In a large multi-ethnic group of adults in the United States without cardiovascular disease, those with work-related stress were more likely to have unfavourable measures of cardiovascular health. The findings are published in the Journal of the American Heart Association.
For the analysis, investigators assessed data collected between 2000 and 2002 for 3579 community-based men and women aged 45–84 years enrolled in the Multi-Ethnic Study of Atherosclerosis. Cardiovascular health was determined based on seven metrics – smoking, physical activity, body mass index, diet, total cholesterol, blood pressure, and blood glucose – with each metric contributing zero points, one point, or two points if in the poor, intermediate, or ideal range, respectively, for a range of 0–14 points.
Work-related stress, which was assessed through a questionnaire, was reported by 20% of participants. After adjusting for potentially influencing factors, individuals with work-related stress, had 25% and 27% lower odds of having average (9–10 points) and optimal (11–14 points) cardiovascular health scores, respectively, compared with individuals without work-related stress.
“To address the public health issue of work-related stress and its detrimental effects on cardiovascular health, future research should prioritise the use of longitudinal studies to identify the mechanisms underlying this association,” said first author Oluseye Ogunmoroti, MD, MPH, of Emory University and senior author Erin Michos, MD, MHS, of Johns Hopkins University. “Additionally, conducting thorough workplace intervention studies is essential for the development and implementation of effective stress management strategies that can enhance employee well-being and improve cardiovascular health.”
More than six sedentary hours per day from childhood through young adulthood may cause an excess increase of 4mmHg in systolic blood pressure, a new study shows. Continuously engaging in light physical activity (LPA) significantly mitigated the rise in blood pressure – while longer bouts of more vigorous exercise . The results were published in the prestigiousJournal of Cachexia, Sarcopenia and Muscle.
In the present study, a collaboration between the Universities of Bristol and Exeter, and the University of Eastern Finland, 2513 children drawn from the Children of the 90s cohort were followed up from age 11 until 24 years. At baseline, the children spent six hours per day sedentary, six hours per day engaging in LPA, and approximately 55 minutes per day in moderate-to-vigorous physical activity (MVPA). At follow-up in young adulthood, nine hours per day were spent sedentary, three hours per day in LPA, and approximately 50 minutes per day in MVPA.
The average blood pressure in childhood was 106/56mmHg which increased to 117/67mmHg in young adulthood, partly due to normal physiological development. Persistent increase in sedentary time from age 11 through 24 years was associated with an average of 4mmHg excess increase in systolic blood pressure. Participating in LPA from childhood lowered the final level by 3mmHg, but engaging in MVPA had no blood pressure-lowering effect.
“Furthermore, when 10 minutes out of every hour spent sedentary was replaced with an equal amount of LPA from childhood through young adulthood in a simulation model, systolic blood pressure decreased by 3mmHg and diastolic blood pressure by 2mmHg. This is significant, as it has been reported in adults that a systolic blood pressure reduction of 5mmHg decreases the risk of heart attack and stroke by ten percent,” says Andrew Agbaje, an award-winning physician and associate professor (docent) of Clinical Epidemiology and Child Health at the University of Eastern Finland.
The current study is the largest and the longest follow-up of accelerometer-measured movement behaviour and blood pressure progression in youth in the world. Measurements of blood pressure, sedentary time, LPA and, MVPA were taken at ages 11, 15, and 24 years. The children’s fasting blood samples were also repeatedly measured for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, glucose, insulin, and high-sensitivity C-reactive protein. Heart rate, socio-economic status, family history of cardiovascular disease, smoking status as well as dual-energy X-ray absorptiometry measured fat mass and lean mass were accounted for in the analyses.
“We have earlier shown that elevated blood pressure and hypertension in adolescence increase the risk of premature cardiac damage in young adulthood. The identification of childhood sedentariness as a potential cause of elevated blood pressure and hypertension with LPA as an effective antidote is of clinical and public health significance. Several MVPA-based randomised controlled trials in the young population have been unsuccessful in lowering blood pressure. We noted an MVPA-induced increase in muscle mass enhanced a physiologic increase in blood pressure explaining why earlier MVPA-based randomised clinical trials were unsuccessful,” says Agbaje.
Adding an extra hour every week of physical activity may lower the chance of developing the most common type of irregular heartbeat (arryhthmia) by 11%, a new study shows.
Led by researchers at NYU Langone Health, the investigation focused on atrial fibrillation. While past studies have linked exercise to reduced risk of this type of arrhythmia, nearly all of these analyses have relied on participants’ often inaccurate estimates of their own activity levels, the authors say.
To avert this flaw, the current study team used data recorded from the fitness tracker Fitbit to objectively measure physical activity in more than 6000 men and women across the United States. The results showed that those with higher amounts of weekly physical activity were less likely to develop atrial fibrillation. Notably, the researchers say, even modest amounts of moderate to vigorous exercise, which can range from taking a brisk walk or cleaning the house to swimming laps or jogging, were associated with reduced risk.
Specifically, study participants who averaged between 2.5 and 5 hours per week, the minimum amount recommended by the American Heart Association, showed a 60% lower risk of developing atrial fibrillation. Those who averaged greater than 5 hours had a slightly greater (65%) reduction.
