<img loading="lazy" decoding="async" class="alignright wp-image-1857 size-medium" title="dutchrations" src="http://35.88.189.111/wp-content/uploads/2008/11/dutchrations-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/dutchrations-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/11/dutchrations.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
We all know that what a mother eats, drinks, smokes and does during pregnancy can affect her child’s prenatal development. But can it actually affect the baby’s DNA?
Animal studies have shown that transient environmental exposures of a pregnant female can produce “epigenetic” changes in her offspring &#8212; chemical modifications superimposed on the DNA sequence that affects how and when genes are expressed.
It would, of course, be highly unethical to purposefully subject human mothers to environmental insults for the purpose of studying DNA effects in developing fetuses. But history has provided researchers a unique opportunity to study how one environmental factor, maternal nutrition, can affect an unborn child at the genetic level.
In the winter of 1944-1945, the Germans imposed a food embargo in the western part of the Netherlands, leading to a period of famine known as the <a href="https://en.wikipedia.org/wiki/Dutch_famine_of_1944" target="_blank" rel="noopener noreferrer">Dutch Hunger Winter</a>. Food was so scarce that the average daily caloric intake was cut to about 667 calories. Despite the desperate times, birth registries and the health care system remained operational, allowing researchers today to trace people who were prenatally exposed to the famine.
Higher rates of schizophrenia, addiction, obesity and heart disease have <a href="https://www.ncbi.nlm.nih.gov/pubmed/16778567?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">previously been associated</a> with people conceived during the Hunger Winter. But new results, published online last week in the <a href="https://dx.doi.org/10.1073/pnas.0806560105" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>, offer some of the first evidence that there were also epigenetic effects in these people.
Heijmans and colleagues found that people who were conceived during the Hunger Winter, and thus exposed to famine very early in their development, to this day have fewer epigenetic markers called methyl groups attached to a gene called IGF2 than their unexposed siblings. People who had been in the late stages of gestation during the famine did not show these differences.
The protein encoded by the IGF2 gene is a key factor in human growth and development. A reduction in the number of methyl groups attached to the gene affects whether the maternal copy of the gene is expressed and has been associated with an increased risk of colorectal cancer.
Although people exposed to famine during the earliest days of their development show evidence of epigenetic changes all these years later, their average recorded birth weight was no different than what was seen in children born before the famine. But the people who were late in gestation during the famine and didn’t show epigenetic effects were lighter at birth. This suggests that low birth weight, a commonly used proxy measure for compromised prenatal development, might not be sufficient for understanding the true extent of how a mother’s environment has impacted her child.
The authors of the study suggest that future research should focus on the epigenetic effects of environmental exposures that are more common in modern societies, such as over-nutrition and assisted reproductive technologies.
“Understanding how epigenetic control depends on early exposure may shed light on the link between development and health over the lifespan and ultimately suggest new ways to prevent human disease,” the authors conclude.
Photo: Sander van der Molne

23andMe Blog

23andMe Blog Team

Mom’s Experience Can Affect Your Genes

It was a great honor to learn yesterday that the 23andMe Personal Genome Serviceâ„¢ has been named TIME Magazine&#8217;s 2008 Invention of the Year. Today the Blog would like to acknowledge several 23andMe partners who contributed to the innovation behind our service.
<img loading="lazy" decoding="async" class="alignright size-full wp-image-68" title="toast" src="https://blog-api.23andme.com/wp-content/uploads/2008/01/toast.png" alt="" width="350" height="219" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/01/toast.png 350w, https://blogcms.23andme.com/wp-content/uploads/2008/01/toast-300x188.png 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
We&#8217;d like to extend our thanks to Illumina, Inc., DNA Genotek, Inc., and LabCorp, and especially to everybody at those companies who shared their ideas, expertise and hard work.
<ul>
<li>DNA Genotek produces the collection system our customers use to collect their saliva samples and ship them to our contracted laboratory. The caps, container and funnel are functional and easy to use.</li>
<li>Illumina is behind the technology we use to generate our customers&#8217; genetic data. The Illumina Human Hap550+ is a customizable DNA array that allows us to determine an individual&#8217;s genetic signature at nearly 600,000 locations on all 23 pairs of chromosomes, plus the mitochondrial DNA. Because Illumina&#8217;s technology lets our scientists select thousands of specific locations in the genome that they want to probe, we think it is the best genotyping platform for personalized genetics.</li>
<li>Labcorp is the company that brings the Spit Kit and the Human Hap550+ together. Their laboratory technicians extract DNA from our customers&#8217; saliva, then run it through Illumina arrays to produce the basic genetic data we use as the starting point for our Personal Genome Service. As a CLIA-certified laboratory with extensive experience in all types of medical diagnostic testing, Labcorp assures our customers genetic data of the utmost accuracy and quality.</li>
</ul>
A big thanks to all who help make our Personal Genome Service possible – including our partners, scientific advisors, investors, team members and customers. We hope everyone is as excited as we are to see not just our service recognized, but also our shared vision of personal genomics for all.

