Publisher Health

A new study from McGill University finds higher incidence of lung cancer and brain tumors in people exposed to wildfires. The study, which tracks over two million Canadians over a period of 20 years, is the first to examine how proximity to forest fires may influence cancer risk.
“Wildfires tend to happen in the same locations each year, but we know very little about the long-term health effects of these events. Our study shows that living in close proximity to wildfires may increase the risk of certain cancers,” says Scott Weichenthal, an Associate Professor in the Department of Epidemiology, Biostatistics, and Occupational Health at McGill University.
Published in The Lancet Planetary Health, the study shows that people living within 50-kilometer of wildfires over the past 10 years had a 10 per cent higher incidence of brain tumors and 4.9 per cent higher incidence of lung cancer, compared to people living further away.
Impacts of climate change on human health
With the changing climate, wildfires are predicted to become more prevalent, severe, and longer in duration in the future — and they are increasingly recognized as a global health problem. “Many of the pollutants emitted by wildfires are known human carcinogens, suggesting that exposure could increase cancer risk in humans,” says Jill Korsiak, a PhD student in Professor Weichenthal’s lab who led the analysis.
Wildfires typically occur in similar regions each year, and as a result, people living in nearby communities might be exposed to carcinogenic wildfire pollutants on a chronic basis, warn the researchers.
Lingering harmful pollutants
In addition to impacts on air quality, wildfires also pollute aquatic, soil, and indoor environments. While some pollutants return to normal concentrations shortly after the fire has stopped burning, other chemicals might persist in the environment for long periods of time, including heavy metals and hydrocarbons. “Exposure to harmful environmental pollutants might continue beyond the period of active burning through several routes of exposure,” adds Professor Weichenthal.
Still, more research is necessary to understand the complex mixture of environmental pollutants released during wildfires, note the researchers. They also note that further work is needed to develop more long-term estimates of the chronic health effects of wildfires.
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Materials provided by McGill University. Note: Content may be edited for style and length.

A group of former heads of state and Nobel laureates are calling on the United States to immediately commit $5 billion to combat the global coronavirus pandemic, and activists are pressing President Biden to take a more forceful leadership role in the response as he convenes world leaders for a Covid-19 summit on Thursday.“I want America to recognize that the disease is not over anywhere until it’s over everywhere,” Gordon Brown, the former British prime minister, who is leading the push for funding, said in an interview Monday, adding, “We must not sleepwalk into the next variant.”But Mr. Biden conceded Monday afternoon that “much needed funding” for the Covid-19 response is not coming anytime soon. In a statement issued by the White House, the president said he had been informed by congressional leaders in both parties that including the funding in a new aid package for Ukraine would “slow down action on the urgently needed Ukrainian aid,” and that he was resigned to having the two packages move separately.“However let me be clear: As vital as it is to help Ukraine combat Russian aggression, it is equally vital to help Americans combat Covid,” Mr. Biden wrote, adding that both the domestic and the global response would suffer if the funding is not approved.Mr. Biden has asked Congress to authorize $22.5 billion in emergency coronavirus aid, including $5 billion for the global pandemic, but the request has stalled on Capitol Hill. A compromise proposal for $10 billion in emergency aid includes no money for the global response, meaning Mr. Biden will almost certainly arrive at his own summit empty-handed. Mr. Brown said in the interview that his appeal is intended to place pressure on Congress to release the funds.The White House said Monday that Mr. Biden will address the summit, and that Vice President Kamala Harris and Dr. Ashish K. Jha, the coronavirus response coordinator will also participate. Both Dr. Jha and Mr. Biden have been working behind the scenes to press lawmakers to authorize the funding, officials said.The summit, a virtual gathering that will be co-hosted by Belize, Germany, Indonesia and Senegal, is aimed at reinvigorating the global response. The need is urgent: The drive to vaccinate the world is losing steam; testing has plummeted around the globe and efforts to bring tests and Covid antiviral pills to low- and middle- income nations are stalled, running into obstacles that recall battles fought 20 years ago around H.I.V.Mr. Brown, now the World Health Organization’s ambassador for global health financing, said he is also encouraging leaders of other wealthy nations to make funding commitments. He is the lead author on a letter to the president whose signatories also include Mary Robinson, a former president of Ireland; Helen Clark, a former prime minister of New Zealand; and Joseph Stiglitz, the Nobel Prize-winning economist.