{"cache":{"posts_f30bc_19c25":{"__typename":"RootQueryToPostConnection","nodes":[{"__typename":"Post","id":"cG9zdDozMjQ2Mw==","databaseId":32463,"featuredImage":{"__typename":"NodeWithFeaturedImageToMediaItemConnectionEdge","node":{"__typename":"MediaItem","id":"cG9zdDozMjQ4MQ==","altText":"","mediaDetails":{"__typename":"MediaDetails","width":800,"height":800,"sizes_cad4b_bf21a":[{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-150x150.webp","name":"thumbnail"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-300x300.webp","name":"medium"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-768x768.webp","name":"medium_large"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-271x271.webp","name":"square_sm"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-372x372.webp","name":"square_md"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-574x574.webp","name":"square_lg"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-271x149.webp","name":"wide_sm"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-372x204.webp","name":"wide_md"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-574x315.webp","name":"wide_lg"},{"__typename":"MediaSize","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail-800x539.webp","name":"wide_xl"}]},"sourceUrl_772ce_bf21a":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail.webp","mediaItemUrl":"https://blog-api.23andme.com/wp-content/uploads/2024/01/Tx-Assets-Homepage-OurScience-Detail.webp","title_b28e9_bf21a":"Tx-Assets-Homepage-OurScience-Detail"}},"author":{"__typename":"NodeWithAuthorToUserConnectionEdge","node":{"__typename":"User","id":"dXNlcjo1","name":"23andMe"}},"date":"2024-01-10T12:00:50","uri":"/articles/the-power-of-large-genetic-datasets","title_b28e9_bf21a":"The Power of Scale in Drug Development","slug":"the-power-of-large-genetic-datasets","categories_3cd3e_bf21a":{"__typename":"PostToCategoryConnection","edges":[{"__typename":"PostToCategoryConnectionEdge","node":{"__typename":"Category","id":"dGVybToyMDAzMA==","name":"Therapeutics","slug":"therapeutics","uri":"/category/therapeutics","seo":{"__typename":"TaxonomySEO","title":"Therapeutics Archives - 23andMe Blog","opengraphTitle":"Therapeutics Archives","metaDesc":"23andMe Therapeutics empowers everyone to be part of finding cures to disease. Our model has the power to transform drug discovery.","opengraphDescription":"23andMe Therapeutics empowers everyone to be part of finding cures to disease. Our model has the power to transform drug discovery.","fullHead":"\n\n\n\n\n\n\n\n\n\n\n\n\n"}}}]},"imageOptions":{"__typename":"Post_Imageoptions","featuredImageSquare":{"__typename":"MediaItem","id":"cG9zdDoyODIzNQ==","mediaDetails":{"__typename":"MediaDetails","sizes_cad4b_bf21a":[{"__typename":"MediaSize","name":"medium","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-300x300.jpg"},{"__typename":"MediaSize","name":"thumbnail","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-150x150.jpg"},{"__typename":"MediaSize","name":"square_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-271x271.jpg"},{"__typename":"MediaSize","name":"square_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-372x372.jpg"},{"__typename":"MediaSize","name":"wide_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-271x149.jpg"},{"__typename":"MediaSize","name":"wide_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-372x204.jpg"},{"__typename":"MediaSize","name":"wide_lg","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO-512x315.jpg"}],"height":512,"width":512},"mediaItemUrl":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO.jpg","sourceUrl_772ce_bf21a":"https://blog-api.23andme.com/wp-content/uploads/2020/04/23ANDME-LOGO.jpg","title_b28e9_bf21a":"23ANDME-LOGO"},"singleTemplateFeaturedImage":"none"},"content_b28e9_bf21a":"\n

Analyses of large genotyped and phenotyped datasets can provide valuable information for therapeutic development and research. Many sizable genetic research data sets have been used for this purpose, such as the UK Biobank, the Million Veterans Project, and the NIH’s All of Us.

\n\n\n\n

What is unique about 23andMe’s approach is that we have data at a scale that significantly exceeds many other entities. The size of our data increases our ability to detect disease associations with a given genotype and identify individuals with unique genomic composition for participation in additional research opportunities.

