Vice president of Genomics Eurie Hong 96 is currently leading a research team at the genealogy company Ancestry to investigate the link between genomics, which is the study of a persons genes and their interactions, and COVID-19 susceptibility and symptom severity.

The research launched in April and has produced several preliminary results and findings that, once confirmed and validated, may accelerate the pace of other COVID-19 research, according to Hong. According to Ancestrys website, the research could also be useful in the development of a cure or vaccine.

Early data has shown that healthcare workers who are directly exposed to the virus are around six times more likely to have a confirmed case than the average person in the survey population, and discovered possible explanations for the appearance of increased susceptibility to the virus in men but not women, among other findings.

Hongs research with Ancestry comes as multiple different genealogy companies mobilize to contribute their unique access to large genetic data pools to the current body of COVID-19 research. 23andMe has also launched a COVID-19 study, and both companies aim to explore why the virus appears to affect different people in very different ways when it comes to symptom severity.

From the early days I think it was clear to all of us that some people were getting very, very sick when they were affected with coronavirus, and some people had hardly any symptoms at all, said Dr. Catherine Ball in an interview with USA Today. Ball is the chief scientific officer at Ancestry.

[The spectrum of human response] is still remarkably divergent in different people, even if they have the same age and have the same overall health, she added. And so to geneticists, that looks like theres a genetic factor in whether people become infected in the first place or have serious or mild symptoms.

Ancestrys research is the result of a collaboration between a range of scientists from geneticists to computational biologists and consists of gathering data through a survey which current AncestryDNA customers of 18 years or older can opt in to. Consenting customers answer a set of questions about their demographics, their exposure to the virus, their testing results and their symptoms, if any. Based on responses to the survey, participants are grouped by several factors including exposure and severity of COVID-19 symptoms.

The different groups may be those who have tested positive for COVID-19 or those who have a severe response to COVID-19 as well as those who have not had COVID-19 or those who were exposed but did not get COVID-19, Hong said.

Within these different groups, the DNA sequences of participants which are already in the Ancestry database since all participants must be customers are compared by researchers. A genome-wide association study (GWAS) is used to compare these sequences and identify common variants in the DNA of one group in comparison to the DNA of another. These common variants point to possible genetic reasoning behind differences in severity of response or vulnerability to COVID-19 from group to group.

The goal is to find regions in the DNA that can help understand why some people become infected or have a more severe disease than others, Hong said.

This survey has already gathered 750,000 participants in a three-month period. The data collected has shown that healthcare workers who are directly exposed to the virus are around six times more likely to have a confirmed case, and those with household members who have contracted the virus are around 121 times more likely to have a confirmed case, compared to the overall Ancestry survey population.

Ancestry believes this information sheds light on the risk of transmission in different settings, and potentially the importance of using PPE, according to its website.

The collected data has also been able to produce some novel findings. Researchers have identified a region on chromosome 1 associated with a 44% increase in odds of susceptibility in males. Near this region is the IVNS1ABP gene, which codes for a protein involved in influenza replication. This association is not present in females. The discovery of the region near this gene could help researchers understand why the virus appears to take a greater toll on men compared to women, and they are currently working to validate this preliminary result.

Since the population participating in the survey is limited to those who are already customers and those who have also opted to participate, the researchers involved have also had to take steps to ensure the collected data is valid.

We evaluated the data against a CDC database of those who have tested positive from hospitals and clinics, Hong explained.

According to Hong, the survey results have matched the CDCs data pretty closely. For example, where the median age of those who self-reported testing positive in the Ancestry survey was 49, the median age in the CDC dataset was 48. Where 10% of positive-testing participants reported being hospitalized in the Ancestry survey, 14% reported the same in the CDC dataset. Other demographics of the positive-testing survey participants also matched the CDC dataset with similar differential margins.

Still, Hong warns against using this research to self-evaluate your own risk.

Our results are preliminary and need to be validated and confirmed, Hong said. The best thing to do now is to wash your hands, follow social distancing guidelines and wear a mask in public areas.

While not to be used to self-diagnose, finding a link between genetics and the virus in the research data has the potential to be used by scientists outside of Ancestry working on vaccines, cures and preventatives for COVID-19.

