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30th August 2023
Women receiving breast cancer therapy across six clinical centres in Europe will be enrolled in a study to determine whether behavioural and psychological interventions can reduce the cardiac damage from anti-cancer therapies.
The innovative CARDIOCARE project, which was launched in 2021 by a consortium of European partners including the European Society of Cardiology (ESC), aims to radically change the management of older women with breast cancer by harnessing the expertise of a multidisciplinary team to improve the monitoring, treatment and care these patients receive.
It is already known that breast cancer survivors have an estimated 32% higher risk of cardiovascular disease.
Now, a clinical trial evaluating the impact of behavioural and psychological interventions on quality of life, physical and mental wellbeing, and the cardiotoxic effects of breast cancer treatment will be conducted in 750 patients with breast cancer.
As part of the trial, all patients will receive the CARDIOCARE mobile app, which includes psychological and behavioural elements called ePsycHeart and eHealtHeart. Participants will be randomly allocated to receive both ePsycHeart and eHealtHeart – the intervention group – or to receive ePsycHeart only.
ePsycHeart monitors quality of life, mobility and mental health using a wearable chest band heart rate sensor, smartwatch and questionnaires. eHealtHeart encourages patients to adopt behaviours such as physical activity, healthy diet, games to improve memory and changing the home environment to reduce the risk of falls.
A further aim of the trial is the early identification of women with breast cancer who are at the greatest risk of cardiac damage from anti-cancer treatments. The trial will utilise cutting-edge technologies, such as next generation sequencing, to pinpoint changes in gut microbe species that signal damage of the heart and blood vessels before symptoms occur. In addition, artificial intelligence will be used to analyse images of the heart to predict the likelihood of heart damage.
Professor Dimitrios Fotiadis, project coordinator and professor of biomedical engineering at the University of Ioannina in Greece, said: ‘Cardiovascular disease is a devastating complication of anti-cancer treatment that affects physical and mental health. CARDIOCARE will provide women over the age of 65 with breast cancer the tools to improve their physical health and to psychologically adapt to the disease.
‘CARDIOCARE is on track to improve the physical and mental health of older women with breast cancer by detecting the cardiovascular side effects of anti-cancer treatment early and providing digital tools to help patients improve their mental and physical wellbeing.‘
Being more sedentary in childhood leads to a higher left ventricular mass in young adulthood, which is an independent risk factor for cardiovascular events. This was the key finding of a study presented at the recent European Society of Cardiology (ESC) Congress 2023 in Amsterdam.
The study also revealed that this increased risk occurred even in those with a normal weight and blood pressure.
The first study to investigate the cumulative effect of smartwatch-assessed sedentary time in young people and cardiac damage later in life, the researchers asked children aged 11 to wear a smartwatch with an activity tracker for seven days. This was repeated at 15 years of age and again at age 24.
Echocardiography which the imaging modality of choice to assess left ventricular end-diastolic and end-systolic volumes, was used assess the mass of the left ventricle. Measurements were undertaken at ages 17 and 24 years of age and reported in grams relative to height (g/m2.7).
The study enrolled 766 children (55% girls). At 11 years of age, the participants were sedentary for an average of 362 minutes a day. This rose to an average of 474 minutes a day in those 15 years of age, and further still to 531 minutes by age 24.
Sedentary time therefore increased by an average of 169 minutes or 2.8 hours per day between childhood and young adulthood.
The researchers calculated that each one-minute increase in sedentary time from 11 to 24 years of age, was associated with a 0.004 g/m2.7 increase in left ventricular mass between the ages of 17 and 24 years.
When multiplied by 169 minutes of additional inactivity, this equates to a 0.7 g/m2.7 daily rise – the equivalent of a 3 g increase in left ventricular mass between echocardiography measurements at the average height gain.
Study author Dr Andrew Agbaje of the University of Eastern Finland in Kuopio, Finland, said: ‘Children were sedentary for more than six hours a day and this increased by nearly three hours a day by the time they reached young adulthood.
‘Our study indicates that the accumulation of inactive time is related to heart damage regardless of body weight and blood pressure. Parents should encourage children and teenagers to move more by taking them out for a walk and limiting time spent on social media and video games’.