“Mr. President — your leadership can revive the global Covid-19 response,” they wrote, adding that “our wholehearted hope is that your administration will step up to provide leadership on financing the global response, encouraging other countries to follow you, as is both urgent and necessary to help save lives across the world.”Global health officials are increasingly concerned about what many are calling “Covid fatigue,” as world leaders deal with crises like the war in Ukraine, or turn to other pressing health concerns.“Donors are predominantly saying, ‘Oh, we want to get back to, you know, whatever it was that they prefer funding like maternal child health, H.I.V., T.B., whatever it is, and they’re saying that there’s a reduced appetite for Covid,” said Dr. Fifa A. Rahman, an adviser to ACT-Accelerator, the consortium backed by the W.H.O. that is leading the global response.The summit is a follow-up to one Mr. Biden convened in September; he will use the gathering to ask wealthy nations to step up their financial contributions for vaccines, tests and treatments. Specifically, he will call on developed nations to donate $2 billion to purchase Covid treatments and $1 billion to purchase oxygen supplies for low- and middle-income countries, according to a senior administration official involved with the planning.The United States, working with international organizations, has donated more vaccine doses than any other nation to the global vaccination effort. Mr. Biden has pledged 1.2 billion doses to other nations; as of Monday, more than 539 million had been shipped, according to the State Department. But countries receiving the doses have had difficulty getting those shots into arms.Activists and advocacy groups are increasingly impatient. Organizations including Public Citizen, the consumer health and safety nonprofit; Prep4All, an AIDS advocacy group; and HealthGAP, a global health advocacy group that operates in Uganda, are circulating a petition that blasts the United States government — though not Mr. Biden personally — for a “lack of leadership” that “is alarming and shortsighted.”The petition urges the president to “act with reinvigorated urgency” and lays out specific demands, including working with international institutions and donor countries to “mobilize $48 billion this year to get the global response on track” and pressing drugmakers to share their intellectual property and technological know-how, not only for vaccines but also for Covid antivirals, which are plentiful in the United States, but not widely available in low- and middle-income countries.“The administration is not spending political capital to demand that Congress act,” Asia Russell, the executive director of Health GAP, said in an interview, adding, “What we know from the global AIDS response is that decades were wasted dithering. Those wasted years translated into human lives lost. President Biden and his Covid chiefs, they have the power to change history.”The administration wants international intellectual property rules to be waived to facilitate the generic manufacture of vaccines. But the waiver request is stalled at the World Trade Organization and does not extend to treatments, drawing objections from a coalition of 170 groups led by Trade Justice Education Fund, a nonprofit that works to advance equitable trade policy.“Americans and people around the world continue to suffer not only preventable deaths and long-term health consequences, but also disruptions to economic activity and global supply chains,” the groups wrote in a letter addressed to Mr. Biden’s trade representative, Katherine Tai, adding “We need every possible tool to overcome barriers and improve equitable access to Covid-19 medical products.”

When cells reproduce, the internal mechanisms that copy DNA get it right nearly every time. Rice University bioscientists have uncovered a tiny detail that helps us understand how the process could go wrong.
Their study of enzymes revealed the presence of a central metal ion critical to DNA replication also appears to be implicated in misincorporation, the faulty ordering of nucleotides on new strands.
The observation reported in Nature Communications could help find treatments for genetic mutations and the diseases they cause, including cancer.
Rice structural biologist Yang Gao, graduate student Caleb Chang and alumna Christie Lee Luo used time-resolved crystallography to analyze the flexible enzymes called polymerase as they bend and twist to rapidly reassemble complete strands of DNA from a pool of C, G, A and T nucleotides.
