Moderate coffee and caffeine consumption is associated with lower risk of developing multiple cardiometabolic diseases, new study finds

Consuming moderate amounts of coffee and caffeine regularly may offer a protective effect against developing multiple cardiometabolic diseases, including type 2 diabetes, coronary heart disease and stroke, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.

Researchers found that regular coffee or caffeine intake, especially at moderate levels, was associated with a lower risk of new-onset cardiometabolic multimorbidity (CM), which refers to the coexistence of at least two cardiometabolic diseases.

The prevalence of individuals with multiple cardiometabolic diseases, or CM, is becoming an increasing public health concern as populations age around the world, notes the study.

Coffee and caffeine consumption could play an important protective role in almost all phases of CM development, researchers found.

“Consuming three cups of coffee, or 200-300 mg caffeine, per day might help to reduce the risk of developing cardiometabolic multimorbidity in individuals without any cardiometabolic disease,” said the study’s lead author Chaofu Ke, M.D., Ph.D., of the Department of Epidemiology and Biostatistics, School of Public Health at Suzhou Medical College of Soochow University, in Suzhou, China.

The study found that compared with non-consumers or consumers of less than 100mg caffeine per day, consumers of moderate amount of coffee (3 drinks per day) or caffeine (200-300 mg per day) had a 48.1% or 40.7% reduced risk for new-onset CM.

Ke and his colleagues based their findings on data from the UK Biobank, a large and detailed longitudinal dietary study with over 500,000 participants aged 37-73 years. The study excluded individuals who had ambiguous information on caffeine intake. The resulting pool of participants included a total of 172,315 individuals who were free of any cardiometabolic diseases at baseline for the analyses of caffeine, and a corresponding 188,091 individuals for the analyses of coffee and tea consumption.

The participants’ cardiometabolic diseases outcomes were identified from self-reported medical conditions, primary care data, linked inpatient hospital data and death registry records linked to the UK Biobank.

Coffee and caffeine intake at all levels were inversely associated with the risk of new-onset CM in participants without cardiometabolic diseases. Those who reported moderate coffee or caffeine intake had the lowest risk, the study found. Moderate coffee or caffeine intake was inversely associated with almost all developmental stages of CM.

“The findings highlight that promoting moderate amounts of coffee or caffeine intake as a dietary habit to healthy people might have far-reaching benefits for the prevention of CM,” Ke said.

Addressing a Research Gap

Numerous epidemiological studies have revealed the protective effects of coffee, tea and caffeine consumption on morbidity of single cardiometabolic diseases. However, the potential effects of these beverages on the development of CM were largely unknown.

The authors reviewed the available research on this topic and found people with single cardiometabolic disease may have a two-fold higher all-cause mortality risk than those free of any cardiometabolic diseases. By contrast, the researchers found individuals with CM may have an almost 4 to 7 times higher risk of all-cause mortality. The researchers also noted that CM may present higher risks of loss of physical function and mental stress than those with single diseases.

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Study shows reduced inflammation in residents after adding trees to their neighborhoods

The University of Louisville's groundbreaking Green Heart Louisville Project has found that people living in neighborhoods where the number of trees and shrubs was more than doubled showed lower levels of a blood marker of inflammation than those living outside the planted areas. General inflammation is an important risk indicator for heart disease and other chronic diseases.

The Christina Lee Brown Envirome Institute launched the first-of-its-kind project in 2018 in partnership with The Nature Conservancy, Washington University in St. Louis, Hyphae Design Laboratory and others to study whether and how living among more densely greened surroundings contributes to better heart health. The design of the study closely mirrors clinical trials which test whether medical treatments are effective. The team applied the treatment -- the addition of large trees and shrubs -- to some participants' neighborhoods but not to others. They then compared residents' health data to see how the addition of the trees affected their health.

"The Green Heart Louisville Project is an excellent example of how our university's innovative and collaborative researchers are working to improve lives in our community and far beyond," UofL President Kim Schatzel said. "Trees are beautiful, but these results show that the trees around us are also beneficial to individual and community health. Through this and many other projects, the Envirome Institute is improving health at the community level, not just for individuals, but for everyone living in a neighborhood."

To understand the state of community's health at the start of the study, researchers took blood, urine, hair and nail samples and documented health data from 745 people living in a four-square-mile area of south Louisville. The researchers also took detailed measurements of tree coverage and levels of air pollution in the area.

Following this baseline data collection, the Envirome Institute worked with The Nature Conservancy and a host of local partners and contractors to plant more than 8,000 large trees and shrubs in designated neighborhoods within the project area. Those living in the greened area were considered the treated population and the results obtained from this population were compared with residents of adjacent neighborhoods, where the project team did not plant any trees.

After the plantings, the research team reassessed residents' health. They found that those living in the greened area had 13-20% lower levels of a biomarker of general inflammation, a measure called high-sensitivity C-reactive protein (hsCRP) than those living in the areas that did not receive any new trees or shrubs. Higher levels of hsCRP are strongly associated with a risk of cardiovascular disease and are an even stronger indicator of heart attack than cholesterol levels. Higher CRP levels also indicate a higher risk of diabetes and certain cancers.

A reduction of hsCRP by this percentage corresponds to nearly 10-15% reduction in the risk of heart attacks, cancer or dying from any disease.

"These results from the Green Heart Louisville Project indicate that trees contribute more to our lives than beauty and shade. They can improve the health of the people living around them," said Aruni Bhatnagar, director of the Envirome Institute and UofL professor of medicine. "Although several previous studies have found an association between living in areas of high surrounding greenness and health, this is the first study to show that a deliberate increase in greenness in the neighborhood can improve health. With these results and additional studies that we hope to report soon, we are closer to understanding the impact of local tree cover on residents' health. This finding will bolster the push to increase urban greenspaces."

As more is known about the health impacts of increased tree cover, increased greening in cities may emerge as a key method to improve public health.

"Most of us intuitively understand that nature is good for our health. But scientific research testing, verifying and evaluating this connection is rare," said Katharine Hayhoe, chief scientist of The Nature Conservancy. "These recent findings from the Green Heart Project build the scientific case for the powerful connections between the health of our planet and the health of all of us."

Earlier in August, the Green Heart Louisville Project was awarded an additional $4.6 million in funding from the National Institute of Environmental Health Sciences to support continued research over the next five years.

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Researchers uncover why light-to-moderate drinking is tied to better heart health

A new study led by investigators from Massachusetts General Hospital, a founding member of the Mass General Brigham healthcare system, offers an explanation for why light-to-moderate alcohol consumption may be associated with lower risk of heart disease. For the first time, researchers found that alcohol, in light to moderate quantities, was associated with long-term reductions in stress signaling in the brain. This impact on the brain's stress systems appeared to significantly account for the reductions in cardiovascular events seen in light to moderate drinkers participating in the study. Findings are published in the Journal of the American College of Cardiology.

"We are not advocating the use of alcohol to reduce the risk of heart attacks or strokes because of other concerning effects of alcohol on health," says senior author and cardiologist Ahmed Tawakol, MD, co-director of the Cardiovascular Imaging Research Center at Massachusetts General Hospital. "We wanted to understand how light to moderate drinking reduces cardiovascular disease, as demonstrated by multiple other studies. And if we could find the mechanism, the goal would be to find other approaches that could replicate or induce alcohol's protective cardiac effects without the adverse impacts of alcohol."

Previous epidemiological studies have suggested that light to moderate alcohol consumption (1 drink per day for women and 1 to 2 drinks per day for men) is associated with a lower risk of cardiovascular disease. But it was unknown whether alcohol was inducing cardiovascular benefits, or whether light/moderate drinkers' health behaviors, socioeconomic status, or other factors protected their hearts.

The study, led by K Mezue and M Osborne, included more than 50,000 individuals enrolled in the Mass General Brigham Biobank. The first part of the study evaluated the relationship between light/moderate alcohol consumption and major adverse cardiovascular events after adjusting for a range of genetic, clinical, lifestyle, and socioeconomic confounders. The researchers found that light/moderate alcohol consumption was associated with a substantial reduction in the risk of cardiovascular disease events, even after accounting for those other factors.

Next, they studied a subset of 754 individuals who had undergone previous PET/CT brain imaging (primarily for cancer surveillance) to determine the effect of light/moderate alcohol consumption on resting stress-related neural network activity.

The brain imaging showed reduced stress signaling in the amygdala, the brain region associated with stress responses, in individuals who were light to moderate drinkers compared to those who abstained from alcohol or who drank little. And when the investigators looked at these individuals' history of cardiovascular events, they found fewer heart attacks and strokes in light to moderate drinkers. "We found that the brain changes in light to moderate drinkers explained a significant portion of the protective cardiac effects," says Tawakol.

It's long been known that alcohol reduces the amygdala's reactivity to threatening stimuli while individuals are drinking. The current study is the first to indicate that light to moderate alcohol consumption has longer-term neurobiological effects in dampening activity in the amygdala, which may have a significant downstream impact on the cardiovascular system.

"When the amygdala is too alert and vigilant, the sympathetic nervous system is heightened, which drives up blood pressure and increases heart rate, and triggers the release of inflammatory cells," explains Tawakol. "If the stress is chronic, the result is hypertension, increased inflammation, and a substantial risk of obesity, diabetes, and cardiovascular disease."

Finally, the investigators examined whether light/moderate alcohol would be even more effective at reducing heart attacks and strokes in people who are prone to a chronically higher stress response, such as those with a history of significant anxiety. They found that, within the 50,000-patient sample, light to moderate drinking was associated with nearly double the cardiac-protective effect in individuals with a history of anxiety compared with others.

