A new thesis by Karolinska Institutet student Tessa Schillemans has found that exposure persistent environmental pollutants did not increase biomarkers of cardiovascular disease risk – rather, exposure reduced them, raising further questions on their complex interactions with the environment and within the human body.
What is the thesis about? The thesis is about a group of environmental pollutants called per- and polyfluoroalkyl substances (PFAS), also called “forever-chemicals”. Since we all are exposed and their chemical structure resembles that of fatty acids, we wanted to investigate whether exposure to PFAS associated with increased risk of cardiovascular disease. Additionally, we also explored if we could gain insight in potential underlying molecular pathways by linking PFAS exposure to biological molecules in the blood.
Can you tell us about some interesting results? We found no evidence that PFAS was linked to increased risk of cardiovascular disease in the general population. If anything, rather the opposite – which also deserves careful consideration. We did observe associations with higher cholesterol, lower triglycerides and with lipid metabolism intermediates, which all point towards potential perturbations in lipid metabolism.
What further research is needed in the area? It is essential to fully understand any adverse consequences that PFAS may have, since they are omnipresent and persistent. Thus, epidemiological studies involving other outcomes and vulnerable subgroups (such as pregnant women and children) should also be performed, as disturbances in lipid metabolism could impact other physiological processes. For a deeper mechanistic understanding, integration of data from different biological systems (genome, epigenome, transcriptome, proteome, metabolome) in human and experimental settings would be optimal. Additionally, since humans are exposed to many different chemicals simultaneously and these could interact with each other, there is a need for studies that investigate multiple exposures at the same time (exposome studies).
Bempedoic acid, a new cholesterol-lowering drug, has the potential to be an effective substitute for patients who can’t tolerate statins. Bempedoic acid is an ATP citrate lyase inhibitor that reduces low-density lipoprotein (LDL) cholesterol levels and is associated with a low incidence of muscle-related adverse events. Its effects on cardiovascular outcomes were uncertain, so researchers used a double-blind, randomised, placebo-controlled trial to determine outcomes on a variety of cardiovascular measures in statins-intolerant patients.
The study, published in the New England Journal of Medicine, recruited patients aged 18–85 years at increased cardiovascular risk and unable or unwilling to take statins due to adverse effects. Patients were first tested with placebo over a 4-week run-in period, and were not randomised if they experience unacceptable adverse effects or if adherence was less than 80%. The 13 970 patients who successfully completed run-in were randomised to receive bempedoic acid 180mg orally per day or matching placebo.
The mean LDL cholesterol level at baseline was 139.0mg/dL in both groups, and after 6 months, the reduction in the level was greater with bempedoic acid than with placebo by 29.2mg/dL; the observed difference in the percent reductions was 21.1 percentage points in favour of bempedoic acid.
Compared to placebo, risk of fatal or nonfatal stroke, death from cardiovascular causes, and death from any cause after significantly were lower by 13%, after a median of 40.6 months of follow-up. The risk of death from cardiovascular causes, nonfatal stroke, or nonfatal myocardial infarction was 15% lower with bempedoic acid than with placebo, and the risks of fatal or nonfatal myocardial infarction and coronary revascularisation were 23% lower and 19% lower, respectively.
The researchers noted that the LDL-cholesterol lowering effects were similar in magnitude and predicted reduction in cardiovascular risks to that observed with statins. In addition, bempedoic acid did not increase glycated haemoglobin levels or the incidence of new-onset diabetes, unlike statins. Due to the demonstrated benefits, those taking placebo were offered the chance to transition to taking bempedoic acid.
A trial limitation was that it only included patients with statins intolerance, and who therefore had higher LDL cholesterol levels at baseline.
Being overweight in childhood and in early adulthood are discrete risk factors for blood clots (thrombi) later in life, according to a study using school health care and military service records, according to a study published in the Journal of Internal Medicine.
The association between obesity and blood clots is already established. However, to date it has been unclear how much influence a raised BMI in childhood and puberty exerts. Thrombi usually arise in the legs, often starting in a blood vessel in the calf. Swelling, pain and redness are common symptoms. Though easily treated if caught early, they can result pulmonary embolism may be life-threatening.
