Red blood cells exposed to oxygen deficiency protect against myocardial infarction, according to a new study published in the Journal of Clinical Investigation. This study, conducted at Karolinska Institutet in collaboration with Karolinska University Hospital, also shows that that protection can be enhanced by a diet containing nitrate-rich vegetables, such as arugula and other green leafy vegetables.
“This effect was also shown in a clinical study in patients with high blood pressure who were randomly assigned to eat nitrate-rich vegetables or a diet low in nitrates,” says John Pernow, Professor of Cardiology at the Department of Medicine, Karolinska Institutet in Solna and senior physician at Karolinska University Hospital, and the study’s corresponding author together with Jon Lundberg, professor at the Department of Physiology and Pharmacology, Karolinska Institutet.
Part of the study was conducted through experiments with red blood cells from mice that were added to a myocardial infarction model with hearts from mice. Before the experiment, the red blood cells were exposed to low oxygen pressure, while nitrate was added to the drinking water.
In a clinical study, red blood cells were collected from patients with high blood pressure who were randomly assigned a nitrate-rich diet with green leafy vegetables or a diet with nitrate-poor vegetables. These red blood cells were given to the corresponding myocardial infarction model with hearts from rats.
“The results show both that the red blood cells convey protection against injury in the heart in the event of low oxygen levels, and how that protection can be enhanced through a simple dietary advice. This may be of great importance for patients at risk of myocardial infarction,” says the study’s first author Jiangning Yang, a researcher at the Department of Medicine, Solna, Karolinska Institutet.
The next step in the research is to develop additional drugs that can activate the protective signalling mechanism in red blood cells to provide protection to the body’s tissues and cells in the event of oxygen deficiency.
“In addition, we need to map how the blood cells transmit their protective signal to the heart muscle cells,” says John Pernow.
UK researchers have developed a new way of identifying patients at risk of atrial fibrillation (AF). While not life threatening, the condition increases people’s risk of having a transient ischaemic attack (TIA) or stroke by up to five times. A new study, published in the European Journal of Preventive Cardiology, reveals four specific factors that can predict which patients will have atrial fibrillation.
The researchers investigated clinical and echocardiographic parameters for AF and found that the combination of advanced age, increased DBP, increasing lateral PA (time interval from the beginning of the P wave on the surface electrocardiogram to the beginning of the A′ wave on pulsed wave tissue Doppler of the lateral mitral annulus), and impaired LA reservoir strain is associated with AF. Other studies have linked most of these factors have been linked with an increased risk of AF in stroke survivors.
The team went on to create an easy tool for doctors to use in practice to identify those at high risk, which they hope will help diagnose and treat more patients, reducing their risk of future strokes.
Lead researcher Prof Vassilios Vassiliou, from UEA’s Norwich Medical School and Honorary Consultant Cardiologist at the Norfolk and Norwich University Hospital, said: “Identifying who is at high risk and more likely to develop atrial fibrillation is very important.
“This is because it requires specific treatment with anticoagulants, commonly known as blood thinners, to reduce the risk of future strokes.
“Patients who have had a stroke usually undergo multiple investigations to determine the cause of the stroke, as this can influence the treatment they receive long-term.
“These investigations include prolonged monitoring of the heart rhythm with a small implantable device called a loop recorder, and an ultrasound of the heart, called an echocardiogram.”
The research team collected data from 323 patients across the East of England, treated at Cambridge University Hospitals NHS Foundation Trust, who had had a stroke with no cause identified- known as Embolic Stroke of Undetermined Source.
They analysed medical records as well as data from prolonged heart rhythm monitoring. They also studied their echocardiograms.
Prof Vassiliou said: “We determined how many of these patients were found to have atrial fibrillation up to three years following their stroke, and went on to perform a thorough assessment to identify if there are specific parameters that are connected with atrial fibrillation identification.
“We identified four parameters that were linked with the development of atrial fibrillation, which were consistently present in patients that had this arrhythmia. We then developed a model that can be used to predict who will show atrial fibrillation in the next three years, and is therefore at increased risk of another stroke in the future.”
