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By Sheel Dandekar

Not convinced that those trips to the gym are making a difference? Think again. In a recent study in PloS Genetics, researchers from Lund University in Sweden found that exercising can change how the DNA in fat cells works.

Fate

With the growing number of links found between genetics and health, it is easy to fall into the trap of thinking that your genes determine your fate. That’s just not the case.

Genetics plays an important role in your health, but so do environmental influences. This includes lifestyle factors, which you have control over (e.g. eating junk food, smoking), and factors that may be difficult to control (e.g. the quality of healthcare you receive). To the extent to which we can dictate our environment, we have the power to change our risk for many common diseases

We frequently think about genetics and environment as two completely separate things — the classic nature vs. nurture debate. However, it turns out that genetics and environment can’t be neatly separated.

Epigenetic

A growing list of studies show that environmental factors can lead to lasting “epigenetic” changes, such as modification of the DNA base. To understand how this can happen, consider that your DNA is just a blueprint, a set of instructions for making the various things your body needs. Not all parts of the blueprint are actively being read in every cell. A complex system of switches controls which parts are being decoded, and which parts remain unread. Environmental factors can epigenetically modify DNA to determine whether or not those switches work. For instance, a famous study of children conceived during times of famine found that a chemical modification known as methylation can last for decades.

So do these epigenetic changes only happen in extreme environmental conditions, such as famine? The Lund study showed that simply exercising can change how the DNA in fat cells is read through the methylation of key genes.

They recruited 31 generally healthy but sedentary men and had them follow an exercise program for 6 months. The program consisted of 1 session of a 1 hour spinning class and 2 sessions of a 1 hour aerobics class each week. As one might expect, a number of clinical measurements (waist circumference, cholesterol, blood pressure) improved after 6 months of working out.

Metabolism

More surprisingly, when they compared the DNA from the men’s fat cells before and after the program, they found that significant portions of the DNA sequence had been methylated. In particular, a number of genes suspected to play a role in obesity and type 2 diabetes were modified, and the authors suggested that these modifications might drive differences in metabolism in fat cells.

In demonstrating that exercise can alter DNA methylation in fat cells, this study raises some interesting questions. Previous work has shown that exercise can lead to epigenetic changes in muscle cells. What other types of cells show epigenetic changes after exercise, and what exercises are best? Finally, how long do these epigenetic changes last?

Further research may help to answer these questions and maximize the benefits of exercise. For now, take solace in the fact that your genetic code is just one factor to consider in your overall health, and that many other factors remain under your control.

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A new study published this week demonstrates just how powerful large-scale genetic research can be when it comes to predicting health traits—like body weight. By combining data from consented 23andMe research participants with the GIANT consortium, an international group of scientists have created the most predictive polygenic score for body mass index (BMI) to date. The study used genetic data from up to 5.1 million individuals from diverse backgrounds, helping push the science forward in important and inclusive ways.

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What’s a Polygenic Score?

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Think of a polygenic score (sometimes called a polygenic risk score or PRS) as a genetic summary. It adds up the small effects of many different genetic variants—often thousands or even millions—that are each linked to a trait, like BMI. The higher your score, the higher your predicted BMI. These scores are increasingly used in research, and even clinical settings, to better understand traits and potential health risks.

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Why This Study Matters

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One of the big takeaways from this research? The more data we include in building a polygenic score, the more accurate the predictions become. Thanks to the massive dataset, this new BMI polygenic score is one of the most accurate developed so far—and it’s also more applicable to people of diverse ancestries than previous versions.

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Still, it’s important to note that while this polygenic score performs better across different populations, its accuracy is still highest in individuals of European descent. That’s because most genetic research to date has been heavily based on European-ancestry populations. Studies like this one help move the field toward more inclusive and equitable research.

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What the Study Found

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Childhood weight gain: A higher BMI polygenic score was linked to faster weight gain starting from age 2.5 onwards and an earlier “adiposity rebound”—a key moment in childhood growth when BMI dips and then begins to increase again. This could help identify children at higher risk of becoming overweight before other warning signs appear.
Adult weight change: Between ages 20 and 50, people with higher BMI polygenic scores were more likely to gain weight. Interestingly, this was especially true for those who started adulthood at a weight lower than what their genetics might predict. It suggests that individuals with a genetic predisposition to higher weight may eventually “catch up” to their genetic set point over time.
Lifestyle changes: In lifestyle intervention studies (think: intensive diet and exercise programs), people with a higher genetic predisposition to obesity tended to lose more weight during the first year—but they were also more likely to regain it. This pattern fits with previous research showing that people who are genetically predisposed to obesity often respond more dramatically to environmental changes, both positive and negative.

