This study examines how medical students and clinicians report experiencing patient medication requests associated with prescription drug direct-to-consumer advertising on social media; survey data from 98 respondents indicate that those providing both in-person and virtual care encounter more frequent requests for medications advertised online, particularly branded glucagon-like peptide-1 (GLP-1) weight loss drugs.
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Heart’s Constant Beating Suppresses Tumor Growth in Cardiac Tissues
The results of a study by researchers at the International Centre for Genetic Engineering and Biotechnology (ICGEB) suggest that the heart’s constant beating may actively suppress tumor growth in cardiac tissues. The collective findings from the team’s research in mouse models and in engineered heart tissues (EHT) suggests that this is because cellular pathways in these tissues alter gene regulation in cancer cells to keep them from proliferating.
Headed by Giulio Ciucci, PhD, and Serena Zacchigna, MD, PhD, at the ICGEB Cardiovascular Biology Laboratory, the scientists say the findings shed light on the role of mechanical forces in protecting the heart from cancer and may pave the way to new cancer therapies based on mechanical stimulation. First author Ciucci, together with senior author Zacchigna and colleagues reported on their findings in Science, in a paper titled “Mechanical load inhibits cancer growth in mouse and human hearts.” In their report the authors concluded “Collectively, the data presented in this work provide evidence that mechanical load in the heart inhibits cancer cell proliferation, likely explaining the low incidence of cardiac tumors.”
Heart cancer is very rare in mammals, but as the authors noted, “The mechanisms that protect the heart remain elusive.” The adult human heart in addition has a limited capacity for self-renewal, with cardiomyocytes regenerating at roughly 1% per year. “This suggests that the same mechanisms that halt the proliferation of cardiac cells could also inhibit the growth of cancer cells in the adult heart,” the authors continued. One proposed explanation for this loss of cardiomyocyte proliferative capacity lies in the intense mechanical demands placed on heart tissues, which must continuously pump blood against significant resistance. “We hypothesized that it could similarly hamper the proliferation of cancer cells in the heart,” the investigators reported.
Using a genetically engineered mouse model, Ciucci et al. first showed that the heart is remarkably resistant to cancer-causing mutations, even when potent oncogenic changes were introduced. To understand why, the authors developed a transplantation model in which the heart’s mechanical workload could be reduced. By grafting a donor heart into the neck of a compatible mouse, they created a “mechanically unloaded” organ, one that remained perfused with blood but did not bear physiological strain. “To assess the contribution of mechanical load to the low incidence and growth of cancer in the heart, we used a model of in vivo cardiac unloading by heterotopically transplanting a donor heart into the neck of a recipient syngeneic mouse,” they explained.
![Image of lung cancer cells (in green) growing in a heart, in which cardiomyocytes are stained in red. Nuclei are stained in blue. [Ciucci et al., Science 2026]](https://www.genengnews.com/wp-content/uploads/2026/04/low-res-4-300x300.jpeg)
After injecting human cancer cells directly into the heart muscle, they compared tumor behavior in the unloaded transplanted heart versus the animal’s native, mechanically active heart. Across their experiments, Ciucci et al. found that mechanical load consistently suppressed the growth of various cancer types, while unloading the heart promoted tumor cell proliferation within cardiac tissue.
According to the study findings, mechanical forces within the tissue reshape the cancer cell genome’s regulatory landscape, influencing whether cells can proliferate. Central to this process is Nesprin-2, a protein that transmits mechanical signals from the cell surface to the nucleus. “Nesprin-2, a protein known to mediate mechanotransduction from the cytoplasm to the nucleus, emerged as a key molecule sensing mechanical forces operating in beating hearts and translating them into reduced cell proliferation,” the scientists reported.
Nesprin-2, a component of the LINC complex, senses the mechanical microenvironment of the heart and functionally alters chromatin structure and histone methylation, reducing gene activity linked to tumor cell proliferation. When Nesprin-2 was silenced in cancer cells, those cells regained the ability to grow in the mechanically active environment of the heart, forming tumors. “Silencing of Nesprin-2 in lung cancer cells prior to their implantation in the heart in vivo restored the capacity of the cells to proliferate in the presence of physiological mechanical load, resulting in the formation of large tumors,” the authors stated.