A genetic study has revealed how the use of clopidogrel in British patients of south Asian ancestry appears to be less effective at preventing recurrent myocardial infarction than in those of European descent.
The study, which was published in the journal JACC: Advances, sought to assess the prevalence of common CYP2C19 genotype polymorphisms in a British south Asian population and correlate these with recurrent myocardial infarction risk in participants prescribed clopidogrel.
Researchers used data from the East London Genes & Health (ELGH) database – a community-based, long-term study of health and disease in British Bangladeshi and British Pakistani people in east London. ELGH incorporates cutting-edge genomics with electronic health record data linkage and targeted recall-by-genotype studies.
Using data from 44,396 individuals, researchers found a high prevalence (57%) of intermediate or poor CYP2C19 metabolisers, with at least one loss-of-function CYP2C19 allele.
In addition, the prevalence of poor metabolisers, characterised by two CYP2C19 loss-of-function alleles was 13%, which was higher than that in previously studied European (2.4%) and central/south Asian populations (8.2%).
In the cohort, 69% were diagnosed with an acute myocardial infarction and prescribed clopidogrel. Poor metabolisers were found to be significantly more likely to have a recurrent myocardial infarction (Odds ratio, OR = 3.1, 95% CI 1.2 – 8.1, p = 0.019).
Dr Emma Magavern, lead author from Queen Mary University of London, said: ‘This study highlights the importance of using genetics to determine who can benefit from clopidogrel after a heart attack, and how not doing so is likely to disproportionately disadvantage specific groups, such as south Asians.
‘British peoples of south Asian ancestry suffer from high rates of cardiovascular disease and therefore have both a high risk of needing an anti-platelet medication and a high risk of treatment failure with clopidogrel.’
The P2Y12-inhibiting agent clopidogrel, which can be used post-myocardial infarction to reduce the risk of a second infarction, as well as to lower the risk of bleeding following a percutaneous coronary invention, is metabolised by the hepatic enzyme CYP2C19. This transformation converts the inactive pro-drug into an active metabolite.
25th August 2023
Survivors of a myocardial infarction (MI) who discontinue aspirin remain at an elevated risk of a subsequent infarction, stroke or even death over the next eight years compared to those who remain adherent to treatment.
These were the findings of a a study presented at the recent European Society of Cardiology (ESC) Congress 2023 in Amsterdam.
While the use of aspirin is no longer recommended for use as a primary preventative strategy, despite continued use, especially in the elderly, it remains an essential component of secondary prevention treatment.
Researchers used Danish nationwide health registries to look at patients aged 40 years and over who had a first MI and were prescribed aspirin during the first year after it. Their aim was to examine the extent to which MI survivors collected a prescription for aspirin over the next two, four, six and eight years and the clinical consequences of not taking the drug.
Adherence to aspirin at each of the four time points was assessed as the proportion of days patients had collected the drug over the preceding two years.
Non-adherence was defined when survivors used aspirin for 80% or less of the time and patients were excluded at each time point if they had experienced another heart attack, a stroke, died, or had been started on other anticoagulants or P2Y12 inhibitors.
The researchers analysed whether patients who did not take aspirin as prescribed had a higher risk of the composite outcome of recurrent heart attack, stroke or death compared with those who consistently took aspirin.
The study included 40,114 patients with a first-time MI. Adherence to aspirin progressively declined with each time point, from 90% at two years post-MI, to 84% at four years, 82% at six years and 81% at eight years.
At each of the time-points, adherence to aspirin was associated with a reduced risk of the composite outcome. For example, when compared to adherent patients, non-adherent patients had a 29%, 40%, 31% and 20% higher likelihood of recurrent heart attack, stroke or death at two, four, six and eight years post-MI, respectively.
Commenting on the findings, study author Dr Anna Meta Kristensen of Bispebjerg and Frederiksberg Hospital, Frederiksberg, Denmark, said: ‘Our findings suggest that not taking aspirin as prescribed after a heart attack is linked to a higher risk of having another heart attack, a stroke or dying.‘
However, she added: ‘Our results should be interpreted with caution because they show an association but do not establish causality. Since the study is registry-based, we do not have information about the specific reasons as to why patients did not take their aspirin.