The present study comprises 37 672 men in Sweden, born between 1945 and 1961. It is based on information about height, weight, and BMI from the men’s records, first from school health care services (at the age of 8 years) and, second, from medical examinations on enrolment in the Armed Services (at age 20), along with register data on any blood clots up to age 62 on average.
Distinctly elevated thrombus risk
The results showed that BMI at both ages 8 and 20, independently of each other, can be linked to venous blood clots. These may occur in, for example, the leg (deep vein thrombosis, DVT) or the lung (pulmonary embolism).
In adulthood, two groups were found to be at a significantly increased risk of venous thrombi. The first was individuals who had been overweight both as children and as young adults, while the second was composed of those whose weight in childhood was normal and who became overweight only in early adulthood.
Moreover, being overweight in both childhood and young adulthood was found to raise the risk of arterial thrombi – clots resulting from constricted blood vessels with fatty deposits and inflammation. Since there were few cases of arterial blood clots in the study, however, further studies are needed to confirm these findings. All comparisons in the study were made with the control group, whose weight was normal at both 8 and 20 years of age.
Overweight in puberty an important factor
The first and corresponding author of the study is Lina Lilja, a doctoral student at Sahlgrenska Academy, University of Gothenburg, and paediatrician. At the time of the study, she worked at the Kungshöjd paediatric clinic in Gothenburg. Today, she is a senior physician in child health care in Region Västra Götaland.
“Our study shows that both overweight in childhood and overweight in young adulthood increase the risk of venous blood clots later in life. The latter, overweight when the men were young adults, proved to be a more influential factor than overweight when they were children,” Lilja notes.
The study includes data from the BMI Epidemiology Study (BEST) in Gothenburg, a population study, and from Swedish national registers.
Regular physical activity can improve young adolescents’ mental health and help with behavioural difficulties, suggests research published in Mental Health and Physical Activity. Investigators found that engaging in regular moderate to vigorous physical activity at age 11 was associated with better mental health between the ages of 11 and 13.
Physical activity was also associated with reduced hyperactivity and behavioural problems, such as loss of temper, fighting with other children, lying, and stealing, in young people.
Researchers from the Universities of Edinburgh, Strathclyde, Bristol, and Georgia in the United States explored data from the Children of the 90s study (also known as the Avon Longitudinal Study of Parents and Children; ALSPAC). They looked at the levels of physical activity of 4755 11-year-olds which was measured using devices.
The devices recorded levels of moderate physical activity, typically defined as brisk walking or cycling, as well as vigorous activity which boosts heart rate and breathing, such as aerobic dancing, jogging or swimming.
The young people and their parents reported on their levels of depressive symptoms from age 11 and at age 13 years. Participants’ parents and teachers were also quizzed about the young people’s general behaviour and emotional difficulties.
In analysing the impact of moderate to vigorous exercise on the young people’s mental health and behaviour, the team also considered factors such as age, sex and socio-economic status.
They found that higher levels of moderate or intense physical activity had a small but detectable association with decreases in depressive symptoms and emotional difficulties.
Regular exercise had a small but detectable association with reduced behavioural problems, even after controlling for other possible influences, the study found.
The findings suggest regular moderate and intense physical activity may have a small protective influence on mental health in early adolescence, researchers say.
Dr Josie Booth, of the University of Edinburgh’s Moray House School of Education and Sport, said: “This study adds to the increasing evidence base about how important physical activity is for all aspects of young people’s development – it can help them feel better, and do better at school. Supporting young people to lead healthy active lives should be prioritised.”
Researchers say the study is the first to offer such a comprehensive approach to examining mental health and exercise in young people.
Professor John Reilly, at the University of Strathclyde, said: “While it might seem obvious that physical activity improves mental health the evidence for such a benefit in children and young people has been scarce, so the study findings are important. The findings are also important because levels of moderate-to-vigorous intensity activity globally are so low in pre-teens globally – less than a third achieve the 60 minutes per day recommended by the WHO and UK Health Departments.”
The study is a long-term health-research project that enrolled more than 14 000 pregnant women in 1991 and 1992.