All of the proteins involved in DNA replication rely on metal ions — either magnesium or manganese — to catalyze the transfer of nucleotides to their proper positions along the strand, but whether there were two or three ions involved has long been a topic of debate.
The Rice team seems to have settled that through studying a polymerase known as eta, a translesion synthesis enzyme that guards against ultraviolet-induced lesions. Those with mutations on the poly-eta gene often have a predisposition for xeroderma pigmentosum and skin cancer, according to the researchers.

Anindya Dutta, MBBS, Ph.D., and colleagues have described a novel form of gene regulation that is altered in bladder cancer, leading to the boosting of a gene pathway that helps the cancer cells survive during rapid growth.
Their work focuses on a 22-base fragment of transfer RNAs known as a tRF-3b, which is modified by an enzyme complex called TRMT6/61A. In bladder cancer, the levels of TRMT6/61A — a methyltransferase enzyme that adds a methyl group onto the fourth base of the tRF-3bs — are elevated. This modification prevents tRF-3bs from silencing the expression of various genes in the unfolded protein response pathway in the cancer cells, resulting in increased expression of those genes.
“To the best of our knowledge, this is the first example of microRNA-like gene silencing being regulated by the TRMT6/61 based on an N1-methyladenosine modification, and our report provides a mechanism by which the elevation of TRMT6/61A seen in cancers can impact gene expression,” Dutta said. “Fast proliferating cancer cells synthesize and fold many more proteins than normal cells and thus need to upregulate the unfolded protein response pathway to maintain protein homeostasis. We find that one way bladder cancer cells activate the pro-survival unfolded protein response to alleviate endoplasmic reticulum stress is by preventing tRFs from silencing the expression of genes involved in this unfolded protein response.”
“The unfolded protein response is tightly linked to many aspects of cancer progression and has emerged as a promising therapeutic target,” Dutta said. “It has been previously noted that unfolded protein response-related genes are globally upregulated in several cancer types, including bladder cancer, and so our results suggest that inhibiting the TRMT6/61A enzyme may be a new approach to treat bladder cancer.”
The study by Dutta and co-corresponding author Rune Ougland, M.D., Ph.D., included analysis of bladder cancer tissue obtained from patients undergoing transurethral resection of bladder tumors. It is published in the journal Nature Communications. Dutta is chair of the University of Alabama at Birmingham Department of Genetics, and Ougland is a urologic surgeon and senior research investigator at Oslo University Hospital Rikshospitalet, Oslo, Norway.
An important advance in the study was the workflow used to create a library from human cells of small RNAs with an N1-methyladenosine modification, or m1A. The workflow combined two independent approaches — enrichment by m1A-antibody, followed by small RNA-sequencing and m1A-induced mismatch signature by sequencing.

If you’ve ever struggled to breathe, you’ve had a moment of hypoxia — a lack of oxygen. Hypoxia can have long-term effects. In fact, doctors describe hypoxia as an “initial insult.”
Experiencing hypoxia is a known trigger for developing and worsening lung conditions such as severe asthma, chronic obstructive pulmonary disease (COPD), and fibrosis. To treat and prevent these diseases, researchers need to understand why a lack of oxygen would affect the immune system.
New research from scientists at La Jolla Institute for Immunology (LJI), shows that hypoxia can activate the same group of immune cells that cause inflammation during asthma attacks. As a person with gasps for breath, these cells flood the airways with molecules that damage the lungs.
“We show how lack of oxygen can be part of a feedback loop that can contribute to even worse inflammation,” says LJI Professor and Chief Scientific Officer Mitchell Kronenberg, Ph.D., a member of the LJI Center for Autoimmunity and Inflammation. “This work gives us insight into the causes of fibrosis of the lung and severe asthma.”
Kronenberg and his colleagues worked with a genetically altered mouse model to mimic the signals of hypoxia in the airway’s epithelial cells, which line the paths to the lungs. They discovered that combining the hypoxia signals with inflammatory signals stimulated the “innate,” or rapidly responding immunity, and an immune cell type called an ILC2.