\n\n\n\n

Early results from a pilot project 23andMe launched this year inspired us to look deeper into our Research Cohort at the gene MAP3K15, where previous research found a loss of function variant that protects people against developing type 2 diabetes.

\n\n\n\n

If someone has a loss of function variant, for example, the MAP3K15 loss of function variant, and they are healthy, it tells scientists that turning off that gene could be safe. Knowing that a loss of function variant is not deleterious is incredibly important for drug development. Understanding this helps not just with target validation but with potentially de-risking and safety concerns around developing therapeutics that might turn off the expression of that gene.

\n\n\n\n

\n\n\n\n

Unique Insights into MAP3K15

\n\n\n\n

Our researchers wanted to see if the size of the 23andMe database could enable additional insight into the metabolic role of MAP3K15 that might not have been discoverable in other datasets. The findings from this work was recently published on the preprint server MedRxiv.

\n\n\n\n

For this study we performed various genetic analyses for MAP3K15 to see what we could learn from the >11 million consented customers in the 23andMe Research Cohort. In addition to confirming the protective effect for diabetes, analysis of our database resulted in several new insights for MAP3K15 loss of function (LoF):

\n\n\n\n

MAP3K15 LoF is associated with an increased risk of high blood pressure
MAP3K15 LoF is associated with a decreased risk of high cholesterol
Among individuals determined to be at a high genetic risk for type 2 diabetes, those who also have MAP3K15 LoF show a potential 4.5-year delay in the median age of disease onset compared to non-carriers

\n\n\n\n

Genetics-driven Recruitment

\n\n\n\n

We wanted to know if we could establish a recruitment capability to obtain clinical laboratory evidence for the new MAP3K15 findings from genetic analyses of the 23andMe database. Because we have a very, very large number of people who have consented to participate in this additional level of research, we could readily identify potential research participants of interest with the protective MAP3K15 loss of function variant.

\n\n\n\n

In this study, we were particularly interested in clinical lab values related to participant blood pressure and high cholesterol in individuals with or without a particular loss of function variant in MAP3K15. To obtain these lab values and biobank blood samples from consented participants, we set up a research protocol to recruit participants nationwide to answer survey questions and participate in a blood draw. This protocol was reviewed and approved by an Institutional Review Board (an independent ethical and regulatory review board) to ensure protection for the rights and welfare of our study participants.

\n\n\n\n

Results from this pilot study enabled us to find evidence supporting our database findings, including elevated systolic blood pressure, reduced cholesterol levels, and lower LDL/HDL ratio in 23andMe participants with the protective variant compared to controls without the variant.

\n\n\n\n

Research Opportunities Based on Your Unreported Genetics\n\n

The participants in this study represent a group of our research participants who’ve gone through an additional layer of consent.

\n\n

For this research, our research participants have opted-in to being contacted by our researchers about research opportunities based on genetic information not included in their 23andMe reports.

\n\n

These research opportunities might be related to specific conditions for which we do not yet have a report. Those who agree to participate and who are contacted for specific studies may only learn about the condition being studied but not the specific variant.

\n\n

Like all our research, participants must opt in to be included, and those currently participating can change their minds and then opt out at any time.

\n\n

Learn more here.

\n\n\n\n

DNA-Driven Discoveries

\n\n\n\n

This recruitment capability opens a whole host of capabilities for researchers. Dubbed “The DNA-Driven Discoveries Study,” this genetics-driven recruitment approach could potentially inform drug target safety concerns, improve patient selection and efficacy in clinical trials while also helping to identify hard-to-find drug targets, rare genetic variants and even reveal more about the underlying biology of certain conditions.

\n\n\n\n

“I’m not aware of any other entity out there with this capability and scale,” said Jen Brady, Ph.D., a senior scientist in 23andMe’s Therapeutics division who helped lead the study. “We’re leveraging the discovery power of what is the world’s largest re-contactable genetic database.

\n\n\n\n

Our (DNA-Driven Discoveries) study allows 23andMe scientists to recontact consented individuals based on genetic variants they may have but do not know about. Contacting these individuals based on their genetics is a key capability for 23andMe. It could help inform drug discovery efforts for 23andMe and our collaborators, improve how we create genetic research hypotheses, and help us build an internal deeply-phenotyped biobank.”

