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Poverty significantly increases heart disease and cancer mortality risk

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Living in poverty with chronic inflammation significantly increases heart disease and cancer mortality risk, a new US study has found.

The University of Florida research showed that health outcomes for Americans living in poverty and with chronic inflammation are significantly worse than expected from their separate health effects.

Lead author Dr Arch Mainou is a professor at the University of Florida.

The researcher said: “Here we show that clinicians need to consider the effect of inflammation on people’s health and longevity, especially on those experiencing poverty.”

Inflammation is a natural physiological reaction to infections or injuries and is essential for healing.

But chronic inflammation – caused by exposure to environmental toxins, certain diets, autoimmune disorders such as arthritis, or other chronic diseases like Alzheimer’s – is a known risk factor for disease and mortality, much like poverty.

In the study, researchers analysed data from adults aged 40 and older, enrolled between 1999 and 2002 in the National Health and Nutrition Examination Survey (NHANES), and followed them until 31 December 2019.

The survey, conducted since 1971 by the National Center for Health Statistics, tracks the health and nutritional status of US adults and children.

The survey allows for estimates of the US population represented by the cohort, and this study represented nearly 95 million adults.

The authors combined NHANES data with records from the National Death Index, to calculate mortality rates over a period of 15 years after enrolment.

NHANES records the household income, among other demographics. The authors divided this by the official poverty threshold to calculate the ‘poverty index ratio’ – a standard measure of poverty.

Whether participants suffered from severe inflammation was deduced from their plasma concentration of high sensitivity C-reactive protein (hs-CRP), which is produced by the liver in response to the secretion of interleukins by immune and fat cells.

The concentration of this protein, included among NHANES data, is a readily available, informative, and well-studied measure of inflammation: for example, elevated concentrations are known to increase the risk of cardiovascular disease and all-cause mortality.

The researchers classified participants in four groups: with or without chronic inflammation, and living below the poverty line or not.

By comparing the 15-year mortality rate between these, they could therefore study the effects of poverty and inflammation separately and jointly.

Dr Frank A. Orlando is an associate professor at the University of Florida and the study’s second author.

He said: “We found that participants with either inflammation or poverty alone each had about a 50 per cent increased risk in all-cause mortality.

In contrast, individuals with both inflammation and poverty had a 127 per cent increased heart disease mortality risk and a 196 per cent increased cancer mortality risk.

“If the effects of inflammation and poverty on mortality were additive, you’d expect a 100 per cent increase in mortality for people where both apply.

“But since the observed 127 per cent and 196 per cent increases are much greater than 100 per cent, we conclude that the combined effect of inflammation and poverty on mortality is synergistic.”

A wide variety of treatments for systemic inflammation exist, ranging from diet and exercise to nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids.

The new findings suggest that clinicians might consider screening socially disadvantaged people – already a medically vulnerable group – for chronic inflammation, and if necessary treat them with such anti-inflammatory drugs.

However, steroids and NSAIDS aren’t without risks when used long-term.

More research will therefore be needed before patients are routinely prescribed them in clinical practice to decrease systemic inflammation.

Mainous said: “It’s important for guidelines panels to take up this issue to help clinicians integrate inflammation screening into their standard of care, particularly for patients who may have factors that place them at risk for chronic inflammation, including living in poverty.

“It is time to move beyond documenting the health problems that inflammation can cause, to trying to fix these problems.”

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Europe: Improving access to early-stage lung cancer care

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Europe: Improving access to early-stage lung cancer care

Researchers from Amsterdam UMC Cancer Center Amsterdam have looked at inequalities in access to early-stage lung cancer care in Europe.

Early-stage lung cancer has stark differences between European countries regarding access and reimbursement.

There are also differences in reimbursement times and indications between the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA).

Researchers from Amsterdam UMC Cancer Center Amsterdam analysed the landscape, publishing their results in The Lancet Regional Health Europe as part of a series on the latest developments in the treatment of this lung cancer.