Yet while light/moderate drinkers lowered their risk for cardiovascular disease, the study also showed that any amount of alcohol increases the risk of cancer. And at higher amounts of alcohol consumption -- more than 14 drinks a week -- heart attack risk started to increase while overall brain activity started to decrease (which may be associated with adverse cognitive health).

The authors concluded that research should focus on finding new interventions that reduce the brain's stress activity without the deleterious effects of alcohol. The research team is currently studying the effect of exercise, stress-reduction interventions such as meditation, and pharmacological therapies on stress-associated neural networks and how they might induce cardiovascular benefits.

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Skipping breakfast may compromise the immune system

Fasting may be detrimental to fighting off infection, and could lead to an increased risk of heart disease, according to a new study by the Icahn School of Medicine at Mount Sinai. The research, which focused on mouse models, is among the first to show that skipping meals triggers a response in the brain that negatively affects immune cells. The results that focus on breakfast were published in the February 23 issue of Immunity, and could lead to a better understanding of how chronic fasting may affect the body long term.

"There is a growing awareness that fasting is healthy, and there is indeed abundant evidence for the benefits of fasting. Our study provides a word of caution as it suggests that there may also be a cost to fasting that carries a health risk," says lead author Filip Swirski, PhD, Director of the Cardiovascular Research Institute at Icahn Mount Sinai. "This is a mechanistic study delving into some of the fundamental biology relevant to fasting. The study shows that there is a conversation between the nervous and immune systems."

Researchers aimed to better understand how fasting -- from a relatively short fast of only a few hours to a more severe fast of 24 hours -- affects the immune system. They analyzed two groups of mice. One group ate breakfast right after waking up (breakfast is their largest meal of the day), and the other group had no breakfast. Researchers collected blood samples in both groups when mice woke up (baseline), then four hours later, and eight hours later.

When examining the blood work, researchers noticed a distinct difference in the fasting group. Specifically, the researchers saw a difference in the number of monocytes, which are white blood cells that are made in the bone marrow and travel through the body, where they play many critical roles, from fighting infections, to heart disease, to cancer.

At baseline, all mice had the same amount of monocytes. But after four hours, monocytes in mice from the fasting group were dramatically affected. Researchers found 90 percent of these cells disappeared from the bloodstream, and the number further declined at eight hours. Meanwhile monocytes in the non-fasting group were unaffected.

In fasting mice, researchers discovered the monocytes traveled back to the bone marrow to hibernate. Concurrently, production of new cells in the bone marrow diminished. The monocytes in the bone marrow -- which typically have a short lifespan -- significantly changed. They survived longer as a consequence of staying in the bone marrow, and aged differently than the monocytes that stayed in the blood.

The researchers continued to fast mice for up to 24 hours, and then reintroduced food. The cells hiding in the bone marrow surged back into the bloodstream within a few hours. This surge led to heightened level of inflammation. Instead of protecting against infection, these altered monocytes were more inflammatory, making the body less resistant to fighting infection.

This study is among the first to make the connection between the brain and these immune cells during fasting. Researchers found that specific regions in the brain controlled the monocyte response during fasting. This study demonstrated that fasting elicits a stress response in the brain -- that's what makes people "hangry" (feeling hungry and angry) -- and this instantly triggers a large-scale migration of these white blood cells from the blood to the bone marrow, and then back to the bloodstream shortly after food is reintroduced.

Dr. Swirski emphasized that while there is also evidence of the metabolic benefits of fasting, this new study is a useful advance in the full understanding of the body's mechanisms.

"The study shows that, on the one hand, fasting reduces the number of circulating monocytes, which one might think is a good thing, as these cells are important components of inflammation. On the other hand, reintroduction of food creates a surge of monocytes flooding back to the blood, which can be problematic. Fasting, therefore regulates this pool in ways that are not always beneficial to the body's capacity to respond to a challenge such as an infection," explains Dr. Swirski. "Because these cells are so important to other diseases like heart disease or cancer, understanding how their function is controlled is critical."

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Custom, 3D-printed heart replicas look and pump just like the real thing

No two hearts beat alike. The size and shape of the the heart can vary from one person to the next. These differences can be particularly pronounced for people living with heart disease, as their hearts and major vessels work harder to overcome any compromised function.

MIT engineers are hoping to help doctors tailor treatments to patients' specific heart form and function, with a custom robotic heart. The team has developed a procedure to 3D print a soft and flexible replica of a patient's heart. They can then control the replica's action to mimic that patient's blood-pumping ability.

The procedure involves first converting medical images of a patient's heart into a three-dimensional computer model, which the researchers can then 3D print using a polymer-based ink. The result is a soft, flexible shell in the exact shape of the patient's own heart. The team can also use this approach to print a patient's aorta -- the major artery that carries blood out of the heart to the rest of the body.

To mimic the heart's pumping action, the team has fabricated sleeves similar to blood pressure cuffs that wrap around a printed heart and aorta. The underside of each sleeve resembles precisely patterned bubble wrap. When the sleeve is connected to a pneumatic system, researchers can tune the outflowing air to rhythmically inflate the sleeve's bubbles and contract the heart, mimicking its pumping action.

The researchers can also inflate a separate sleeve surrounding a printed aorta to constrict the vessel. This constriction, they say, can be tuned to mimic aortic stenosis -- a condition in which the aortic valve narrows, causing the heart to work harder to force blood through the body.

Doctors commonly treat aortic stenosis by surgically implanting a synthetic valve designed to widen the aorta's natural valve. In the future, the team says that doctors could potentially use their new procedure to first print a patient's heart and aorta, then implant a variety of valves into the printed model to see which design results in the best function and fit for that particular patient. The heart replicas could also be used by research labs and the medical device industry as realistic platforms for testing therapies for various types of heart disease.

"All hearts are different," says Luca Rosalia, a graduate student in the MIT-Harvard Program in Health Sciences and Technology. "There are massive variations, especially when patients are sick. The advantage of our system is that we can recreate not just the form of a patient's heart, but also its function in both physiology and disease."

Rosalia and his colleagues report their results in a study appearing today in Science Robotics. MIT co-authors include Caglar Ozturk, Debkalpa Goswami, Jean Bonnemain, Sophie Wang, and Ellen Roche, along with Benjamin Bonner of Massachusetts General Hospital, James Weaver of Harvard University, and Christopher Nguyen, Rishi Puri, and Samir Kapadia at the Cleveland Clinic in Ohio.

Print and pump

In January 2020, team members, led by mechanical engineering professor Ellen Roche, developed a "biorobotic hybrid heart" -- a general replica of a heart, made from synthetic muscle containing small, inflatable cylinders, which they could control to mimic the contractions of a real beating heart.

Shortly after those efforts, the Covid-19 pandemic forced Roche's lab, along with most others on campus, to temporarily close. Undeterred, Rosalia continued tweaking the heart-pumping design at home.

"I recreated the whole system in my dorm room that March," Rosalia recalls.

Months later, the lab reopened, and the team continued where it left off, working to improve the control of the heart-pumping sleeve, which they tested in animal and computational models. They then expanded their approach to develop sleeves and heart replicas that are specific to individual patients. For this, they turned to 3D printing.

"There is a lot of interest in the medical field in using 3D printing technology to accurately recreate patient anatomy for use in preprocedural planning and training," notes Wang, who is a vascular surgery resident at Beth Israel Deaconess Medical Center in Boston.

An inclusive design

In the new study, the team took advantage of 3D printing to produce custom replicas of actual patients' hearts. They used a polymer-based ink that, once printed and cured, can squeeze and stretch, similarly to a real beating heart.

As their source material, the researchers used medical scans of 15 patients diagnosed with aortic stenosis. The team converted each patient's images into a three-dimensional computer model of the patient's left ventricle (the main pumping chamber of the heart) and aorta. They fed this model into a 3D printer to generate a soft, anatomically accurate shell of both the ventricle and vessel.

The team also fabricated sleeves to wrap around the printed forms. They tailored each sleeve's pockets such that, when wrapped around their respective forms and connected to a small air pumping system, the sleeves could be tuned separately to realistically contract and constrict the printed models.

The researchers showed that for each model heart, they could accurately recreate the same heart-pumping pressures and flows that were previously measured in each respective patient.

"Being able to match the patients' flows and pressures was very encouraging," Roche says. "We're not only printing the heart's anatomy, but also replicating its mechanics and physiology. That's the part that we get excited about."

Going a step further, the team aimed to replicate some of the interventions that a handful of the patients underwent, to see whether the printed heart and vessel responded in the same way. Some patients had received valve implants designed to widen the aorta. Roche and her colleagues implanted similar valves in the printed aortas modeled after each patient. When they activated the printed heart to pump, they observed that the implanted valve produced similarly improved flows as in actual patients following their surgical implants.

Finally, the team used an actuated printed heart to compare implants of different sizes, to see which would result in the best fit and flow -- something they envision clinicians could potentially do for their patients in the future.

"Patients would get their imaging done, which they do anyway, and we would use that to make this system, ideally within the day," says co-author Nyugen. "Once it's up and running, clinicians could test different valve types and sizes and see which works best, then use that to implant."

Ultimately, Roche says the patient-specific replicas could help develop and identify ideal treatments for individuals with unique and challenging cardiac geometries.