The team noted that their collective results shed light on the role of mechanical forces in protecting the heart from cancer and may pave the way to new approaches to cancer therapy. “This offers fundamental insights into the biology of cell proliferation within the myocardium, and additionally, the mechanical stimuli that operate in a beating heart could be exploited for the development of a mechanical therapy for cancer.”
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New Markers of Diabetes and Heart Disease Revealed via Genetic Study in Indians
A study in 3,000 Punjabi Sikhs has identified previously unreported molecular pathways that contribute to cardiometabolic disease. Published today in PLOS Medicine, these findings highlight the benefits of including diverse participants in these types of studies, which have historically centered on individuals of European ancestry.
“Genetic mechanisms that predispose people to type 2 diabetes and cardiovascular disease remain poorly understood, partly because of a lack of sufficient data on non-European ethnic groups,” write the authors of the study, who were led by Dharambir K. Sanghera, PhD, director of the Genetic Epidemiology Laboratory at the University of Oklahoma Health Sciences Center. “Extending these evaluations to diverse cohorts is essential for gaining insights into the molecular pathways involved in disease.”
Sanghera and colleagues conducted a metabolite genome-wide association study to look for links between the human lipidome and cardiometabolic disorders in a Punjabi population originating from Northern India. Epidemiological studies have repeatedly shown that South Asians living abroad experience a higher incidence of type 2 diabetes and are more susceptible to cardiovascular disease compared to other ethnic groups. However, the exact mechanism responsible for this increased risk remains unknown and lipidomic and genome-wide data is lacking for Indian populations.
“Genome-wide studies have shown that genes influencing blood lipid metabolites are often linked to different diseases,” write the study authors. “However, most of this research has been done on people of European ancestry. Studying more diverse populations is important to better understand how these genetic pathways contribute to disease in different ethnic groups.”
The study looked at genetic influences on 516 lipids in 3,000 Punjabi Sikh individuals and then validated the results in larger cohorts, with both European and non-European ancestry, using data from UK Biobank, GeneRISK, DIAMANT, PROMIS, and other studies. After multiple rounds of testing and correction, results showed strong associations in 36 pairs of lipid metabolites and single nucleotide polymorphisms (SNPs). Among them, 33 had not been reported before, and three were confirmed to be ancestry-specific.
Further investigation identified a causal association between type 2 diabetes and the metabolite LPC O-16:0, which was paired with a genetic variant in the gene encoding for CD45, a key regulator of immune signaling. Another possible causal relationship was found with PC 38:4, a metabolite shown to protect against coronary artery disease in Indian populations that was paired with a genetic variant in an untranslated region of the FADS1/2 genes.
“Our study has discovered new metabolite markers and genes that intersect with pathways of inflammation and immuno-vascular diseases, which have not been reported in previous European studies, specifically emphasizing how immune system signaling affects metabolic health,” state the authors. “By identifying unique genetic signatures in Asian Indians, the research advocates for ancestry-specific medical approaches to address chronic immuno-vascular conditions in cardiometabolic disease. These advances could be beneficial in clinical practice, enabling effective personalized therapies and preventive strategies.”
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Vitamin D Linked to Lower Diabetes Risk in People with VDR Gene Variant
A genetic analysis of a large U.S. clinical trial suggests that vitamin D supplementation may reduce the risk of progression from prediabetes to type 2 diabetes, but only for those people who harbor specific variants of the vitamin D receptor gene. The study, led by researchers at Tufts University and published in JAMA Network Open, found that daily high-dose vitamin D lowered diabetes risk by 19% in participants with certain genotypes, opening the possibility of using vitamin D as a diabetes prevention strategy.
The new findings build on data from the Vitamin D and Type 2 Diabetes (D2d) clinical trial, a multi-site randomized study that enrolled more than 2,000 U.S. adults with prediabetes. Study participants were assigned to receive either 4,000 IU of vitamin D3 daily or a placebo. The subjects were then followed for a median of 2.5 years to assess progression to diabetes. The original trial did not show a statistically significant reduction in diabetes risk across all participants.