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What This Study Doesn’t Say

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This research doesn’t mean that lifestyle doesn’t matter. In fact, it’s just the opposite. Even with a high genetic predisposition to obesity, lifestyle choices—like diet, physical activity, sleep, and stress management—still have a meaningful impact. What polygenic scores offer is insight into who may be at higher risk and might benefit most from early interventions or targeted prevention strategies.

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Final Thoughts

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Your genes are only one part of the story. While this research gives us a clearer picture of how genetics influence weight over time, it also highlights the importance of using that information wisely. At 23andMe, we believe that understanding your genetics can empower you to make informed health decisions—not define your destiny. As science continues to evolve, so do the tools we have to support healthier, more personalized approaches to wellness.

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by Destiny Gordon

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We often blame everything on not getting enough sleep—feeling foggy, moody, exhausted, or just off. And while sleep quantity matters, what many of us don’t realize is that it’s not only about how much sleep we get—but when we get it. At the core of it all is your body’s internal clock, known as your circadian rhythm. This quiet, biological timekeeper is constantly at work, regulating everything from hormone release and metabolism to mood and energy. And when it falls out of sync—whether due to shift work, late nights, excessive screen time, or simply inconsistent routines—your health can start to feel out of balance in ways that go far beyond basic tiredness.

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What is circadian rhythm?

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Circadian rhythm is the natural cycle your body goes through in a 24-hour period. Genetics plays a key role in determining circadian rhythm. In fact, the researchers who first uncovered the genetic basis of circadian rhythm won the Nobel Prize in Physiology or Medicine in 2017. Your circadian rhythm influences when your brain is sharp, when your body digests food efficiently, and when it needs deep rest. And for women, the interaction between daily circadian rhythms and monthly hormone fluctuations creates a unique layer of complexity. At different points in the menstrual cycle, shifts in estrogen and progesterone can make your body more sensitive to sleep disruption, stress, and energy dips. So if your daily rhythm is already out of sync, those hormonal shifts can hit harder—amplifying symptoms like fatigue, mood swings, poor focus, or disrupted sleep. It’s a compounding effect that makes it even more important to stay in rhythm.

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What happens when you’re misaligned to your circadian rhythm?

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Research has shown that disruptions to this internal rhythm—like being awake when your body naturally wants to be asleep, sleeping at inconsistent times due to shift work, or missing natural light cues—can throw off the timing of critical biological processes. This circadian misalignment can increase the risk of real, long-term health issues for both men and women. These shifts are linked to mood disorders like anxiety and depression, weight gain, insulin resistance, cardiovascular issues, irregular menstrual cycle, and even fertility challenges. And because these symptoms often start subtly, it’s easy to miss the connection until the effects become harder to ignore.

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What can we do to keep our lives aligned to our circadian rhythm?

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The tricky part? Circadian disruption often hides in plain sight. It doesn’t always feel like a big, dramatic problem. It can look like staying up a little too late, skipping meals, waking up at inconsistent times, or scrolling in bed just a bit too long. These small habits may not seem like much, but if they happen repeatedly over time, they chip away at your body’s natural rhythm.

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The good news? Once you start to tune in, you can make small, manageable changes to help bring your body back into sync. Things like going to bed and waking up at the same time every day (yes, even on weekends), getting exposure to natural light in the morning, limiting caffeine later in the day, and avoiding screens at least an hour before bed can all support a healthier rhythm. It’s not about being perfect—it’s about creating enough consistency that your body knows when to rise, when to rest, and everything in between.

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Because when your body runs in rhythm, everything works better. Your mind feels clearer. Your energy lasts longer. Your health feels like it’s working with you, not against you. So maybe it’s not just about getting more sleep. Maybe it’s time to get back in sync.

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About Destiny: Destiny Gordon is a rising second-year medical student at Morehouse School of Medicine, originally from Jacksonville, Florida. She is the founder of InnerLight ATL, a youth mental health initiative focused on building safe, supportive spaces for emotional wellness. With over three years of experience in cancer research and a passion for community-centered care, Destiny is dedicated to blending science, advocacy, and storytelling to inform and inspire.