Finding a genetic component could help better understand how our immune systems work against the Sars-CoV-2 virus that causes COVID-19 or identify potential targets for development of treatments, Hong said.

The survey data has not yet been peer-reviewed, but Ancestry is preparing a detailed report of its approach and findings for peer review and invites scientists from around the world to determine whether this finding holds up to rigorous scientific scrutiny, according to a press release.

According to Ball, the team at Ancestry is doing their best to publish [their] findings as quickly as possible and [make] them as useful to clinicians and other researchers as quickly as possible.

In order to do this, Ancestry plans to submit the data from the survey to the European Genome-Phenome Archive, an international data archive, where qualified researchers working on preventatives and vaccines can access and use it.

Many doctors are grateful for any research contributing to the defeat of COVID-19.

As a physician, its the moments of hope when medicine finds a way to address a pressing human need that matter the most, wrote Ancestrys vice president of Health and DNA Dr. Ron Park in a blog for Ancestrys website.

The power of the Ancestry and scientific communities, in collaboration together, gives us continued reason to hope, Park added.

Hong is primarily excited to work with such a diverse range of scientists from all different disciplines, and her day-to-day is always a little different from giving feedback to training the next generation of scientific leaders, to tackling the complexities of scale. Still, the main goal remains [unlocking] the power of human genetics for everyone.

[Ancestrys] COVID-19 research study is an example of partnering with our customers and mobilizing our expertise to help combat this pandemic, Hong said. We are just one part of a global scientific community and proud to help advance what we know about COVID-19.

Contact Joelle Chien at joelle.chien2 at gmail.com.

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Stanford alum investigates link between genomics and COVID-19 vulnerability - The Stanford Daily

Humans getting into interspecies dating? Not on this planet oh wait, that already happened.While there was really no such thing as dating hundreds of thousands of years ago, when it was more of a find your mate and dont get eaten sort of thing, there is evidence that Homo sapiens interbred with other proto-human species in the distant past.

Neanderthals were one of those species (and also the butt of endless caveman jokes). Denisovans were another. Geneticist and computer scientistAdam Siepel developed an algorithm to trace human genetics and recently published a study in PLOS Genetics. He andhis research teamhave now found that these groups gave us more of their DNA than we thought, and thatsome of us have genes from a mysterious ancestral hominid, possibly Homo erectus. There was only one way for that to happen. But why did Homo sapiens end up taking over while Neanderthals and Denisovans eventually vanished?

"That is a great matter of speculation among both archaelogists and geneticistscould be disease, conquest, out-competition for scarce resources, or perhaps the modern humans simply absorbed them.There is little hard evidence,"Siepeltold SYFY WIRE."But the one thing that we can see, as geneticists, is that these Neanderthal and Denisovan populations had relatively low levels of genetic diversity, suggesting they may have been prone to genetic diseases and/or particularly susceptible to infectious diseases."

Hybridization of a species results in introgression, or the genetic exchange which occurs in interbreeding species. Humans migrated out of Africa to Eurasia about 50,000 years ago and interbred with the Neanderthal population there. This is the migration and subsequent genetic merging that is the most recognized example of such a phenomenon. What Siepel found, using an updated ancestral recombination graph (ARG) algorithm called ARGweaver-D, is that they were already headed elsewhere much earlier, around 200,000-300,000 years ago. The algorithm also revealed interbreeding between mystery super-archaic ancestors with both Neanderthals and Denisovans before either of those species interbred with ancient Homo sapiens.

Homo erectus is the most likely ancient relative of humans to be that ancestor. Now extinct except for fragments of DNA that show up in some modern human samples, these proto-humans were the first Homo sapiensrelatives that showed body proportions similar to what you see when you look in the mirror. Unlike earlier hominids, the arms and legs of Homo erectus had evolved to be shorter than its torso. They were also the first hominids believed to have migrated out of Africa. This strengthens the case for interbreeding with Denisovans and Neanderthals, especially Denisovans.

That has to make you wonder. If you've ever taken a commercial DNA test and your results came back with a small percentage labeled "unknown", could that be a connection to the mystery ancestor?