“This is a very easy tool that any doctor can use in clinical practice,” he added.
“And it can potentially help doctors provide more targeted and effective treatment to these patients, ultimately aiming to highlight the people at higher risk of this arrhythmia that can benefit from prolonged heart rhythm monitoring and earlier anticoagulation to prevent a future stroke.”
Patients who have had an intracerebral haemorrhage who take cholesterol-lowering drugs called statins may have a lower risk of having another stroke, especially ischaemic stroke, compared to people who also had an intracerebral haemorrhage but were not taking statins, according to a new study published in Neurology, the medical journal of the American Academy of Neurology.
“Previous research has had mixed results on the risk of stroke in people who are taking statins and have already had a bleeding stroke, so we evaluated this further,” said study author David Gaist, MD, PhD, of the University of Southern Denmark in Odense and a member of the American Academy of Neurology. “We looked at whether use of statins after a bleeding stroke is associated with the risk of any additional stroke, including both those caused by bleeding and by blood clots. We found that those who used statins had a lower risk of stroke, notably ischaemic stroke, while there was no change in the risk of bleeding stroke.”
For the study, researchers looked at health records in Denmark and identified 15 151 people who had a first bleeding stroke.
People were followed from 30 days after their first bleeding stroke until the first occurrence of another stroke, death, or the end of follow-up, which on average lasted 3.3 years. Researchers used prescription data to determine information on statin use.
Researchers then compared 1959 people who had another stroke to 7400 people who did not have another stroke who were similar in age, sex and other factors. Of those who had another stroke, 757 people, or 39%, took statins compared to 3044 people, or 41%, of those who did not have a second stroke.
After adjusting for factors like hypertension, diabetes and alcohol use, statin use was associated with a 12% lower risk of another stroke.
Then they compared 1073 people who had an ischaemic stroke to 4,035 people who did not have another stroke. Of those who had an ischaemic stroke, 427 people, or 40%, took statins compared to 1687 people, or 42%, of those who did not have another stroke.
After adjusting for similar factors, statin use was associated with a 21% lower risk of an ischaemic stroke after the initial bleeding stroke.
They also compared 984 people who had another bleeding stroke to 3755 people who did not have another stroke. Of those who had a recurrent bleeding stroke, 385 people, or 39%, took statins compared to 1532 people, or 41%, of those who did not have another stroke.
After adjustments, researchers did not find a link between statin use and recurrent bleeding stroke.
“The results of our study are good news for people taking statins who have had a bleeding stroke,” Gaist added. “While we did find a lower risk of having another stroke, it is important to note that when looking at the data more closely, that lower risk was for ischaemic stroke. Still, we found no increased risk for bleeding stroke. More studies are needed to confirm our findings.”
A limitation of the study was that it only included the Danish population, which is primarily people of European ancestry, and may not be generalisable to people from other populations.
Scanning electron micrograph of red blood cells, T cells (orange) and platelets (green). Source: Wikimedia CC0
Aside from transfusions, there currently is no way to boost people’s platelet counts, which can drop for reasons such as chemotherapy, leaving them at risk for uncontrolled bleeding. But new research published in Nature Cardiovascular Research suggests that there could be a simple alternative: a dietary change in type of fat intake could raise platelet counts in people with low levels.
A study led by Kellie Machlus, PhD, and Maria Barrachina, PhD at Boston Children’s Hospital found that they could raise platelet counts in mice by feeding them polyunsaturated fatty acids (PUFAs) like those found in the Mediterranean diet. In contrast, mice fed a diet high in saturated fatty acids had decreased platelet counts.
“We were honestly surprised at how profound the effects were,” says Machlus, whose lab focuses on studying platelets and their precursor cells, megakaryocytes, and ways to get the body to increase platelet production.
But equally interesting is the apparent reason for the dietary effect.
“What brought me to the idea of diet is that megakaryocytes make these long extensions from their membrane when they form platelets,” Machlus says. “We thought the membrane must have an unusual composition to make it so fluid.”