An ILC2’s job is to make signaling molecules (called cytokines) that quickly alert other immune cells to react to a pathogen. Unfortunately, ILC2s sometimes over-react and respond to harmless environmental allergens. In these cases, ILC2s churn out cytokines that drive mucus production and inflammation in the lungs. All this swelling and mucus leads to hypoxia.

Epigenetic drugs that have shown promise in cancer trials significantly reduce scarring in the cells of patients with scleroderma, an incurable and life-threatening autoimmune disease, a new study shows.
Scleroderma is a chronic disease that affects the immune system, causing a buildup of scar-like tissues in the skin and internal organs known as fibrosis. This process occurs when cells that make up connective tissue, called fibroblasts, produce too much collagen that causes the skin and organs of patients to harden — resulting in tissue damage and organ failure.
In a recent study, Michigan Medicine researchers focused on BETs, which are proteins that regulate gene expression by binding to modifications on proteins around which DNA wraps, a process called epigenetic regulation. Drugs targeting BETs, specifically an isoform called BRD4, have been developed by various pharmaceutical companies for cancer treatment.
Results published in JCI Insight reveal that drugs that inhibit BRD4, known to play a role in cancer, also affect fibrosis in scleroderma. Researchers tested BRD4 inhibitors on the skin fibroblasts of scleroderma patients and in mouse models of skin fibrosis. They found that the treatment stopped scarring in both human-derived cells and in animals.
The inhibitors used by Michigan Medicine researchers have shown promise for treating various cancers in preclinical studies. Specifically, one drug used in the recent study, called AZD5153, is being tested in a Phase I clinical trial for sarcomas and lymphomas.
“Through this study, we have uncovered a new class of epigenetic drugs that can be used in scleroderma fibrosis,” said Pen-Suen Tsou (Eliza), Ph.D., senior author of the paper and a rheumatology researcher at Michigan Medicine. “If we can repurpose these drugs and get them through development more quickly, we can provide faster relief for patients who struggle with debilitating symptoms of this autoimmune disease. The process can typically take around 10 years, but our patients cannot wait that long.”
The study is a collaborative effort with Michigan Medicine’s Scleroderma Program. Tsou’s team also found that a calcium signaling protein, called CaMKII, affects fibrosis in scleroderma, which researchers had previously not seen.
“Right now, we are doing some follow up studies to see if inhibitors of this protein can block scarring for scleroderma,” Tsou said. “This opens up a brand-new direction for us to offer a novel target for this disease.”
Additional authors include: Sirapa Vichaikul, B.S., Mikel Gurrea-Rubio, Ph.D., M. Asif Amin, M.D., Phillip L. Campbell, B.S., Qi Wu, Ph.D., Megan N. Mattichak, William D. Brodie, Pamela J. Palisoc, B.S., Mustafa Ali, B.S., Sei Muraoka, M.D., Ph.D., Jeffrey H. Ruth, Ph.D., Ellen N. Model, B.S., Dallas M. Rohraff, B.S., M.P.H., Jonatan L. Hervoso, B.S., Yang Mao-Draayer, M.D., Ph.D., David A. Fox, M.D., Dinesh Khanna, M.B.B.S., M.Sc., all of Michigan Medicine, and Amr H. Sawalha, M.D., University of Pittsburgh.

Most cancer treatments are based on using the maximum tolerated dose of a drug to kill as many cancer cells as possible. While this approach has led to patients achieving good responses to therapy, most patients develop drug resistance and disease recurrence. Researchers in the Center of Excellence for Evolutionary Therapy at Moffitt Cancer Center have been investigating an alternative treatment approach called adaptive therapy that focuses on maintaining disease control instead of complete tumor cell elimination. In a new study published in Communications Medicine, the researchers used mathematical modeling to reveal that the spatial organization of a tumor is an important factor that governs how cells compete with one another and the effectiveness of adaptive therapy.
The development of drug resistance is one of the primary concerns in the oncology field. As each new targeted therapy is added to the arsenal of potential therapeutics, scientists are already addressing how to tackle inevitable drug resistance that occurs through a variety of different mechanisms. Drug resistance is common when using a maximum tolerated dose of a drug because this approach provides a growth advantage to existing resistant cells as they become free from competition with sensitive cells.
