̽��ֱ�� of Cambridge - British Heart Foundation

High cholesterol levels at a young age significant risk factor for atherosclerosis

cjb250 — Wed, 04 Sep 2024 15:00:18 +0000

̽��ֱ��research also suggests that people who are taking lipid-lowering drugs such as statins to lower their cholesterol levels should remain on them, even if their cholesterol levels have fallen, as stopping treatment could increase their risk of atherosclerosis.

Atherosclerosis is one of the major causes of heart and circulatory disease. It involves the hardening and narrowing of the vessels that carry blood to and from the heart. It is caused by the build-up of abnormal material called plaques – collections of fat, cholesterol, calcium and other substances circulating in the blood.

Atherosclerosis is largely considered a disease of the elderly and so most screening, prevention and intervention programmes primarily target those with high cholesterol levels, generally after the age of 50.

But in a study published today in Nature, a team led by scientists at the ̽��ֱ�� of Cambridge shows that high cholesterol levels at a younger age – particularly if those levels fluctuate – can be even more damaging than high cholesterol levels that only begin in later life.

To study the mechanisms that underlie atherosclerosis, scientists often use animal modes, such as mice. ̽��ֱ��mice will typically be fed a high fat diet for several weeks as adults to see how this leads to the build up of the plaques characteristic of the condition.

Professor Ziad Mallat and colleagues at the Victor Phillip Dahdaleh Heart and Lung Research Institute at the ̽��ֱ�� of Cambridge decided to explore a different approach – to see whether giving mice the same amount of high fat food but spread over their lifetime changed their atherosclerosis risk.

“When I asked my group and a number of people who are experts in atherosclerosis, no one could tell me what the result would be,” said Professor Mallat, a British Heart Foundation (BHF) Professor of Cardiovascular Medicine.

“Some people thought it would make no difference, others thought it would change the risk. In fact, what we found was that an intermittent high fat diet starting while the mice were still young – one week on, a few weeks off, another week on, and so on – was the worst option in terms of atherosclerosis risk.”

Armed with this information, his team turned to the Cardiovascular Risk in Young Finns Study, one of the largest follow-up studies into cardiovascular risk from childhood to adulthood. Participants recruited in the 1980s returned for follow-up over the subsequent decades, and more than 2,000 of them had received ultrasound scans of their carotid arteries when they were aged around 30 years and again at around 50 years.

Analysing the data, the team found that those participants who had been exposed to high cholesterol levels as children tended to have the biggest build of plaques, confirming the findings in mice.

“What this means is that we shouldn’t leave it until later in life before we start to look at our cholesterol levels,” Professor Mallat said. “Atherosclerosis can potentially be prevented by lowering cholesterol levels, but we clearly need to start thinking about this much earlier on in life than we previously thought.”

̽��ֱ��mouse studies showed that fluctuating levels of cholesterol appeared to cause the most damage. Professor Mallat says this could explain why some people who are on statins but do not take them regularly remain at an increased risk of heart attack.

“If you stop and start your statin treatment, your body is being exposed to a yo-yo of cholesterol, which it doesn’t like, and it seems this interferes with your body’s ability to prevent the build-up of plaques,” he added.

̽��ֱ��reason why this is so damaging may come down to the effect that cholesterol has on specific types of immune cells known as ‘resident arterial macrophages’. These reside in your arteries, helping them to clear damaged cells and fatty molecules known as lipids, which include cholesterol, and stopping the build-up of plaques.

When the team examined these macrophages in their mouse models, they found that high cholesterol levels – and in particular, fluctuating cholesterol levels – changed them physically and altered the activity of their genes. This meant that the cells were no longer protective, but were instead detrimental, accelerating atherosclerosis.

̽��ֱ��research was funded by the British Heart Foundation.

Reference
Takaoka, M et al. Early intermittent hyperlipidaemia alters tissue macrophages to boost atherosclerosis. Nature; 4 Sept 2024; DOI: 10.1038/s41586-024-07993-x

Our risk of developing atherosclerosis – ‘furring’ of the arteries – can begin much earlier in life than was previously thought, highlighting the need to keep cholesterol levels low even when we are young, new research has discovered.