\n\n\n\n

Next Steps

\n\n\n\n

We believe the ability to identify, recruit, and characterize research participants based on genetics unknown to them is a critical capability for 23andMe to inform drug development and genetics research.

\n\n\n\n

Future studies using this method could enable similar recruitment and study designs for other conditions. They could also potentially help in clinical trials as we determine a drug’s efficacy and potential toxicity, modeling control and treatment arms. It may also help recruit family members, which could increase power for studying, especially rare variants that might run in families. We may also use this genetic-driven research to test the validity or interpretation of some self-reported data from research participants.

\n\n\n\n

These DNA-driven discoveries will improve our important work and may lead to important insights into the treatment and diagnosis of disease.

\n\n\n\n

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Familial hypercholesterolemia (FH) is one of the most common genetic conditions, which is associated with very high levels of “bad” cholesterol. Elevated levels of cholesterol can lead to a higher risk for early cardiovascular disease, and, in turn, an increased risk for heart attacks.

Even though FH is relatively common — affecting about 1 in 250 people worldwide — awareness of the condition is very low. That combined with the lack of symptoms, means that people with FH often go undiagnosed.

In fact, as many as 90 percent of people with FH don’t know they have it. If left untreated, men with the condition have a 50 percent chance of having a heart attack by age 50, while untreated women with the condition have about a 30 percent risk of a heart attack by age 60, according to published studies.

$\"\"$

A Positive First Step for FH

Today 23andMe added a new Genetic Health Risk* report on FH* which can tell individuals about their risk of developing high cholesterol associated with the condition. Given its expertise as the leading research and patient advocacy organization for the FH community, the FH Foundation provided input on the patient journey, the report’s content and associated educational resources.

This new report could give an early warning for people who otherwise wouldn’t know of their risk, given the lack of awareness around the condition. Because there are few physical signs or symptoms, many people don’t know they have FH and how it can affect their cholesterol levels. However, when diagnosed early in life, the condition can be treated effectively to substantially reduce the risk of heart attack.

“Nine out of ten people born with familial hypercholesterolemia in the United States are undiagnosed, leaving them at risk for heart disease in the prime of life. Unlike many genetic conditions, FH is highly actionable. Early diagnosis and appropriate medical treatment save lives,” said Katherine Wilemon, Founder and CEO of the FH Foundation, a global research and advocacy organization. “The new 23andMe report, will not find everyone with an FH mutation, but it can be a positive first step for prevention by providing early detection for those who have one of the FH variants reported on.”

A New Genetic Health Risk Report for Familial Hypercholesterolemia

23andMe’s new Familial Hypercholesterolemia Genetic Health Risk report looks at 24 variants in the LDLR and APOB genes linked to the condition that have been shown to increase one’s risk of elevated levels of LDL cholesterol, and as a result, aggressive and premature cardiovascular disease. 23andMe’s report looks at some of the more common variants in people of European and Lebanese ancestry, as well as people from the “Old Order Amish” community. The variants in the report are also found in people of other ethnicities. Our team of scientists conducted an extensive review of the currently available peer-reviewed publications on the genetic variants associated with FH. We determined that those included in this report are among some of the more common in certain populations and well-studied.

“Through this report, 23andMe is providing individuals with potentially life-saving information about their risk for high LDL cholesterol levels associated with FH. We are grateful for the input from the FH Foundation on the patient journey and how we can continue to educate individuals about their risk for this often undiagnosed genetic condition,” said Arin Assero, Director of Advocacy at 23andMe.

FH and LDL

People with FH have very high levels of low-density lipoprotein (LDL) — so-called “bad cholesterol.” This is because genetic variants, or mutations, associated with the condition decrease the liver’s ability to remove excess LDL cholesterol from the blood. The result is often much higher LDL levels in the bloodstream. This in turn can lead to cardiovascular disease and a higher risk for heart attack. Other factors influence a person’s chances for heart disease or high cholesterol such as smoking, diet, exercise, and weight. However 23andMe’s report focuses specifically on genetic factors for FH and its influence on the risk for high cholesterol and cardiovascular disease.