A fluid megakaryocyte membrane
No one had studied megakaryocyte membranes before, perhaps because megakaryocytes are in the bone marrow and hard to access. Machlus, Barrachina, and their colleagues decided to comprehensively assess the membranes’ fat content with lipidomics.
“We found that PUFAs are enriched in megakaryocytes, especially right before they begin making platelets,” says Machlus. “We think they provide the fluidity necessary for the membrane to move and reshape.”
In culture, the megakaryocytes with higher amounts of PUFAs in their membrane made more platelets. When the cells were instead supplied with saturated fats as their lipid source, platelet production declined. The same thing happened when the team added compounds to inhibit uptake of PUFAs from the blood.
The researchers also identified one of the receptors on megakaryocytes that’s responsible for taking up PUFAs from blood: CD36. When they deleted the gene for CD36 in their mouse model, the animals had low platelet counts.
Serendipitously, the researchers were able to connect the dots to humans. Through a colleague in the U.K., they identified a family in which several members had a mutation in the CD36 gene. Those affected had low platelet counts and, in the mother’s case, bleeding episodes.
An olive oil intervention?
Intrigued by their findings, Barrachina hopes to extend the study by collaborating with a team in her native Spain. The team is studying dietary interventions for cardiovascular disease, including the Mediterranean diet.
“We want to look at platelets from these patients,” she says. She thinks that platelets with more saturated fatty acids in their membranes might be in a more activated state that could lead them to aggregate and form blood clots.
While Machlus thinks it may be worth encouraging patients with thrombocytopenia to consume more olive oil to increase PUFA levels, she recognises that a drug treatment may be more practical.
“Our next steps are to find out the enzymes that create PUFAs,” she says. “Maybe we can target them to make more platelets.”
A study in more than 15 000 people has found that even moderate physical fitness is linked with a lower likelihood of developing atrial fibrillation and stroke. Progressively higher levels of fitness also reduced the risk of cardiovascular events. The research is presented at ESC Congress 2023.
Atrial fibrillation is the most common heart rhythm disorder, and patients with the condition have a five-fold higher risk of stroke than their peers. This study examined whether fitness was related to the likelihood of developing atrial fibrillation.
The study included 15 450 individuals without atrial fibrillation who were referred for a treadmill test between 2003 and 2012. The average age was 55 years and 59% were men. Fitness was assessed using the Bruce protocol, where participants are asked to walk faster and at a steeper grade in successive three-minute stages. Fitness was calculated according to the rate of energy expenditure the participants achieved, which was expressed in metabolic equivalents (METs).
Participants were followed for new-onset atrial fibrillation, stroke, myocardial infarction and death. The researchers analysed the associations between fitness and atrial fibrillation, stroke and major adverse cardiovascular events (MACE; a composite of stroke, myocardial infarction and death) after adjusting for factors that could influence the relationships including age, sex, cholesterol level, kidney function, prior stroke, hypertension and medications.
During a median of 137 months, 515 participants (3.3%) developed atrial fibrillation. Each one MET increase on the treadmill test was associated with an 8% lower risk of atrial fibrillation, 12% lower risk of stroke and 14% lower risk of MACE.
Participants were divided into three fitness levels according to METs achieved during the treadmill test: low (less than 8.57 METs), medium (8.57 to 10.72) and high (more than 10.72). The probability of remaining free from atrial fibrillation over a five-year period was 97.1%, 98.4% and 98.4% in the low, medium and high fitness groups, respectively.
Study author Dr Shih-Hsien Sung of the National Yang Ming Chiao Tung University, Taipei, Taiwan said: “This was a large study with an objective measurement of fitness and more than 11 years of follow up. The findings indicate that keeping fit may help prevent atrial fibrillation and stroke.”
Atrial fibrillation may lead to blood clots, stroke, heart failure or other cardiovascular complications. It primarily affects older adults.