"Some of the commercial tests specifically look for Neanderthal ancestry, but yes, it is possible that superarchaic ancestry, or ancestry from a highly divergent branch of Neanderthals or Denisovans, would be labeled 'unknown'by a commercial test," Siepel said.

The most common genetic transfers happened between Neanderthals and Denisovans, Neanderthals and ancient Homo sapiens, super-archaic ancestors and ancient Homo sapiens who stayed in Africa, and super-archaic ancestors and Denisovans. Alleles, or alternate versions of genes, shared by Denisovans and the mystery ancestor support super-archaic DNA making its way into the modern gene pool when that species interbred with Denisovans. Unfortunately, so did mutations.

"It appears that Neanderthals and Denisovansintroduced deleterious mutations into modern human populations when they interbred with them," Siepel explained."Many of these mutations gradually fadedover time, but some undoubtedly persist.Interestingly, however, we could not find clear evidence of the reverse effectof modern humans introducing deleterious mutations into Neanderthals through this interbreeding.It is possible, though, that we do not yet have enough sensitivity to detect this phenomenon."

Even with an advanced algorithm, it still proved more difficult to identify when and where super-archaic human ancestors interbred with Denisovans than it was to find the same information about Neanderthal or Denisovan interbreeding with Homo sapiens. This is probably because no sequence exists for the genes of the super-archaic ancestor yet, and also because they have been broken over and over again by recombining with the genes of ancient humans and the other two hominid groups so many times. Will we ever really know who the super-archaic ghosts of our ancestors were?

"That is the big question we are all wondering about," said Siepel."It is conceivable that it could be done, at least in principle,if very well-preserved remains were recovered from permafrost or from a cave that is well protected from the environment. But I do not know of any promising leads at present."

So dont be offended if someone calls you a Neanderthal. Just tell them science says you probably are to some extent, and so are they.

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Humans have had mystery DNA for 300,000 yearsand now we might finally know what it is - SYFY WIRE

The first time I heard nematode worms can teach us something about human longevity, I balked at the idea. How the hell can a worm with an average lifespan of only 15 days have much in common with a human who lives decades?

The answer is in their genesespecially those that encode for basic life functions, such as metabolism. Thanks to the lowly C. elegans worm, weve uncovered genes and molecular pathways, such as insulin-like growth factor 1 (IGF-1) signaling that extends healthy longevity in yeast, flies, and mice (and maybe us). Too nerdy? Those pathways also inspired massive scientific and popular interest in metformin, hormones, intermittent fasting, and even the ketogenic diet. To restate: worms have inspired the search for our own fountain of youth.

Still, thats just one success story. How relevant, exactly, are those genes for humans? Were rather a freak of nature. Our aging process extends for years, during which we experience a slew of age-related disorders. Diabetes. Heart disease. Dementia. Surprisingly, many of these dont ever occur in worms and other animals. Something is obviously amiss.

In this months Nature Metabolism, a global team of scientists argued that its high time we turn from worm to human. The key to human longevity, they say, lies in the genes of centenarians. These individuals not only live over 100 years, they also rarely suffer from common age-related diseases. That is, theyre healthy up to their last minute. If evolution was a scientist, then centenarians, and the rest of us, are two experimental groups in action.

Nature has already given us a genetic blueprint for healthy longevity. We just need to decode it.

Long-lived individuals, through their very existence, have established the physiological feasibility of living beyond the ninth decade in relatively good health and ending life without a period of protracted illness, the authors wrote. From this rare but valuable population, we can gain insight into the physiology of healthy aging and the development of new therapies to extend the human healthspan.

While it may seem obvious now, whether genes played a role in longevity was disputed for over a century. After all, rather than genes, wouldnt access to health care, socioeconomic status, diet, smoking, drinking, exercise, or many other environmental and lifestyle factors play a much larger role? Similar to height or intelligence (however the latter is assessed), the genetics of longevity is an enormously complicated and sensitive issue for unbiased studying.

Yet after only a few genetic studies of longevity, a trend quickly emerged.