TIME to Thank Our Friends

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1782" title="phoeniciantrade" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/phoeniciantrade.png" alt="" width="300" height="225" />
About 3,500 years ago, the Phoenicians expanded from their homeland in present-day Syria and Lebanon, using their superior maritime technology to establish trading posts across southern Europe and North Africa.
<h2>The Rise and Fall of the Phoenicians</h2>
They traded silver from Iberia, copper from Cyprus, and textiles from Morocco. They built cities in Sicily, Malta, and Tunisia that rivaled those in Greece and Rome. However, by the 1st century BC, nearly all evidence of their power and authority over Mediterranean trade routes had vanished.
The Phoenicians&#8217; fate as a maritime power is well documented. The Persians conquered the Phoenician homeland in 539 BC. Two centuries later, Alexander the Great&#8217;s army swept in from the west. Finally, the Roman Empire conquered—and destroyed—the Phoenician city of Carthage in 146 BC following the Third Punic War.
<h2>The Disappearance of the Phoenicians</h2>
But what happened to the Phoenicians themselves? Were they wiped out, too? Or are their descendants still alive today?
In a study published this week, researchers identify Phoenician-specific DNA markers in present-day Mediterranean populations, demonstrating that genetic traces of the ancient civilization still exist in some modern-day peoples. These people could be descendants of the Phoenicians themselves.

It has always been difficult to use genetics to trace specific historical migrations, such as the Jewish Diaspora, the Norman invasion of Britain, or even the Viking expansions into Western Europe.
<h2>Using DNA to Tell a Story</h2>
Attempting to trace migrations across the Mediterranean is even more arduous, as there have been multiple migrations at different times throughout history. How do scientists sort out each unique migration event over the long and complex population history of the region? A team of geneticists from National Geographic and IBM’s Genographic Project believes they have found a way to do just that. They discuss their research in the latest American Journal of Human Genetics issue.
Traditionally, when scientists want to understand the genetic history of an area, they collect DNA samples from the entire region of interest. But in this case, the authors of the AJHG paper collected samples from specific towns and cities that are believed to have been built on or near ancient Phoenician archaeological sites, including Carthage, Cyprus, and Sicily. They reasoned that if descendants of the Phoenicians do indeed exist, they would more likely be found near these sites.
<h2>Tracing Paternal Lines</h2>
Armed with this newly collected data, the authors focused on the Y-chromosome to trace the Phoenicians’ genetic history. According to Chris Tyler-Smith, one of the study’s authors, “We chose the Y-chromosome because its male-specificity means that it would have been carried by the predominantly male Phoenician traders.” They then used a newly devised analytical method of distinguishing any Phoenician migration from other geographically similar migrations. Their results are surprisingly informative.
The authors found a weak — but significant — genetic signature among their samples that could not be explained by chance. Many of the samples belonged to a particular branch of haplogroup J2, which the authors believe points back to distinct migrations by Phoenician traders from the Middle East into Europe and North Africa more than 3,000 years ago.
The applications of the authors’ new approach to studies of population history are incredibly far-reaching. Perhaps similar analyses could be used to trace the genetic footprints of Alexander the Great and his army into Persia during the 4th century BC or migrations along the Silk Road from China during the Middle Ages. The authors even propose that their technique could be used within populations to discover historical migrations that we never even knew existed.
Photograph courtesy of Wikimedia Commons.

