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Being underweight a risk factor for mortality after heart attack
Low body mass index (BMI) increases risk mortality after acute myocardial infarction (AMI), even after adjustment for other health factors that affect body weight, according to a study published in PLOS Medicine. Researchers from Yale University in the US conducted a prospective cohort study of 57 574 elderly patients hospitalised for AMI, analysing short- and long-term mortality among underweight and normal weight patients (as measured by BMI) while controlling for comorbid illness and frailty. Crude mortality (deaths from all causes without adjustment for other factors likely to affect the risk of death) was higher among underweight patients than among normal weight patients at 30 days and 1, 5 and 17 years after AMI. After adjustment for comorbidities that cause cachexia (for example, cancer and chronic liver disease), variables reflecting frailty (such as mobility), and two laboratory measures of nutritional status, underweight patients had a 13% higher risk of death at 30 days and a 26% higher risk of death over 17 years than normal weight patients. Among patients without comorbidity, underweight patients had a 21% higher risk of death over 17 years than normal weight patients. These findings suggest that while coexisting illnesses that contribute to cachexia may contribute additional risk, being underweight on its own is an important independent risk factor for death after AMI, even years later.
Loneliness is, literally, heartbreaking
Loneliness and social isolation are linked to around a 30% increased risk of having a stroke or developing coronary artery disease — the two leading causes of illness and death in high income countries — according to an analysis of the available evidence, published in Heart. The size of the effect is comparable to that of other recognised risk factors, such as anxiety and a stressful job, the findings indicate. Researchers from the University of York in the UK trawled 16 research databases for relevant studies published up to May 2015 and found 23 that were eligible. These studies, which involved more than 181 000 adults, included 4628 coronary heart disease events (heart attacks, angina attacks, death) and 3002 strokes recorded during monitoring periods ranging from 3 to 21 years. Analysis of the pooled data showed that loneliness/social isolation was associated with a 29% increased risk of a heart or angina attack and a 32% heightened risk of having a stroke. In a linked editorial, Drs Julianne Holt-Lunstad and Timothy Smith of Brigham Young University in the US pointed out that social factors should be included in medical education, individual risk assessment, and guidelines and policies applied to populations and the delivery of health services.
Cancer gene mutation linked to reduced ovarian reserve
Women with a gene mutation known to increase their cancer risk may have reduced ovarian reserve which may have implications for family planning, according to an Australian study published in Human Reproduction. The international study led by Peter MacCallum Cancer Centre oncologist and National Breast Cancer Foundation Fellow Professor Kelly-Anne Phillips checked the levels of anti-Müllerian hormone (AMH), which is an indicator of egg count, in women with either the BRCA1 or BRCA2 mutation. Women with a BRCA2 mutation were found to have similar AMH levels to women of the same age who did not carry either mutation (non-carriers). However, women with a BRCA1 mutation had AMH concentrations that were, on average, 25% lower than women of the same age who did not carry the mutation. The study analysed AMH levels from almost 700 women, aged 25-45 years, and who were enrolled in kConFab (the Kathleen Cuningham Foundation Consortium for research into Familial Breast cancer), a study supported by a grant from the National Breast Cancer Foundation. The researchers adjusted their analysis to take account of age, oral contraceptive use, BMI and smoking. In addition to BRCA1 mutation carriers having 25% lower AMH concentrations, on average, than non-carriers, they were also more likely to have AMH concentrations that placed them in the lowest quarter for age when the women were divided into four groups according to the AMH levels. This was not seen in BRCA2 mutation carriers.
Screening young athletes’ hearts of little benefit
Young athletes should not undergo screening to prevent sudden cardiac arrest because it is not proven to save lives, suggests an analysis of the available evidence published in The BMJ. The authors conclude that the harms are likely to outweigh any benefits, and no robust evidence exists to confirm it actually prevents deaths. Researchers from the Belgian Health Care Knowledge Centre estimated that around 0.001% of young athletes experience sudden cardiac death every year, often caused by an underlying cardiovascular condition. Pre-participation screening is an attempt to identify these conditions and prevent deaths. But there are disagreements about the harms and benefits, and national guidelines make different recommendations on types of screening. The authors carried out a detailed review of the literature on the harms and benefits of such pre-participation screening programs to prevent cardiac arrest in non-professional athletes aged 14-34 years. Overall, 25% of people with a condition that may lead to a sudden cardiac death would not be identified, the authors wrote. At the same time, there are a high number of false positives associated with screening programs, meaning healthy people are inappropriately identified as having a potential condition, leading to overdiagnosis and overtreatment. Up to 5% of healthy people can be suspected of having disease following electrocardiograms, and up to 30% of those screened may be referred for additional cardiovascular testing. These additional tests can lead to unnecessary harms associated with anxiety and psychological trauma, overdiagnosis and overtreatment. And athletes can be subjected to temporary or lifelong restrictions and exclusion from sport, and impediments to insurability or employment opportunities.
HIV infection may prematurely age humans 5 years
A study published in Molecular Cell has applied a highly accurate biomarker to measure just how much HIV infection ages people at the biological level – an average of almost 5 years. Researchers from the US used a tool which looks at epigenetic changes in people’s cells. Epigenetic changes affect the DNA, but not the DNA sequence. Once they occur, they are passed down from one generation of cell to the next, influencing how genes are expressed. The particular epigenetic change used as a biomarker in this research was methylation, the process by which small chemical groups are attached to DNA. Methylation of DNA can impact how genes get translated into proteins. The 137 male patients included in the analysis were enrolled in CHARTER (the CNS Antiretroviral Therapy Effects Research study), a long-term study aimed at monitoring HIV-infected individuals who are being treated with combination antiretroviral therapy. Subjects who were chosen didn’t have other health conditions that could skew the results. Forty-four HIV-negative control subjects were also included in the initial analysis. An independent group of 48 subjects, both HIV positive and negative, was used to confirm the findings. In addition to the discovery that HIV infection led to an average advance in biological aging of 4.9 years, the researchers note that such a change correlates with an increased expected risk of mortality of 19%.