“Tackling inequalities in access to care must be a common European priority,” says Amsterdam UMC pulmonologist Idris Bahce. In collaboration with colleagues from seven European countries, Bahce used a literature review to map out the latest developments and analyse access to these new treatments from a European perspective.

“The existing differences in healthcare systems and reimbursement structures between European countries threaten to exacerbate healthcare inequalities at both European and national level. We therefore call for a collective European approach to reduce these inequalities,” says Bahce.

He suggests measures such as more international cooperation between the EMA and other registration authorities, harmonising cost-effectiveness procedures in European countries, a more critical evaluation of reimbursement criteria and improving multidisciplinary collaborations around the patient.

The standard treatment for fit patients with early-stage lung cancer has always been surgery, sometimes combined with pre- or post-operative chemotherapy. Recently, the EMA has approved new treatments such as immunotherapy, which appear to significantly improve survival rates after surgery. More approvals of innovative treatments are expected, potentially further exacerbating existing inequalities within Europe.

In addition to the Dutch hospitals Amsterdam UMC and Erasmus MC, colleagues from Spain, France, Germany, England, Italy and Poland also contributed to this international study as well as a Review and a Viewpoint in The Lancet Regional Health Europe.

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Study looks at link between adversity and cognitive decline

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A new paper has examined the relationship between childhood adversity and psychiatric decline, as well as adult adversity and psychiatric and cognitive decline. 

The findings revealed just one instance of adversity in childhood can increase cases of mental illness later in life. It also revealed that adverse events in adults can lead to a greater chance of both mental illness and cognitive decline later in life. 

The paper has been published by Saint Louis University associate professor of health management and policy in the College for Public Health and Social Justice, SangNam Ahn, Ph.D., in Journal of Clinical Psychology.

Ahn stated: “Life is very complicated, very dynamic. I really wanted to highlight the importance of looking into the lasting health effect of adversity, not only childhood but also adulthood adversity on health outcomes, especially physical health and psychiatric and cognitive health. 

“There have been other studies before, but this is one of the first that looks into these issues comprehensively.” 

Ahn, along with his team of researchers, examined data from nearly 3500 individuals over the course of 24 years. The group took the longitudinal data and evaluated it using a list of lifetime potential traumatic events.

The research team included childhood adversity events such as moving due to financial difficulties, family requiring financial help, a parent experiencing unemployment, trouble with law enforcement before the age of 18, repeating school, physical abuse and parental abuse of drugs or alcohol. 

Adulthood adversity events included the death of a child, the death of a spouse, experiencing a natural disaster after age 17, firing a weapon in combat, a partner abusing drugs or alcohol, being a victim of a physical attack after age 17, a spouse or child battling a serious illness, receiving Medicaid or food stamps and experiencing unemployment. 

The study determined that nearly 40% of all individuals experienced a form of childhood adversity, while that number climbed to nearly 80% for adulthood adversity. Those who experienced childhood adversity were also 17% more likely to experience adulthood adversity. Only 13% of individuals sampled reported two or more forms of childhood adversity, while 52% of adults experienced two or more forms of adult adversity. 

In cases of either childhood adversity or adulthood adversity, researchers found individuals who experienced adversity were also more likely to experience anxiety and depression later in life, and in the case of adulthood adversity, were also more likely to experience cognitive decline later in life. 

Individuals with one childhood adversity experience saw a 5% higher chance of suffering from anxiety, and those with two or more childhood adversity experiences had 26% and 10% higher chances of depression and anxiety, respectively. Individuals who experienced two adulthood adversities had a 24% higher chance of depression, while also experiencing a 3% cognitive decline later in life. 

While most of the results were expected or unsurprising, one area that stood out to Ahn was education. Those individuals studied who reported higher levels of education saw a reduction in the number of adversity experiences. Ahn hopes to study this avenue more to learn how education may be able to mitigate or prevent these declines. 