Importantly, since FH is an inherited condition, each child of a person with FH has a 50 percent chance of inheriting the disorder so it is essential to screen parents, siblings and children of a person diagnosed with FH. This will aid in finding others who may have inherited the condition.

Limitations

There are limitations to the 23andMe report. It looks at only a few select variants of the more than 1,000 associated with the condition. About 30-35 percent of people who are of European descent with a variant linked to FH have one of the variants in this report. In the case of individuals with FH of Lebanese ancestry, about 80 percent have one of the variants in this report. About 15-20 percent of Latinos and people of East Asian ancestry with a variant linked to FH have one of the variants in 23andMe’s report.

Given the report’s limitations, many 23andMe customers will receive a 0 variant result. This does not mean they have no risk for the condition. It also doesn’t mean they should forgo regular screening for cholesterol particularly if they have a family history of high cholesterol or early heart disease. In addition, the report is unable to detect if a person has two copies of a variant. Having two copies of a variant is associated with the more severe form of FH called homozygous FH. The FH Foundation can provide more resources on FH. It can also serve as a care navigator for individuals with a positive or negative test result.

There are currently effective treatments that can lower the risks associated with FH. However, early detection is critical. 23andMe and the FH Foundation are committed to raising awareness of familial hypercholesterolemia. We are working to advocate for access to early detection and treatment.

The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. The test is not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment. The Familial Hypercholesterolemia genetic health risk report is indicated for reporting of one variant in the APOB gene and 23 variants in the LDLR gene and describes if a person has variants associated with an increased risk of developing very high LDL cholesterol, which can lead to heart disease. The majority of the variants included in this report have been most studied in people of European and Lebanese descent, as well as in the Old Order Amish.

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$\"High$ For the live-updated, fully-labelled, interactive version of this infographic, click here.

By Alex Carmichael, Co-Founder of CureTogether

If part of your plan for 2014 is to eat healthier, exercise, and lower your cholesterol, this post is for you! Some of the most popular treatments for High Cholesterol are not necessarily the most effective, according to a new study by CureTogether, a free resource owned by 23andMe that allows people to share information about their health and treatments.

Participants in the study said they found that some drugs – including Statins, Crestor, and Lipitor – were the most effective. Conversely some popular treatments such as Fish oil and Vitamin D were among the least effective, according to the study. High Cholesterol affects millions of Americans. Finding treatments that work well is important to improve quality of life, so CureTogether asked people living with High Cholesterol to rate the effectiveness of different treatments.

CureTogether’s study compiled responses from 1,862 people with High Cholesterol, who rated the effectiveness of 19 different treatments. Among the most helpful treatments were statin drugs, weight loss, exercise, and quitting smoking. Also effective for those in the study were diet changes including reducing carbohydrates. The people in the study also said that cinnamon and garlic – both folk remedies – were not as effective.

Most Effective Rated Treatments for People with High Cholesterol
\n1. Statins
\n2. Crestor
\n3. Lipitor
\n4. Quit smoking
\n5. Zocor
\n6. Weight loss
\n7. Niaspan
\n8. No carbohydrates
\n9. Exercise
\n10. Red yeast rice

Where did this data come from? This is the result of a four-year CureTogether study on High Cholesterol, in which people suffering from the condition shared information about their symptoms and what treatments worked best for them. We’d like to thank those who participated. And just as they shared their experience with High Cholesterol treatments, we’re freely and openly sharing the results of the High Cholesterol study.

This is part of a regular series of CureTogether research findings. CureTogether’s research findings are different than those made by 23andMe, which look at genetic associations with illness, traits and drug response. But as we continue our work with the CureTogether community, 23andMe hopes to incorporate more of this kind of self-reported information into our own research. CureTogether present its findings just as they are — patient-reported data — to stimulate discussion and generate new insights for further research.

Please tweet, blog, or pass this along to anyone who can benefit or is interested in High Cholesterol. Thank you!

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high cholesterol

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What Patients Say Works For High Cholesterol

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