Alternatively, the emerging concept of adaptive therapy is based on ecological principles that predict that maintaining a population of cancer cells that is sensitive to therapies will keep the development of resistance in check through competition. Similar approaches are used in other biological situations, such as insecticide use. It is now well accepted that using a less aggressive spraying approach and maintaining a “refuge” insecticide-free spot allows insecticide-sensitive insects to breed with resistant populations, which limits the propagation of resistant groups.
These ecological concepts are now being more fully investigated in cancer. Promising results were observed from a recent early-stage clinical trial of prostate cancer patients treated with adaptive therapy, and additional larger clinical studies of adaptive therapy are underway in prostate cancer and melanoma. While these investigations continue, scientists need to improve their understanding of the cellular interactions that impact adaptive therapy.
Previous studies have revealed that adaptive therapy depends on the competitive interactions of sensitive and resistance cells within a spatially constrained tumor; however, it is unknown how competition occurs and how it is impacted by the spatial arrangement of cells within the tumor. Rather than using typical cell or mouse models to study adaptive therapy, the Moffitt research team is using mathematical modeling that can better incorporate the numerous variables that impact adaptive therapy.
In their study, the researchers used a two-dimensional model of a tumor composed of drug sensitive and resistant cells to directly quantify how different cells compete for space.
“While competition is thought to be the driving mechanism behind adaptive therapy, it is challenging to assert its role in real tumors. This is because it is difficult to rule out confounding factors, such as treatment induced changes in the tumor vasculature or the immune response,” said Maximilian Strobl, Ph.D., a postdoctoral researcher at Moffitt and first author of the study. “However, in our computational model we can control and monitor the cells in a way not possible in the wet lab. We seized this opportunity to explicitly measure how often a resistant cell is blocked from division during adaptive therapy. The results of these experiments were surprising.”
Currently, it is believed that adaptive therapy permits drug sensitive cells to keep resistant cells in check through competition, but the Moffitt team discovered that competition between resistant cells themselves and their distribution across a tumor are important factors that also impact adaptive therapy. The researchers showed that adaptive therapy will be most effective when resistant cells are clustered in a single area and surrounded by sensitive cells. This scenario will allow resistant cells to be kept in check by sensitive cells and other resistant cells.
These results suggest that it will be important to understand how resistant cells are spatially organized to determine the appropriate adaptive therapy treatment schedule; however, determining cell resistance patterns may require tissue biopsies that would be invasive and impractical. As an alternative approach, the researchers used response data from prostate cancer patients undergoing adaptive therapy to demonstrate that it may be possible to use mathematical modeling to determine spatial organization patterns. Patients who cycled through therapy quickly had more diffuse tumors, while patients who cycled through therapy more slowly tended to have more compact tumors that may be better suited to adaptive therapy.
While additional studies are needed to more fully understand adaptive therapy, these results provide new insights into factors that are critical in determining its success.
“We have shown that the spatial organization of resistant populations is an important and understudied factor in cancer treatment. This strengthens the argument for patient-specific, adaptive therapy protocols that explicitly consider not only a tumor’s evolution but also its ecology,” said Sandy Anderson, Ph.D., director of the Center of Excellence for Evolutionary Therapy and chair of the Department of Integrated Mathematical Oncology.