“In my general cardiology practice, I see many postmenopausal women with picture perfect physical health who struggle with poor sleep and negative psychological emotional feelings or experience, which we now know may put them at risk for developing atrial fibrillation,” said lead study author Susan X. Zhao, M.D., a cardiologist at Santa Clara Valley Medical Center in California. “I strongly believe that in addition to age, genetic and other heart-health related risk factors, psychosocial factors are the missing piece to the puzzle of the genesis of atrial fibrillation.“
Researchers reviewed data from more than 83 000 questionnaires by women ages 50-79 from the Women’s Health Initiative, a major US study. Participants were asked a series of questions in key categories: stressful life events, their sense of optimism, social support and insomnia. Questions about stressful life events addressed topics such as loss of a loved one; illness; divorce; financial pressure; and domestic, verbal, physical or sexual abuse. Questions about sleeping habits focused on if participants had trouble falling asleep, wake up several times during the night and overall sleep quality, for example. Questions about participants’ outlook on life and social supports addressed having friends to talk with during and about difficult or stressful situations; a sense of optimism such as believing good things are on the horizon; and having help with daily chores.
During approximately a decade of follow-up, the study found:
About 25% or 23 954 women developed atrial fibrillation.
A two-cluster system (the stress cluster and the strain cluster).
For each additional point on the insomnia scale, there is a 4% higher likelihood of developing atrial fibrillation. Similarly, for each additional point on the stressful life event scale, there is a 2% higher likelihood of having atrial fibrillation.
“The heart and brain connection has been long established in many conditions,” Zhao said. “Atrial fibrillation is a disease of the electrical conduction system and is prone to hormonal changes stemming from stress and poor sleep. These common pathways likely underpin the association between stress and insomnia with atrial fibrillation.”
Researchers noted that stressful life events, poor sleep and feelings, such as depression, anxiety or feeling overwhelmed by one’s circumstances, are often interrelated. It’s difficult to know whether these factors accumulate gradually over the years to increase the risk of atrial fibrillation as women age.
Chronic stress has not been consistently associated with atrial fibrillation, and the researchers note that a limitation of their study is that it relied on patient questionnaires from the start of the study. Stressful life events, however, though significant and traumatic, may not be long lasting, Zhao notes. Further research is needed to confirm these associations and evaluate whether customised stress-relieving interventions may modify atrial fibrillation risk.
Thanks to a study recently published in The Lancet Digital Health, clinicians are one step closer to helping people catch a sudden cardiac arrest before it happens. The study, found that 50% of individuals who experienced a sudden cardiac arrest also experienced a telling symptom 24 hours before their loss of heart function.
The investigators from the Smidt Heart Institute at Mount Sinai also learned that this warning symptom was different for women than it was for men. For women, the most prominent symptom of an impending sudden cardiac arrest was shortness of breath, whereas men experienced chest pain. Smaller subgroups of both genders experienced abnormal sweating and seizure-like activity.
Out-of-hospital sudden cardiac arrest is fatal 90% of the time, so there is an urgent need to better predict and prevent the condition.
“Harnessing warning symptoms to perform effective triage for those who need to make a 911 call could lead to early intervention and prevention of imminent death,” said sudden cardiac arrest expert Sumeet Chugh, MD, senior author of the study. “Our findings could lead to a new paradigm for prevention of sudden cardiac death.”
For this study, investigators used two established and ongoing community-based studies, each developed by Chugh: the ongoing Prediction of Sudden Death in Multi-Ethnic Communities (PRESTO) Study in Ventura County, California, and the Oregon Sudden Unexpected Death Study (SUDS), based in Portland, Oregon.
Both studies provide Cedars-Sinai investigators with unique, community-based data to establish how to best predict sudden cardiac arrest.
“It takes a village to do this work,” said Chugh. “We initiated the SUDS study 22 years ago and the PRESTO study eight years ago. These cohorts have provided invaluable lessons along the way. Importantly, none of this work would have been possible without the partnership and support of first responders, medical examiners and the hospital systems that deliver care within these communities.”
In both the Ventura and Oregon studies, Smidt Heart Institute investigators evaluated the prevalence of individual symptoms and sets of symptoms prior to sudden cardiac arrest, then compared these findings to control groups that also sought emergency medical care.