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By Jalen Robinson

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Personalized medicine is increasingly becoming recognized as a necessary evolution of the standard of care. One key aspect of this shift is a dual understanding: that medical care based on race, ethnicity, or outward appearance is inaccurate and can lead to harm, and at the same time knowledge of genetic, cultural, and environmental factors together provide a more nuanced and complete picture of a person’s health risks and potential intervention strategies.

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In this article, we explore a few health conditions—uterine fibroids, metabolic dysfunction-associated steatotic liver disease (MASLD), gestational diabetes, and atrial fibrillation—that have meaningful connections with ancestry, environment, or cultural factors. We also examine diseases such as G6PD deficiency and Tay-Sachs disease—conditions that are primarily genetic and therefore closely linked to genetic ancestry. By understanding different ways in which their unique background might influence their health, individuals and their healthcare providers can make more informed health decisions for themselves and their families.

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Uterine Fibroids: An African Connection

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Uterine fibroids are non-cancerous growths that develop in the wall of the uterus. These growths can vary in size, ranging from small, undetectable nodules to large masses that distort the uterus. Symptoms of fibroids include heavy menstrual bleeding, pelvic pain, bloating, and complications with fertility and pregnancy. Risk factors include race and ethnicity, age, family history, hormonal factors, obesity, diet, environmental toxins, and stress.

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While many women may experience fibroids at some point in their lives, this condition affects women with African ancestry more commonly and severely. African American women have a three-times higher risk of developing fibroids than women from other groups. Black women are also more likely to be diagnosed at younger ages, experience more severe symptoms such as infertility and pregnancy loss, and face worse outcomes, including higher rates of hospitalization. Although there are likely many contributing factors, vitamin D deficiency may play a role: this nutrient helps regulate how cells grow and divide, but people with darker skin produce less vitamin D from sunlight.

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Maintaining a healthy weight, limiting processed foods and red meat, and managing stress are beneficial in reducing risk for uterine fibroids, but there are also specific proactive steps women can take. These include reducing exposure to endocrine-disrupting chemicals like those found in personal care products and hair relaxers, and ensuring adequate levels of vitamin D in their diet. As with any health condition, regular medical check-ups are important for early detection and management of fibroids and for maintaining overall reproductive health.

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Liver Disease: An Indigenous American Connection

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Metabolic dysfunction-associated steatotic liver disease (MASLD, also known as non-alcoholic fatty liver disease or NAFLD) is the most common liver disease worldwide, marked by excess fat in the liver unrelated to alcohol use. While often silent, it can progress to metabolic dysfunction-associated steatohepatitis (MASH), which can lead to cirrhosis and liver cancer. MASLD is strongly linked to metabolic syndrome—a group of conditions including a large waist circumference, high blood sugar levels, high blood pressure, and abnormal cholesterol levels.

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Indigenous peoples of the Americas are disproportionately affected by MASLD and MASH. This elevated risk is influenced by both genetic and environmental factors. A genetic variant in the PNPLA3 gene, known as I148M, has been linked to a higher risk of developing MASLD, and is particularly common in Indigenous populations and regions with high proportions of Indigenous American ancestry. Indigenous communities also report higher rates of metabolic syndrome compared to other groups.

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Historically, many Indigenous societies had diets and lifestyles that may have protected against metabolic diseases. These societies typically consumed diets high in fiber, with a wide variety of seasonal plant-based foods, and maintained regular physical activity through subsistence living. However, the rapid shift away from these traditional patterns, especially in North America—driven by violent colonization, forced displacement, and systemic marginalization—has created a potential mismatch between genetic predispositions and modern environments.

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Addressing the risk of MASLD today may benefit from restoring access to healthy foods, revitalizing traditional food systems, and encouraging physical activity in ways that respect Indigenous culture. Additionally, ensuring culturally respectful, community-led healthcare is essential for addressing MASLD risk and improving long-term outcomes for Indigenous populations.

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Gestational Diabetes: An Asian Connection

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Gestational diabetes mellitus (GDM) is a form of diabetes that develops during pregnancy when the body cannot produce or effectively use enough insulin. This leads to elevated blood glucose levels, which increases the chances of preeclampsia (dangerously high blood pressure), preterm birth, and complications during labor. People who experience GDM are also at higher risk of developing type 2 diabetes later in life, while their children are more likely to develop obesity and metabolic disorders.