Children of the 90s has been following the health and development of the parents and their children in detail and is currently recruiting the children and the siblings of the original children into the study. It receives core funding from the Medical Research Council, the Wellcome Trust and the University of Bristol.
Scientific evidence that supports vaping as an additional approach to tackle smoking-related morbidity and mortality is fast growing. The time is ripe for decisionmakers to embrace tobacco harm reduction and to steer away from precautionary principle-based tobacco control policies. This is according to Dr Riccardo Polosa, Founder of the Centre of Excellence for the Acceleration of Harm Reduction (CoEHAR) and Professor of Internal Medicine of the University of Catania, Italy.
Towards the end of 2022, the South African Tobacco Products and Electronic Delivery Systems Control Bill was officially introduced into parliament by the Minister of Health. Now, in the coming months, it will be discussed and possibly amended by a portfolio committee.
With this Bill lumping Electronic Nicotine Delivery Systems (ENDS, i.e. e-cigarettes and vapes) in the same category as smoking, Kurt Yeo, co-founder of consumer advocacy group Vaping Saved My Life (VSML), explains that it is essential for those involved in this process to consider the mounting scientific evidence demonstrating that vaping is far less harmful than tobacco smoking and is an effective way to support smokers seeking less risky alternatives and/or wanting to quit.
Dr Colin Mendelsohn is an Australian academic, researcher and clinician, who has helped smokers quit for over 30 years, says that vaping nicotine is a more effective quitting aid than nicotine replacement products such as patches and gums and is the most popular aid for quitting or reducing smoking globally. “It has the potential to save the lives of hundreds of thousands of South African smokers and prevent untold disease and suffering.”
He adds that vaping has been estimated to cause no more than 5% of the harm from smoking. “While the long-term effects have not yet been established, e-cigarettes are certain to be far less harmful than smoking. Vaping carries only a small fraction of the risk of tobacco smoking and is an effective quitting aid or long-term safer substitute for smoking. Vaping should be easily accessible to help adult smokers to quit deadly cigarettes.”
Dr Polosa highlights that decisionmakers and the public should also beware of many flawed articles scientific and fake news that are propagating ‘findings’ of potential harms, thus feeding the counter-narrative that e-cigarettes are ‘not as safe as promoted’. “Proliferation of poor-quality science and fake news need to be actively contrasted by good quality science and by correct information/education.”
The proof is in the numbers
“Countries which have supported vaping such as the United Kingdom and New Zealand have had accelerated declines in smoking rates,” explains Dr Mendelsohn. “For example, in New Zealand the national adult smoking rate fell by an unprecedented 33% in the two years between 2020 and 2022 after vaping was legalised.”
Illustrating this point further, Dr Polosa says that according to the same national surveys used for reporting smoking prevalence to the World Health Organization (WHO), these countries show faster declines in smoking prevalence compared with neighbouring countries with lower uptake of these alternatives. “In Sweden and Norway, eradication of smoking is now almost a reality with a daily smoking prevalence among Norwegian and Swedish youth close to zero (1% and 3%, respectively). Widespread diffusion of e-cigarettes in New Zealand and the United States is also contributing to the historical acceleration in the downward trend in daily prevalence of smoking among young people (1.3% and 1.9%, respectively).”
Regulation is essential, but the proposed Bill is deeply flawed
When it comes to regulation, Dr Polosa asserts that vaping and smoking are completely different animals. “Smoking kills. Vaping does not.”
Therefore, to regulate vaping in the same way as smoking does not make any sense, says Dr Polosa. “Doing so denies smokers access to much lower risk products. Rather, the South African government should table a risk-proportionate approach where the main regulatory levers are applied differentially.”
“This means that the most stringent and restrictive regulation would be applied to the most harmful products: tobacco cigarettes. Regulation of the smoke-free alternatives would focus on consumer protection (i.e., benefits to the consumer) and control of uptake by adolescents in a way that does not cause significant harm to adult smokers. This would meet the demands of people who cannot or do not wish to quit completely, but with much less cancer, cardiovascular and respiratory disease as a result,” Dr Polosa explains.