‘Furthermore, our findings cannot be generalised to all patients who experience a heart attack, as our study specifically focused on those who received treatment with a coronary stent and were not taking other medications to prevent blood clot formation.
‘With that in mind, the results support current guidelines recommending long-term aspirin after a heart attack.‘
Recognising the signs and symptoms of a myocardial infarction is linked with faster life-saving treatment and reduced in-hospital mortality, according to a recent study presented at the 2023 European Society of Cardiology (ESC) congress in Amsterdam.
Researchers in the Republic of Korea have found a correlation between symptom recognition, time to treatment and mortality in those experiencing a myocardial infarction.
Although AI-based tools are becoming potentially valuable as an aid to quickly diagnose a myocardial infarction, if patients are capable of recognising the most common symptoms, this too could ensure they receive prompt treatment.
The current study, ‘Effect of symptoms recognition in patients with recurrent acute myocardial infarction: from KRAMI-RCC stratification in acute coronary syndromes’, used data from KRAMI-RCC – a registry of myocardial infarction patients in the Republic of Korea.
Trained nurses consulted with survivors of myocardial infarction, asking them if they recognised six sets of symptoms: chest pain; shortness of breath; cold sweat; radiating pain to the jaw, shoulder or arm; dizziness, vertigo, lightheadedness, loss of consciousness; and stomach ache.
Patients were then classified as ‘recognised symptoms‘ if they could identify at least one symptom, otherwise they were classified as ‘did not recognise symptoms‘.
The study included 11,894 myocardial infarction patients, of whom 90.4% had a first-time event and 9.6% a repeat event. Overall, just over half (52.3%) of patients recognised the symptoms.
The majority of patients (92.9%) could identify chest pain as a symptom. However, only a third (32.1%) identified shortness of breath and cold sweats (31.4%) and just 1.3% recognised stomach ache.
Among 57.4% of patients who correctly identified the symptoms, treatment was received within two hours, compared to 47.2% of those who did not recognise the symptoms.
Moreover, the in-hospital mortality rate was much lower for those able to recognise symptoms (1.5% vs 6.7%).
For patients with recurrent myocardial infarction, the recognition rate was 57.5% for those previously enrolled in KRAMI-RCC and just 14.4% of patients with a first-time myocardial infarction could identify the symptoms.
Study author Dr Kyehwan Kim of Gyeongsang National University Hospital in Jinju, Republic of Korea, said: ‘The findings indicate that education is needed for the general public and heart attack survivors on the symptoms that should trigger calling an ambulance.
‘In our study, patients who knew the symptoms of a heart attack were more likely to receive treatment quickly and subsequently survive. Women, older patients, those with a low level of education and people living alone may particularly benefit from learning the symptoms to look out for.‘
24th August 2023
Artificial intelligence technologies could be utilised to reduce the time needed for contouring during radiotherapy treatment planning, according to draft guidance from NICE.
In June 2023, NICE guidance suggested lower intensity and shorter duration radiotherapy in breast cancer did not impact on breast cancer-related mortality or disease recurrence and therefore served as a suitable alternative to the current standard care.
Now, related draft guidance proposes that artificial intelligence (AI) technologies have the potential to help healthcare professionals to produce contours more quickly, which could improve workflow efficiency.
Evidence made available to NICE’s independent medical technologies advisory committee indicates how AI technologies generally produce similar quality contours of organs at risk as those carried out manually, with most only needing minor edits.
Currently, following a CT or MRI scan, a radiographer has to manually contour an image to highlight organs at risk of radiation damage, lymph nodes and the site of the cancer. The dose of radiotherapy is not only calculated to target the tumour site but also to prevent organs and healthy tissue from being damaged.
Clinical experts advising the independent NICE committee estimated a time saving of 10-30 minutes per plan, depending on the amount of editing needed, while the clinical evidence presented to the committee suggests it may range between three and 80 minutes of time saved per plan.
Sarah Byron, programme director for health technologies at NICE, said: ‘NHS colleagues working on the front line in radiotherapy departments are under severe pressure with thousands of people waiting for scans.
