also reveal the subtle differences in the types of bacteria we all carry.
<h6>Human Microbiome</h6>
The NIH has initiated a large project to explore the so-called “human microbiome” and its implications for our health.   Other projects are using bacteria to trace ancient migrations and human interactions.
Today scientists published the first in-depth study of global diversity in a specific human microbiome — the mouth. There is wide variety around the world in dietary and other cultural factors that could influence the types of bacteria found in a person’s mouth. However, the researchers discovered that the an individual’s “salivary microbiome” is likely to be just as different from a neighbor’s as it is from someone on the other side of the world.
“[T]here is significantly more diversity in bacterial genera [types of bacteria] compared from different individuals than from the same individual,&#8221; the authors write. &#8220;[But] the diversity among individuals from the same location is nearly the same as the diversity among individuals from different locations.”
Their results appear online in <a href="https://genome.cshlp.org/content/early/2009/02/23/gr.084616.108" target="_blank" rel="noopener">Genome Research</a>.
<h6>Oral Bacteria</h6>
The researchers studied the oral bacteria of 120 people — 10 individuals from each of 12 worldwide locations: Oakland, CA; Baton Rouge, LA; La Paz, Bolivia; Buenos Aires, Argentina; Pointe Noire, Congo; Johannesburg, Sought Africa; Surigao, Philippines; Shanghai, China; Batumi, Georgia; Ankara, Turkey; Warsaw, Poland; and Dessau/Leipzig, Germany.
Overall, DNA analysis identified a total of 101 known types of bacteria. Thirty-nine of those had not previously been found in the human mouth.   The scientists also found evidence for another 64 unknown bacterial types lurking in people’s mouths.
Their results lay the groundwork for future studies that will explore the influence of environmental, dietary and genetic factors on the types of bacteria found in a person’s saliva.   This may lead to a better understanding of the role of saliva bacteria in mouth diseases. It can also shed light on the interaction of the salivary microbiome with other microbial environments in the body, such as the intestines.
Their work could also help expand the use of bacteria in the study of human history. The stomach bacteria H. pylori has already been used in several studies to investigate human history. Just last month a study using this bacteria revealed new information about <a href="https://blog.23andme.com/2009/01/22/thinking-outside-the-box-bacterial-genetics-and-the-peopling-of-the-pacific/" target="_blank" rel="noopener">how Polynesia was colonized</a>.   But while these H. pylori studies have been impressive, they do have a downside: a stomach biopsy is needed to get the samples.
“There would be obvious advantages if similarly-informative bacterial species could be identified in saliva,” the authors write, suggesting that their work might help identify just such a species.

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