Dr Mendelsohn agrees and says that the preferred regulatory model is for nicotine liquids for vaping to be sold as adult consumer products from licensed premises, with strict age verification, like cigarettes and alcohol. “Regulation of e-cigarettes should be proportionate to risk and a light touch approach is more appropriate. A balanced regulatory model is needed which allows adult smokers easy access to regulated vaping products while restricting access to underage users. The current proposals will restrict adult smokers’ access to an effective quitting aid which can save lives and prevent smoking-related illness.”
“A precautionary approach to prevent the use of much less harmful smoke-free products is unjustified in the face of the massive burden of smoked tobacco products, which are widely available. This principle requires policymakers to compare the risks of introducing a product with the risks of delaying its introduction. In the case of vaping, the relatively small risks of harm will be outweighed by the far more substantial harms from delaying access to current smokers,” Dr Mendelsohn explains.
He points out that harsh restrictions on the sale and marketing of electronic cigarettes will have negative unintended consequences and will lead to black market sales of unregulated products to both adults and children. “The public health goal should be to encourage smokers who are unable to quit to switch to vaping, a far safer alternative.”
Yeo concludes by saying: “With the Bill aiming to reduce the incidence of tobacco-related illness, disability and death, regulations should be drawn up based on all available research and case studies to ensure South Africa’s smokers are truly helped.”
A new study details the step-by-step cascade that allows bacteria to break through the brain’s protective layers, the meninges, and cause meningitis, a highly fatal disease. Published inNature, the mouse-based research shows that bacteria exploit nerve cells in the meninges to suppress the immune response and allow the infection to spread into the brain.
“We’ve identified a neuroimmune axis at the protective borders of the brain that is hijacked by bacteria to cause infection – a clever manoeuvre that ensures bacterial survival and leads to widespread disease,” said study senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at Harvard Medical School.
The study identifies two central players in this molecular chain of events that leads to infection – a chemical released by nerve cells and an immune cell receptor blocked by the chemical. The study experiments show that blocking either one can interrupt the cascade and thwart the bacterial invasion.
If replicated through further research, the new findings could lead to much-needed therapies for this hard-to-treat condition that often leaves those who survive with serious neurologic damage.
Such treatments would target the critical early steps of infection before bacteria can spread deep into the brain.
“The meninges are the final tissue barrier before pathogens enter the brain, so we have to focus our treatment efforts on what happens at this border tissue,” said study first author Felipe Pinho-Ribeiro, a former post-doctoral researcher in the Chiu lab, now an assistant professor at Washington University in St. Louis.
A recalcitrant disease in need of new treatments
More than 1.2 million cases of bacterial meningitis occur globally each year, according to the US Centers for Disease Control and Prevention. Untreated, it kills seven out of 10 people who contract it. Treatment can reduce mortality to three in 10. However, among those who survive, one in five experience serious consequences, including hearing or vision loss, seizures, chronic headache, and other neurological problems.
The meninges are three membranes that lie atop one another, wrapping the brain and spinal cord to shield the central nervous system from injury, damage, and infection. The dura mater, outermost of the three layers, contains pain neurons that detect signals. Such signals could come in the form of mechanical pressure: blunt force from impact or toxins that make their way into the central nervous system through the bloodstream. The researchers focused on the dura mater as the site of initial interaction between bacteria and protective border tissue.
Recent research has revealed that the dura mater also harbours a wealth of immune cells, and that immune cells and nerve cells reside right next to each other – a clue that captured Chiu’s and Pinho-Ribeiro’s attention.
“When it comes to meningitis, most of the research so far has focused on analysing brain responses, but responses in the meninges – the barrier tissue where infection begins – have remained understudied,” Ribeiro said.
What exactly happens in the meninges when bacteria invade? How do they interact with the immune cells residing there? These questions remain poorly understood, the researchers said.
How bacteria break through the brain’s protective layers
In this particular study, the researchers focused on two pathogens – Streptococcus pneumoniae and Streptococcus agalactiae, leading causes of bacterial meningitis in humans. In a series of experiments, the team found that when bacteria reach the meninges, the pathogens trigger a chain of events that culminates in disseminated infection.