Ripples in the Mediterranean: Tracing the Genetic Origins of the Phoenicians

<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-1818" title="grouptwo" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/grouptwo.jpg" alt="" width="500" height="333" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/grouptwo.jpg 1000w, https://blogcms.23andme.com/wp-content/uploads/2008/10/grouptwo-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/10/grouptwo-768x511.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2008/10/grouptwo-880x586.jpg 880w" sizes="auto, (max-width: 500px) 100vw, 500px" />
Editor&#8217;s Note: This week TIME Magazine is naming the 23andMe Personal Genome Service, its Invention of the Year, an honor that the publication has previously bestowed on innovations such as the iPhone and YouTube. This post by Director of Products Alex Wong (back row, second from right) offers a glimpse at how 23andMe came to be, and what makes it such a powerful tool for exploring your DNA.
We&#8217;re thrilled that our product has been named TIME Magazine&#8217;s 2008 Invention of the Year. But what exactly did we invent? To answer that question, let&#8217;s to go back to the early days of 23andMe … .
I first met our co-founders Anne and Linda, together with Serge and Brian, our first two employees, in the summer of 2006 at a bakery in downtown Palo Alto, Calif.. As they were explaining the basic concept behind the company, Linda reached into her bag and pulled out a CD with &#8220;Aveys&#8221; written on it in magic marker.
&#8220;What&#8217;s that?&#8221;, I asked.
Her reply: &#8220;It&#8217;s my family&#8217;s genomes!&#8221;
That&#8217;s a first, I thought to myself – pulling genomes from a handbag. I was hooked. I knew I wanted to join 23andMe and help make this possible for everyone and their family.

But we had a long way to go. DNA chip technology was still fairly new, something that only researchers had access to. Linda, having worked at a DNA chip company, was able to get her own family genotyped. But unless you had an in at a research lab or one of these companies, getting your own genome just was not possible. Even if you did manage to get the genomes of you and yours on a CD, all you&#8217;d find when you looked at it would be a bunch of giant, indecipherable text files filled with &#8220;rs&#8221; numbers and A&#8217;s and B&#8217;s. These are the raw data files of SNP information that the DNA chip analysis produces.
How to make sense of all that data? The good news was that years of research, starting with the <a href="https://www.genome.gov/10001772" target="_blank" rel="noopener">Human Genome Project</a> and the International HapMap Project, had produced a wealth of publicly available information about human genetics. The bad news was, it was all locked inside databases designed by researchers, for researchers. Want to know what one of your SNPs means? A logical place to start, you would think, would be <a href="https://www.ncbi.nlm.nih.gov/projects/SNP/" target="_blank" rel="noopener">dbSNP</a>, a massive database of SNPs run by the National Institutes of Health.
Good luck. Assuming you can wade through its dense user interface, make sure you get your alignment, genome build, major and minor alleles, orientation, and stranding right, or you&#8217;re liable to get your interpretation backwards and think you&#8217;re supposed to have wet earwax when you really have dry! Don&#8217;t know what stranding, genome builds, or any of those other things are? Trust me, you&#8217;d rather not.
Not only did these government and academic databases sport slow and unfriendly user interfaces, but some of them also had data quality and consistency problems and few of them were linked together.
So it was going to require more than just building a website to make all the fruits of ongoing genetic research accessible, useful, and compelling to regular people like you and me. We had to create a whole architecture and process for cleaning up, aggregating and integrating all of this human genetic information, combining it with an individual&#8217;s own genotype data, running comparisons and algorithms on it, blending it with great educational content, and serving it back to our customers through a friendly user interface – all in under 500 milliseconds, which is how long you have before people start to complain that your website is slow.
On top of that, we wanted personal genetics to be social, so our customers could see their genetic data in context and learn about what makes us all different and similar at the same time. That meant building in the ability for customers to share their data with family or friends without sacrificing privacy or security.
It&#8217;s taken the combined talents of all the different kinds of people we have at our company, from bioinformaticians, to engineers, to writers, to UI designers, but we&#8217;re all so excited about having made it possible in 2008 for anyone with $399 to explore their own genome.
Of course, if you&#8217;d like to rock it 2006-style, you can still get your own gigantic text file full of SNPs using our Download Your Raw Data feature. You can even burn it onto a CD and stick it in your handbag!