Atherosclerosis can potentially be prevented by lowering cholesterol levels, but we clearly need to start thinking about this much earlier on in life

Ziad Mallat

SolStock (Getty Images)

Teenagers eating pizza by the river

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Anti-inflammatory drug could reduce future heart attack risk

Anonymous — Mon, 02 Sep 2024 10:52:31 +0000

A cancer drug that unlocks the anti-inflammatory power of the immune system could help to reduce the risk of future heart attacks, according to research part-funded by the British Heart Foundation. By repurposing an existing drug, researchers hope it could soon become part of routine treatment for patients after a heart attack.

̽��ֱ��findings will be presented at the European Society of Cardiology Congress in London by Dr Rouchelle Sriranjan, NIHR Clinical Lecturer in Cardiology at the ̽��ֱ�� of Cambridge.

High levels of inflammation in blood vessels are linked to an increased risk of heart disease and heart attacks. After a heart attack, the body’s immune response can aggravate existing inflammation, causing more harm and increasing risk even further. However, NICE guidelines don’t currently recommend the use of any anti-inflammatory drugs to reduce future risk.

Now, a team of researchers, led by Dr Joseph Cheriyan from Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust, have found that low doses of an anti-inflammatory drug called aldesleukin, injected under the skin of patients after a heart attack, significantly reduces inflammation in arteries.

̽��ֱ��researchers are currently following up patients to investigate the longer-term impact of this fall in inflammation. To date, in the two and a half years after their treatment, there have been no major adverse cardiac events in the group that received aldesleukin, compared to seven in the group that received the placebo.

Professor Ziad Mallat, BHF Professor of Cardiovascular Medicine at the ̽��ֱ�� of Cambridge who developed the trial, said: “We associate inflammation with healing – an inbuilt response that protects us from infection and injury. But it’s now clear that inflammation is a culprit in many cardiovascular conditions.

“Early signs from our ongoing trial suggest that people treated with aldesleukin may have better long-term outcomes, including fewer heart attacks. If these findings are repeated in a larger trial, we’re hopeful that aldesleukin could become part of routine care after a heart attack within five to 10 years.”

Aldesleukin is already used to treat kidney cancer, as high doses stimulate the immune system to attack cancer cells. ̽��ֱ��Cambridge team previously found that doses one thousand times lower than those used in cancer treatment increased the number of regulatory T cells – a type of anti-inflammatory white blood cell – in patients’ blood compared to a placebo.

In the current trial at Addenbrooke's and Royal Papworth hospitals in Cambridge, 60 patients admitted to hospital with a heart attack or unstable angina received either low dose aldesleukin or placebo. Patients received an injection once a day for the first five days, then once per week over the next seven weeks. Neither the participants nor their doctors knew whether they had received the drug or placebo.

At the end of treatment, Positron Emission Tomography (PET) scans showed that inflammation in the artery involved in patients’ heart attack or angina was significantly lower in the group treated with aldesleukin, compared to those who received the placebo.

̽��ֱ��anti-inflammatory effect of aldesleukin appeared even more striking in the most inflamed arteries, leading to a larger reduction in inflammation levels in these vessels and a bigger difference between the two groups by the end of the study.

Dr Sonya Babu-Narayan, Associate Medical Director at the British Heart Foundation and consultant cardiologist said: “Thanks to research, we have an array of effective treatments to help people avoid heart attacks and strokes and save lives. But, even after successful heart attack treatment, unwanted inflammation in the coronary arteries can remain, which can lead to life-threatening complications.

“A treatment to reduce inflammation after a heart attack could be a game-changer. It would help doctors to interrupt the dangerous feedback loop that exacerbates inflammation and drives up risk. This research is an important step towards that treatment becoming a reality.”

̽��ֱ��study was predominantly funded by the Medical Research Council, with significant support from the BHF and National Institute for Health and Care Research Cambridge Biomedical Research Centre (NIHR-BRC).

Originally published by the British Heart Foundation.

Repurposed cancer drug helps to calm inflammation in arteries.