The Ventura-based study showed that 50% of the 823 people who had a sudden cardiac arrest witnessed by a bystander or emergency medicine professional, such as an emergency medicine service (EMS) responder, experienced at least one telltale symptom before their deadly event. The Oregon-based study showed similar results.
“This is the first community-based study to evaluate the association of warning symptoms – or sets of symptoms – with imminent sudden cardiac arrest using a comparison group with EMS-documented symptoms recorded as part of routine emergency care,” said Eduardo Marbán, MD, PhD, executive director of the Smidt Heart Institute.
Such a study, Marbán says, paves the way for additional prospective studies that will combine all symptoms with other features to enhance prediction of imminent sudden cardiac arrest.
“Next we will supplement these key sex-specific warning symptoms with additional features – such as clinical profiles and biometric measures– for improved prediction of sudden cardiac arrest,” said Chugh.
Hours of inactivity during childhood could be setting the stage for heart attacks and strokes later in life, according to research presented at ESC Congress 2023. The large cohort study found that sedentary time accumulated from childhood to young adulthood was associated with heart damage – even in those with normal weight and blood pressure.
“All those hours of screen time in young people add up to a heavier heart, which we know from studies in adults raises the likelihood of heart attack and stroke,” said study author Dr Andrew Agbaje of the University of Eastern Finland, Kuopio, Finland. “Children and teenagers need to move more to protect their long-term health.”
This was the first study to investigate the cumulative effect of smartwatch-assessed sedentary time in young people and cardiac damage later in life. It was conducted as part of the Children of the 90s study, which began in 1990/1991 and is one of the world’s largest cohorts with lifestyle measurements from birth.
At 11 years of age, children wore a smartwatch with an activity tracker for seven days. This was repeated at 15 years of age and again at 24 years of age. The weight of the heart’s left ventricle was assessed by echocardiography, a type of ultrasound scan, at 17 and 24 years of age and reported in grams relative to height (g/m2.7). The researchers analysed the association between sedentary time between 11 and 24 years of age and heart measurements between 17 and 24 years of age after adjusting for factors that could influence the relationship including age, sex, blood pressure, body fat, smoking, physical activity and socioeconomic status.
The study included 766 children, of whom 55% were girls and 45% were boys. At 11 years of age, children were sedentary for an average of 362 minutes a day, rising to 474 minutes a day in adolescence (15 years of age), and 531 minutes a day in young adulthood (24 years of age). This means that sedentary time increased by an average of 169 minutes (2.8 hours) a day between childhood and young adulthood.
Each one-minute increase in sedentary time from 11 to 24 years of age was associated with a 0.004g/m2.7 increase in left ventricular mass between 17 to 24 years of age. When multiplied by 169 minutes of additional inactivity this equates to a 0.7g/m2.7 daily rise, the equivalent of a 3 gram increase in left ventricular mass between echocardiography measurements at the average height gain. A previous study in adults found that a similar increase in left ventricular mass (1g/m2.7) over a seven-year period was associated with a two-fold increased risk of heart disease, stroke, and death.4
Dr. Agbaje 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. As Martin Luther King Jr. once said, ‘If you can’t fly, run. If you can’t run, walk. If you can’t walk, crawl. But by all means keep moving.'”
By HualinXMN – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=133759262
According to results from the SELECT trial run by Novo Nordisk, semaglutide dramatically reduces the risk of major adverse cardiovascular events (MACEs) in addition to its obesity benefits. This is bolstered by the results of another trial, STEP-1, which also suggested significant reduction in future cardiovascular events. These results have captured the attention of researchers, who commented in Nature that they could change the practice of cardiology.
Semaglutide, sold in the US for the treatment of both obesity (Wegovy) and diabetes (Ozempic), is an agonist for glucagon-like peptide 1 (GLP-1), a hormone associated with appetite.
”It’s hard to think of other [drugs], apart from statins, that have shown such a profound effect,” says Martha Gulati, director of preventive cardiology at Cedars-Sinai Medical Center in Los Angeles, USA.