Creating the Invention of the Year: A Look Behind the Scenes

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1787" title="276px-finland-cia_wfb_map" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/276px-finland-cia_wfb_map.png" alt="" width="276" height="600" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/276px-finland-cia_wfb_map.png 276w, https://blogcms.23andme.com/wp-content/uploads/2008/10/276px-finland-cia_wfb_map-138x300.png 138w" sizes="auto, (max-width: 276px) 100vw, 276px" />
Even though European populations have been studied for years, there are still many lingering questions as to the continent’s population history — especially with regards to isolated peoples.   Understanding the history of the Basque of northern Spain has long been a topic of interest among geneticists, as has the origins of the indigenous Saami of northern Finland.
Now, a study published by geneticists at the University of Helsinki supports the conclusion of <a id="k1oa" title="Some recent studies" href="../2008/08/13/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe/" target="_blank" rel="noopener">some recent studies</a> that have hinted that the Finnish people themselves are more genetically isolated than other European populations.
Traditional methods of examining genetic ancestry are focused on two areas of our genome: our mitochondrial DNA, which is passed down from mothers to children, revealing information on our maternal ancestry, and the Y-chromosome, which is passed down from fathers to sons, revealing our paternal ancestry.
But these are only two relatively small regions of our entire genome, and geneticists have often said that to truly understand a person’s ancestry we must examine human DNA much more broadly.   One way to do this is to use a genome-wide analysis, examining hundreds of thousands of genetic markers.   The new University of Helsinki <a id="bt3m" title="study" href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003519" target="_blank" rel="noopener">study</a> did just that, analyzing more than 250,000 unique SNPS across the entire human genome.
What the researchers found was quite intriguing.   First they investigated German and British populations as a basis for comparison and found them to be genetically close to one another – hardly a surprise considering their historical closeness.   But when the researchers looked at populations from Finland in comparison to other parts of Europe, they found few enough similarities to conclude that Finnish people are genetically isolated from other parts of Europe.

This study is important for a few reasons.   First, it illustrates that using genome-wide analysis, rather than only using the Y-chromosome or the mitochondrial DNA, can reveal much about population history.   Second, it confirms previous hypotheses that Finland — which is both geographically and linguistically isolated from other parts of Europe — is genetically isolated as well.
The ancestors of the modern Finns, once they arrived in this cold land thousands of years ago, remained relatively separate from even their closest European neighbors.   Although modern travel and telecommunications have likely reduced this isolation, the remnants of it are still evident in the genetics.

Not So Close Neighbors: The Genetically Isolated People of Finland

The Blog has pointed out several times in the last few months that when researchers look for evidence of interbreeding between early humans and Neanderthals, they often fail to find any.
But there are still several geneticists who would like us to heed the words of former defense secretary Donald Rumsfeld, who once pointed out that &#8220;the absence of evidence is not evidence of absence.&#8221;
During a briefing for science writers this morning at Stanford University, geneticist Bruce Lahn argued that interbreeding with Neanderthals may have introduced a mutation that appears to confer an evolutionary advantage about brain development into the human gene pool.
&#8220;We argue that in modern humans, there may actually be some Neanderthal genes,&#8221; Lahn said at the Council for the Advancement of Science Writing&#8217;s New Horizons in Science briefings.

Lahn based his argument on a gene known as microcephalin. Because certain gene mutations can cause brain underdevelopment, microcephalin is assumed to be involved in that organ&#8217;s development.
Lahn described research he and several colleagues first described two years ago in the <a href="https://www.pnas.org/content/103/48/18178.full?sid=a8247834-aa24-4260-b390-4213ac428291" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>. The researchers sequenced microcephalin in 89 people from populations around the world. They found that the sequences fell into two very different groups – so different, in fact, that they apparently traced back to a common ancestor older than the human species itself.
Moreover, each of the two groups appeared to have a very distinct history. One appeared to have arisen about a million years ago and diversified at a steady pace since then. The other group appeared to have arisen just 37,000 years ago and spread rapidly throughout 70% of the human population. That kind of pattern suggests what evolutionary biologists call a &#8220;selective sweep,&#8221; the introduction of an advantageous genetic variant that quickly wipes out older versions of the gene.
Usually, when geneticists see a selective sweep in action, the new variant appears to arise out of the pre-existing one. But in this case, Lahn argues, the new genetic variation traces back to a common ancestor that precedes both populations. He believes Neanderthals could have been that population and that they could have transferred the &#8220;new&#8221; variation into the human gene pool through interbreeding about 40,000 years ago.
It&#8217;s just a hypothesis at this point – and one that many geneticists consider challenging to <a href="https://www.nature.com/hdy/journal/v98/n4/full/6800953a.html" target="_blank" rel="noopener noreferrer">confirm</a>. But suppose ongoing efforts to sequence the Neanderthal genome find a version of the microcephalin gene identical to the one currently sweeping through the human population. In that case, Lahn will have strong evidence for his claim.