Sebastian Kaulitzki/Science Photo Library via Getty Images

Illustration of human heart

Yes

Incidence of heart attacks and strokes was lower after COVID-19 vaccination

cjb250 — Wed, 31 Jul 2024 09:00:37 +0000

̽��ֱ��study, published today in Nature Communications, showed that the incidence of arterial thromboses, such as heart attacks and strokes, was up to 10% lower in the 13 to 24 weeks after the first dose of a COVID-19 vaccine. Following a second dose, the incidence was up to 27% lower after receiving the AstraZeneca vaccine and up to 20% lower after the Pfizer/Biotech vaccine.

̽��ֱ��incidence of common venous thrombotic events – mainly pulmonary embolism and lower limb deep venous thrombosis – followed a similar pattern.

Research led by the Universities of Cambridge, Bristol and Edinburgh and enabled by the British Heart Foundation (BHF) Data Science Centre at Health Data Research UK analysed de-identified health records from 46 million adults in England between 8 December 2020 and 23 January 2022. Data scientists compared the incidence of cardiovascular diseases after vaccination with the incidence before or without vaccination, during the first two years of the vaccination programme.

Co-first author Dr Samantha Ip, Research Associate at the Department of Public Health and Primary Care, ̽��ֱ�� of Cambridge, said: “We studied COVID-19 vaccines and cardiovascular disease in nearly 46 million adults in England and found a similar or lower incidence of common cardiovascular diseases, such as heart attacks and strokes, following each vaccination than before or without vaccination. This research further supports the large body of evidence on the safety of the COVID-19 vaccination programme, which has been shown to provide protection against severe COVID-19 and saved millions of lives worldwide.”

Previous research found that the incidence of rare cardiovascular complications is higher after some COVID-19 vaccines. For example, incidence of myocarditis and pericarditis have been reported following mRNA-based vaccines such as the Pfizer/Biotech vaccine, and vaccine-induced thrombotic thrombocytopenia following adenovirus-based vaccines such as the AstraZeneca vaccine. This study supports these findings, but importantly it did not identify new adverse cardiovascular conditions associated with COVID-19 vaccination and offers further reassurance that the benefits of vaccination outweigh the risk.

Incidence of cardiovascular disease is higher after COVID-19, especially in severe cases. This may explain why incidence of heart attacks and strokes is lower in vaccinated people compared with unvaccinated people, but further explanations are beyond the scope of this study.

Professor William Whiteley, Associate Director at the BHF Data Science Centre and Professor of Neurology and Epidemiology at the ̽��ֱ�� of Edinburgh, said: “ ̽��ֱ��COVID-19 vaccination programme rollout began strongly in the UK, with over 90% of the population over the age of 12 vaccinated with at least one dose by January 2022.

“This England-wide study offers patients reassurance of the cardiovascular safety of first, second and booster doses of COVID-19 vaccines. It demonstrates that the benefits of second and booster doses, with fewer common cardiovascular events include heart attacks and strokes after vaccination, outweigh the very rare cardiovascular complications.”

̽��ֱ��research team used de-identified linked data from GP practices, hospital admissions and death records, analysed in a secure data environment provided by NHS England.

Co-last author Dr Venexia Walker, Research Fellow at the ̽��ֱ�� of Bristol, said: “Given the critical role of COVID-19 vaccines in protecting people from COVID-19, it is important we continue to study the benefits and risks associated with them. ̽��ֱ��availability of population-wide data has allowed us to study different combinations of COVID-19 vaccines and to consider rare cardiovascular complications. This would not have been possible without the very large data that we are privileged to access and our close cross-institution collaborations.”

Reference
Ip, S et al. Cohort study of cardiovascular safety of different COVID-19 vaccination doses among 46 million adults in England. Nat Comms; 31 Jul 2024; DOI: 10.1038/s41467-024-49634-x

Adapted from a press release from Health Data Research UK

̽��ֱ��incidence of heart attacks and strokes was lower after COVID-19 vaccination than before or without vaccination, according to a new study involving nearly the whole adult population of England.

This research further supports the large body of evidence on the effectiveness of the COVID-19 vaccination programme, which has saved millions of lives worldwide

Samantha Ip

Paul_McManus

Vial of the AstraZeneca COVID-19 vaccine

Yes

Licence type:

Public Domain

Cambridge research receives £5 million boost for ‘world-leading’ cardiovascular research

cjb250 — Tue, 28 May 2024 11:10:58 +0000

̽��ֱ��funding will support the university to cultivate a world-class research environment that encourages collaboration, inclusion and innovation, and where visionary scientists can drive lifesaving breakthroughs.