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Oral bacteria may increase heart disease risk

Infection with a bacterium that causes gum disease and bad breath may increase the risk of heart disease, shows a study published today in eLife.

The study suggests another potential risk factor that physicians might screen for to identify individuals at risk of heart disease. It may also indicate that treatments for colonisation or infection with the oral bacterium Fusobacterium nucleatum may help reduce heart disease risk.

A combination of genetic and environmental risk factors contributes to heart disease, which is responsible for about one-third of all deaths worldwide. A build-up of plaque in the arteries that supply the heart with blood causes coronary heart disease -- the most common type of heart disease -- and can also lead to blockages that cause heart attacks. Previous studies have linked certain infections to an increased risk of plaque build-up.

"Although enormous progress has been made in understanding how coronary heart disease develops, our understanding of how infections, inflammation, and genetic risk factors contribute is still incomplete," says lead author Flavia Hodel, former PhD student at the School of Life Sciences of EPFL, Switzerland. "We wanted to help fill some of the gaps in our understanding of coronary heart disease by taking a more comprehensive look at the role of infections."

Hodel and colleagues analysed genetic information, health data, and blood samples from a subset of 3,459 people who participated in the CoLaus|PsyCoLaus Study -- a Swiss population-based cohort. Of the 3,459 participants, around 6% experienced a heart attack or another harmful cardiovascular event during the 12-year follow-up period. The team tested participants' blood samples for the presence of antibodies against 15 different viruses, six bacteria, and one parasite.

Once the authors adjusted the results for known cardiovascular risk factors, they found that antibodies against F. nucleatum, a sign of previous or current infection by the bacterium,were linked with a slightly increased risk of a cardiovascular event.

"F. nucleatum might contribute to cardiovascular risk through increased systemic inflammation due to bacterial presence in the mouth, or through direct colonisation of the arterial walls or plaque lining the arterial walls," Hodel explains.

The authors also confirmed that individuals with high genetic risk scores for coronary heart disease are at elevated risk for cardiovascular events, as previous studies have shown.

If future studies confirm the link between F. nucleatum and heart disease, the authors say it may lead to new approaches to identifying those at risk or preventing cardiovascular events.

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Vitamin D benefits and metabolism may depend on body weight

Researchers from Brigham and Women's Hospital, a founding member of the Mass General Brigham healthcare system, have found new evidence that vitamin D may be metabolized differently in people with an elevated body mass index (BMI). The study, appearing in JAMA Network Open, is a new analysis of data from the VITAL trial, a large nationwide clinical trial led by Brigham researchers that investigated whether taking vitamin D or marine omega-3 supplements could reduce the risk of developing cancer, heart disease, or stroke.

"The analysis of the original VITAL data found that vitamin D supplementation correlated with positive effects on several health outcomes, but only among people with a BMI under 25," said first author Deirdre K. Tobias, ScD, an associate epidemiologist in Brigham's Division of Preventive Medicine. "There seems to be something different happening with vitamin D metabolism at higher body weights, and this study may help explain diminished outcomes of supplementation for individuals with an elevated BMI."

Vitamin D is an essential nutrient involved in many biological processes, most notably helping our body absorb minerals, such as calcium and magnesium. While some of the vitamin D we need is made in the body from sunlight, vitamin D deficiencies are often treated with supplementation. Evidence from laboratory studies, epidemiologic research and clinical research has also suggested that vitamin D may play a role in the incidence and progression of cancer and cardiovascular disease, and it was this evidence that prompted the original VITAL trial.

The VITAL trial was a randomized, double-blind, placebo-controlled trial in 25,871 U.S. participants, which included men over the age of 50 and women over the age of 55. All participants were free of cancer and cardiovascular disease at the time of enrollment. While the trial found little benefit of vitamin D supplementation for preventing cancer, heart attack, or stroke in the overall cohort, there was a statistical correlation between BMI and cancer incidence, cancer mortality, and autoimmune disease incidence. Other studies suggest similar results for type 2 diabetes.

The new study aimed to investigate this correlation. The researchers analyzed data from 16,515 participants from the original trial who provided blood samples at baseline (before randomization to vitamin D), as well as 2,742 with a follow-up blood sample taken after two years. The researchers measured the levels of total and free vitamin D, as well as many other novel biomarkers for vitamin D, such as its metabolites, calcium, and parathyroid hormone, which helps the body utilize vitamin D.

"Most studies like this focus on the total vitamin D blood level," said senior author JoAnn E. Manson, MD, DrPH, chief of the Division of Preventive Medicine at the Brigham and principal investigator of VITAL. "The fact that we were able to look at this expanded profile of vitamin D metabolites and novel biomarkers gave us unique insights into vitamin D availability and activity, and whether vitamin D metabolism might be disrupted in some people but not in others."

The researchers found that vitamin D supplementation increased most of the biomarkers associated with vitamin D metabolism in people, regardless of their weight. However, these increases were significantly smaller in people with elevated BMIs.

"We observed striking differences after two years, indicating a blunted response to vitamin D supplementation with higher BMI," Tobias said. "This may have implications clinically and potentially explain some of the observed differences in the effectiveness of vitamin D supplementation by obesity status."

"This study sheds light on why we're seeing 30-40 percent reductions in cancer deaths, autoimmune diseases, and other outcomes with vitamin D supplementation among those with lower BMIs but minimal benefit in those with higher BMIs, suggesting it may be possible to achieve benefits across the population with more personalized dosing of vitamin D," said Manson. "These nuances make it clear that there's more to the vitamin D story."

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Potential threat to heart health from extreme weather

An analysis in nearly 2.3 million Europeans has found detrimental associations between cold weather and deaths from heart disease, particularly in poor neighbourhoods. The late-breaking research is presented at ESC Congress 2022.1 Hot weather was linked with excess deaths from heart disease and stroke in patients with heart conditions.

Study author Professor Stefan Agewall of the University of Oslo, Norway said: "Climate change is leading to a rise in the average global temperature but also extreme cold in some regions. More than 70,000 excess deaths occurred across Europe during the summer of 2003 due to intense heatwaves.2 Cold weather also accounts for excess deaths and hospital admissions.3,4 Previously studies on the cardiovascular effects of heat and cold mainly used aggregated data, such as daily deaths in a city. The EXHAUSTION project used individual data, enabling us to identify vulnerable subgroups for protective interventions, thereby increasing resilience for future weather events."

The analysis included 2.28 million adults from five cohort studies conducted in Italy, Germany, the UK, Norway, and Sweden between 1994 and 2010. The average age ranged from 49.7 years to 71.7 years and the proportion of women ranged from 36.0% to 54.5%. Participants with and without cardiovascular disease at baseline were included. Data on mortality and new-onset disease were collected through death and disease registries and follow up surveys. Daily average air temperatures at participants' home addresses were collected from local weather stations or estimated using modelling of temperature data from weather stations

The relationships between temperature and cardiovascular conditions and death were analysed for all participants and in subgroups with particular characteristics. A time-stratified case-crossover study design was used where for each participant, the researchers compared the temperature on the day of the week an adverse event occurred (e.g. Monday) with the temperature on the same day of the week without an adverse event (e.g. all remaining Mondays) within the same month. Using within-participant comparisons between days in the same month eliminated the potential confounding effects of participant characteristics and time trends.

The analysis found increased risks of death from cardiovascular disease overall and ischaemic heart disease in particular, as well as an elevated risk of new-onset ischaemic heart disease, associated with cold weather. With an approximately 10°C temperature drop, from 5°C to -5°C, there was a 19% greater risk of death from cardiovascular disease (relative risk [RR] 1.19; 95% confidence interval [CI] 1.04-1.36) and a 22% elevated likelihood of death from ischaemic heart disease (RR 1.22; 95% CI 1.07-1.38). There was a 4% higher risk of new-onset ischaemic heart disease associated with an approximately 11°C temperature drop, from 2°C to -9°C (RR 1.04; 95% CI: 1.01-1.08).

Professor Agewall said: "The relationships between cold temperatures and deaths were more pronounced in men and people living in neighbourhoods with a low socioeconomic status. The links between cold and new-onset ischaemic heart disease were stronger among women and people older than 65 years."

Heat was not related to detrimental effects in the overall study population. However, temperature rises from 15°C to 24°C were associated with 25% (RR 1.25; 95% CI 1.12-1.39) and 30% (RR 1.30; 95% CI 1.10-1.53) elevated risks of death from cardiovascular disease and stroke, respectively, in people with heart disease at baseline.

Professor Agewall said: "Clinicians can use this information to provide tailored advice to those most at risk of adverse health outcomes during hot and cold days. Patients with heart conditions should stay hydrated in hot weather and adhere to advice from their cardiologist on medication use. We can all check the news for extreme heat and cold alerts and follow safety tips from local authorities."

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Good sleepers have lower risk of heart disease and stroke

Nine in ten people do not get a good night's sleep, according to research presented at ESC Congress 2022.1 The study found that suboptimal sleep was associated with a higher likelihood of heart disease and stroke. The authors estimated that seven in ten of these cardiovascular conditions could be prevented if everyone was a good sleeper.

"The low prevalence of good sleepers was expected given our busy, 24/7 lives," said study author Dr. Aboubakari Nambiema of INSERM (the French National Institute of Health and Medical Research), Paris, France. "The importance of sleep quality and quantity for heart health should be taught early in life when healthy behaviours become established. Minimising night-time noise and stress at work can both help improve sleep."