“Our findings make clear that you do not need to start running marathons to help prevent atrial fibrillation and other forms of heart disease,” said preventive cardiologist Sean P. Heffron, MD, the study senior author. “Just keeping moderately active can, over time, add up to major benefits for maintaining a healthy heart,” added Dr Heffron, an assistant professor in the Department of Medicine at NYU Grossman School of Medicine.
Dr. Heffron notes that in the sole earlier study that used activity monitors to investigate atrial fibrillation, researchers provided Fitbit-style monitors to the participants and tracked them for only a week, an approach that may not have accurately captured their normal workout habits. The new investigation, which the authors say is the largest of its kind to date, assessed participants for a full year and included only those who already owned the devices.
A report on the findings will be presented at the annual meeting of the American Heart Association on November 16.
From data collected as part of the All of Us Research Program, the authors of the current study assessed physical activity in the subset (6086 people) who used a Fitbit device and permitted their Fitbit and electronic health records to be linked to their All of Us data. The team tracked activity information for a year as a baseline and then followed up for another five years to identify those who were diagnosed with atrial fibrillation. The researchers also took into account factors known to contribute to the condition, such as age, sex, and a history of high blood pressure.
“These results highlight the value of Fitbits and similar monitors in medical research,” said study lead author Souptik Barua, PhD, an assistant professor in the Department of Medicine at NYU Grossman School of Medicine. “By offering an objective way to measure exercise for years at a time, these tools can provide deeper insight into how different patterns of activity can impact health.”
For example, says Dr Barua, the research team next plans to explore whether working out in the morning or at night may have different effects on heart health.
He cautions that since many Fitbit owners in the study were college-educated White women, the investigation assessed a less-diverse group than that of the overall All of Us population. The program is now providing free devices to participants in underrepresented communities for future investigations.
Dr. Barua also cautions that the study was not designed to tell whether exercise alone directly reduced the risk of atrial fibrillation, nor to detect how that might come about or what other factors, such as income or educational status, might be in play in the reduced risk. However, the association between exercise “doses” and the development of the condition in the study participants was strong.
A new study from researchers at Wilmer Eye Institute, Johns Hopkins Medicine explains not only why some patients with wet age-related macular degeneration (or “wet” AMD) fail to have vision improvement with treatment, but also how an experimental drug could be used with existing wet AMD treatments to save vision.
Wet AMD, one of two kinds of AMD, is a progressive eye condition caused by an overgrowth of blood vessels in the retina. Such blood vessels – caused by an overexpression of a protein known as VEGF that leads to blood vessel growth – then leak fluid or bleed and damage the retina, causing vision loss.
Despite the severe vision loss often experienced by people with wet AMD, less than half of patients treated with monthly eye injections, known as anti-VEGF therapies, show any major vision improvements. Additionally, for those who do benefit with improved vision, most will lose those gains over time.
Now, in the full report published November 4 in the Proceedings of the National Academy of Sciences, the Wilmer-led team of researchers share how such anti-VEGF therapies may actually contribute to lack of vision improvements by triggering the overexpression of a second protein. Known as ANGPTL4, the protein is similar to VEGF, as it can also stimulate overproduction of abnormal blood vessels in the retina.
“We have previously reported that ANGPTL4 was increased in patients who did not respond well to anti-VEGF treatment,” says Akrit Sodhi, MD, PhD, corresponding author and associate professor of ophthalmology at the Johns Hopkins University School of Medicine and the Wilmer Eye Institute. “What we saw in this paper was a paradoxical increase of ANGPTL4 in patients that received anti-VEGF injections – the anti-VEGF therapy itself turned on expression of this protein.”
The team compared VEGF and ANGPTL4 levels in the eye fluid of 52 patients with wet AMD at various stages of anti-VEGF treatment. Prior to anti-VEGF injections, patients with wet AMD had high levels of ANGPTL4 and VEGF proteins. After treatment, their VEGF levels predictably decreased, yet ANGPTL4 levels rose higher, indicating ANGPTL4 remained active following the anti-VEGF injections and the treatments contributed to an increase in ANGPTL4. Such ANGPTL4 activity can lead to blood vessel overgrowth and lack of vision improvement.
The team then investigated ways to bridge the gap between patients with increased ANGPTL4 following anti-VEGF treatments by testing the experimental drug 32-134D in mice with wet AMD. The drug decreases levels of a third protein, HIF-1, known to be involved in wet AMD and diabetic eye disease for its role in switching on VEGF production. Researchers believed the HIF-inhibitor 32-134D would have a similar effect on ANGPTL4 following anti-VEGF treatment, since ANGPTL4 production is also turned on by HIF-1.
In mice treated with 32-134D, the team observed a decrease in HIF-1 levels and VEGF, as well as decreased levels of ANGPTL4 and blood vessel overgrowth. Mice treated only with anti-VEGF therapies corroborated the team’s findings in human patients: levels of VEGF were lower, yet ANGPTL4 levels rose, preventing anti-VEGF therapies from fully working to prevent blood vessel growth (and vision loss). Researchers also determined that combining 32-134D with anti-VEGF treatments prevented the increase in HIF-1, VEGF and ANGPTL4. This treatment combination was more effective than either drug alone, showing promise for treating wet AMD.
“This work exposes a way to improve anti-VEGF therapy for all patients and potentially help a subset of patients with wet AMD who still lose vision over time despite treatment,” Sodhi says. “Our hope is that this [project] will further the three goals we have related to wet AMD: make current therapies as effective as possible, identify new therapies, and prevent people from ever getting wet AMD.”