Professor Martin Bennett, BHF Professor of Cardiovascular Sciences at the ̽��ֱ�� of Cambridge, said: “This is a fantastic achievement from the whole Cambridge team. This award will support our multiple research programmes identifying new targets and treatments for vascular disease and heart failure, new ways to reduce the consequences of diabetes and obesity, and how we can get our research used to treat patients.”

̽��ֱ��Cambridge award is part of a £35 million boost to UK cardiovascular disease research from the British Heart Foundation. It comes from the charity’s highly competitive Research Excellence Awards funding scheme. ̽��ֱ��£5 million award to the ̽��ֱ�� of Cambridge will support researchers to:

Combine their expertise to work on cardiovascular diseases and in populations with high unmet need.
Identify new markers and disease targets for a wide range of cardiovascular diseases, and test new drugs in clinical trials.
Develop new ways to diagnose cardiovascular disease and harness the power of artificial intelligence from imaging and health records to identify people at highest risk.
Generate user-friendly risk communication and management tools to improve the prevention and management of cardiovascular disease.

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: “We’re delighted to continue to support research at the ̽��ֱ�� of Cambridge addressing the biggest challenges in cardiovascular disease. This funding recognises the incredible research happening at Cambridge and will help to further its reputation as a global leader in the field.

“With generous donations from our supporters, this funding will attract the brightest talent, power cutting-edge science, and unlock lifesaving discoveries that can turn the tide on the devastation caused by heart and circulatory diseases.”

Research Excellence Awards offer greater flexibility than traditional research funding, allowing scientists to quickly launch ambitious projects that can act as a springboard for larger, transformative funding applications.

̽��ֱ��funding also aims to break down the silos that have traditionally existed in research, encouraging collaboration between experts from diverse fields. From clinicians to data scientists, biologists to engineers, the funding will support universities to attract the brightest minds, nurture new talent and foster collaboration to answer the biggest questions in heart and circulatory disease research.

̽��ֱ�� ̽��ֱ�� of Cambridge has previously been awarded £9 million funding through the BHF’s Research Excellence Awards scheme. This funding has supported research that will lay the foundations for future breakthroughs, including:

Research showing that low doses of a cancer drug could improve recovery after a heart attack. ̽��ֱ��drug boosts activity of anti-inflammatory immune cells that can cause harmful inflammation in blood vessels supplying the heart. It’s currently being tested in clinical trials to see if it benefits patients.
A new risk calculator to enable doctors across the UK and Europe predict who is at risk of having a heart attack or stroke in the next 10 years with greater accuracy. ̽��ֱ��calculator has been adopted by the European Guidelines on Cardiovascular Disease Prevention in Clinical Practice.
Developing imaging and artificial intelligence tools to improve diagnosis of heart and vascular disease by enhancing analysis of scans for disease activity and high-risk fatty plaques. These tools can be rapidly implemented to support diagnosis, treatment and prevention.
A study investigating whether an epilepsy medication could help to prevent strokes in people with a common gene variant. ̽��ֱ��change in the gene HDAC9 can cause it to become ‘overactive’ and increase stroke risk. ̽��ֱ��epilepsy medication sodium valproate blocks the HDAC9 activity, so could reduce stroke risk in people with the variant.
Discovery of rare and common changes in the genetic code that influences proteins and small molecules in the blood, helping us understand the development of cardiovascular diseases and identify novel drug targets.

Adapted from a press release by BHF

̽��ֱ�� ̽��ֱ�� of Cambridge has received £5 million funding from the British Heart Foundation (BHF) to support its world-class cardiovascular disease research over the next five years, the charity has announced.

This is a fantastic achievement from the whole Cambridge team. This award will support our multiple research programmes.

Martin Bennett

Lloyd Mann

Professor Martin Bennett standing outside the Victor Phillip Dahdaleh Heart and Lung Research Institute

Yes

Lab-grown ‘small blood vessels’ point to potential treatment for major cause of stroke and vascular dementia

cjb250 — Thu, 16 Nov 2023 16:00:19 +0000

̽��ֱ��study, published today in Stem Cell Reports, also identifies a drug target to ‘plug’ these leaks and prevent so-called small vessel disease in the brain.