Previous studies on sleep and heart disease have generally focused on one sleep habit, such as sleep duration or sleep apnoea, where breathing stops and starts while sleeping. In addition, prior studies have often assessed sleep at baseline only. The current study used a healthy sleep score combining five sleep habits. The researchers investigated the association between the baseline sleep score, and changes over time in the sleep score, and incident cardiovascular disease.

This study included 7,200 participants of the Paris Prospective Study III (PPP3), an observational community-based prospective cohort. Men and women aged 50 to 75 years and free of cardiovascular disease were recruited in a preventive medical centre between 2008 and 2011. The average age was 59.7 years and 62% were men. Participants underwent a physical examination and completed questionnaires on lifestyle, personal and family medical history, and medical conditions.

Questionnaires were used to collect information on five sleep habits at baseline and two follow up visits. Each factor was given 1 point if optimal and 0 if not. A healthy sleep score ranging from 0 to 5 was calculated, with 0 or 1 considered poor and 5 considered optimal. Those with an optimal score reported sleeping 7 to 8 hours per night, never or rarely having insomnia, no frequent excessive daytime sleepiness, no sleep apnoea, and an early chronotype (being a morning person). The researchers checked for incident coronary heart disease and stroke every two years for a total of 10 years.

At baseline, 10% of participants had an optimal sleep score and 8% had a poor score. During a median follow up of eight years, 274 participants developed coronary heart disease or stroke. The researchers analysed the association between sleep scores and cardiovascular events after adjusting for age, sex, alcohol consumption, occupation, smoking, body mass index, physical activity, cholesterol level, diabetes, and family history of heart attack, stroke or sudden cardiac death. They found that the risk of coronary heart disease and stroke decreased by 22% for every 1 point rise in the sleep score at baseline. More specifically, compared to those with a score of 0 or 1, participants with a score of 5 had a 75% lower risk of heart disease or stroke.

The researchers estimated the proportion of cardiovascular events that could be prevented with healthier sleep. They found that if all participants had an optimal sleep score, 72% of new cases of coronary heart disease and stroke might be avoided each year.

Over two follow ups, almost half of participants (48%) changed their sleep score: in 25% it decreased whereas in 23% it improved. When the researchers examined the association between the change in score and cardiovascular events, they found that a 1 point increment over time was associated with a 7% reduction in the risk of coronary heart disease or stroke.

Dr. Nambiema said: "Our study illustrates the potential for sleeping well to preserve heart health and suggests that improving sleep is linked with lower risks of coronary heart disease and stroke. We also found that the vast majority of people have sleep difficulties. Given that cardiovascular disease is the top cause of death worldwide, greater awareness is needed on the importance of good sleep for maintaining a healthy heart."

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New research may explain unexpected effects of common painkillers

Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and aspirin are widely used to treat pain and inflammation. But even at similar doses, different NSAIDs can have unexpected and unexplained effects on many diseases, including heart disease and cancer.

Now, a new Yale-led study has uncovered a previously unknown process by which some NSAIDs affect the body. The finding may explain why similar NSAIDs produce a range of clinical outcomes and could inform how the drugs are used in the future.

The study was published May 23 in the journal Immunity.

Until now, the anti-inflammatory effects of NSAIDs were believed to arise solely through the inhibition of certain enzymes. But this mechanism does not account for many clinical outcomes that vary across the family of drugs. For example, some NSAIDs prevent heart disease while others cause it, some NSAIDs have been linked to decreased incidence of colorectal cancer, and various NSAIDs can have a wide range of effects on asthma.

Now, using cell cultures and mice, Yale researchers have uncovered a distinct mechanism by which a subset of NSAIDs reduce inflammation. And that mechanism may help explain some of these curious effects.

The research showed that only some NSAIDs -- including indomethacin, which is used to treat arthritis and gout, and ibuprofen -- also activate a protein called nuclear factor erythroid 2-related factor 2, or NRF2, which, among its many actions, triggers anti-inflammatory processes in the body.

"It's interesting and exciting that NSAIDs have a different mode of action than what was known previously," said Anna Eisenstein, an instructor at the Yale School of Medicine and lead author of the study. "And because people use NSAIDs so frequently, it's important we know what they're doing in the body."

The research team can't say for sure that NSAIDs' unexpected effects are due to NRF2 -- that will require more research. "But I think these findings are suggestive of that," Eisenstein said.

Eisenstein is now looking into some of the drugs' dermatological effects -- causing rashes, exacerbating hives, and worsening allergies -- and whether they are mediated by NRF2.

This discovery still needs to be confirmed in humans, the researchers note. But if it is, the findings could have impacts on how inflammation is treated and how NSAIDs are used.

For instance, several clinical trials are evaluating whether NRF2-activating drugs are effective in treating inflammatory diseases like Alzheimer's disease, asthma, and various cancers; this research could inform the potential and limitations of those drugs. Additionally, NSAIDs might be more effectively prescribed going forward, with NRF2-activating NSAIDs and non-NRF2-activating NSAIDs applied to the diseases they're most likely to treat.

The findings may also point to entirely new applications for NSAIDs, said Eisenstein.

NRF2 controls a large number of genes involved in a wide range of processes, including metabolism, immune response, and inflammation. And the protein has been implicated in aging, longevity, and cellular stress reduction.

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From cavefish to humans: Evolution of metabolism in cavefish may provide insight into treatments for a host of diseases such as diabetes, heart disease, and stroke

New research from the Stowers Institute for Medical Research examines how cavefish, surface-dwelling river fish that flooded into underground cave systems over 100,000 years ago, developed unique metabolic adaptations to survive in nutrient-scarce environments. The study, published online in Nature Genetics on May 12, 2022, led by Jaya Krishnan, PhD, a senior research associate in the lab of Nicolas Rohner, PhD, created a genome-wide map of liver tissue for two independent colonies of cavefish along with river fish to understand how cavefish metabolism evolved and how this may be applicable for humans.

Historically, humans have been able to adapt during periods of feast or famine. Today, however, feast has replaced famine in many regions around the globe leading to a rise in a host of diseases related to metabolism such as diabetes, heart disease and stroke. Collectively called metabolic syndrome, these conditions are associated with genetic mutations in regions of DNA that regulate how our genes work to keep us healthy; on an evolutionary timescale, the constant "feast state" is in its infancy, which for humans, means disease rather than adaptation.

This study marks the first time genetic mapping of the non-coding regions of liver DNA that act to regulate gene activity and expression have been performed. The new data is a now valuable resource for the scientific community studying starvation resistance and metabolism.

"It's a very good foundation for us or anyone to now ask relevant questions in relation to metabolism, diet, and adaptation," said Krishnan.

Metabolism, or the way in which we utilize and store energy, is an integral part of health in all species. Cavefish are ideal for studying metabolism; during periodic flooding of caves, these fish intake and store all the nutrition they need to survive until the next nutrient inundation, which may not be for another year. "They can shed light on metabolic disorders such as diabetes and obesity," said Krishnan, because, despite elevated fat and blood glucose levels, these fish remain vibrant and healthy.

"The fact that these fish are apparently healthy, despite having these extreme traits is, by definition, a good place to ask how they deal with that," said Rohner.

What is truly remarkable is that the two independently derived cavefish colonies examined in this study evolved strikingly similar metabolic adaptations to survive in dark, nutrient-scarce environments. This raises the question, what can we learn from animals who have had the time to evolve? And even further, if multiple cavefish populations evolved in a very similar manner completely independently from each other, are there universal adaptation mechanisms that could potentially be triggered in other species like humans?

"We know only a handful of genes that could be therapeutic targets," said Krishnan. "This means we need to adopt novel ways to identify such potential genes so that we can investigate them, and cavefish are a very powerful system for us to do that."

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New miniature heart could help speed heart disease cures

There's no safe way to get a close-up view of the human heart as it goes about its work: you can't just pop it out, take a look, then slot it back in. Scientists have tried different ways to get around this fundamental problem: they've hooked up cadaver hearts to machines to make them pump again, attached lab-grown heart tissues to springs to watch them expand and contract. Each approach has its flaws: reanimated hearts can only beat for a few hours; springs can't replicate the forces at work on the real muscle. But getting a better understanding of this vital organ is urgent: in America, someone dies of heart disease every 36 seconds, according to the Centers for Disease Control and Prevention.

Now, an interdisciplinary team of engineers, biologists, and geneticists has developed a new way of studying the heart: they've built a miniature replica of a heart chamber from a combination of nanoengineered parts and human heart tissue. There are no springs or external power sources -- like the real thing, it just beats by itself, driven by the live heart tissue grown from stem cells. The device could give researchers a more accurate view of how the organ works, allowing them to track how the heart grows in the embryo, study the impact of disease, and test the potential effectiveness and side effects of new treatments -- all at zero risk to patients and without leaving a lab.

The Boston University-led team behind the gadget -- nicknamed miniPUMP, and officially known as the cardiac miniaturized Precision-enabled Unidirectional Microfluidic Pump -- says the technology could also pave the way for building lab-based versions of other organs, from lungs to kidneys. Their findings have been published in Science Advances.

"We can study disease progression in a way that hasn't been possible before," says Alice White, a BU College of Engineering professor and chair of mechanical engineering. "We chose to work on heart tissue because of its particularly complicated mechanics, but we showed that, when you take nanotechnology and marry it with tissue engineering, there's potential for replicating this for multiple organs."

According to the researchers, the device could eventually speed up the drug development process, making it faster and cheaper. Instead of spending millions -- and possibly decades -- moving a medicinal drug through the development pipeline only to see it fall at the final hurdle when tested in people, researchers could use the miniPUMP at the outset to better predict success or failure.