“But the D2d results raised an important question: Could vitamin D still benefit some people?” said lead author Bess Dawson-Hughes, MD, a senior scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University. “Diabetes has so many serious complications that develop slowly over years. If we can delay the time period that an individual will spend living with diabetes, we can stop some of those harmful side effects or lessen their severity.”
In their follow-on research, the Tufts noted that subsequent analysis of the D2d trial data showed that outcomes varied based on achieved blood levels of vitamin D in participants. The new study also found a genetic link to those who had improved outcomes.
To explore the role genetics might play, the investigators conducted a post hoc analysis of 2,098 D2d participants who consented to genetic testing. They focused on three common polymorphisms in the vitamin D receptor (VDR) gene: ApaI, BsmI, and FokI. The researchers first examined how vitamin D levels correlated with diabetes risk across genotypes, then evaluated how genetic variants influenced response to supplementation.
The data showed that the ApaI polymorphism is a key determinant of response. Participants with the AA genotype, which was about 30% of the cohort, did not experience a reduction in diabetes risk with vitamin D supplementation. By comparison, those with the AC or CC genotypes, the remaining 70% of participants, showed a 19% lower risk of developing diabetes when treated with vitamin D compared with placebo.
The biological basis for this effect is linked to the role the VDR gene plays in pancreatic β cells, where it influences insulin secretion and glucose regulation. Variations in the receptor may alter how effectively vitamin D exerts these effects, explaining why some individuals benefit from supplementation while others do not.
Earlier research has suggested there is a connection between vitamin D and diabetes risk. In earlier analyses of the D2d trial, participants who maintained higher blood levels of vitamin D experienced substantial reductions in diabetes incidence. These findings were supported by meta-analyses and observational studies, including research from the UK Biobank, which found that genetic variation in VDR could modify its activity.
“We hypothesized that VDR gene variants modify the association between achieved intratrial 25-hydroxyvitamin D (25(OH)D) level and diabetes risk and may modify the effect of vitamin D3 supplementation on the risk of developing diabetes,” the researchers wrote. 25(OH)D is the main form of vitamin D circulating in the blood.
The current study broadens knowledge on the role vitamin D can play in diabetes prevention by identifying the specific polymorphisms at play. The overlap between ApaI and BsmI variants provides further evidence of the role of VDR genetics, although the researchers noted that ApaI alone may be sufficient to identify likely responders.
“This genetic association analysis of the D2d study suggests that genetic variation in the VDR, specifically the ApaI polymorphism, is associated with diabetes risk at higher intratrial 25(OH)D levels and is associated with response to 4000 IU/d of vitamin D3 supplementation among adults with prediabetes,” the researchers wrote.
The implications for clinical care include the potential use of genetic testing to guide preventive treatment. A single test for the ApaI polymorphism could help identify patients with prediabetes who are most likely to benefit from higher-dose vitamin D supplementation.
While the results have established a link between variations in the VDR gene and diabetes development, the research noted that the study was not designed to assess the mechanisms underlying the genetic effects. Further, its sample size limited subgroup analyses by race and ethnicity.
“Our findings suggest we may eventually be able to identify which patients with prediabetes are most likely to benefit from additional vitamin D supplementation,” Dawson-Hughes said. “In principle, this could involve a single, relatively inexpensive genetic test.”
Next steps in this line of research include replicating the findings in independent cohorts and conducting prospective trials designed to test genotype-guided supplementation strategies.
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Heart’s beat may help it beat cancer, mouse research suggests
Heart disease and cancer are the leading causes of death in the United States, but it is rare that cancer makes its way to the heart.
It’s an observation that clinicians have been grateful for, though largely unable to explain. But in a paper published Thursday in Science, researchers propose one potential explanation: The constant pressure that the organ is under from beating thousands of times a day and pushing gallons of blood creates an environment that is hostile to cancers. The study, which was conducted in mice, is preliminary, but outside experts said it points to potential new approaches for cancer treatments.