The natural lifespan in humans, even under optimal conditions in modern societies, varies considerably, the authors said. One study, for example, found that centenarians lived much longer than people born around the same time in the same environment. The offspring of centenarians also have lower chances of age-related diseases and exhibit a more youthful profile of metabolism and age-related inflammation than others of the same age and gender.

Together, about 25 to 35 percent of the variability in how long people live is determined by their genesregardless of environment. In other words, rather than looking at nematode worm genes, we have a discrete population of humans whove already won the genetic lottery when it comes to aging. We just need to parse what winning means in terms of biology. Genes in hand, we could perhaps tap those biological phonelines and cut the wires leading to aging.

Identification of the genetic factors that underlie extreme human lifespan should provide insights into the mechanisms of human longevity and disease resistance, the authors said.

Once scientists discovered that genes play a large role in aging, the next question was which ones are they?

They turned to genome-wide association studies, or GWAS. This big data approach scans existing genomic databases for variations in DNA coding that could lead to differences in some outcomefor example, long versus short life. The differences dont even have to be in so-called coding genes (that is, genes that make proteins). They can be anywhere in the genome.

Its a powerful approach, but not that specific. Think of GWAS as rudimentary debugging software for biological code: it only looks for differences between different DNA letter variants, but doesnt care which specific DNA letter swap most likely impacts the final biological program (aging, in this case).

Thats a huge problem. For one, GWAS often finds dozens of single DNA letter changes, none powerful enough to change the trajectory of aging by itself. The technique highlights a village of DNA variants, that together may have an effect on aging by controlling the cells course over a lifetime, without indicating which are most important. Its also hard to say that a DNA letter change causally leads to (or protects against) aging. Finally, GWAS studies are generally performed on populations of European ancestry, which leaves out a huge chunk of humansfor example, the Japanese, who tend to produce an outsized percentage of centenarians.

So what needs to change?

Rather than focusing on the general population, the key is to home in on centenarians of different cultures, socioeconomic status, and upbringing. If GWAS are like fishing for a rare species in several large oceans, then the authors point is to focus on pondsdistributed across the worldwhich are small, but packed with those rare species.

Extremely long-lived individuals, such as centenarians, compose only a tiny proportion (~0.01 percent to 0.02 percent) of the United States population, but their genes contain a biological blueprint for healthy aging and longevity, the authors said. Theyre spared from usual age-related diseases, and this extreme and extremely rare phenotype is ideal for the study of genetic variants that regulate healthspan and lifespan.

Its an idea that would usually make geneticists flinch. Its generally thought that the larger the study population, the better the result. Here, the recommendation is to narrow our focus.

And thats the point, the authors argue.

Whatever comes out of these studies will likely have a much larger impact on aging than a GWAS fishing experiment. Smaller (genomic) pond; larger (pro-youth) fish. Whats more, a pro-youth gene identified in one European-based long-living population can be verified in another group of centenarianssay, Japaneseensuring that the gene candidates reflect something fundamental about human aging, regardless of race, culture, upbringing, and wealth.

A genomic screen of centenarians can easily be done these days on the cheap. But thats only the first step.

The next step is to validate promising anti-aging genetic differences, similar to how scientists validated such differences in nematode worms during classic longevity studies. For example, a promising pro-youth gene variant can be genetically edited into mice using CRISPR or some other tool. Scientists can then examine how the mice grow up and grow old, compared to their non-edited peers. Does the gene make these mice more resilient to dementia? What about muscle wasting? Or heart troubles? Or hair greying and obesity?

From these observations, scientists can then use an enormous selection of molecular tools to further dissect the molecular pathways underlying these pro-youth genetic changes.

The final step? Guided by centenarian genes and validated by animal models of aging, we can design powerful drugs that sever the connection between the genes and proteins that drive aging and its associated diseases. Metformin is an experimental pill that came out of aging studies in nematode wormsimagine what studies in human centenarians will yield.

Despite enormous improvements in human health over the past century, we remain far from a situation in which living to 100 years of age in fairly good health is the norm, the authors said.

But as centenarians obviously prove, this is possible. By digging into their genes, scientists may find a path towards healthy longevitynot just for the genetically fortunate, but for all of us.