‘The role imaging plays in radiotherapy treatment planning is quite pivotal, so recommending the use of AI technologies to help support treatment planning alongside clinical oversight by a trained healthcare professional could save both time and money.‘
Health and social care secretary Steve Barclay added: ‘It’s hugely encouraging to see the first positive recommendation for AI technologies from a NICE committee, as I’ve been clear the NHS must embrace innovation to keep fit for the future.
‘These tools have the potential to improve efficiency and save clinicians’ thousands of hours of time that can be spent on patient care. Smart use of tech is a key part of our NHS Long Term Workforce Plan, and we’re establishing an expert group to work through what skills and training NHS staff may need to make best use of AI.‘
Patients with greater levels of self-reported pain one year after a myocardial infarction (MI) have a significantly higher risk of subsequent mortality, according to a new study.
It is recognised that in patients with symptomatic chest pain, markers such as coronary artery calcium score and cystatin C levels are linked to a higher risk of all-cause mortality.
In addition, self-reported chronic pain is also linked to a higher risk of adverse cardiovascular outcomes including MI and stroke, independently of established cardiovascular risk factors. The extent to which any post-MI pain impacts on subsequent mortality is to be determined.
To this end, in the recent study, published in the Journal of the American Heart Association, Swedish researchers aimed to examine various levels of pain severity one year after an MI as a potential risk for all-cause mortality.
The team collated data from patients who had a registered MI event between 2004 and 2013 with measurements of potential cardiovascular risk indicators at hospital discharge from the Swedish quality register SWEDEHEART database.
Self-reported levels of experienced pain according to EuroQol-5 dimension instrument were recorded in secondary prevention clinics one year after their hospital discharge. The researchers set the primary outcome as all‐cause mortality.
A total of 18,376 patients with complete data were included in the analysis, and all-cause mortality data were collected up to 8.5 years (median 3.4 years) after the one-year visit. There were 1,067 recorded deaths.
Self-reported moderate pain and extreme pain were reported by 38.2% and 4.5% of included patients, respectively.
In fully adjusted models, the mortality risk among those with self-reported moderate severity pain was 35% higher than for those not reporting pain (hazard ratio, HR = 1.35, 95% CI 1.18 – 1.55, p < 0.0001).
But in those reporting severe pain, the risk was more than doubled (HR = 2.06, 95% CI 1.63 – 2.60, p < 0.0001). In fact, pain was a stronger mortality predictor than smoking.
The researchers suggested that clinicians managing post-MI patients should recognise the need to consider those with self-reported pain as a prognostic factor, which is comparable to persistent smoking, and to address this when tailoring secondary prevention treatments.
17th August 2023
JAK inhibitors are known to increase the risk of major adverse cardiovascular events when used in rheumatoid arthritis, but does this elevated risk also apply when this class of drugs is used in atopic eczema? Clinical writer Rod Tucker investigates.
Since the 1990s, the treatment of severe rheumatoid arthritis (RA) has centred on biologics such as tumour necrosis factor (TNF) inhibitors. However, a better understanding of cell signalling pathways and, in particular, intracellular signal transduction, led to the development of alternative therapies, one of which being oral Janus kinase (JAK) inhibitors. Several of these have been approved for use in RA since 2011.
What’s more, as JAK inhibitors disrupt intracellular signalling through a variety of cytokine and haematopoietic growth factor receptors, this mode of action suggests the drug class may have a much wider role in a number of immune-mediated inflammatory diseases. As such, approvals for JAK inhibitors in Crohn‘s disease, psoriasis and atopic eczema have been seen in recent years.
Despite their apparent effectiveness in RA, a recent post-marketing study has raised safety concerns over JAK inhibitors compared to TNF inhibitors. The Oral Rheumatoid Arthritis Trial (ORAL) was a randomised, post-authorisation, non-inferiority trial designed to evaluate the safety and efficacy of the JAK inhibitor tofacitinib compared to a TNF inhibitor such as etanercept or adalimumab. It focused on patients with RA who were aged 50 or older and had at least one additional cardiovascular risk factor.