The project is part of CELL-MET, a multi-institutional National Science Foundation Engineering Research Center in Cellular Metamaterials that's led by BU. The center's goal is to regenerate diseased human heart tissue, building a community of scientists and industry experts to test new drugs and create artificial implantable patches for hearts damaged by heart attacks or disease.

"Heart disease is the number one cause of death in the United States, touching all of us," says White, who was chief scientist at Alcatel-Lucent Bell Labs before joining BU in 2013. "Today, there is no cure for a heart attack. The vision of CELL-MET is to change this."

Personalized Medicine

There's a lot that can go wrong with your heart. When it's firing properly on all four cylinders, the heart's two top and two bottom chambers keep your blood flowing so that oxygen-rich blood circulates and feeds your body. But when disease strikes, the arteries that carry blood away from your heart can narrow or become blocked, valves can leak or malfunction, the heart muscle can thin or thicken, or electrical signals can short, causing too many -- or too few -- beats. Unchecked, heart disease can lead to discomfort -- like breathlessness, fatigue, swelling, and chest pain -- and, for many, death.

"The heart experiences complex forces as it pumps blood through our bodies," says Christopher Chen, BU's William F. Warren Distinguished Professor of Biomedical Engineering. "And while we know that heart muscle changes for the worse in response to abnormal forces -- for example, due to high blood pressure or valve disease -- it has been difficult to mimic and study these disease processes. This is why we wanted to build a miniaturized heart chamber."

At just 3 square centimeters, the miniPUMP isn't much bigger than a postage stamp. Built to act like a human heart ventricle -- or muscular lower chamber -- its custom-made components are fitted onto a thin piece of 3D-printed plastic. There are miniature acrylic valves, opening and closing to control the flow of liquid -- water, in this case, rather than blood -- and small tubes, funneling that fluid just like arteries and veins. And beating away in one corner, the muscle cells that make heart tissue contract, cardiomyocytes, made using stem cell technology.

"They're generated using induced pluripotent stem cells," says Christos Michas (ENG'21), a postdoctoral researcher who designed and led the development of the miniPUMP as part of his PhD thesis.

To make the cardiomyocyte, researchers take a cell from an adult -- it could be a skin cell, blood cell, or just about any other cell -- reprogram it into an embryonic-like stem cell, then transform that into the heart cell. In addition to giving the device literal heart, Michas says the cardiomyocytes also give the system enormous potential in helping pioneer personalized medicines. Researchers could place a diseased tissue in the device, for instance, then test a drug on that tissue and watch to see how its pumping ability is impacted.

"With this system, if I take cells from you, I can see how the drug would react in you, because these are your cells," says Michas. "This system replicates better some of the function of the heart, but at the same time, gives us the flexibility of having different humans that it replicates. It's a more predictive model to see what would happen in humans -- without actually getting into humans."

According to Michas, that could allow scientists to assess a new heart disease drug's chances of success long before heading into clinical trials. Many drug candidates fail because of their adverse side effects.

"At the very beginning, when we're still playing with cells, we can introduce these devices and have more accurate predictions of what will happen in clinical trials," says Michas. "It will also mean that the drugs might have fewer side effects."

Thinner than a Human Hair

One of the key parts of the miniPUMP is an acrylic scaffold that supports, and moves with, the heart tissue as it contracts. A series of superfine concentric spirals -- thinner than a human hair -- connected by horizontal rings, the scaffold looks like an artsy piston. It's an essential piece of the puzzle, giving structure to the heart cells -- which would just be a formless blob without it -- but not exerting any active force on them.

"We don't think previous methods of studying heart tissue capture the way the muscle would respond in your body," says Chen, who's also director of BU's Biological Design Center and an associate faculty member at Harvard University's Wyss Institute for Biologically Inspired Engineering. "This gives us the first opportunity to build something that mechanically is more similar to what we think the heart is actually experiencing -- it's a big step forward."

To print each of the tiny components, the team used a process called two-photon direct laser writing -- a more precise version of 3D printing. When light is beamed into a liquid resin, the areas it touches turn solid; because the light can be aimed with such accuracy -- focused to a tiny spot -- many of the components in the miniPUMP are measured in microns, smaller than a dust particle.

The decision to make the pump so small, rather than life-size or larger, was deliberate and is crucial to its functioning.

"The structural elements are so fine that things that would ordinarily be stiff are flexible," says White. "By analogy, think about optical fiber: a glass window is very stiff, but you can wrap a glass optical fiber around your finger. Acrylic can be very stiff, but at the scale involved in the miniPUMP, the acrylic scaffold is able to be compressed by the beating cardiomyocytes."

Chen says that the pump's scale shows "that with finer printing architectures, you might be able to create more complex organizations of cells than we thought was possible before." At the moment, when researchers try to create cells, he says, whether heart cells or liver cells, they're all disorganized -- "to get structure, you have to cross your fingers and hope the cells create something." That means the tissue scaffolding pioneered in the miniPUMP has big potential implications beyond the heart, laying the foundation for other organs-on-a-chip, from kidneys to lungs.

Refining the Technology

According to White, the breakthrough is possible because of the range of experts on CELL-MET's research team, which included not just mechanical, biomedical, and materials engineers like her, Chen, and Arvind Agarwal of Florida International University, but also geneticist Jonathan G. Seidman of Harvard Medical School and cardiovascular medicine specialist Christine E. Seidman of Harvard Medical School and Brigham and Women's Hospital. It's a breadth of experience that's benefited not just the project, but Michas. An electrical and computer engineering student as an undergraduate, he says he'd "never seen cells in my life before starting this project." Now, he's preparing to start a new position with Seattle-based biotech Curi Bio, a company that combines stem cell technology, tissue biosystems, and artificial intelligence to power the development of drugs and therapeutics.

"Christos is someone who understands the biology," says White, "can do the cell differentiation and tissue manipulation, but also understands nanotechnology and what's required, in an engineering way, to fabricate the structure."

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Good news for coffee lovers: Daily coffee may benefit the heart

Drinking coffee -- particularly two to three cups a day -- is not only associated with a lower risk of heart disease and dangerous heart rhythms but also with living longer, according to studies being presented at the American College of Cardiology's 71st Annual Scientific Session. These trends held true for both people with and without cardiovascular disease. Researchers said the analyses -- the largest to look at coffee's potential role in heart disease and death -- provide reassurance that coffee isn't tied to new or worsening heart disease and may actually be heart protective.

"Because coffee can quicken heart rate, some people worry that drinking it could trigger or worsen certain heart issues. This is where general medical advice to stop drinking coffee may come from. But our data suggest that daily coffee intake shouldn't be discouraged, but rather included as a part of a healthy diet for people with and without heart disease," said Peter M. Kistler, MD, professor and head of arrhythmia research at the Alfred Hospital and Baker Heart Institute in Melbourne, Australia, and the study's senior author. "We found coffee drinking had either a neutral effect -- meaning that it did no harm -- or was associated with benefits to heart health."

Kistler and his team used data from the UK BioBank, a large-scale prospective database with health information from over half a million people who were followed for at least 10 years. Researchers looked at varying levels of coffee consumption ranging from up to a cup to more than six cups a day and the relationship with heart rhythm problems (arrhythmias); cardiovascular disease, including coronary artery disease, heart failure and stroke; and total and heart-related deaths among people both with and without cardiovascular disease. Patients were grouped by how much coffee they reported drinking each day: 0, <1, 1, 2-3, 4-5, >5 cups/day. Coffee drinking was assessed from questionnaires completed upon entry into the registry. Overall, they either found no effect or, in many cases, significant reductions in cardiovascular risk after controlling for exercise, alcohol, smoking, diabetes and high blood pressure that could also play a role in heart health and longevity.

For the first study, researchers examined data from 382,535 individuals without known heart disease to see whether coffee drinking played a role in the development of heart disease or stroke during the 10 years of follow up. Participants' average age was 57 years and half were women. In general, having two to three cups of coffee a day was associated with the greatest benefit, translating to a 10%-15% lower risk of developing coronary heart disease, heart failure, a heart rhythm problem, or dying for any reason. The risk of stroke or heart-related death was lowest among people who drank one cup of coffee a day. Researchers did observe a U-shaped relationship with coffee intake and new heart rhythm problems. The maximum benefit was seen among people drinking two to three cups of coffee a day with less benefit seen among those drinking more or less.

The second study included 34,279 individuals who had some form of cardiovascular disease at baseline. Coffee intake at two to three cups a day was associated with lower odds of dying compared with having no coffee. Importantly, consuming any amount of coffee was not associated with a higher risk of heart rhythm problems, including atrial fibrillation (AFib) or atrial flutter, which Kistler said is often what clinicians are concerned about. Of the 24,111 people included in the analysis who had an arrhythmia at baseline, drinking coffee was associated with a lower risk of death. For example, people with AFib who drank one cup of coffee a day were nearly 20% less likely to die than non-coffee drinkers.

"Clinicians generally have some apprehension about people with known cardiovascular disease or arrhythmias continuing to drink coffee, so they often err on the side of caution and advise them to stop drinking it altogether due to fears that it may trigger dangerous heart rhythms," Kistler said. "But our study shows that regular coffee intake is safe and could be part of a healthy diet for people with heart disease."

Although two to three cups of coffee a day seemed to be the most favorable overall, Kistler said that people shouldn't increase their coffee intake, particularly if it makes them feel anxious or uncomfortable.