Image credit:Cristian Newman / Unsplash

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The Secret to a Long, Healthy Life Is in the Genes of the Oldest Humans Alive - Singularity Hub

I WAS one of the first two Jeffrey Cheah Professorial Fellows to be appointed at Gonville and Caius College, Cambridge.

Founded in 1348, Caius is one of the most illustrious Cambridge Colleges, founded by John Caius, a medical doctor.

The colleges reputation in medical education is unparalleled. Fourteen Nobel prizewinners are closely associated with Caius, including Francis Crick, a fellow who elucidated the structure of DNA with James Watson.

When I moved to the Nuffield Department of Medicine in Oxford in 2018, I placed such value on my link with Tan Sri Dr Jeffrey Cheah that I was able to secure a highly-prized Jeffrey Cheah Fellowship in Brasenose College an ancient and distinguished college, and sister college of Caius. Tan Sri Dr Jeffrey had forged a relationship with Brasenose, similar to Caius.

I was drawn to the Jeffrey Cheah professorship because of the extraordinary reputation of Tan Sri Dr Jeffrey Cheah as entrepreneur, philanthropist and educationalist who has an abiding interest in the development and welfare of his countrymen and women.

He also has an abiding interest in providing the best possible education to the youth of his country, especially those from less advantaged backgrounds. He set up Sunway College in 1986, with a vision that this beginning would lead to Sunway University and the Harvard of the East.

Of particular attraction to me was Tan Sri Dr Cheahs interest in developing a world-class reputation in the provision of medical care through his Sunway Medical hospital system, and his wish to set up an associated medical school in Sunway University.

I was well aware of the tenacity with which Tan Sri Dr Cheah pursues his aims, and my field diabetes research seemed particularly relevant to these ambitions in a country with one of the highest incidence of the disease in South-East Asia.

Early into my appointment as Jeffrey Cheah Professorial Fellow at Caius I was asked to co-ordinate what turned out to be a very successful joint Cambridge-Oxford-Sunway symposium on precision medicine, held at the impressive Sunway University campus. This was followed by a second symposium on stem cells, and the third in 2019 on diabetes.

In all of these activities it was the reputation of Tan Sri Dr Cheah and Sunway that persuaded leading experts from Cambridge, Oxford and other renowned universities to come to Malaysia for three days to bring state of the art theory and technique to these exciting areas of medical research and practice.

The symposia have put Sunway on the world stage and introduced leading experts from around the world to the wonderful city that Tan Sri Dr Cheah has created from a disused tin mine.

I find it most fulfilling to hold a professorship named after Tan Sri Dr Jeffrey Cheah. His eminence as a Malaysian statesman, a successful entrepreneur and benefactor lends great credibility to my efforts to extend my work on diabetes, and its relation to dementia, and my work on novel pathogens, into a new region that has significant health challenges.

The potential for joint research, and access to high tech facilities in Oxford, is of great mutual benefit and through his ambition, foresight and willingness to invest in the future, Tan Sri Dr Cheah has laid the foundations for the Harvard (or Oxbridge) of the East that has always been his vision.

Prof John Todd FRS

About Prof John Todd FRS

Prof John Todd FRS is Jeffrey Cheah Fellow in Medicine at Brasenose College, Oxford. He was previously Jeffrey Cheah Professorial Fellow at Gonville and Caius College, Cambridge, before he transferred to Oxford in 2018. He is a leading pioneer researcher in the fields of genetics, immunology and diabetes, and is a Professor of Precision Medicine at the University of Oxford.

In his former role as a Professor of Human Genetics and a Wellcome Trust Principal Research Fellow at Oxford, he helped pioneer genome-wide genetic studies, first in mice and then in humans.

His research areas include type 1 diabetes (T1D) genetics and disease mechanisms with the aim of clinical intervention.

Prof Todd holds senior roles as the director of the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory (DIL) at the Universitys Wellcome Trust Centre for Human Genetics, and is senior investigator of the UKs National Institute for Health Research.

He founded and deployed the Cambridge BioResource, a panel of around 17,500 volunteers, both with and without health conditions, to participate in research studies investigating the links between genes, the environment, health and disease.