STAT+: Trump’s boosting of psychedelics, cannabis signal a new era in GOP drug policy
The days of “Just Say No,” it seems, are long gone.
Over the weekend, President Trump signed an executive order to increase the availability of certain psychedelics as treatments for mental health conditions, ordering that $50 million be spent, and that the Food and Drug Administration fast-track reviews to usher in their approval. At one point, the president joked to the motley assembly of administration officials, a former Navy SEAL, and the podcaster Joe Rogan: “Can I have some, please?”
On Wednesday, the Trump administration announced it had downgraded medical marijuana from the highest tier of controlled substances, and was pushing the Drug Enforcement Administration to do the same for recreational marijuana.
The president’s lenient tack on some mind-altering drugs ushers in a new world of right-wing drug policy. While the administration has emphasized hardline, militaristic tactics when it comes to fentanyl, its recent actions on “softer” drugs could represent a new era not just for Republican politics but also for American drug policy writ large.
“With this imminent move, we are now confronted with the most pro-drug administration in our history,” Kevin Sabet, the CEO of the anti-legalization advocacy group Smart Approaches to Marijuana, said in a statement. “Policy is now being dictated by marijuana CEOs, psychedelics investors, and podcasters in active addiction — it is a travesty and injustice to the American people of unprecedented proportions. The marijuana industry is the new Big Tobacco, and President Trump is welcoming them to the homes of families across this country with open arms.”
Regenerative Medicine: Promise, Hype, and What Actually Works
From stem cells to platelet-rich plasma, regenerative medicine is often positioned as the future of healthcare. But not all approaches deliver on that promise. As interest grows, so do questions regarding what actually works. GEN’s Editor in Chief John Sterling spoke with Thomas Buchheit, MD, founder and medical director of the Triangle Regen Medicine and Biologics Center in Chapel Hill, NC, in relation to the science, the hype, and the realities shaping the field today.
GEN: How do you define regenerative medicine?
Buchheit: Many people think of regenerative medicine as growing new organs, but I define it more broadly as any therapy that improves tissue health or function. With that definition, we can include platelet-rich plasma (PRP), stem cells, and autologous conditioned serum (ACS). These approaches aim to enhance tissue health and improve function.
GEN: The field is promising, but also sometimes criticized as overhyped. Which areas deserve that criticism, and which have gained credibility through clinical validation?
Buchheit: Some criticism is valid, especially around stem cells. We’ve all seen claims over “miracle” stem cells that regrow cartilage. In reality, while these cells can be therapeutic, they typically don’t survive long after injection. Instead, they work by activating the body’s immune-based healing mechanisms. They can improve tissue health, but they’re not the miracle cures they were once portrayed to be.
On the other hand, therapies like PRP and ACS have gained credibility when properly applied and studied, particularly in musculoskeletal conditions.
GEN: How do you incorporate regenerative medicine into your practice?
Buchheit: I focus on patient function—what people can do now and what they want to achieve. Then tailor therapies accordingly. I prioritize treatments with strong evidence. One example is ACS, also known as the Regenokine* program. It’s highly standardized and supported by over 20 years of research in osteoarthritis, sciatica, and radiculopathy.
I also use PRP, which can be effective, but only when properly dosed. That’s been a major challenge since there are many ways to prepare PRP. We now know that dose matters. For example, treating knee osteoarthritis typically requires close to 10 billion platelets. At our clinic, we measure platelet counts before and after preparation to ensure accuracy, something often not done enough or at all.
GEN: Where did these approaches originate, and how widely are they used?
Buchheit: ACS originated in Germany in the 1990s with Dr. Peter Wehling. It was initially developed as an alternative to steroids for treating sciatica. The process involves incubating whole blood under controlled conditions, which stimulates the release of anti-inflammatory proteins, growth factors, and exosomes.
It became popular as patients, including athletes, traveled to Germany for treatment. Today, it’s available in the United States, though still more common in Europe. We now better understand how it works. Our research shows that exosomes play a key role in long-term benefits. If you remove them, effectiveness drops significantly.