Did Neanderthals and Humans Mate?

<img loading="lazy" decoding="async" width="300" height="385" class="alignright size-full wp-image-1744" title="467px-charles_darwin_011" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/467px-charles_darwin_011.jpg" alt="" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/467px-charles_darwin_011.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/10/467px-charles_darwin_011-234x300.jpg 234w" sizes="auto, (max-width: 300px) 100vw, 300px" />
In the year 1831, two very important events happened to 22-year-old biologist Charles Darwin. &nbsp;
The first was that he boarded the Beagle, a research vessel upon which he would embark on a five-year journey to Central and South America. &nbsp; There he would collect mountains of data on hundreds of plant and animal species, which he would then use to develop his theory of evolution by natural selection – the cornerstone of modern biology.
The second event was that – just before boarding the Beagle – he fell extremely ill. &nbsp;
Darwin kept his condition secret for fear of being removed from the passenger list. &nbsp; But this early bout of illness was just the beginning in a series of ailments that would continually affect nearly every aspect of Darwin’s life for the next 40 years.

<h6>The Symptoms</h6>
The list of symptoms that plagued Darwin for the majority of his adult life included everything from chronic fatigue, severe abdominal pain, nausea and vomiting, headaches, insomnia, mouth ulcers, boils, anxiety, heart palpitations, and depression (just to name a few). &nbsp; In his many letters to friends and colleagues, he constantly mentioned the wretched state of his health. &nbsp;
“I have been [for] five or six wretched days miserable from morning to night and unable to do anything,” Darwin wrote in 1865 to naturalist and friend William Hooker.
Just a year earlier he had told Hooker, “for five months I have done nothing but be sick.” &nbsp;
His illness often precluded him from many public lectures and events expected of eminent scientists of the time. &nbsp; His wife, Emma, tried to care for Darwin, as did numerous physicians, but his poor health remained until his death in 1882.
The importance of Charles Darwin as a father of modern biology, combined with the complex and intriguing nature of his chronic illness, have led to many hypotheses as to why he suffered as he did. &nbsp;
Everything from heart disease to arsenic poisoning to a variety of psychosomatic causes has been proposed since his death. &nbsp; However, it is only within the last several years that these hypotheses have focused on the gastrointestinal symptoms that seemed to plague Darwin most consistently. &nbsp; Unable to examine the man himself, scientists have pored over his medical records, letters, and personal diaries, in order to posthumously diagnose Darwin’s debilitating illness.
<h6>The Case for Lactose Intolerance</h6>
During the mid-19th century, lactose intolerance had not yet been described in great detail. &nbsp; Most gastrointestinal problems were written off as ‘indigestion’ or &#8216;dyspepsia&#8217;. &nbsp; Indeed, the genetics of lactose intolerance would not be discovered until more than 70 years after Darwin’s death.
People diagnosed as lactose intolerant often suffer severe lower abdominal cramping and diarrhea after consuming milk or other dairy products (including some cheeses and various kinds of cream). Because the majority of Darwin’s symptoms appear to be centered around the digestive tract, a group of researchers from <a id="a-hb" title="Cardiff University" href="https://www.ncbi.nlm.nih.gov/pubmed/15811889?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&amp;linkpos=1&amp;log$=relatedarticles&amp;logdbfrom=pubmed" target="_blank" rel="noopener noreferrer">Cardiff University</a> proposed in 2005 that the best explanation for Darwin&#8217;s symptoms was lactose intolerance.
It is far more common to find lactose intolerance among South and East Asian populations, though it is not unheard of to find it among Europeans, where it reaches levels of about 8%. &nbsp; Researchers, digging through his written correspondence, have found many key passages that hint at Darwin being lactose intolerant. For example, in 1865, Darwin wrote to H.B. Jones, his physician, recounting that “on most days, three hours after luncheon or dinner I have a sharpish headache on one side, and with bad flatulence last to the next meal.” &nbsp; He also wrote to his friend and colleague, William Hooker, “I have had a bad spell. &nbsp; Vomiting every day for eleven days, and some days after every meal.”