His significant contribution in genetics and diabetes research has seen him receive several awards and prizes including Fellowship of the Royal Society of London.

In his lifetime, Prof Todd has supervised 29 PhD students with three in progress, garnering over 36,000 total citations.

With a h-index of 93, Prof Todd is considered a truly unique individual. The index is an author-level metric that measures both the productivity and citation impact of the publications of a scientist or scholar.

Brought to you by Jeffrey Cheah Foundation in conjunction with its 10th anniversary.

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BUILDING THE NATION WITH QUALITY EDUCATION - The Star Online

For many years, researchers and clinicians assumed that nutrition was a one-size-fits-all affair. Everybody needs the same nutrients from their food, they thought, and a vitamin pill or two could help dispense with any deficiencies.

But now scientists are learning that our genes and environment, along with the microbes that dwell in us and other factors, alter our individual abilities to make and process nutrients. These differences mean that two given people can respond to identical diets in different ways, contributing to varied health outcomes and patterns of disease.

Until recently, scientists didn't fully appreciate that individual metabolic differences can have a big impact on how diet affects the risk for chronic diseases, says Steven Zeisel, director of the Nutrition Research Institute at the University of North Carolina, Chapel Hill. The new knowledge is resolving long-standing mysteries about human health and paving the way toward a world of "precision nutrition," Zeisel writes in a recent article in the Annual Review of Food Science and Technology.

Although the findings are unlikely to lead all the way to hyper-individualized dietary recommendations, they could help to tailor nutrition to subsets of people depending on their genetics or other factors: Zeisel's company, SNP Therapeutics, is working on a test for the genetic patterns of 20-odd variants that can identify individuals at risk of fatty liver disease, for example. Knowable Magazine spoke with Zeisel about our developing understanding of precision nutrition.

This interview has been edited for length and clarity.

Why has nutrition lagged behind other research areas in medicine?

Nutrition studies have always had a problem with variability in experimental results. For instance, when infants were given the fatty acid DHA [docosahexaenoic acid], some had an improvement in their cognitive performance and others didn't. Because some showed improvements, it was added to infant formula. But we didn't understand why they were responding differently, so scientists continued to debate why we did this if only 15 percent of children improved and 85 percent showed no response.

The confusion came from an expectation that everybody was essentially the same. People didn't realize that there were predictable sources of variation that could separate those who responded to something from those who did not. For DHA, it turned out that if the mother had a difference in her genes that made her slow to produce DHA, then her baby needed extra DHA and responded when given it. That gene difference occurs in about 15 percent of women and, it turns out, it's their babies that get better when given DHA.

How are researchers starting to make sense of this variability?

Studying differences in human genetics is one way. We conducted a series of studies that found a good deal of variation in the amounts of choline [an essential nutrient] that people required: Men and postmenopausal women got sick when deprived of it, but only half of young women became sick.

We found that some women can make choline because the hormone estrogen turns on the gene to make choline. Other women have a difference in this gene that makes it unresponsive to estrogen. Men and postmenopausal women need to get the nutrient another way by eating it because they have minimal amounts of estrogen.

If I had initially done the choline study and chosen only young women participants, I would have found that half needed choline, half didn't, and had a lot of noise in my data. Now that we can explain it, it makes sense. What seemed to be noisy data can be better described using a precision nutrition approach.

Are there other nutritional conundrums that suggest these sorts of variations are common?

There are some things for which we already know the underlying genetic reasons. For example, there's a great deal of information on genetic differences that make some people's cholesterol go up when they eat a high-fat diet while other people's doesn't. Researchers are discovering genetic variants that account for why some people need more vitamin D than others to get the same levels in their blood.

Every metabolic step is controlled by such variants. So, when we find people who seem to be responding differently in our studies, that's a hint that there is some underlying variation. Rather than throwing the data away or saying participants didn't comply with the study protocol, we can look at the data to discover some of the genetic reasons for these differences. Precision nutrition is really a change in how we do nutrition research, in that we're starting to identify why some people respond and some don't.

Besides genetic variants, are there other factors that precision nutrition needs to take into account?

Right now, much of our ability to be more precise comes from better tools to understand genetic variation. But genetics alone doesn't determine your response to nutrients. It interacts with other factors too.