This work was supported by the Engineering and Physical Sciences Research Council and the Medical Research Council (EP/L016044/1), the National Cancer Institute (U01CA232382 and U54CA193489) and the Moffitt Center of Excellence for Evolutionary Therapy.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesMajor US pharmacies have restricted sales of baby formula in response to a worsening shortage of the special milk.CVS and Walgreens are among the big chains to have imposed limits in recent weeks on how many cans customers can buy at a time.The shortages intensified after Abbott – which makes top brand Similac – shut a key factory and issued a recall in February after finding contamination.Pressure is building on the Biden administration to respond to the issue.Republicans, such as Senator Tom Cotton, have called it a “national crisis” that the White House must address.Democratic Representative Rosa DeLauro also said she was concerned the Food and Drug Administration – which regulates formula makers – had responded “far too slowly” to the issue, and to the reports of problems at the Abbott factory in Michigan, which remains closed. Abbott – the main supplier of baby formula to many of the state government programmes for low income women and children – said it was working with regulators to get the plant re-opened. It has been sending extra shipments from a plant in Ireland to try to address the problem, expecting shipments from the country to double this year, it added.”We know that our recent recall caused additional stress and anxiety in an already challenging situation of a global supply shortage,” the company said in a recent statement. “We are working hard to help moms, dads and caregivers get the high-quality nutrition they need for their babies.”‘Increased demand and supplier challenges’Abbott issued the recall of certain batches of powdered formula in February after reports that four babies who had been fed from cans from the factory became sick, including two who died. The Centers for Disease Control and Protection said they were investigating a possible link, but that testing so far had found the strain of bacteria detected at the factory did not match that found in the sickened babies. Separately, the FDA criticised Abbott for unsanitary conditions.But the shortage pre-dates those issues and has been building since last year due to supply chain and other factors, according to research firm Datasembly, which tracks 11,000 stores across the US. The situation deteriorated further last month, as publicity of the problem grew and parents raced to stock up. Image source, Getty ImagesAs of 24 April, the average out-of-stock rate across the country had jumped to 40%, up from just 30% a few weeks earlier – and 11% in November, according to Datasembly.There were 26 states with out of stock rates higher than 40% – compared to just seven states three weeks earlier, it said.”Due to increased demand and various supplier challenges, infant and toddler formulas are seeing constraint across the country,” the major pharmacy chain Walgreens said in a statement. “We continue to work diligently with our supplier partners to best meet customer demands.”Walgreens has limited families to buying three cans at a time – similar to other retailers. A 12.4 ounce can of formula typically lasts for about 15 bottles – or just a few days’ worth of supply.Companies that produce items like baby formula – in which demand is typically steady over time – have troubles catching up when there is disruption, said Rudi Leuschner, director of the masters in supply chain management programme at Rutgers Business School.And as parents rush to buy as stories of empty shelves spread, that only makes the problem worse, he warned.”It’s not a situation where you can just snap out of it,” he said. “It was designed to run at one speed.”While this year’s formula shortage may expose the fragility of the supply chain, it may not be enough to make a business case for backup inventories, Prof Leuschner added. Overall, birth rates are falling, reaching the lowest point on record in the US in 2020. Studies have also found that consumption of infant formula has been declining in favour of breast milk. More on this storyThe shortages hitting countries around the worldUS birth rate falls 4% to its lowest point ever

An international team of researchers, led by scientists at University of California San Diego School of Medicine, report that a gene therapy that inhibits targeted nerve cell signaling effectively reduced neuropathic pain with no detectable side effects in mice with spinal cord or peripheral nerve injuries.
The findings, published in the May 5, 2022 online issue of Molecular Therapy, represent a potential new treatment approach for a condition that may affect more than half of patients who suffer spinal cord injuries. Neuropathy involves damage or dysfunction in nerves elsewhere in the body, typically resulting in chronic or debilitating numbness, tingling, muscle weakness and pain.
There are no singularly effective remedies for neuropathy. Pharmaceutical therapies, for example, often require complex, continuous delivery of drugs and are associated with undesirable side effects, such as sedation and motor weakness. Opioids can be effective, but can also lead to increased tolerance and risk of misuse or abuse.
Because physicians and researchers are able to pinpoint the precise location of a spinal cord injury and origin of neuropathic pain, there has been much effort to develop treatments that selectively target impaired or damaged neurons in the affected spinal segments.
In recent years, gene therapy has proven an increasingly attractive possibility. In the latest study, researchers injected a harmless adeno-associated virus carrying a pair of transgenes that encode for gamma-aminobutyric acid or GABA into mice with sciatic nerve injuries and consequential neuropathic pain. GABA is a neurotransmitter that blocks impulses between nerve cells; in this case, pain signals.