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Though GDM affects pregnancies globally, rates of GDM are highest in individuals of East and South Asian descent, despite generally lower BMI. This heightened risk may be linked to both genetic predisposition to type 2 diabetes as well as greater insulin resistance and a tendency to store fat in the abdomen (also known as visceral fat, associated with cardiometabolic disease) even at lower BMIs. Dietary patterns may compound these risks, and limited access to healthcare and low awareness of GDM may further contribute to poorer outcomes in some communities.

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Prioritizing a diet high in whole grains and vegetables, avoiding refined carbohydrates and sugar, and incorporating regular physical activity—even modest forms like daily walking or yoga—can significantly improve the body’s ability to control blood sugar. Awareness and early screening are also important, especially given the higher rates of GDM even among those with lower BMIs.

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Atrial Fibrillation: A European Connection

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Atrial fibrillation (AFib) is the most common heart rhythm disorder, marked by an irregular and often rapid heartbeat that can reduce blood flow and increase the risk of stroke, heart failure, and other complications. Symptoms may include palpitations, fatigue, shortness of breath, or dizziness, though some people remain asymptomatic. AFib risk rises with age, and conditions such as high blood pressure, obesity, diabetes, and excessive alcohol use are major contributors.

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In multiple studies, AFib shows the highest prevalence in White populations, Scandinavian countries, and countries with high proportions of European ancestry. The higher prevalence does not appear to be explained by differences in lifestyle risk factors or by differences in diagnosis rates. Although the genetic variants identified to date are not especially frequent in European populations compared to other groups, one intriguing study has shown an association between AFib risk and degree of European genetic ancestry. Additionally, individuals with Northern European ancestry tend to be taller on average, and increased height and body size are associated with a greater risk of AFib, perhaps due to greater load on the heart.

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To help mitigate the risk of atrial fibrillation, there are several strategies people can adopt. Maintaining a healthy weight, engaging in moderate physical activity, managing other health conditions, limiting alcohol intake, and avoiding smoking are all important. Since rates of AFib remain high even in Scandinavian countries known for healthy lifestyles, individuals with known genetic risk factors or a family history of AFib should consider regular heart rhythm monitoring and consult with a healthcare provider for personalized screening.

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Genetic Ancestry and Health

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Some health conditions are primarily genetic, meaning they are caused by inherited changes in specific genes rather than lifestyle or environmental factors. Because these variations are passed down through families, the risk of developing or carrying certain genetic disorders can vary significantly depending on one’s ancestry. These inherited conditions often reflect patterns shaped over thousands of years by human migration, geographic isolation, and natural selection—making genetic ancestry a powerful lens through which to understand personal health risks.

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Take glucose-6-phosphate dehydrogenase (G6PD) deficiency, for example. This inherited condition affects how red blood cells function, potentially leading to fatigue, jaundice, or anemia—especially when triggered by certain foods, medications, or infections. G6PD deficiency is particularly common in people of African, Middle Eastern, Mediterranean, and Southeast Asian descent, with prevalence rates as high as 25% in some regions. Just like sickle cell trait, the high frequency of G6PD deficiency is thought to stem from a genetic advantage: people who carry a G6PD variant are more resistant to certain forms of malaria, an infectious disease that historically plagued these areas. Similarly, Tay-Sachs disease is a rare but serious neurodegenerative disorder that is more prevalent in Ashkenazi Jewish, French Canadian, and Cajun populations. This is largely due to what geneticists call a founder effect, where a small ancestral group passes on a limited set of genes—some of which may carry disease-causing variants.

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In communities where certain genetic risks are more common, genetic screening and counseling have already made a major impact. However, understanding your genetic ancestry—rather than making assumptions based on appearance, social identity, or cultural heritage—is what really matters for identifying these inherited health risks. As our knowledge and the cost of mapping genetic ancestry and health predispositions continues to improve, so does our potential to address inherited health risks in more personalized and proactive ways.

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Personalizing Health

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Our DNA plays a key role in health, offering insights into inherited traits and potential risks. Together with cultural background and lived experiences, these factors all shape our health in ways unique to each of us. Understanding both your genetic ancestry and cultural context can support proactive care through early screenings, personalized lifestyle choices, and more informed conversations with healthcare providers. As populations grow more diverse, moving beyond outdated assumptions based on race and focusing on the full picture—biology, ancestry, and culture—can help improve care and reduce health disparities.