The microbiome [the community of bacteria and other microbes that live in and on our body] clearly also affects how nutrients work. Most microbiome research until now has been to name the organisms in the gut, but it's now getting to the point where researchers can measure what microbial genes are switched on, what nutrients are made by gut microbes, and so on. As that research matures, we'll be able to get much better recommendations than we do now.

Our environment could be a very important factor as well. We're starting to be able to measure different environmental exposures by testing for thousands of chemicals in a drop of blood. Epigenetics, which is the science of chemical marks placed on DNA to turn genes on and off, will also likely contribute to important differences. It's been a hard field because these marks vary in different tissues, and we can't easily get a sample of liver or heart tissue for a nutrition test. We have to track these changes in the bloodstream, and estimate whether they're the same changes that occurred in the organs themselves.

We'll have to include each of these factors to improve our predictions of who will or won't respond to a certain nutrient. Eventually, precision nutrition will have all of these inputs at its early stages.

There are various precision nutrition tests now being sold by different companies. Do they have anything useful to offer?

Right now, most tests look at one gene at a time in a database and say, "You have this gene difference and it makes you more susceptible to something." But the metabolic pathways for most nutrients are not controlled by a single gene. There may be 10 or 20 steps that all add up to how you respond to sugars, for example, and any one of those steps can cause a problem. Knowing where you have variations all along the pathway can help us predict how likely you are to have a problem metabolizing sugar. It's more sophisticated, but it's also harder to do.

Are there ethical concerns with precision nutrition?

Once I know something about a person's genetics for nutrition, I may be able to predict that they're more likely to develop a disease or a health problem. That could change whether an insurance company wants to cover them. We have to try to make that risk clear to people, and also work on improving privacy so their information isn't available to anybody but them.

The other problem is that wealthier people can afford to do these genetic tests and others can't. But we can use precision nutrition to find alternate solutions. For instance, women who can't turn choline production genes on with the hormone estrogen are at higher risk of having babies with neural tube defects and poor brain development. If we need a test for only that one gene difference, a test like that could be reduced to a few dollars and made widely available. Or we might choose to just give everybody choline supplements, if that proves to be a more cost-effective solution.

In the long run, will these discoveries help prevent disease?

There is an advantage in seeking more precise advice for some problems right now. With obesity, for instance, we know that as people gain weight, they develop a group of problems called metabolic syndrome that's related to the accumulation of fat in the liver. We know that because of genetic differences, about 20 percent of the population is much more likely to develop fatty liver and is at higher risk for developing these related problems. If we can test for these gene differences, then we can identify those who will benefit the most from changes in diet and weight loss and treat them, either with supplements, drugs or lifestyle changes.

Salt sensitivity is another example. About 10 percent of people have higher blood pressure when they eat high-salt diets. Right now, because we don't know the metabolic differences that contribute, we say everybody should stay away from salt. But the truth is, only about 10 percent of people are benefiting from that recommendation, and 90 percent are getting bland food that they don't like. If we could do genetic testing and tell whether a person is salt-sensitive, then they know that effort is worth it for their health. I think that helps to make people comply with recommendations and change their lifestyles.

Unlike some drugs, which have an all-or-nothing effect, nutrition's effects tend to be modest. But it's clearly an important, easy intervention. And if we don't fix a diet, then we have to treat the problems that arise from a bad diet.

Nutrition is always going to be a tough field to get precise results. It isn't going to be perfect until we can get all the variables identified. Part of what precision nutrition is doing is helping to refine the tools we have to understand these complex systems.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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'Precision nutrition': Are hyper-individualized diets the future of eating? - The Week Magazine

When the sons and grandsons of Genghis Khan ruled the Mongol empire in the thirteenth century, it stretched from eastern Europe to the Pacific Ocean, and encompassed Persia in the south and Russia to the north. How did this nomadic culturethe third such empire to rise from the arid grasslands of the Eurasian Steppe since 200 b.c.conquer and cohere across such vast distances? And how did these nomads predecessors, pastoralists with ox-drawn carts, spread swiftly east and west to forever change the genetic structure of Europe and Asia?