The delivery and expression of the transgenes — GAD65 and VGAT — was restricted to the area of sciatic nerve injury in the mice and, as a result, there were no detectable side effects, such as motor weakness or loss of normal sensation. The production of GABA by the transgenes resulted in measurable inhibition of pain-signaling neurons in the mice, which persisted for at least 2.5 months after treatment.
“One of the prerequisites of a clinically acceptable antinociceptive (pain-blocking) therapy is minimal or no side effects like muscle weakness, general sedation or development of tolerance for the treatment,” said senior author Martin Marsala, MD, professor in the Department of Anesthesiology in the UC San Diego School of Medicine.
“A single treatment invention that provides long-lasting therapeutic effect is also highly desirable. These finding suggest a path forward on both.”
Co-authors include: Takahiro Tadokoro, UC San Diego, University of Ryukyus, Japan and Neurgain Technologies, San Diego; Mariana Bravo-Hernandez, Yoshiomi Kobayashi, Oleksandr Platoshyn, Michael Navarro, Atsushi Miyanohara, Tetsuya Yoshizumi, Michiko Shigyo, Rajiv Reddy and Joseph Ciacci, all at UC San Diego; Silvia Marsala, UC San Diego and Neurgain Technologies, San Diego; Kirill Agashkov and Volodymyr Krotov, both at Bogomoletz Institute of Physiology, Ukraine; Stefan Juhas, Jana Juhasova, Duong Nguyen, Helena Kupcova Skalnikova and Jan Motlik, all at Czech Academy of Sciences; Shawn P. Driscoll, Thomas D. Glenn and Samuel L. Pfaff, all at Salk Institute for Biological Studies; Taratorn Kemthong and Suchinda Malaivijitnond, both at Chulalongkorn University, Thailand; Zoltan Tomori and Ivo Vanicky, both at Slovak Academy of Sciences; Manabu Kakinohana. University of Ryukyus; and Pavel Belan, Kyiv Academic University, Ukraine.

Women who experienced complications related to developing high blood pressure, or hypertension, during pregnancy had a 63% increased risk for developing cardiovascular disease later in life, according to research funded by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health.
While hypertensive pregnancy complications previously have been linked to increased cardiovascular risks, the current study controlled for pre-pregnancy shared risk factors for these types of complications and cardiovascular disease. Researchers also found that high blood pressure, high cholesterol, type 2 diabetes, or being overweight or obese after pregnancy accounted for most of the increased risk between pregnancy complications and future cardiovascular events.
The findings, published in the Journal of the American College of Cardiology, could support healthcare providers in developing personalized heart disease prevention and monitoring strategies for women who had hypertension during pregnancy. The information could also help bridge the gap that often occurs after a woman ends obstetric care and resumes or starts care with another provider.
Using health data shared by more than 60,000 participants in the Nurses’ Health Study II, the research represents one of the most comprehensive reviews evaluating links between future cardiovascular events in women who have had preeclampsia or gestational hypertension. Gestational hypertension is characterized by an increase in blood pressure during pregnancy. Preeclampsia is a more severe complication marked by a sudden rise in blood pressure that can affect the organs and be dangerous for both mother and baby. Both conditions are often diagnosed after 20 weeks of pregnancy.
“Women with a history of gestational hypertension or preeclampsia should be informed that they have an increased risk for cardiovascular disease,” said Jennifer J. Stuart, Sc.D., a study author and associate epidemiologist in the Division of Women’s Health at Brigham and Women’s Hospital and Harvard Medical School, Boston. “While the American Heart Association and American College of Cardiology recognize these conditions as cardiovascular risk factors, women and their providers have lacked clear direction on what to do in the intervening years between delivery of a hypertensive pregnancy and the onset of cardiovascular disease.”
The researchers’ analysis showed that early screening and monitoring in four targeted areas — blood pressure, cholesterol and glucose levels, and body mass index — could provide even more personalized targets to help delay or possibly prevent future cardiovascular events among these women.