"There is a whole range of mechanisms through which coffee may reduce mortality and have these favorable effects on cardiovascular disease," he said. "Coffee drinkers should feel reassured that they can continue to enjoy coffee even if they have heart disease. Coffee is the most common cognitive enhancer -- it wakes you up, makes you mentally sharper and it's a very important component of many people's daily lives."

So how might coffee beans benefit the heart? People often equate coffee with caffeine, but coffee beans actually have over 100 biologically active compounds. These substances can help reduce oxidative stress and inflammation, improve insulin sensitivity, boost metabolism, inhibit the gut's absorption of fat and block receptors known to be involved with abnormal heart rhythms, Kistler said.

In a third study, researchers looked at whether there were any differences in the relationship between coffee and cardiovascular disease depending on whether someone drank instant or ground coffee or caffeinated or decaf. They found, once again, two to three cups a day to be associated with the lowest risk of arrhythmias, blockages in the heart's arteries, stroke or heart failure regardless of whether they had ground or instant coffee. Lower rates of death were seen across all coffee types. Decaf coffee did not have favorable effects against incident arrhythmia but did reduce cardiovascular disease, with the exception of heart failure. Kistler said the findings suggest caffeinated coffee is preferable across the board, and there are no cardiovascular benefits to choosing decaf over caffeinated coffees.

There are several important limitations to these studies. Researchers were unable to control for dietary factors that may play a role in cardiovascular disease, nor were they able to adjust for any creamers, milk or sugar consumed. Participants were predominantly white, so additional studies are needed to determine whether these findings extend to other populations. Finally, coffee intake was based on self-report via a questionnaire fielded at study entry. This should be considered when interpreting the study findings, though Kistler noted that research suggests people's dietary habits don't change much in adulthood or over time. Kistler said the results should be validated in randomized trials.

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Poor sleep can triple risk for heart disease

Individual aspects of poor sleep can be detrimental to heart health. But if you combine them, the risk of heart disease can increase by as much as 141 percent. That's the finding of a new study published in the journal Scientific Reports.

The University of South Florida-led study reviewed sleep data of 6,820 U.S. adults with an average age of 53 who self-reported their sleep characteristics and heart disease history. Among the participants, 633 also wore a research device (actigraphy) around their wrist that captured sleep activity.

Researchers focused on multiple aspects of sleep health, such as regularity, satisfaction, alertness during waking hours, timing of sleep, sleep efficiency and sleep duration and linked them to physician-diagnosed heart disease. They found that each additional increase in self-reported sleep health problems was associated with a 54 percent increased risk of heart disease. The estimated risk of heart disease associated with an increase in sleep health problems was much higher for those who provided sleep data by both self-report and the research device. They had a 141 percent increase -- a figure that could be perceived to be more accurate.

"These findings show the importance of assessing 'co-existing sleep health problems' within an individual to capture the risk of heart disease. This is one of the first studies showing that, among well-functioning adults in midlife, having more sleep health problems may increase the risk of heart disease," said lead author Soomi Lee, assistant professor of aging studies and director of the STEALTH lab at USF. "The higher estimated risk in those who provided both self-report and actigraphy sleep data suggests that measuring sleep health accurately and comprehensively is important to increase the prediction of heart disease."

The research team asked participants about their health, including if their physician confirmed a heart condition such as arrythmia, heart murmur or an enlarged heart. High blood pressure was not considered a diagnosis as it's labeled a risk factor for heart disease rather than a heart disease condition. They also controlled for family history of heart disease and sociodemographic factors, such as race, sex, smoking, depression and physical activity.

Researchers found that while women reported having more sleep health problems, men were more likely to suffer heart disease -- yet gender did not impact the overall correlation between the two factors. They also found that Black participants had more sleep health problems and a higher prevalence of heart disease than white participants, but the strong association between sleep health and heart disease did not differ by race in general.

Lee says while sleep health is important for all ages, the team focused on middle adulthood as it spans for a longer period of time and consists of diverse and more stressful life experiences due to work and family roles. This is also when precursors for heart disease and age-related sleep issues begin to arise.

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Tweaked genes borrowed from bacteria excite heart cells in live mice

Biomedical engineers at Duke University have demonstrated a gene therapy that helps heart muscle cells electrically activate in live mice. The first demonstration of its kind, the approach features engineered bacterial genes that code for sodium ion channels and could lead to therapies to treat a wide variety of electrical heart diseases and disorders.

The results appeared online February 2 in the journal Nature Communications.

"We were able to improve how well heart muscle cells can initiate and spread electrical activity, which is hard to accomplish with drugs or other tools," said Nenad Bursac, professor of biomedical engineering at Duke. "The method we used to deliver genes in heart muscle cells of mice has been previously shown to persist for a long time, which means it could effectively help hearts that struggle to beat as regularly as they should."

Sodium-ion channels are proteins in the outer membranes of electrically excitable cells, such as heart or brain cells, that transmit electrical charges into the cell. In the heart, these channels tell muscle cells when to contract and pass the instruction along so that the organ pumps blood as a cohesive unit. Damaged heart cells, however, whether from disease or trauma, often lose all or part of their ability to transmit these signals and join the effort.

One approach researchers can take to restoring this functionality is gene therapy. By delivering the genes responsible for creating sodium channel proteins, the technique can produce more ion channels in the diseased cells to help boost their activity.

In mammals, sodium channel genes are unfortunately too large to fit within the viruses currently used in modern gene therapies in humans. To skirt this issue, Bursac and his laboratory instead turned to smaller genes that code for similar sodium ion channels in bacteria. While these bacterial genes are different than their human counterparts, evolution has conserved many similarities in the channel design since multi-cellular organisms diverged from bacteria hundreds of millions of years ago.

Several years ago, Hung Nguyen, a former doctoral student in Bursac's laboratory who now works for Fujifilm Diosynth Biotechnologies, mutated these bacterial genes so that the channels they encode could become active in human cells. In the new work, current doctoral student Tianyu Wu further optimized the content of the genes and combined them with a "promoter" that exclusively restricts channel production to heart muscle cells. The researchers then tested their approach by delivering a virus loaded with the bacterial gene into veins of a mouse to spread throughout the body.

"We worked to find where the sodium ion channels were actually formed, and, as we hoped, we found that they only went into the working muscle cells of the heart within the atria and ventricles," Wu said. "We also found that they did not end up in the heart cells that originate the heartbeat, which we also wanted to avoid."

This gene therapy approach only delivers extra genes within a cell; it does not attempt to cut out, replace or rewrite the existing DNA in any way. Scientists believe these types of delivered genes make proteins while floating freely within the cell, making use of the existing biochemical machinery. Previous research with this viral gene delivery approach suggests the transplanted genes should remain active for many years.

As a proof of concept, tests on cells in a laboratory setting suggest that the treatment improves electrical excitability enough to prevent human abnormalities like arrhythmias. Within live mice, the results demonstrate that the sodium ion channels are active in the hearts, showing trends toward improved excitability. However, further tests are needed to measure how much of an improvement is made on the whole-heart level, and whether it is enough to rescue electrical function in damaged or diseased heart tissue to be used as a viable treatment.

Moving forward, the researchers have already identified different bacterial sodium channel genes that work better in preliminary benchtop studies. The team is also working with the laboratories of Craig Henriquez, professor of biomedical engineering at Duke, and Andrew Landstrom, director of the Duke Pediatric Research Scholars Program, to test the ability of these genes to restore heart functionality in mouse models that mimic human heart diseases.

Read more at Science Daily

Using the eye as a window into heart disease

Scientists have developed an artificial intelligence (AI) system that can analyse eye scans taken during a routine visit to an optician or eye clinic and identify patients at a high risk of a heart attack.

Doctors have recognised that changes to the tiny blood vessels in the retina are indicators of broader vascular disease, including problems with the heart.

In the research, led by the University of Leeds, deep learning techniques were used to train the AI system to automatically read retinal scans and identify those people who, over the following year, were likely to have a heart attack.

Deep learning is a complex series of algorithms that enable computers to identify patterns in data and to make predictions.

Writing in the journal Nature Machine Intelligence, the researchers report that the AI system had an accuracy of between 70% and 80% and could be used as a second referral mechanism for in-depth cardiovascular investigation.

The use of deep learning in the analysis of retinal scans could revolutionise the way patients are regularly screened for signs of heart disease.

Professor Alex Frangi, who holds the Diamond Jubilee Chair in Computational Medicine at the University of Leeds and is a Turing Fellow at the Alan Turing Institute, supervised the research. He said: "Cardiovascular diseases, including heart attacks, are the leading cause of early death worldwide and the second-largest killer in the UK. This causes chronic ill-health and misery worldwide.

"This technique opens-up the possibility of revolutionising the screening of cardiac disease. Retinal scans are comparatively cheap and routinely used in many optician practices. As a result of automated screening, patients who are at high risk of becoming ill could be referred to specialist cardiac services.

"The scans could also be used to track the early signs of heart disease."

The study involved a worldwide collaboration of scientists, engineers and clinicians from the University of Leeds; Leeds Teaching Hospitals' NHS Trust; the University of York; the Cixi Institute of Biomedical Imaging in Ningbo, part of the Chinese Academy of Sciences; the University of Cote d'Azur, France; the National Centre for Biotechnology Information and the National Eye Institute, both part of the National Institutes for Health in the US; and KU Leuven in Belgium.

The UK Biobank provided data for the study.