An analysis of his Diary of Health indicates that foods such as sugar, bacon, butter, and any desserts seemed to intensify his symptoms. &nbsp; Unfortunately, Darwin had a sweet tooth, and the majority of his wife’s recipes involved heavy cream. &nbsp; To make matters worse, when Darwin was feeling particularly ill he was often given warm milk as a nightcap, a typical remedy during the mid-19th century. &nbsp; This may have exacerbated his abdominal pain and discomfort.
In fact, the only treatment that appeared to work was something called “hydrotherapy” in which the patient bathed and drank copious amounts of cold water. &nbsp; Milk was not allowed. &nbsp; This, some argue, is additional evidence in support of lactose intolerance being the primary cause of Darwin’s symptoms.
<h6>The Case for Crohn’s Disease</h6>
However, while most agree that the majority of Darwin’s symptoms were gastrointestinal in nature, some remain unconvinced that the best explanation was that Darwin was lactose intolerant. &nbsp; Instead, they point to a more serious disorder known as Crohn’s Disease. &nbsp; This new diagnosis is garnering much support within the medical community, in that Crohn’s — even more so than lactose intolerance — accounts for the vast majority of Darwin’s incapacitating symptoms.
Crohn’s disease is a chronic autoimmune disease of the digestive tract. &nbsp; It is found in about 1-2% of people of European descent and can affect an individual&#8217;s entire digestive system, from the mouth to the anus and everything in between. &nbsp; Additional symptoms include skin rashes, arthritis, and inflammation of the eye. &nbsp; It usually first presents itself in early adulthood as a severe gastrointestinal infection. &nbsp; Individuals suffering from the disease often have a series of flare-ups and remissions throughout their lives. &nbsp; Crohn’s disease is believed to be a largely genetic disorder, though not all genetic markers have been identified.
Various factors can influence the timing and frequency of flare-ups for sufferers of Crohn’s, including stress, nutrition, and other health issues. &nbsp; Indeed, Darwin often noted worsening symptoms during periods of high stress, especially when he had to give public appearances or lectures.
Upon close examination of Darwin’s correspondence and diaries by scientists at the <a id="h6:5" title="University of Chile," href="https://www.ncbi.nlm.nih.gov/pubmed/17575947?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&amp;linkpos=1&amp;log$=relatedarticles&amp;logdbfrom=pubmed" target="_blank" rel="noopener noreferrer">University of Chile,</a> his most severe symptoms included abdominal pain and vomiting, but virtually no mention of diarrhea, which is the main symptom of lactose-intolerant individuals. &nbsp; In fact, Darwin had reported regular bowel movements for the majority of his adult life. &nbsp; It was the abdominal pain, nausea, and vomiting that plagued him for so many years, and these symptoms are key when diagnosing Crohn’s Disease.
In addition, and perhaps more importantly, Darwin had several other health issues seemingly unrelated to the digestive tract, namely skin, and eye irritation. Symptoms such as these are often found in patients diagnosed with Crohn’s Disease. &nbsp; And the fact that there are conflicting reports on the kinds of foods that upset his illness (Darwin also reported getting sick after eating sugar, bacon, and salads), lends additional support that his illness was not related to a specific type of food (i.e. dairy).
There is, of course, the possibility that Darwin suffered from both lactose intolerance AND Crohn’s Disease. &nbsp; In fact, there is an 83% chance that individuals with Crohn’s Disease are also lactose intolerant. &nbsp; However, the reverse is not also true, meaning the root cause of lactose intolerance among people with both conditions usually traces back to their Crohn&#8217;s.
It also appears that there is some genetic aspect to Darwin’s illness, as many of his family members suffered chronic health problems. &nbsp; In fact, the Darwin family was famous throughout the 19th and early 20th centuries as having overall poor health. &nbsp; Darwin’s family history points to some kind of genetic disorder, and the symptoms of Crohn’s disease appear to be the most comprehensive explanation.
The mystery surrounding Darwin’s chronic illness has mystified researchers for over 100 years. &nbsp; If he were alive today, it is likely that physicians would have no trouble diagnosing what ailed him.