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Learn more about Jalen Robinson, a student at Morehouse School of Medicine and former Research Diversity intern at 23andMe, who helped develop our African American Genetic Groups

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This is part of an ongoing series of posts we plan to publish in order to help raise further awareness of lung cancer. We hope to highlight the work of the 20+ lung cancer patient advocacy organizations collaborating with us on our recently launched Lung Cancer Genetics Study.

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It’s not as if lung cancer is an obscure disease, and yet facts about lung cancer are not well known.

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23andMe wants to spotlight the disease while also highlighting our efforts with our Lung Cancer Genetics Study and the work of more than 20 organizations collaborating with us on this important new research, which aims to identify genetic risk factors that contribute to lung cancer. Ultimately the goal of the study is to improve prevention, detection and treatment for lung cancer.

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Read our previous post: A Legacy of Hope in the Fight Against Lung Cancer

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Lung cancer is the leading cause of cancer death worldwide. In the US, it accounts for one in five cancer deaths and kills nearly as many people each year as colon, breast, and prostate cancer combined. These staggering statistics underscore the urgent need for greater awareness and more research.

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Dispelling Common Myths About Lung Cancer

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Our first post in this series looked at the origins of our Lung Cancer Genetics Study and how the collaboration started. This one focuses on myths and facts about lung cancer, and we are again leaning on the expertise of some of our collaborators. This time, we talked to leaders from the LUNGevity Foundation and Upstage Lung Cancer. They shared some common misconceptions about lung cancer and some facts they wished more people knew.

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Myth: Only People Who Smoke Get Lung Cancer

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No, it’s not just people with a history of tobacco exposure who get lung cancer.

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Among lung cancer survivors and advocates, this pervasive myth about lung cancer being only a disease for people who have smoked is particularly vexing, and it’s not true.

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Indeed, cigarette smoking is strongly linked to lung cancer, but as advocates like to say, “anyone with lungs can get lung cancer, but no one deserves it.”

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Fact: Many Risk Factors Play a Role in Lung Cancer

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“All the warnings about the dangers of tobacco exposure, which are totally legitimate, got people to make this very powerful association — tobacco exposure leads to cancer, but it’s not the only cause. Making this connection, we often ignore other causes,” said Upal Basu Roy, PhD, MPH, Executive Director of Research for the non-profit LUNGevity Foundation. “It’s hard to see beyond tobacco exposure.”

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“Active tobacco exposure is indeed an important risk factor that’s been well-studied. However, other risk factors, such as radon exposure, passive (or secondhand) tobacco exposure, occupational exposures, air pollution, and genetics, all can play a role in lung cancer development. Often, it is a complex mix of many of those factors that contribute to why some people develop lung cancer”, said Upal.

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In 2019, nearly 15% of lung cancers were not related to direct tobacco exposure. To put that into perspective, lung cancer in people who never smoked cigarettes, or LCINS, would be ranked in the top ten causes of cancer deaths if ranked separately from tobacco exposure–related lung cancer. LCINS is on the rise, and more research is needed to have an accurate estimate of the true numbers of LCINS today.

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“80 to 90% of people with tobacco exposure never get lung cancer, while many people without tobacco exposure get the disease,” said Upal. “It’s incredibly complex. We haven’t unpacked how much a role all these contributing factors play, and that’s why this genetic study is so interesting. It offers a chance to learn more about the nature of the disease and how these factors might interact.”

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Lung Cancer Screening and Early Detection

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Myth: There’s No Way to Detect Lung Cancer Early

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Current US screening recommendations include:

Ages 50–80

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20-pack-year cigarette smoking history
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Currently smoking or having quit within the last 15 years

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Lung cancer screening exists — but not everyone at risk is eligible. There is a strong association between tobacco use and lung cancer, and current guidelines consider this history for screening eligibility. Current US guidelines recommend screening for people ages 50 to 80 who have a 20-pack-year cigarette smoking history and currently smoke tobacco or have quit within the last 15 years.

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Unfortunately, the vast majority of people who are eligible for lung cancer screening don’t receive it. According to the American Lung Association, only 16% of eligible people were screened for lung cancer in 2024. Much work remains to ensure everyone eligible for screening knows about and has access to this life-saving healthcare measure. And additional progress is needed to expand lung cancer screening to include others at high risk, like those who have never smoked.

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Fact: Not Everyone at Risk of Lung Cancer is Currently Eligible for Screening

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While lung cancer in people with a smoking history is more common in men, two-thirds of people diagnosed with LCINS are women. Hildy Grossman, who describes herself as a clinical psychologist by day and a jazz singer by night, is one of those women diagnosed with lung cancer who’d smoked cigarettes as a teenager but quit at age twenty.