Cerebral small vessel disease (SVD) is a leading cause of age-related cognitive decline and contributes to almost half (45%) of dementia cases worldwide. It is also responsible for one in five (20%) ischemic strokes, the most common type of stroke, where a blood clot prevents the flow of blood and oxygen to the brain.

̽��ֱ��majority of cases of SVD are associated with conditions such as hypertension and type 2 diabetes, and tend to affect people in their middle age. However, there are some rare, inherited forms of the disease that can strike people at a younger age, often in their mid-thirties. Both the inherited and ‘spontaneous’ forms of the disease share similar characteristics.

Scientists at the Victor Phillip Dahdaleh Heart and Lung Research Institute, ̽��ֱ�� of Cambridge, used cells taken from skin biopsies of patients with one of these rare forms of SVD, which is caused by a mutation in a gene called COL4.

By reprogramming the skin cells, they were able to create induced pluripotent stem cells – cells that have the capacity to develop into almost any type of cell within the body. ̽��ֱ��team then used these stem cells to generate cells of the brain blood vessels and create a model of the disease that mimics the defects seen in patients’ brain vessels.

Dr Alessandra Granata from the Department of Clinical Neurosciences at Cambridge, who led the study, said: “Despite the number of people affected worldwide by small vessel disease, we have little in the way of treatments because we don’t fully understand what damages the blood vessels and causes the disease. Most of what we know about the underlying causes tends to come from animal studies, but they are limited in what they can tell us.

“That’s why we turned to stem cells to generate cells of the brain blood vessels and create a disease model ‘in a dish’ that mimics what we see in patients.”

Our blood vessels are built around a type of scaffolding known as an extracellular matrix, a net-like structure that lines and supports the small blood vessels in the brain. ̽��ֱ��COL4 gene is important for the health of this matrix.

In their disease model, the team found that the extracellular matrix is disrupted, particularly at its so-called ‘tight junctions’, which ‘zip’ cells together. This leads to the small blood vessels becoming leaky – a key characteristic seen in SVD, where blood leaks out of the vessels and into the brain.

̽��ֱ��researchers identified a class of molecules called metalloproteinases (MMPs) that play a key role in this damage. Ordinarily, MMPs are important for maintaining the extracellular matrix, but if too many of them are produced, they can damage the structure – similar to how in ̽��ֱ��Sorcerer’s Apprentice, a single broom can help mop the floor, but too many wreak havoc.

When the team treated the blood vessels with drugs that inhibit MMPs – an antibiotic and anti-cancer drug – they found that these reversed the damage and stopped the leakage.

Dr Granata added: “These particular drugs come with potentially significant side effects so wouldn’t in themselves be viable to treat small vessel disease. But they show that in theory, targeting MMPs could stop the disease. Our model could be scaled up relatively easily to test the viability of future potential drugs.”

̽��ֱ��study was funded by the Stroke Association, British Heart Foundation and Alzheimer’s Society, with support from the NIHR Cambridge Biomedical Research Centre and the European Union’s Horizon 2020 Programme.

Reference
Al-Thani, M, Goodwin-Trotman, M. A novel human 1 iPSC model of COL4A1/A2 small vessel disease unveils a key pathogenic role of matrix metalloproteinases. Stem Cell Reports; 16 Nov 2023; DOI: https://doi.org/10.1016/j.stemcr.2023.10.014

Cambridge scientists have grown small blood vessel-like models in the lab and used them to show how damage to the scaffolding that supports these vessels can cause them to leak, leading to conditions such as vascular dementia and stroke.

Despite the number of people affected worldwide by small vessel disease, we have little in the way of treatments because we don’t fully understand what damages the blood vessels and causes the disease

Alessandra Granata

Alessandra Granata/ ̽��ֱ�� of Cambridge

Disease mural cells stained for calponin (mural cells marker, green), collagen IV (magenta) and DAPI (nuclei, blue)

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Licence type:

Attribution

Cancer drug could hold hope for treating inflammatory diseases including gout and heart diseases

cjb250 — Wed, 01 Nov 2023 08:00:30 +0000

In a study published on 1 November in the Journal of Clinical Investigation, the researchers have identified a molecule that plays a key role in triggering inflammation in response to materials in the body seen as potentially harmful.