GEN: Your new book Healing Joints and Nerves—who is it for?
Buchheit: It’s written for patients and a broad audience. I focused on authoring a book on regenerative medicine based on scientific accuracy and depth. I wanted to create a resource that explains these therapies clearly and truthfully—what they can and cannot do. It took over six years to complete. The book covers the history of stem cells and concludes with ACS, including both research and my personal experience with it as an avid runner and bicycle rider.
GEN: You often mention “good” vs. “bad” inflammation. What’s the difference?
Buchheit: Chronic inflammation is harmful. It damages tissue, drives pain, and contributes to diseases like osteoarthritis. But acute, controlled inflammation is essential for healing. It triggers the body’s repair processes. Exercise is a good example. It creates cycles of inflammation and recovery that make us stronger. Regenerative therapies aim to harness this same mechanism.
Interestingly, suppressing inflammation too aggressively can backfire. Studies show that patients who take anti-inflammatories after acute injuries may have a higher risk of chronic pain. Repeated steroid injections can also worsen joint damage over time.
GEN: Does all PRP work for osteoarthritis?
Buchheit: No. PRP must contain a sufficient platelet dose to be effective. Research shows that below approximately three billion platelets, it’s unlikely to work. Above four billion, effectiveness improves, and near 10 billion provides optimal results.
A practical tip: patients should ask how much blood is drawn. If only 10 mL is used to produce PRP, it’s mathematically impossible to achieve a high dose. Proper preparation typically requires 60–120 mL. Patients should also ask whether platelet counts are measured.
GEN: Please talk a bit more about Regenokine.
Buchheit: The program is based on ACS, enhanced through a controlled incubation process. This stimulates cells to release anti-inflammatory proteins, growth factors, and exosomes. Treatment typically takes roughly a week. Patients often come to the clinic for that duration. We’ve seen strong results in osteoarthritis and spine conditions, especially in patients who haven’t responded to other treatments, including stem cells.
GEN: What about safety, efficacy, and durability of results?
Buchheit: Outcomes vary by patient, but the primary goal is restoring function—whether that’s walking a dog or running a marathon. My approach is to stay as evidence-based as possible. That’s critical in a field where there is some overpromise or poorly validated treatments.
There are real concerns regarding product quality, sourcing, and transparency in some parts of the market. We need to know exactly what we’re using, how it works, and what evidence supports it. That’s how regenerative medicine will continue to advance responsibly.
Thomas Buchheit, MD, founded the Triangle Regen Medicine and Biologics Center in Chapel Hill, NC, to bring a range of regenerative therapies to patients. He now serves as an adjunct associate professor at Duke and continues to work with scientists at the Center for Translational Pain Medicine.
Buchheit began studying nerve injury pain and served as chief of pain medicine at Duke University Medical Center. He investigated the immune basis of pain relief following injury and the mechanisms behind regenerative therapies, including platelet-rich plasma, stem cells, and autologous conditioned serum. He has led several studies funded by the NIH and the Department of Defense.
*Regenokine was developed by Peter Wehling, MD, in Germany, originally in the 1990s. It utilizes a patient’s own blood to create a serum rich in anti-inflammatory proteins, particularly the interleukin 1 receptor antagonist (IL-1Ra), which helps reduce inflammation and promote healing in joints and tendons. The treatment is used for conditions like osteoarthritis and has gained popularity among athletes seeking pain relief. While it has shown promise in small studies, it is not yet FDA-approved and is not covered by insurance in the United States.
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How Geospatial Science is Reshaping Cancer Epidemiology: Three Perspectives from the Front Lines
The intersection of geography and oncology is no longer a speculative frontier—it is rapidly becoming the new standard in understanding who gets cancer, who survives it, and why. At a recent session at AACR 2026 bringing together leading researchers from the Fred Hutch Cancer Center, Harvard, and UCSF, the consensus was clear: geospatial methods are fundamentally altering how epidemiologists interrogate the cancer continuum, from incidence to mortality, from prevention to palliative care.