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Hildy was diagnosed in December of 2006 by chance. She’d slipped on the threshold of a narrow stairway, resulting in pain in her wrist. After a series of missed diagnoses, Hildy eventually had an MRI to determine if a pinched nerve in her back was causing the pain. Instead, the MRI showed two spots on her lungs. A biopsy revealed it was lung cancer. Her doctor told her how lucky she’d been that they caught it early, saying, “Somebody up there likes you!” Since her tumor was diagnosed so early (stage 1A), her treatment only required surgery, which she had in January 2007.

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“As I came to terms with (the diagnosis), I asked myself, ‘Why me?’ Not ‘why did I get lung cancer,’ but ‘why was I able to find it so early and survive,’” Hildy said. The question prompted her to start Upstage Lung Cancer, an organization using music and the performing arts to raise awareness and support lung cancer research. Hildy is both the founder and president of the board.

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The Need for Expanded Screening Criteria

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While current lung cancer screening guidelines have saved many lives by detecting cancer early, they also miss many others who may be at risk but who never smoked, or like Hildy, who quit cigarette smoking many years earlier. The problem is that there aren’t yet criteria outside of tobacco use for identifying those who are at the highest risk and could benefit most from screening. Without early detection, many lung cancers are not diagnosed before symptoms appear, such as a persistent cough or coughing up blood. And by the time symptoms occur, it’s likely the cancer has spread and will be harder to treat. In contrast, people diagnosed with cancer in its earlier stages tend to live longer or can even be cured. Lingering misconceptions about who is at risk leave many people vulnerable.

\n\n\n\n

“That’s why early detection research (part of the Lung Cancer Genetics Study) is so important,” Hildy said.

\n\n\n\n

Beyond One Disease

\n\n\n\n

Myth: All Lung Cancer is the Same

\n\n\n\n

There are two main types of lung cancer — non-small cell lung cancer and small cell lung cancer. Eighty to 85%of lung cancer cases are non-small cell, and 10 to 15% are small cell. Then, there are numerous subtypes within those types of lung cancer, said Upal.

\n\n\n\n

“And the biology is different, which has implications for how the lung cancer is treated,” said Upal.

\n\n\n\n

Fact: Biomarker Testing Can Identify Lung Cancer Subtypes and Guide Treatment

\n\n\n\n

Some lung cancer subtypes are defined by specific changes in the cancer cells, known as oncogenic driver mutations. These mutations speed up cancer growth. Some of these subtypes can be identified through biomarker testing, which looks for genetic changes in specific genes like EGFR, ALK, RET, or HER2. Discovering whether a tumor has one of these mutations — a biomarker — can help doctors choose the best treatment options, including targeted therapies for specific mutations.

\n\n\n\n\n\n\n \n \n Table Example\n \n\n\n \n \n \n \n \n \n \n \n \n \n \n \n

\n \n Biomarker tests for non-small cell lung cancer (NSCLC)\n \n
ALK BRAF	EGFR ERBB2 / HER2	KRAS MET	NRG1* NTRK	PD-L1 RET	ROS1

\n\n\n\n\n\n

*A targeted therapy for NRG1 mutations was also recently approved by the FDA.

\n\n\n\n

However, only some people who might benefit from biomarker testing receive it. For example, one study examined rates of biomarker testing in more than 17,000 people who were diagnosed with advanced non-small cell lung cancer between 2015 and 2021. This study found that while testing rates increased over time, nearly one-third of people did not receive comprehensive biomarker testing by 2020. Barriers to biomarker testing are complex and include issues like cost, time, tumor sample quality, and lack of awareness of the value of testing. These challenges emphasize the importance of insurance coverage for biomarker testing and approved targeted therapies, increased education of healthcare providers, and self-advocacy by patients and caregivers.

\n\n\n\n

Continuing the Conversation on Lung Cancer Awareness

\n\n\n\n

Misconceptions like the ones addressed here represent just some of the many challenges faced by people diagnosed with lung cancer. As part of our lung cancer blog series, we will continue to amplify the voices of patient advocates and raise awareness of these and other little-known facts about the disease.

\n\n\n\n

Visit our Lung Cancer Genetics Study page to learn more about the 23andMe study, our collaborators, and eligibility criteria.

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