We are born with a defence system known as innate immunity, which acts as the first line of defence against harmful materials in the body. Some of these materials will come from outside, such as bacterial or viral infections, while others can be produced within the body.

Innate immunity triggers an inflammatory response, which aims to attack and destroy the perceived threat. But sometimes, this response can become overactive and can itself cause harm to the body.

One such example of this is gout, which occurs when urate crystals build up in joints, causing excessive inflammation, leading to intense pain. Another example is heart attack, where dead cell build up in the damaged heart – the body sees itself as being under attack and an overly-aggressive immune system fights back, causing collateral damage to the heart.

Several of these conditions are characterised by overactivation of a component of the innate immune response known as an inflammasome – specifically, the inflammasome NLRP3. Scientists at the Victor Phillip Dahdaleh Heart and Lung Research Institute at Cambridge have found a molecule that helps NLRP3 respond.

This molecule is known as PLK1. It is involved in a number of processes within the body, including helping organise tiny components of our cells known as microtubules cytoskeletons. These behave like train tracks inside of the cell, allowing important materials to be transported from one part of the cell to another.

Dr Xuan Li from the Department of Medicine at the ̽��ֱ�� of Cambridge, the study’s senior author, said: “If we can get in the way of the microtubules as they try to organise themselves, then we can in effect slow down the inflammatory response, preventing it from causing collateral damage to the body. We believe this could be important in preventing a number of common diseases that can cause pain and disability and in some cases can lead to life-threatening complications.”

But PLK1 also plays another important role in the body – and this may hold the key to developing new treatments for inflammatory diseases.

For some time now, scientists have known that PLK1 is involved in cell division, or mitosis, a process which, when it goes awry, can lead to runaway cell division and the development of tumours. This has led pharmaceutical companies to test drugs that inhibit its activity as potential treatments for cancer. At least one of these drugs is in phase three clinical trials – the final stages of testing how effective a drug is before it can be granted approval.

When the Cambridge scientists treated mice that had developed inflammatory diseases with a PLK1 inhibitor, they showed that it prevented the runaway inflammatory response – and at a much lower dose than would be required for cancer treatment. In other words, inhibiting the molecule ‘calmed down’ NLRP3 in non-dividing cells, preventing the overly aggressive inflammatory response seen in these conditions.

̽��ֱ��researchers are currently planning to test its use against inflammatory diseases in clinical trials.

“These drugs have already been through safety trials for cancer – and at higher doses than we think we would need – so we’re optimistic that we can minimise delays in meeting clinical and regulatory milestones,” added Dr Li.

“If we find that the drug is effective for these conditions, we could potentially see new treatments for gout and inflammatory heart diseases – as well as a number of other inflammatory conditions – in the not-too-distant future.”

̽��ֱ��research was funded by the British Heart Foundation. Professor James Leiper, Associate Medical Director at the British Heart Foundation said: “This innovative research has uncovered a potential new treatment approach for inflammatory heart diseases such as heart failure and cardiomyopathy. It’s promising that drugs targeting PLK1 – that work by dampening down the inflammatory response – have already been proven safe and effective in cancer trials, potentially helping accelerate the drug discovery process.

“We hope that this research will open the door for new ways to treat people with heart diseases caused by overactive and aggressive immune responses, and look forward to more research to uncover how this drug could be could be repurposed.”

Reference
Baldrighi, M et al. PLK1 inhibition dampens NLRP3 inflammasome-elicited response in inflammatory disease models. JCI; 1 Nov 2023; DOI: 10.1172/JCI162129

A cancer drug currently in the final stages of clinical trials could offer hope for the treatment of a wide range of inflammatory diseases, including gout, heart failure, cardiomyopathy, and atrial fibrillation, say scientists at the ̽��ֱ�� of Cambridge.