Trang VoPham, PhD, from Fred Hutch opened proceedings with a sweeping overview of how location data is being weaponized against cancer disparities. Her team’s work exemplifies the field’s evolution beyond crude ecological fallacies toward granular, individual-level exposure assessment. “We linked geospatial data on agricultural pesticide operations with all death certificates in the U.S. from 1989 to 2023,” she explained, detailing their findings that higher linuron use correlated with a 16% increased risk of colorectal cancer mortality among under-50s—higher than the 11% seen in older populations. The precision matters: “It is absolutely critical… can you access or generate residential address histories, not just baseline, not just at diagnosis, to consider life course exposures, timing of exposures, during relevant and critical time periods?”
VoPham’s lab is already translating these insights into population health interventions. Their GeoXMap web application—developed with community advisory boards across Washington State—enables neighborhood-level mapping of over 175 health variables, each paired with actionable mitigation strategies. “When you map radon, you can click on the tips button and see strategies for exposure mitigation, like where to get free radon test kits,” she noted. During 2023’s wildfire season, her team used Epic electronic health records to identify and contact 64,000 high-risk patients, resulting in over 4,000 same-day virtual primary care appointments. “This approach could absolutely be scaled to target other populations… to empower high-risk patients with information to help protect themselves from environmental hazards.”
Jaime Hart, ScD, from Harvard, shifted focus to the atmospheric dimensions of cancer risk, tracing how air pollution research has matured since IARC’s 2013 carcinogen declaration. She noted that evidence at the time was largely restricted to lung cancer data. Today, the picture has broadened considerably. Hart highlighted recent consortium work linking traffic-related nitrogen dioxide with premenopausal and Black women’s breast cancer risk—”mostly being driven by premenopausal breast cancer and breast cancer among Black women and non-Hispanic white women”—while PM2.5 associations remain more equivocal for this site.
The mechanistic sophistication has advanced in parallel. Hart detailed how particulate matter can “translocate across your lungs, get into your circulation and deposit in every tissue in your body,” even ascending the nasal pathway to breach the blood-brain barrier. Her collaboration with VoPham on wildfire-specific PM2.5 revealed that “even for the same increase in air pollution exposure… if that PM2.5 is coming more from wildfires than not, you saw an elevated risk,” suggesting source-specific toxicity profiles that carry profound regulatory implications.
Iona Cheng, PhD, from University of California, San Francisco, anchored the session in the structural determinants that underlie these spatial patterns. Her work on redlining—historical mortgage discrimination encoded into contemporary health disparities—demonstrates how geospatial tools can excavate systemic injustice. “In Detroit… about 70% [of non-Hispanic white men with prostate cancer] do live in an area that has not been redlined, in contrast to about 30%,” she reported, whereas “almost 60%” of African American patients resided in the most heavily denied neighborhoods. The mortality gradient was stark: “Higher prostate cancer mortality, or lower survival, associated with living in neighborhoods with more redlining, for both Black and white men.”
Cheng emphasized that these are not proxy measures for individual behavior but independent contextual effects. “We do see that the neighborhood itself has contributions,” she said, describing how her team is developing racially-ethnic-specific composite indices of structural racism across housing, education, employment, and judicial domains. The community-engaged methodology proved essential: working with Hawaiian advisory boards revealed that non-Hispanic white reference groups made little demographic sense for the islands, prompting recalibration.
The session closed with a palpable sense of acceleration. From Google’s nascent geospatial reasoning AI to wearable sensor validation of satellite models; from street-view imagery classifying 350 million U.S. locations to ecological momentary assessment tracking real-time exposures, the toolkit is expanding exponentially. As Hart observed: “The places where we live, work, and play influence our risk of cancer, impose diagnostic outcomes. There are robust biological mechanisms that underlie this.” The geospatial revolution in cancer epidemiology, it seems, is only getting started.
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AACR 2026 Video Update: Cancer Research Edges Toward an AI-Driven Era
SAN DIEGO – At the American Association for Cancer Research (AACR) Annual Meeting 2026, the conversation around AI-driven cancer research has moved decisively past theory. Now the focus is on what’s being deployed and how to gain researchers’ and clinicians’ trust.