The findings were somewhat disturbing. JAK inhibitor use led to a significantly higher incidence of both major adverse cardiovascular events (MACE) and cancers compared to a TNF inhibitor, even though the efficacies were broadly similar.
The ORAL trial served to highlight how JAK inhibitors may increase the risk of MACE when used in patients with RA who are already at an elevated risk due to their condition. Indeed, a meta-analysis of 24 studies with over 111,000 RA patients estimated a 50% higher risk of cardiovascular mortality.
So, with three JAK inhibitors (upadacitinib, baricitinib and abrocitinib) approved for atopic eczema, and representing an important and promising development for its treatment, should dermatologists be concerned over the risk of MACE when using this class of drugs?
Before considering whether JAK inhibitors might increase the risk of adverse cardiovascular sequelae in those with atopic eczema, its worth exploring whether atopic eczema, itself an inflammatory condition, is linked to a higher risk of MACE. After all, such a risk is theoretically possible, given the emerging evidence of the pivotal role of inflammation in the development and progression of both cardiac and vascular diseases.
The current evidence of an association between atopic eczema and MACE is equivocal. Some work, for instance, clearly demonstrates that atopic eczema is associated with increased risk of myocardial infarction compared to the general population. In contrast, another study found no such independent association in women.
Nevertheless, pooling data from several studies does suggest a positive relationship. For example, a 2018 meta-analysis of 15 studies, which included over 3.5 million participants, did show that atopic eczema was independently associated with an increased risk of stroke and myocardial infarction, especially in male subjects and those with more severe disease.
In addition, a recent Danish study, looked at what happened to patients over time following a diagnosis of atopic eczema. It included over 40,000 atopic eczema patients and an equal number of matched controls and found that adults were at a significantly higher risk of experiencing a subsequent cardiovascular disease.
Finally, a UK prospective study including 387,439 patients with atopic eczema followed for over five years, concluded that severe active atopic eczema was associated with an increased risk of cardiovascular outcomes.
While prospective studies are subject to confounding, Mendelian randomisation studies, are able to provide an estimate causality without the influence of confounders. One such study showed that asthma and atopic eczema were causal risk factors for heart failure and suggested that the underlying inflammatory nature of both diseases was a major contributory factor.
As ever, things are never that straightforward. In a recent bidirectional Mendelian randomisation study, it was found that there was no robust association between cardiovascular disease and atopic eczema.
In trying to establish if there was a higher risk of MACE in patients with atopic eczema prescribed a JAK inhibitor, researchers recently undertook a systematic review and meta-analysis. The findings were published in July 2023 in the British Journal of Dermatology and included phase 2b or 3 randomised controlled trials and controlled cohort studies.
The primary outcome was the occurrence of MACE, which the researchers defined as a composite of acute coronary syndrome (ACS), ischaemic stroke and CV death.
A total of 23 studies were included in the analysis. Very few cases of MACE were found, leading the researchers to suggest that JAK inhibitors may have little-to-no effect on the occurrence of MACE in patients with atopic eczema compared to placebo. However, they did add the caveat that the evidence was uncertain.
In addition, MACE generally occurred in patients at a high cardiovascular risk and not in the younger, healthy patients typically seen in routine clinical practice.
Further and reassuring evidence of the absence of a possible association with MACE comes from real-world studies on the use of JAK inhibitors in atopic eczema. There have been at least four such studies, none of which have identified any cases of MACE, even though some have been conducted in patients with more severe disease.
Although patients with atopic eczema may have a higher risk of MACE, this is more likely to occur either in those with severe disease or for patients at a greater risk of cardiovascular disease. Over time, pharmacovigilance data will no doubt shed further light on the level of risk associated with JAK inhibitors.
For now, the European Medicines Agency (EMA) issued advice in January 2023 on the use of JAK inhibitors in all chronic inflammatory disorders, including atopic eczema. This recommended avoiding against the use of a JAK inhibitor in those aged 65 years or above, in patients at an increased risk of major cardiovascular problems, smokers and individuals at a higher risk of cancer, unless there are no suitable alternatives.