We believe [our findings] could be important in preventing a number of common diseases that can cause pain and disability and in some cases can lead to life-threatening complications

Xuan Li

kazuma seki (Getty Images)

̽��ֱ��feet of a man suffering from gout - stock photo

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Type 2 diabetes diagnosis at age 30 can reduce life expectancy by up to 14 years

cjb250 — Tue, 03 Oct 2023 09:00:51 +0000

Even people who do not develop the condition until later in life – with a diagnosis at age 50 years – could see their life expectancy fall by up to six years, an analysis of data from 19 high-income countries found.

̽��ֱ��researchers say the findings, published in ̽��ֱ��Lancet Diabetes & Endocrinology, highlight the urgent need to develop and implement interventions that prevent or delay onset of diabetes, especially as the prevalence of diabetes among younger adults is rising globally.

Increasing levels of obesity, poor diet and increased sedentary behaviour are driving a rapid rise in the number of cases of type 2 diabetes worldwide. In 2021, 537 million adults were estimated to have diabetes worldwide, with an increasing number diagnosed at younger ages.

Type 2 diabetes increases an individual’s risk of a range of complications including heart attack and stroke, kidney problems, and cancer. Previous estimates have suggested that adults with type 2 diabetes die, on average, six years earlier than adults without diabetes. There is uncertainty, however, about how this average reduction in life expectancy varies according to age at diagnosis.

To answer this question, a team led by scientists at the ̽��ֱ�� of Cambridge and ̽��ֱ�� of Glasgow examined data from two major international studies – the Emerging Risk Factors Collaboration and UK Biobank – comprising a total of 1.5 million individuals.

̽��ֱ��earlier an individual was diagnosed with type 2 diabetes, the greater the reduction in their life expectancy. Overall, every decade of earlier diagnosis of diabetes was associated with about four years of reduced life expectancy.

Using data from US population it was estimated that, individuals with type 2 diabetes diagnosed at ages 30, 40, and 50 years died on average about 14, 10, and 6 years earlier, respectively, than individuals without the condition. These estimates were slightly higher in women (16, 11, and 7 years, respectively) than they were in men (14, 9, and 5 years, respectively).

̽��ֱ��findings were broadly similar in analyses using EU data, with corresponding estimates being about 13, 9, or 5 years earlier death on average.

Professor Emanuele Di Angelantonio from the Victor Phillip Dahdaleh Heart and Lung Research Institute (VPD-HLRI), ̽��ֱ�� of Cambridge, said: “Type 2 diabetes used to be seen as a disease that affected older adults, but we’re increasingly seeing people diagnosed earlier in life. As we’ve shown, this means they are at risk of a much shorter life expectancy than they would otherwise have.”

Dr Stephen Kaptoge, also from the VPD-HLRI, said: “Type 2 diabetes can be prevented if those at greatest risk can be identified and offered support – whether that’s to make changes to their behaviour or to provide medication to lower their risk. But there are also structural changes that we as a society should be pursuing, including relating to food manufacturing, changes to the built environment to encourage more physical activity, and so on.

“Given the impact type 2 diabetes will have on people’s lives, preventing – or at least delaying the onset – of the condition should be an urgent priority.”

̽��ֱ��researchers found that the majority of the reduction in life expectancy associated with diabetes was due to ‘vascular deaths’ – deaths related to conditions such as heart attack, stroke and aneurysms. Other complications such as cancer also contributed to lowering life expectancy.

Professor Naveed Sattar from the Institute of Cardiovascular & Medical Sciences, ̽��ֱ�� of Glasgow, added: “Our findings support the idea that the younger an individual is when they develop type 2 diabetes, the more damage their body accumulates from its impaired metabolism. But the findings also suggest that early detection of diabetes by screening followed by intensive glucose management could help prevent long-term complications from the condition.”

̽��ֱ��Cambridge team was supported by the Medical Research Council, British Heart Foundation, Health Data Research UK and NIHR Cambridge Biomedical Research Centre.

Reference
Emerging Risk Factors Collaboration. Life expectancy associated with different ages at diagnosis of diabetes: 23 million person-years of observation. Lancet Diabetes & Endocrinology; 11 Sept 2023; DOI: 10.1016/S2213-8587(23)00223-1

An individual diagnosed with type 2 diabetes at age 30 years could see their life expectancy fall by as much as 14 years, an international team of researchers has warned.