Chris Gale, Professor of Cardiovascular Medicine at the University of Leeds and a Consultant Cardiologist at Leeds Teaching Hospitals NHS Trust, was one of the authors of the research paper.

He said: "The AI system has the potential to identify individuals attending routine eye screening who are at higher future risk of cardiovascular disease, whereby preventative treatments could be started earlier to prevent premature cardiovascular disease."

Deep learning

During the deep learning process, the AI system analysed the retinal scans and cardiac scans from more than 5,000 people. The AI system identified associations between pathology in the retina and changes in the patient's heart.

Once the image patterns were learned, the AI system could estimate the size and pumping efficiency of the left ventricle, one of the heart's four chambers, from retinal scans alone. An enlarged ventricle is linked with an increased risk of heart disease.

With information on the estimated size of the left ventricle and its pumping efficiency combined with basic demographic data about the patient, their age and sex, the AI system could make a prediction about their risk of a heart attack over the subsequent 12 months.

Currently, details about the size and pumping efficiency of a patient's left ventricle can only be determined if they have diagnostic tests such as echocardiography or magnetic resonance imaging of the heart. Those diagnostic tests can be expensive and are often only available in a hospital setting, making them inaccessible for people in countries with less well-resourced healthcare systems -- or unnecessarily increasing healthcare costs and waiting times in developed countries.

Read more at Science Daily

Successful transplant of porcine heart into adult human with end-stage heart disease

In a first-of-its-kind surgery, a 57-year-old patient with terminal heart disease received a successful transplant of a genetically-modified pig heart and is still doing well three days later. It was the only currently available option for the patient. The historic surgery was conducted by University of Maryland School of Medicine (UMSOM) faculty at the University of Maryland Medical Center (UMMC), together known as the University of Maryland Medicine.

This organ transplant demonstrated for the first time that a genetically-modified animal heart can function like a human heart without immediate rejection by the body. The patient, David Bennett, a Maryland resident, is being carefully monitored over the next days and weeks to determine whether the transplant provides lifesaving benefits. He had been deemed ineligible for a conventional heart transplant at UMMC as well as at several other leading transplant centers that reviewed his medical records.

"It was either die or do this transplant. I want to live. I know it's a shot in the dark, but it's my last choice," said Mr. Bennett, the patient, a day before the surgery was conducted. He had been hospitalized and bedridden for the past few months. "I look forward to getting out of bed after I recover."

The U.S. Food and Drug Administration granted emergency authorization for the surgery on New Year's Eve through its expanded access (compassionate use) provision. It is used when an experimental medical product, in this case the genetically-modified pig's heart, is the only option available for a patient faced with a serious or life-threatening medical condition. The authorization to proceed was granted in the hope of saving the patient's life.

"This was a breakthrough surgery and brings us one step closer to solving the organ shortage crisis. There are simply not enough donor human hearts available to meet the long list of potential recipients," said Bartley P. Griffith, MD, who surgically transplanted the pig heart into the patient. Dr. Griffith is the Thomas E. and Alice Marie Hales Distinguished Professor in Transplant Surgery at UMSOM. "We are proceeding cautiously, but we are also optimistic that this first-in-the-world surgery will provide an important new option for patients in the future."

Considered one of the world's foremost experts on transplanting animal organs, known as xenotransplantation, Muhammad M. Mohiuddin, MD, Professor of Surgery at UMSOM, joined the UMSOM faculty five years ago and established the Cardiac Xenotransplantation Program with Dr. Griffith. Dr. Mohiuddin serves as the program's Scientific/Program Director and Dr. Griffith as its Clinical Director.

"This is the culmination of years of highly complicated research to hone this technique in animals with survival times that have reached beyond nine months. The FDA used our data and data on the experimental pig to authorize the transplant in an end-stage heart disease patient who had no other treatment options," said Dr. Mohiuddin. "The successful procedure provided valuable information to help the medical community improve this potentially life-saving method in future patients."

About 110,000 Americans are currently waiting for an organ transplant, and more than 6,000 patients die each year before getting one, according to the federal government's organdonor.gov. Xenotransplantation could potentially save thousands of lives but does carry a unique set of risks, including the possibility of triggering a dangerous immune response. These responses can trigger an immediate rejection of the organ with a potentially deadly outcome to the patient.

Xenotransplants were first tried in the 1980s, but were largely abandoned after the famous case of Stephanie Fae Beauclair (known as Baby Fae) at Loma Linda University in California. The infant, born with a fatal heart condition, received a baboon heart transplant and died within a month of the procedure due to the immune system's rejection of the foreign heart. However, for many years, pig heart valves have been used successfully for replacing valves in humans.

Before consenting to receive the transplant, Mr. Bennett, the patient, was fully informed of the procedure's risks, and that the procedure was experimental with unknown risks and benefits. He had been admitted to the hospital more than six weeks earlier with life-threatening arrythmia and was connected to a heart-lung bypass machine, called extracorporeal membrane oxygenation (ECMO), to remain alive. In addition to not qualifying to be on the transplant list, he was also deemed ineligible for an artificial heart pump due to his arrhythmia.

Revivicor, a regenerative medicine company based in Blacksburg, VA, provided the genetically-modified pig to the xenotransplantation laboratory at UMSOM. On the morning of the transplant surgery, the surgical team, led by Dr. Griffith and Dr. Mohiuddin, removed the pig's heart and placed it in the XVIVO Heart Box, perfusion device, a machine that keeps the heart preserved until surgery.

The physician-scientists also used a new drug along with conventional anti-rejection drugs, which are designed to suppress the immune system and prevent the body from rejecting the foreign organ. The new drug used is an experimental compound made by Kiniksa Pharmaceuticals.

"This unprecedented and historic procedure highlights the importance of translational research which lays the groundwork for patients to benefit in the future. It is the culmination of our longstanding commitment to discovery and innovation in our xenotransplantation program," said E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. "Our transplant surgeon-scientists are among the most talented in the country, and are helping to bring the promise of xenotransplantation to fruition. We hope it will one day become a standard of care for patients in need of organ transplants. As has happened throughout our history, the University of Maryland School of Medicine continues to address the most complex medical and scientific problems."

Bruce Jarrell, MD, President of the University of Maryland, Baltimore, who himself is a transplant surgeon, recalled: "Dr. Griffith and I began as organ transplant surgeons when it was in its infancy. Back then, it was the dream of every transplant surgeon, myself included, to achieve xenotransplantation and it is now personally gratifying to me to see this long-sought goal clearly in view. It is a spectacular achievement."

"This is truly a historic, monumental step forward. While we have long been at the forefront of research driving progress toward the promise of xenotransplantation as a viable solution to the organ crisis, many believed this breakthrough would be well into the future," said Bert W. O'Malley, MD, President and CEO, University of Maryland Medical Center. "I couldn't be more proud to say the future is now. Our skilled team of UMMC and UMSOM physician-scientists will continue to advance and adapt medical discovery for patient care that could offer a lifeline for more patients in dire need."

Mohan Suntha, MD, MBA, President and CEO, University of Maryland Medical System, added: "The University of Maryland Medical System is committed to working with our University of Maryland School of Medicine partners to explore, research, and in many cases implement the innovations in patient care that make it possible to improve quality of life and save lives. We appreciate the tremendous courage of this live recipient, who has made an extraordinary decision to participate in this groundbreaking procedure to not only potentially extend his own life, but also for the future benefit of others."

Organs from genetically modified pigs have been the focus of much of the research in xenotransplantation, in part because of physiologic similarities between pigs, human, and nonhuman primates. UMSOM received $15.7 million sponsored research grant to evaluate Revivicor genetically-modified pig UHearts™ in baboon studies.

Three genes -- responsible for rapid antibody-mediated rejection of pig organs by humans -- were "knocked out" in the donor pig. Six human genes responsible for immune acceptance of the pig heart were inserted into the genome. Lastly, one additional gene in the pig was knocked out to prevent excessive growth of the pig heart tissue, which totaled 10 unique gene edits made in the donor pig.

"We are thrilled to support the world-class team of transplant surgeons led by Dr. Griffith and Dr. Mohiuddin at the University of Maryland School of Medicine," said David Ayares, PhD, Chief Scientific Officer of Revivicor, Inc. "This transplant is groundbreaking, and is another step in the investigation of xeno organs for human use."

Dr. Mohiuddin, Dr. Griffith, and their research team spent the past five years perfecting the surgical technique for transplantation of pig hearts into non-human primates. Dr. Mohiuddin's xenotransplant research experience spans over 30 years during which time he demonstrated in peer-reviewed research that genetically-modified pig's hearts can function when placed in the abdomen for as long as three years. Success was dependent on the right combination of genetic modifications to the experimental donor pig UHeart™ and anti-rejection drugs, including some experimental compounds.

"As a cardiothoracic surgeon who does lung transplants, this is an amazing moment in the history of our field. Decades of research here at Maryland and elsewhere have gone into this achievement. This has the potential to revolutionize the field of transplantation by eventually eliminating the organ shortage crisis," said Christine Lau, MD, MBA the Dr. Robert W. Buxton Professor and Chair of the Department of Surgery at UMSOM and Surgeon-in-Chief at UMMC. "This is a continuation of steps to making xenotransplantation a life-saving reality for patients in need."

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Fewer than 1 in 5 adults with Type 2 diabetes in the U.S. are meeting optimal heart health targets

Fewer than 1 in 5 adults with Type 2 diabetes in the U.S. are meeting targets to reduce heart disease risk. Fortunately, available therapies can help when combined with new approaches that address social determinants of health and other barriers to care, according to a new American Heart Association scientific statement published today in the Association's flagship journal Circulation. A scientific statement is an expert analysis of current research and may inform future clinical practice guidelines.