For most patients with atopic eczema, JAK inhibitors represent a potentially game-changing addition to a dermatologist’s armamentarium for their treatment. Provided that clinicians heed the current safety guidance, those prescribed a JAK inhibitor for atopic eczema have much to gain but without the attendant risk of MACE.
15th August 2023
With a recent study suggesting that components within espresso coffee extract nullified the adverse effects of the Alzheimer‘s-associated tau protein, is drinking coffee a potential lifestyle preventative measure for reducing the risk of such neurodegenerative conditions? Clinical writer Rod Tucker takes a look at the evidence.
There’s no doubt that coffee is a widely consumed beverage and coffee culture has taken the world by storm from the espresso bars of Italy to the commercial giants on seemingly every street corner. Deemed to be one of the most widely traded commodities in the world, around two billion cups of coffee are consumed worldwide each day, according to the British Coffee Association.
Coffee is prepared and drunk in a number of different ways from dehydrated instant varieties revived by adding boiling water, to the perfect European espresso in which high pressure hot water is passed through 5-7g of finely-ground powder to produce an energising 30 ml serving.
For many years, a large proportion of healthcare professionals advised against drinking coffee, particularly for those with anxiety, arrhythmias, palpitations or tachycardia. This was based on the premise that the stimulant effects of caffeine – of which there’s just over 60mg in a single espresso shot – would most likely exacerbate cardiac arrhythmias. However, there is a lack of evidence to support this view. In fact, it seems that the opposite may be true.
For instance, a meta-analysis of seven observational studies including 115,993 individuals concluded that caffeine exposure is not associated with increased risk of atrial fibrillation, and that it may even be protective.
More recently, a 2022 analysis of data from the UK Biobanks, suggested that two to three daily cups of coffee was associated with a lower incidence of cardiac arrhythmias. But coffee is purported to have a plethora of health benefits, which were extolled in a 2017 umbrella review, which concluded that there were large risk reductions for a range of health outcomes when consuming three to four cups of coffee per day.
One of the intriguing findings identified in the umbrella review was habitual coffee drinking being linked to a 27% lower risk of developing Alzheimer‘s disease. Some of the earliest evidence identifying a possible protective effect against Alzheimer‘s disease, came from a study in 2002.
Using a case-control study, researchers observed a significant and inverse association between caffeine exposure and Alzheimer‘s disease (odds ratio, OR = 0.40, 95% CI 0.25 – 0.67). Moreover, other work appeared to confirm this benefit, with a further study reporting that drinking three to five cups of coffee a day during midlife was associated with a 65% lower risk of developing dementia or Alzheimer‘s disease during later life.
But this observational study evidence can only be used to demonstrate correlation and not causation. That is to say, just because the two factors of coffee and Alzheimer‘s disease are correlated does not mean that one either causes or protects against the other. However, evidence of a plausible biological mechanism, which accounts for this correlation, helps to support the observed relationship.
For instance, it has been found that caffeine prevents the β-amyloid-induced neurotoxicity in cultured cerebellar neurons of rats via blockade of adenosine A2A. In fact, the authors concluded that their study constituted the first in vitro evidence to suggest that blockade of adenosine A2A receptors, may be the molecular target for the observed beneficial effects of consuming caffeine in relation to the development of Alzheimer’s disease.
Despite this biological plausibility, not all observational studies demonstrate a positive relationship between caffeine intake and cognitive disorders. In a 2015 meta-analysis of 19 studies, the authors found that in all 19 studies caffeine intake was not significantly associated with the risk of cognitive disorders including dementia, Alzheimer’s disease, cognitive impairment and cognitive decline (OR = 0.82, 95% CI 0.67 – 1.01).
But if coffee does offer protection against Alzheimer‘s disease, could this arise from components other than caffeine?
With a good deal of research focusing on the possible protective role of coffee, it has also been recognised that coffee is actually a mixture of a number of bioactive compounds. These include polyphenols, especially chlorogenic acids and caffeic acid in roasted coffee beans; alkaloids, such as caffeine and trigonelline; and the diterpenes cafestol and kahweol. So, is it possible that some of these bioactive agents are responsible for the purported protective effect against Alzheimer’s disease?