Fay Lin, PhD, senior editor, technology at GEN, and Jonathan D. Grinstein, PhD, North American editor at Inside Precision Medicine, discuss how AI is increasingly embedded across cancer research areas, from organoid models to pathology. Yet challenges such as data integration, longitudinal patient tracking, and clinician confidence continue to hinder its impact on patient outcomes.
Watch the full discussion below for a clearer view of the trends, tensions, and inflection points in AI shaping the future of cancer research:
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Prediabetes Genotyping Identifies Who Benefits from Vitamin D
Genotyping could help identify people who would most benefit from vitamin D supplements to prevent their progression to diabetes, further analysis of a clinical trial suggests.
The genetic association study indicated that individuals with glycemic indicators of prediabetes could benefit from supplementation with 4000 IU/d of vitamin D3 if they carried specific genetic polymorphisms.
Two genotypes of the ApaI vitamin D receptor polymorphism (VDR) were linked to a risk reduction when these vitamin supplements were taken compared with placebo, according to the report in JAMA Open.
“Our exploratory findings, if confirmed, hold promise for high-dose vitamin D3 as a targeted, personalized approach to reducing the risk of type 2 diabetes among selected adults with prediabetes,” reported Bess Dawson-Hughes, MD, from the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, and co-workers.
“The magnitude of the observed risk reduction among participants with AC and CC alleles of the ApaI polymorphism, if confirmed in an independent clinical trial, would have clinical implications for the management of prediabetes.”
There are four major polymorphisms in the vitamin D receptor: FokI, BsmI, ApaI, and TaqI. While the FokI polymorphism produces a shorter vitamin D receptor with enhanced transcriptional activity, the BsmI, ApaI, and TaqI polymorphisms influence mRNA stability, posttranscriptional regulation, and translational efficiency.
ApaI is strongly associated with metabolic syndrome and obesity, which are both major risk factors for type 2 diabetes.
In an extended analysis of the Vitamin D and Type 2 Diabetes (D2d) trial, researchers examined whether VDR gene variants modified the results of the trial.
The primary outcome of the original trial, conducted in people who achieved at least two of the three glycemic criteria for prediabetes, did not reach statistical significance in the intention-to-treat analysis. However, further examination revealed that the effect of vitamin D3 depended on the achieved intratrial serum 25-hydroxyvitamin D (25[OH]D) levels.
Dawson-Hughes and team therefore examined common VDR polymorphisms in the D2d trial to see whether these polymorphisms were associated with reduced diabetes risk among participants who achieved higher intratrial mean 25(OH)D level, in a discovery-level analysis.
They then conducted a test phase to determine whether participants’ VDR genetic profile modified the response to vitamin D3 supplementation compared with placebo.
Among 2098 participants in the D2d trial, the 618 carrying the AA alleles experienced no reduction in risk of progression to type 2 diabetes either when achieving higher intratrial 25(OH)D concentrations or when using vitamin D3 4000 IUs per day for a median of 2.5 years after adjusting for race, sex, and body mass index, among other variables.
However, the 1480 participants with ApaI AC and CC genotypes—representing 71% of the study population—had a progressively lower risk of type 2 diabetes at intratrial 25(OH)D levels of 40 ng/ml or higher.
Participants with these genotypes had a 19% reduction in the risk of progressing to type 2 diabetes over the same period (Hazard ratio=0.81).
“If confirmed, a 19% risk reduction in conversion to type 2 diabetes with vitamin D3 supplementation would not be trivial,” the authors concluded, noting that assessment of a single VDR polymorphism is inexpensive and now widely available.
In a Commentary article accompanying the study, Michael Holick, PhD, and Arash Shirvani, PhD, both from Boston University, added: “The enormity of the disease burden of diabetes worldwide and the confirmation that vitamin D supplementation of 4000 IUs per day markedly reduces risk of developing it should be a wake-up call and the impetus for health organizations to develop strategies to improve vitamin D status for children and adults with food fortification programs, implementation of supplementation, and sensible sun exposure recommendations for those who are at risk.”
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