“Before including education, there was a significant association between childhood adversity and cognitive impairment,” Ahn said. 

“But when including education as a covariate, that significant association disappeared. Interesting. So there were important implications here. Education and attending school, people could be better off even if they were exposed to childhood adversity. They’re likely to learn positive coping mechanisms, which may help avoid  relying on unhealthy coping mechanisms, such as smoking or excessive drinking or drug use.

“Education is quite important in terms of health outcomes. If I am educated, I’m likely to get a better job, have a higher income, and live in areas with less crime. I’m likely to buy gym membership or regularly exercise. I’m likely to shop at Whole Foods and get proper nutrition. All of which help combat these adversities we hinted at in the study. So the education and health outcomes are already closely related, and that is what we saw in our study.”

Ahn also encourages clinicians and everyday people alike to discuss their stress. Clinicians can learn more about their patients and have a better approach when it comes to their physical and mental health, while others could potentially relate to shared experiences. But through awareness and recognition, these adverse experiences could potentially have less serious, lasting effects. 

“Public health is very interested in stress,” Ahn said. “But we’re still examining how daily stress impacts our long term health outcomes. So to see the effects here in the study, I want people to pay attention to their stress and proactively address it. Clinicians should have deep discussions with their patients about their stress and mental state. And those topics can be approached in other areas too, like the classroom or the dining room table. The more we are aware of stress and discuss our stress, the better we can handle any adversities we find in life.”

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New tool to explore mechanisms of age-related diseases

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New tool to explore mechanisms of age-related diseases

A new screening tool has been developed that will investigate the mechanisms behind conditions such as cancer, arthritis, neurodegeneration and cardiovascular disease.

Wellcome Sanger Institute researchers and their collaborators at Open Targets and EMBL’s European Bioinformatics Institute (EMBL-EBI) have developed the screening tool called scSNV-seq.

The tool has been designed to uncover how genetic changes affect gene activity that can lead to diseases such as cancer, autoimmunity, cardiovascular disease and neurodegenerative diseases such as Alzheimer’s and Parkinson’s. 

The tool enables the investigation of thousands of DNA mutations identified by genetic studies in one experiment, and will help to guide the development of advanced diagnostics and treatments.

scSNV-seq allows the rapid assessment of the impact of thousands of genetic changes in cells that have never been screened before, directly connecting these changes to how those same cells operate. 

This technique helps researchers to pinpoint mutations that contribute to disease, which will offer crucial insights for developing targeted therapies.

In a new study, published in Genome Biology, the team applied scSNV-seq to the blood cancer gene, JAK1, accurately assessing the impact of JAK1 mutations.

The assessment revealed for the first time that certain mutations caused a “halfway house” phenotype cycling between different states which was not possible under previous approaches.

The technique is designed to demonstrate versatility across cell types, including hard-to-culture primary cells like T cells and stem-cell derived neurons, as well as various editing methods such as base editing and prime editing. 

Applied on a large scale, scSNV-seq could transform understanding of the genetic changes driving cancer and decoding genetic risk for Alzheimer’s, arthritis, diabetes and other complex diseases.

Dr Sarah Cooper, first author of the study at the Wellcome Sanger Institute, stated: “In an era where the rate of genetic variant discovery outpaces our ability to interpret their effects, scSNV-seq fills a major gap for studying challenging cells like T cells and neurons. 

“We are already using it to shed light on the impact of Alzheimer’s and Parkinson’s risk variants on brain cells.”

Dr Andrew Bassett, senior author of the study at the Wellcome Sanger Institute, said: “Our technique is able to directly connect effects of mutations to how a cell behaves, revealing downstream impacts that previous technologies alone cannot deliver. 

“The technique speeds up the identification of causal genetic mutations, which will allow better diagnosis and deepens our molecular understanding of diseases, paving the way for more targeted and effective treatments.”

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