First, researchers found that bacteria release a toxin that activates pain neurons in the meninges. The activation of pain neurons by bacterial toxins, the researchers noted, could explain the severe, intense headache that is a hallmark of meningitis. Next, the activated neurons release a signalling chemical called CGRP. CGRP attaches to an immune-cell receptor called RAMP1. RAMP1 is particularly abundant on the surface of immune cells called macrophages.
Once the chemical engages the receptor, the immune cell is effectively disabled. Under normal conditions, as soon as macrophages detect the presence of bacteria, they spring into action to attack, destroy, and engulf them. Macrophages also send distress signals to other immune cells to provide a second line of defence. The team’s experiments showed that when CGRP gets released and attaches to the RAMP1 receptor on macrophages, it prevented these immune cells from recruiting help from fellow immune cells. As a result, the bacteria proliferated and caused widespread infection.
To confirm that the bacterially induced activation of pain neurons was the critical first step in disabling the brain’s defences, the researchers checked what would happen to infected mice lacking pain neurons.
Mice without pain neurons developed less severe brain infections when infected with two types of bacteria known to cause meningitis. The meninges of these mice, the experiments showed, had high levels of immune cells to combat the bacteria. By contrast, the meninges of mice with intact pain neurons showed meagre immune responses and far fewer activated immune cells, demonstrating that neurons get hijacked by bacteria to subvert immune protection.
To confirm that CGRP was, indeed, the activating signal, researchers compared the levels of CGRP in meningeal tissue from infected mice with intact pain neurons and meningeal tissue from mice lacking pain neurons. The brain cells of mice lacking pain neurons had barely detectable levels of CGRP and few signs of bacterial presence. By contrast, meningeal cells of infected mice with intact pain neurons showed markedly elevated levels of both CGRP and more bacteria.
In another experiment, the researchers used a chemical to block the RAMP1 receptor, preventing it from communicating with CGRP, the chemical released by activated pain neurons. The RAMP1 blocker worked both as preventive treatment before infection and as a treatment once infection had occurred.
Mice pretreated with RAMP1 blockers showed reduced bacterial presence in the meninges. Likewise, mice that received RAMP1 blockers several hours after infection and regularly thereafter had milder symptoms and were more capable of clearing bacteria, compared with untreated animals.
A path to new treatments
The experiments suggest drugs that block either CGRP or RAMP1 could allow immune cells to do their job properly and increase the brain’s border defenses.
Compounds that block CGRP and RAMP1 are found in widely used drugs to treat migraine, a condition believed to originate in the top meningeal layer, the dura mater. Could these compounds become the basis for new medicines to treat meningitis? It’s a question the researchers say merits further investigation.
One line of future research could examine whether CGRP and RAMP1 blockers could be used in conjunction with antibiotics to treat meningitis and augment protection.
“Anything we find that could impact treatment of meningitis during the earliest stages of infection before the disease escalates and spreads could be helpful either to decrease mortality or minimize the subsequent damage,” Pinho-Ribeiro said.
More broadly, the direct physical contact between immune cells and nerve cells in the meninges offers tantalizing new avenues for research.
“There has to be an evolutionary reason why macrophages and pain neurons reside so closely together,” Chiu said. “With our study, we’ve gleaned what happens in the setting of bacterial infection, but beyond that, how do they interact during viral infection, in the presence of tumour cells, or the setting of brain injury? These are all important and fascinating future questions.”
Heart disease is the leading cause of death worldwide, and statins are a vital medication against it – but they are notoriously unpopular, leading to poor adherence. Investigators from Brigham and Women’s Hospital conducted the first population-based study on patients’ nonacceptance of statin therapy recommendations, and published their results in JAMA Network Open.
The study found that in patients at high risk of developing cardiovascular disease, over 20% refused to take statin medications. They were particularly surprised to see that women were about 20% more likely than men to refuse statin therapy when it was first suggested by their physician, and 50% more likely than men to never accept the recommendation. The study also showed that all patients who refused statin therapy developed higher LDL cholesterol levels, likely increasing their risk even further.