A recent study set out to address this issue. The researchers used nuclear magnetic resonance to characterise the molecular composition of an espresso coffee extract. Since aggregation of the protein tau is implicated in the pathophysiology of Alzheimer’s disease, the researchers focused on any components that affected this process. In particular, they considered whether any components in the espresso extract could prevent tau aggregation, condensation – which is a purported mechanism initiating aggregation – and the seeding activity of the tau protein whereby further aggregation occurs once tau fibrils have been formed.
The research uncovered several important actions of the espresso coffee extract in relation to tau. First, the extract had an inhibitory effect on tau fibril formation, preventing aggregation and the ability to induce intracellular tau fibrillisation. Second, the extract interfered with early events (condensation), which led to the accumulation of tau. Finally, the tau fibrils that were formed in the presence of the espresso extract not only had a reduced ability to aggregate, but the resulting species displayed either reduced or no cellular toxicity and were unable to ‘seed‘ further aggregation.
Taken together, the findings suggested that the espresso extract was neuro-protective against tau-induced toxicity in cultured cells. In fact, the authors even suggested that ‘based on the bioavailability of coffee components in the brain, and on the results of our study, we expect that moderate coffee consumption may provide a sufficient amount of bioactive molecules to act separately or synergistically as modulators of tau protein aggregation and toxicity‘.
The evidence to date indicates that coffee intake may be a protective factor against Alzheimer‘s disease. Moreover, there is data showing neuro-protective effects for many of the bioactive components within coffee. While much of the evidence is derived from observations studies, one Mendelian randomisation study that avoids the influence of confounders, has shown that genetically predicted higher plasma caffeine levels were associated with a non-significant lower risk of Alzheimer’s disease.
With the totality of the evidence appearing to suggest a possible benefit from drinking coffee in relation to the development of Alzheimer‘s disease, the espresso research was cell-based and therefore preliminary in nature.
Nevertheless, whether drinking espresso coffee over a lifetime might reduce the risk of developing Alzheimer‘s disease remains an intriguing thought and certainly provides basis for future studies.
14th August 2023
Patients who have low vitamin K levels have a reduced ventilatory capacity and are more likely to self-report asthma, COPD or wheezing, according to a study by researchers from Copenhagen University Hospital and the University of Copenhagen.
The study, which was published in the journal ERJ Open Research, set out to assess whether lower vitamin K status was associated with lung function and lung disease/symptoms. The researchers focused on the measurement of dephosphorylated-uncarboxylated MGP (dp-ucMGP), which serves as an inverse plasma biomarker for vitamin K status.
The team recruited members of the general population and invited them to a health examination to complete questionnaires and undergo spirometry, together with measurement of plasma dp-ucMGP. Lung function assessments were the forced expiratory volume during the first second (FEV1) and forced vital capacity (FVC). FEV1/FVC-ratio was calculated as the ratio between these two measurements.
In the questionnaires, researchers asked participants whether they had ever been diagnosed with either asthma or COPD, or whether they had experienced wheezing during the last 12 months. They then used multivariable logistic regression to assess the associations between dp-ucMGP and the dichotomous variables, COPD, asthma and wheezing.
A total of 4,092 individuals aged 24-77 years were included in the analysis.
Lower vitamin K status, reflected by higher dp-ucMGP levels, was associated with lower FEV1 and FVC. However, dp-ucMGP was not associated with the FEV1/FVC-ratio. A lower status was significantly associated with COPD (Odds ratio, OR = 2.24, 95% CI 1.53 – 3.27), wheezing (OR = 1.81 95% CI 1.44 – 2.28) and asthma (OR = 1.44 95% CI 1.12 – 1.83).
Lead author of the study, Dr Torkil Jespersen, said: ‘We already know that vitamin K has an important role in the blood, and research is beginning to show that it’s also important in heart and bone health, but there’s been very little research looking at vitamin K and the lungs.
‘To our knowledge, this is the first study on vitamin K and lung function in a large general population. Our results suggest that [it] could play a part in keeping our lungs healthy.‘
The vitamin is found in leafy green vegetables, vegetable oils and cereal grains. It plays a role in blood clotting, although, clinically, vitamin K antagonists are used as anticoagulants to control bleeding.
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