"This new scientific statement is an urgent call to action to follow the latest evidence-based approaches and to develop new best practices to advance Type 2 diabetes treatment and care and reduce CVD risk," said Joshua J. Joseph, M.D., M.P.H., FAHA, chair of the statement writing group and an assistant professor of medicine in the division of endocrinology, diabetes and metabolism at The Ohio State University College of Medicine in Columbus, Ohio. "Far too few people -- less than 20% of those with Type 2 diabetes -- are successfully managing their heart disease risk, and far too many are struggling to stop smoking and lose weight, two key CVD risk factors. Health care professionals, the health care industry and broader community organizations all have an important role to play in supporting people with Type 2 diabetes."

Type 2 diabetes is the most common form of diabetes, affecting more than 34 million people in the U.S., representing nearly 11% of the U.S. population, according to the U.S. Centers for Disease Control and Prevention's 2020 National Diabetes Statistics Report, and cardiovascular disease (CVD) is the leading cause of death and disability among people with Type 2 diabetes (T2D). Type 2 diabetes occurs when the body is unable to efficiently use the insulin it makes or when the pancreas loses its capacity to produce insulin. People with T2D often have other cardiovascular disease risk factors, including overweight or obesity, high blood pressure or high cholesterol. Adults with T2D are twice as likely to die from CVD -- including heart attacks, strokes and heart failure -- compared to adults who do not have T2D.

The new scientific statement, based on the writing group's extensive review of clinical trial results through June 2020, addresses the gap between existing evidence on how best to lower cardiovascular risk in people with T2D and the reality for people living with T2D. Targets to reduce CVD risk among people with T2D include managing blood glucose, blood pressure and cholesterol levels; increasing physical activity; healthy nutrition; obesity and weight management; not smoking; not drinking alcohol; and psychosocial care. Greater adherence to an overall healthy lifestyle among people with T2D is associated with a substantially lower risk of CVD and CVD mortality.

"In the United States, less than 1 in 5 adults with T2D not diagnosed with cardiovascular disease are meeting optimal T2D management goals of not smoking and achieving healthy levels of blood sugar, blood pressure and low-density lipoprotein (LDL) cholesterol, also known as 'bad' cholesterol," Joseph said.

A surprisingly large proportion -- as high as 90% -- of factors to effectively manage CVD with T2D includes modifiable lifestyle and societal factors. "Social determinants of health, which includes health-related behaviors, socioeconomic factors, environmental factors and structural racism, have been recognized to have a profound impact on cardiovascular disease and Type 2 diabetes outcomes," he said. "People with T2D face numerous barriers to health including access to care and equitable care, which must be considered when developing individualized care plans with our patients."

Shared decision-making among patients and health care professionals is essential for successfully managing T2D and CVD. A comprehensive diabetes care plan should be tailored based on individual risks and benefits and in consideration the patient's preferences; potential cost concerns; support to effectively manage T2D and take medications as prescribed, including diabetes self-management education and support; promotion and support of healthy lifestyle choices that improve cardiovascular health including nutrition and physical activity; and treatment for any other CVD risk factors.

"One avenue to continue to address and advance diabetes management is through breaking down the four walls of the clinic or hospital through community engagement, clinic-to-community connections and academic-community-government partnerships that may help address and support modifiable lifestyle behaviors such as physical activity, nutrition, smoking cessation and stress management," Joseph said.

The statement also highlights recent evidence on treating T2D that may spur clinicians and patients to review and update their T2D management plan to also address CVD risk factors:

New ways to control blood sugar

The American Heart Association's last scientific statement on blood sugar control was published in 2015, just as research was starting to suggest that glucose-lowering medications may also reduce the risk of heart attack, stroke, heart failure or cardiovascular death.

"Since 2015, a number of important national and international clinical trials that specifically examined new T2D medications for lowering cardiovascular disease and cardiovascular mortality risk among people with Type 2 diabetes have been completed," Joseph said. "GLP-1 (glucagon-like pepdite-1) receptor agonists have been found to improve blood sugar and weight, and they have been game changers in reducing the risk of heart disease, stroke, heart failure and kidney disease." GLP-1 medications (injectable synthetic hormones such as liraglutide and semaglutide) stimulate the release of insulin to control blood sugar, and they also reduce appetite and help people feel full, which may help with weight management or weight loss.

In addition, SGLT-2 (sodium-glucose co-transporter 2) inhibitors (oral medications such as canaglifozin, dapagliflozin, ertugliflozin and empagliflozin) have also been found to be effective in reducing the risks of CVD and chronic kidney disease. SGLT-2 inhibitors spur the kidneys to dispose of excess glucose through the urine, which lowers the risk of heart failure and slows the decrease in kidney function that is common among people with T2D.

"Cost may be a barrier to taking some T2D medications as prescribed, however, many of these medications are now more commonly covered by more health insurance plans," Joseph said. "Another barrier is recognition by patients that these newer T2D medications are also effective in reducing the risk of heart disease, stroke, heart failure and kidney disease. Increasing public awareness about the link between CVD and T2D and provide support, education and tools that help improve T2D and reduce CVD risk are at the core of the Know Diabetes by Heart™ initiative, from the American Heart Association and American Diabetes Association."

Personalized blood pressure control

The statement highlights that individualized approaches to treating high blood pressure are best. These approaches should consider ways to minimize the side effects of hypertension treatment and avoid potentially over-treating frail patients.

Importance of lowering cholesterol levels

Statin medications remain the first line of lipid-lowering therapy, and the Association suggests other types of medications may be considered for people unable to tolerate a statin or who aren't reaching their LDL cholesterol targets with a statin. These medications may include ezetimibe, bempodoic acid, bile acid resins, fibrates and PCSK-9 inhibitors, depending on the individual's overall health status and other health conditions.

Re-thinking aspirin use

Older adults (ages 65 years and older) with T2D are more likely than those who do not have T2D to take a daily low-dose aspirin to help prevent cardiovascular disease. However, it may be time to review if daily low-dose aspirin is still appropriate. Recently published research suggests the increased risk of major bleeding from aspirin may outweigh the benefits, and newer, more potent antiplatelet medications may be more effective for some people.

The statement reinforces the importance of a comprehensive, multidisciplinary and individualized approach to reduce CVD risk among people with T2D. Optimal care should incorporate healthy lifestyle interventions, and medications and/or treatments including surgery that improve T2D management and support healthy weight and weight loss. Social determinants of health, structural racism and health equity are important factors that must also be considered and addressed.

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Daytime meals may reduce health risks linked to night shift work

A small clinical trial supported by the National Institutes of Health has found that eating during the nighttime -- like many shift workers do -- can increase glucose levels, while eating only during the daytime might prevent the higher glucose levels now linked with a nocturnal work life. The findings, the study authors said, could lead to novel behavioral interventions aimed at improving the health of shift workers -- grocery stockers, hotel workers, truck drivers, first responders, and others -- who past studies show may be at an increased risk for diabetes, heart disease, and obesity.

The new study, which the researchers noted is the first to demonstrate the beneficial effect of this type of meal timing intervention in humans, appears online in the journal Science Advances. It was funded primarily by the National Heart, Lung, and Blood Institute (NHLBI), part of NIH.

"This is a rigorous and highly controlled laboratory study that demonstrates a potential intervention for the adverse metabolic effects associated with shift work, which is a known public health concern," said Marishka Brown, Ph.D., director of the NHLBI's National Center on Sleep Disorders Research. "We look forward to additional studies that confirm the results and begin to untangle the biological underpinnings of these findings."

For the study, the researchers enrolled 19 healthy young participants (seven women and 12 men). After a preconditioning routine, the participants were randomly assigned to a 14-day controlled laboratory protocol involving simulated night work conditions with one of two meal schedules. One group ate during the nighttime to mimic a meal schedule typical among night workers, and one group ate during the daytime.

The researchers then evaluated the effects of these meal schedules on their internal circadian rhythms. That's the internal process that regulates not just the sleep-wake cycle, but also the 24-hour cycle of virtually all aspects of your bodily functions, including metabolism.

The researchers found that nighttime eating boosted glucose levels -- a risk factor for diabetes -- while restricting meals to the daytime prevented this effect. Specifically, average glucose levels for those who ate at night increased by 6.4% during the simulated night work, while those who ate during the daytime showed no significant increases.

"This is the first study in humans to demonstrate the use of meal timing as a countermeasure against the combined negative effects of impaired glucose tolerance and disrupted alignment of circadian rhythms resulting from simulated night work," said study leader Frank A.J.L. Scheer, Ph.D., professor of medicine at Harvard Medical School and director of the Medical Chronobiology Program at Brigham & Women's Hospital in Boston.

The researchers said that the mechanisms behind the observed effects are complex. They believe that the nighttime eating effects on glucose levels during simulated night work are caused by circadian misalignment. That corresponds to the mistiming between the central circadian "clock" (located in the brain's hypothalamus) and behavioral sleep/wake, light/dark, and fasting/eating cycles, which can influence peripheral "clocks" throughout the body. The current study shows that, in particular, mistiming of the central circadian clock with the fasting/eating cycles plays a key role in boosting glucose levels. The work further suggests the beneficial effects of daytime eating on glucose levels during simulated night work may be driven by better alignment between these central and peripheral "clocks."

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