“Our study highlights the alarming number of patients who refuse statins and signals that physicians must have discussions with patients about why,” says Alex Turchin, MD, MS, an associate professor at Harvard Medical School and director of quality in the Brigham’s Division of Endocrinology, Diabetes, and Hypertension. “We need to better understand what our patients’ preferences are and to be able to provide more patient-centered care.”
After Turchin began noticing that many of his patients with high cholesterol, including those with diabetes, were opting not to take safe and beneficial medications like statins that can lower cholesterol and bring down the risk of heart attack and stroke, he developed a system to more closely study the phenomenon by analysing the text of provider notes.
The study focused on high-risk patients who either had coronary artery or vascular disease, diabetes, very high cholesterol, or had suffered a stroke. All were recommended statin medications by their physicians to reduce their risk of heart attack and stroke and reduce cholesterol levels. The retrospective study included more than 24 000 patients who were seen at Mass General Brigham between January 1, 2000, and December 31, 2018.
“Even in this higher-risk patient population, so many people did not accept statin therapy,” Turchin said. The study found that while about two-thirds of the patients who were being recommended statin therapy eventually tried it, about one-third never did. And it took three times as long for people in the study who initially said no to taking statin medications to reduce their LDL cholesterol levels to less than 100, compared to people who initially said yes.
The study’s biggest surprise, however, was the much higher rate of refusal by women than men. Turchin and his colleagues wonder if this might be due in part to a false misconception that heart disease impacts men more than women, and plan to further research the reasons underlying these results.
“Ultimately, we need to talk to our patients and find out in more detail why they would prefer not to take statins,” Turchin says. He is currently looking at the impacts of nonacceptance of statin therapy on outcomes that matter to most to patients including heart attacks, strokes, and death. “I think people underestimate how much of a difference modern medicine has made in extending people’s lives, and their quality of life, and medications can play a big role in that.”
From back pain to achy joints, musculoskeletal pain, while common, can be life-changing and debilitating. A recent study published by the Journal of Biomechanical Engineering reveals that, in spinal degeneration, stiffening ligaments can alter mechanical loading on joints resulting in facet joint pain. This research may help to develop new treatments for musculoskeletal pain.
“Our goal is to understand the degeneration process of musculoskeletal tissues, including cartilage, ligaments, and intervertebral discs, using advanced mechanics techniques,” says Jill Middendorf, an assistant professor of mechanical engineering at Johns Hopkins University. “If we understand why this process is happening, we hope to translate our findings into new methods to repair damaged tissues and prevent more pain,”
Middendorf and collaborators sought to understand how the soft tissues of the spine change as spinal discs break down, or degenerate, over time.
Specifically, they looked at the facet capsular ligament, a soft tissue that holds the two sides of the facet joint together and is thought to be a common cause of lower back pain. Previous studies suggest this could be related to mechanical changes that occur in this ligament during spinal degeneration, though it’s not clear exactly why, Middendorf says.
To find out, the team extracted facet capsular ligaments from cadaver spines and ran experiments to measure the ligament’s mechanical properties, like stress and strain, under different loading conditions. By comparing MRI images of the spine and their experimental results, the team discovered that the tissues in the ligament became stiffer as the spine degenerated.
The researchers think this increased stiffness causes altered loading in surrounding tissues, and may explain why some people experience facet joint pain.
“Here we show that there is a correlation between the mechanics of the ligament and spine degeneration, which brings us even closer to being able determine if this ligament is causing pain or if it’s some other part of the spine,” Middendorf says.
With insights gathered from their tissue experiments, researchers in Middendorf’s lab plan to work next on furthering our understanding of spinal degeneration and creating engineered musculoskeletal tissue that can be implanted to replace damaged or diseased tissue.
However, when it comes to pain, answers aren’t always easy to find.
“‘One of the challenges associated with diagnosing and treating spine pain is determining the source of the pain,” Middendorf says. “But we can understand more about the causes and mechanisms of tissue damage, and that means we will someday be able to reverse engineer a solution.”
Following pharmaceutical company Eli Lilly’s much-lauded move to cut US prices for its insulin products, US President Joe Biden is calling on other drugmakers to make similar reductions for the vital medication.