Charles Darwin’s Mysterious Illness

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1733" title="aspergillus" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/aspergillus.jpg" alt="" width="290" height="193" />
Invasive aspergillosis (IA) is a common and life-threatening infection among bone marrow transplant patients caused by the fungus Aspergillus fumigatus.
About 10% of bone marrow transplant recipients are affected by IA. An estimated 30% of those affected die within three months.
In June, researchers showed that a <a href="https://blog.23andme.com/2008/06/24/snpwatch-genetic-variant-may-influence-risk-of-fungal-infection-after-bone-marrow-transplant/" target="_blank" rel="noopener noreferrer">genetic variant in bone marrow recipients</a> could increase their risk of developing IA almost six-fold. New research published online today in the <a href="http://content.nejm.org/cgi/content/short/359/17/1766" target="_blank" rel="noopener noreferrer">New England Journal of Medicine</a> shows that genetic variants in the bone marrow donor may also increase the risk of this potentially deadly infection.
<h6>Variants Identified</h6>
Pierre-Yves Bochud and colleagues from the Fred Hutchinson Cancer Research Center and the University of Washington School of Medicine suggest that identifying IA-associated genetic variants in bone marrow donors could help doctors develop more effective prevention strategies for at-risk recipients.
Using a sample of 242 bone marrow transplant donor/recipient pairs, the researchers found that each a certain variant in a bone marrow donor increased the risk the recipient would develop IA more than four times compared to donors with two Cs.
A follow up study of 366 donors/recipients showed that this effect was seen only when the donors and recipients were unrelated. When a patient received a transplant from a relative, that variant had no effect on the risk of IA. The researchers suggest that recipients of familial donations may require lower amounts of immunosuppressive drugs, thus decreasing their risk of all types of infections.

Bone Marrow Donor’s DNA May Affect Recipient’s Risk of Fungal Infection

<img loading="lazy" decoding="async" class="size-full wp-image-1715" title="altman" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/altman.jpg" alt="Russ Altman" width="130" height="170" />Russ Altman.
In a recent post on his &#8220;<a href="http://rbaltman.wordpress.com/" target="_blank" rel="noopener noreferrer">Building Confidence</a>&#8221; blog, 23andMe scientific advisor Russ Altman recounts an experience that should be familiar to 23andMe customers who regularly read The Blog.
After reading a recent New England Journal of Medicine paper about a genetic variant associated with the development of side effects among people taking cholesterol-lowering statin drugs, Altman logged into his 23andMe account and checked his own genotype at the SNP in question.
&#8220;In about 30 seconds I went from reading an article of potential interest to checking my genotype and drawing a preliminary conclusion,&#8221; Altman wrote. &#8220;I must say it was quite quick, informative, even fun.&#8221;

Russ discovered that his genotype does not put him at elevated risk for statin-induced muscle soreness – not an earth-shattering realization, but one that he said might make him more comfortable with taking cholesterol-lowering drugs should he ever need them.
Now, most of us don&#8217;t scour the New England Journal looking for papers that might have relevance to our own health. That&#8217;s why The Blog publishes SNPWatch posts that announce the latest findings and identify the SNPs that 23andMe customers can use to see how that research might apply to them. In fact, we published a <a href="https://blog.23andme.com/2008/07/24/snpwatch-gene-variant-may-increase-risk-for-rare-side-effect-of-cholesterol-lowering-drugs/" target="_blank" rel="noopener noreferrer">post</a> on the statin-induced myopathy paper when it first came out back in July.
So if you&#8217;re a 23andMe customer who is interesting in learning about a particular topic, don&#8217;t forget to check The Blog as well as your account – because the latest research often appears here first.

Latest Posts — Page 204