Answers have been hard to come by, in part because nomadic cultures leave only limited archaeological evidence of their lifeways behindmortuary mounds with occasional animal-bone offerings are the prime archaeological feature of the Eastern Steppe. Now a scientist interested in reconstructing ancient diets and understanding the evolution of the human microbiome has begun to assemble new types of evidence suggesting that the ability to build a succession of empires on the Eurasian Steppe has been predicated, at least in part, on dairying: the widespread production and consumption of horse, sheep, goat, cow, and other milks and milk products that sustained and tied nomadic tribes together culturally across vast distances. And the record showing the origin, extent, and diversity of this custom lies in a durable and extraordinarily representative source: ancient dental plaque.

Dental calculus is fascinating because its like the kitchen sinka time capsule of your mouth and everything that goes into it, says assistant professor of anthropology Christina Warinner, who is also a Seaver assistant professor at the Radcliffe Institute. Ancient tartar, once discarded, is now regarded by archaeologists as a vital archive that preserves individuals DNA, their oral microbiome, and traces of what they ateall thanks to Warinner, who first began exploring its potential while a Harvard graduate student. In 2014, she and her colleagues showed that milk proteins can become trapped in calcifying human dental plaque, enabling researchers to determine when livestock milk first began appearing in human diets. In addition, the specific amino acid sequences of the recovered milk proteins act as a kind of fingerprint that can reveal which livestock species were being milked.

Warinner is using plaque analysis, together with a little genetics, a bit of microbiology, history, social archaeology, and ethnography to pursue a larger goal: understanding the origins and global spread of dairying. How did we end up with this crazy food that adult humans arent meant to digest, she asks, and how have we made it work? Dairying, well-studied in Western European cultures, was once thought to have spread alongside a genetic mutation that makes it possible to digest lactose, a milk sugar, into adulthood. This correlation between culture and a genetic trait, driven by natural selection, appears to have been the dominant pattern for dairyings spread in the British Isles and Scandinavia, where a majority of people now carry the gene variant. But most of the worlds populationincluding the nomads of the Eurasian Steppelack such a mutation. Warinners work nevertheless provides direct evidence that this did not hinder the rapid adoption of domesticated milk production in that region.

In new research described in Nature Ecology & Evolution, Warinner and her coauthors use dental calculus to show that around 3000 b.c., ruminant dairying rapidly spread thousands of kilometers across the Eurasian Steppe, from the north Caucusus region near the Black Sea to as far east as Mongolia, in the span of only a few centuries. There, the grasslands, although inhospitable to grain agriculture, provided abundant nutrition for grazing animals and supported the production of a wide variety of dairy-based foods for humans.

But not until 1200 b.c., coincident with the first plaque-protein evidence for horse-milk consumption, does mobile pastoralism reach its height, says Warinner. Mares milk was probably used almost exclusively for alcohol production, to make a drink that is still used today to cement contracts and social ties, but the use of horses led to a transformative expansion of dairying culture. Horses travel farther and faster than other ruminants, she points out, thereby enhancing herding capacity, access to pasturage, and the control of larger territories. And in winter, they dig instinctually for snow-covered grasses, exposing it for sheep, goats, and cattle, which would otherwise starve. Horses, explains Warinner, made the whole dairy-based economy work better and more efficiently. The stage was set for the rise of nomadic empires.

But at least one mystery remains. Although 95 percent of the Eastern Steppe population lacks the gene variant for digesting lactose, ethnographic studies of modern nomadic herders show that between 30 percent and 50 percent of their summertime dietary calories come from dairy products. These range from mares milk (men will consume up to eight liters of fermented airag a day), to lightweight, calorie-dense curds that can be transported and stored for up to two yearsin all, more than 20 different dairy-based foods. How these nomads cope with such extreme levels of lactose in their diet is unknown, but Warinner suspects they may have highly altered gut microbiomes that could be adaptive. This summer, she is beginning to test that hypothesis, working remotely from Cambridge with her field collection team in COVID-free Mongolia. She just might find that the Mongol empire was built on milk and microbes.

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Dairy culture on the Eurasian Steppe - Harvard Magazine