According to Euronews, Lilly is directly slashing its insulin prices by about 70%, since many patients cannot access discounts, and is capping consumer costs at US$35 (R635) a month.
Biden is driving a push for cheaper insulin, signing a law that capped insulin at US$35 a month for senior citizens on Medicare, and urged companies to lower prices on their own. “For far too long, American families have been crushed by drug costs many times higher than what people in other countries are charged for the same prescriptions,” Biden said.
“Insulin costs less than US$10 to make, but Americans are sometimes forced to pay over US$300 for it. It’s flat wrong”.
Biden has called for a national cap on insulin prices, but his current Act does not extend to that.
A Lilly press release revealed that the price of Humalog® (insulin lispro injection) 100 units/mL (Lilly’s most commonly prescribed insulin) and Humulin® (insulin human) injection 100 units/mL by would be cut by 70%. This price change would take effect around the end 2023. Lilly also said it would cut the price for the generic Lispro to US$25 a vial starting in May. In South Africa, a Humulin® 10mL vial costs R525.28, or US$28.08, according to Health-e’s medicine price registry.
Lilly CEO David Ricks said his company was bringing the changes as not all patients could benefit through discounts through insurers or pharmacy benefit managers.
“We are driving for change in repricing older insulins, but we know that 7 out of 10 Americans don’t use Lilly insulin. We are calling on policymakers, employers and others to join us in making insulin more affordable,” said Ricks. “For the past century, Lilly has focused on inventing new and improved insulins and other medicines that address the impact of diabetes and improve patient outcomes. Our work to discover new and better treatments is far from over. We won’t stop until all people with diabetes are in control of their disease and can get the insulin they need.”
Since insurers and pharmacies will take a while to implement the price cuts, Lilly will immediately cap monthly out-of-pocket costs at $35 for people who are not covered by Medicare’s prescription drug programme.
Child obesity is linked to increased risk of developing diabetes in adulthood, both autoimmune forms of diabetes and different forms of type 2 diabetes, according to a new study in the journal Diabetologia. The risk of developing the most insulin-resistant form of diabetes is, for example, three times as high in children with obesity.
Diabetes affects ~7% of the adult population and is one of the world’s fasted growing diseases. It has traditionally been divided into two subgroups – type 1 and type 2 diabetes – but research suggests that this is a simplification.
In 2018, a Swedish study identified five subgroups of adult-onset diabetes, characterised by auto-immunity, severe insulin deficiency, serious insulin resistance, overweight and advanced age.
One way the researchers say that the relevance of these subgroups can be highlighted is to examine if the influence of known risk factors for diabetes differs between the proposed diabetes types.
“Our study is one of the first attempts to find this out,” says the study’s first author Yuxia Wei, doctoral student at Karolinska Institutet. “Childhood obesity has been linked to several chronic diseases, but has never been studied in relation to the recently proposed diabetes subgroups.”
Wanted to investigate the effect of child obesity
The purpose of the present study was therefore to see if the effect of childhood obesity differs. The researchers used a method called Mendelian randomisation, which uses genetic information to study the correlation between an environmental risk factor and disease risk while taking into account the impact of other risk factors.
Basing their analysis on genetic data from over 400 000 UK Biobank participants, the researchers compared children who considered themselves larger than other children with children who rated their weight as normal.
The results showed that overweight/obesity in childhood was linked to a 62% higher risk of autoimmune diabetes, a doubling of the risk of diabetes characterised by insulin deficiency, almost a tripling of the risk of the most insulin-resistant form of diabetes and a seven-times higher risk of the form of diabetes primarily characterised by overweight.
“Our analyses show that children who are larger than others are more likely to develop four of the five proposed new subgroups of adult-onset diabetes,” says Wei. “In other words, obesity in childhood seems to be a risk factor in effectively all types of adult diabetes, with the exception of age-related diabetes. This underscores how important it is to prevent obesity in children since it can have lasting effects on their future health.”
The study was a collaboration among researchers at Karolinska Institutet, Bristol University (UK) and Sun Yat-Sen University (China).