Given the impact type 2 diabetes will have on people’s lives, preventing – or at least delaying the onset – of the condition should be an urgent priority

Stephen Kaptoge

Elva Etienne (Getty Images)

Man using blood sugar measurement device to monitor diabetes - stock photo

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

£16million gift to support Europe’s largest heart and lung research centre

cjb250 — Thu, 23 Mar 2023 14:00:31 +0000

̽��ֱ��Victor Phillip Dahdaleh Heart and Lung Research Institute (HLRI) is home to the largest concentration of scientists and clinicians in heart and lung medicine in Europe. It opened in July 2022 with the ambitious goal of identifying ten new potential treatments or diagnostic tests for heart and lung diseases within five years.

̽��ֱ��HLRI is located on Cambridge’s rapidly expanding Biomedical Campus, immediately adjacent to Royal Papworth Hospital. ̽��ֱ��institute brings together population health, laboratory and clinical scientists, with NHS clinicians and patients, with the aim of improving outcomes for people with cardiovascular and lung diseases such as heart attacks, pulmonary hypertension, lung cancers, cystic fibrosis and acute respiratory distress syndrome.

Dr Dahdaleh said: “Cambridge is one of the greatest Universities in the history of civilisation and, 800 years on, it is at the cutting edge of scientific progress. Over the years in which I have been supporting education and medical research around the world, I have realised the UK is a global leader in the prevention, identification and treatment of heart and lung diseases.

“I’m supporting this new Institute because, through collaboration with Royal Papworth Hospital and other leading institutions, it will enable a concentration of expertise that will make medical advances in these fields that are of international importance.”

Dr Dahdaleh has previously supported research at the ̽��ֱ�� of Cambridge looking into COVID-19 and national research on mesothelioma, a type of lung cancer linked to asbestos exposure. Cardiovascular and lung diseases kill more than 26 million people a year and have a major impact on the quality of life of many more. Alongside the immense human cost, the economic burden of these diseases – an estimated annual global cost of £840 billion – is already overwhelming and unsustainable. Yet declining air quality and increasing rates of obesity are set to compound the scale of the challenge faced worldwide.

Dr Anthony Freeling, Acting Vice-Chancellor of the ̽��ֱ�� of Cambridge, said: “We are truly grateful to Victor for his generous donation. There has never been a more pressing need to develop new approaches and treatments to help us tackle the heart and lung diseases that affect many millions of people worldwide. ̽��ֱ��Victor Phillip Dahdaleh Heart and Lung Research Institute is in a strong position to make a major difference to people’s lives.”

Professor John Wallwork, Chair of Royal Papworth Hospital NHS Foundation Trust, said: “When we moved our hospital to the Cambridge Biomedical Campus in 2019, one of our ambitions was to collaborate with partners to create a research and education institute on this scale. Victor’s kind donation will support all the teams working in HLRI to develop new treatments in cardiovascular and respiratory diseases, improving the lives of people in the UK and around the globe.”

̽��ֱ��HLRI includes state-of-the-art research facilities, space for collaboration between academia, healthcare providers and industry, conference and education facilities. It also includes a special 10-bed clinical research facility where the first-in-patient studies of new treatments are being conducted.

Professor Charlotte Summers, Interim Director of the HLRI, said: “We have set ourselves ambitious goals because of the urgent need to improve cardiovascular and lung health across the world. Victor’s generous gift will help us realise our ambitions. Collaboration is at the heart of our approach, with our researchers and clinicians working with patient, academic, charity and industry partners within the Cambridge Cluster, nationally and internationally.”

Dr Dahdaleh is also a significant supporter of the Duke of Edinburgh awards, York and McGill universities in his homeland of Canada, and the British Lung Foundation. Dr Dahdaleh and his wife Mona, via the Victor Dahdaleh Foundation, have a commitment to supporting scholarships for disadvantaged students pursuing higher education in addition to their extensive philanthropic support for research into cancer, lung and heart disease.

̽��ֱ��HLRI has already raised £30 million from the UK Research Partnership Investment Fund and £10 million from the British Heart Foundation, with additional funding from the Wolfson Foundation, Royal Papworth Hospital Charity and the ̽��ֱ�� of Cambridge. Additional support has been provided by the Cystic Fibrosis Trust for a Cystic Fibrosis Trust Innovation Hub within the institute.