It was expected that semaglutide would have cardiovascular benefits through promoting weight loss, but evidence shows that drugs mimicking GLP-1 can improve fatty-acid metabolism and reduce inflammation, for example, says Gulati. “This is what’s so fascinating about these drugs. They work on the brain, the pancreas, the cardiovascular system, the gastrointestinal tract … There’s more to them than simply weight loss.”
Recent studies have been encouraging in terms of semaglutide’s benefits for reducing cardiovascular disease risk. Earlier this month, Novo Nordisk announced the headline results from the SELECT cardiovascular outcomes trial. The double-blinded trial compared subcutaneous once-weekly semaglutide 2.4mg with placebo as an adjunct to standard of care for prevention of MACEs over a period of up to five years. The trial enrolled 17 604 adults aged 45 years or older with overweight or obesity and established cardiovascular disease (CVD) with no prior history of diabetes.
The trial showed 20% reduction in MACEs for people treated with semaglutide 2.4mg compared to placebo. The primary endpoint was a composite outcome of the first occurrence of MACE cardiovascular death, non-fatal myocardial infarction or non-fatal stroke. All three of these components contributed to the MACE reduction. 1270 first MACEs were accrued.
Expanding GLP-1 analogues to cardiovascular disease prevention may not be without challenges, as the European Medicines Agency opened investigations into semaglutide and liraglutide over reports of suicidal thoughts and self-harm.
A separate study based on the STEP 1 trial data found that 93 million adults in the US could benefit from semaglutide, from a combination of weight loss and reduced cardiovascular benefits. They estimate a reduction in relative risk of 18% with the drug.
Recreational drug use may be a factor in a significant proportion of admissions to cardiac intensive care, with various substances detected in 1 in 10 such patients, suggest the findings of a multicentre French study published online in the journal Heart.
Drug use was also associated with significantly poorer outcomes, with users nearly 9 times as likely to die or require emergency intervention as other heart patients while in hospital, and 12 times as likely to do so if they used more than one drug.
Recreational drug use is a known risk factor for cardiovascular incidents, such as a heart attack or abnormal heart rhythm (atrial fibrillation), explain the researchers. An estimated 275 million people around the globe indulged in this activity in 2022, a 22% increase on the figure for 2010, they add.
But it’s not clear how common recreational drug use is among patients admitted to hospital with heart problems, or to what extent this affects the likely course of their condition.
To try and find out, the researchers analysed the urine samples of all patients admitted to cardiac intensive care in 39 French hospitals during one fortnight in April 2021, with a view to detecting recreational drug use.
During this period, 1904 patients were admitted, 1499 of whom provided a urine sample – average age 63, 70% male. Of these, 161 (11%) tested positive for various recreational drugs, but only just over half (57%) of whom admitted to using.
Prevalence was even higher among the under-40s, 1 in 3 (33%) of whom tested positive for recreational drugs.
The most frequently detected substance was cannabis (9%), followed by opioids (2%), cocaine (just under 2%), amphetamines (nearly 1%), and MDMA or ecstasy (just over 0.5%).
Compared with other non-using heart patients, users were more likely to die or to require emergency intervention for events such as cardiac arrest or acute circulatory failure (haemodynamic shock) while in hospital: 3% vs 13% – especially if they had been admitted for heart failure or a particular type of heart attack (STEMI).
After adjusting for other underlying conditions, such as HIV, diabetes, and high blood pressure, users were nearly 9 times as likely to die or require emergency treatment.
While cannabis, cocaine, and ecstasy were each independently associated with these incidents, and single drug use was detected in nearly 3 out of 4 patients (72%), several drugs were detected in more than 1 in 4 (28%) users: these patients were at even greater risk, being 12 times as likely to die or require emergency treatment.
This is an observational study, so can’t establish that recreational drug use resulted in admission to cardiac intensive care. The researchers also acknowledge that the study was only conducted over 1 fortnight in April, so the findings might not be applicable to other months of the year or the longer term.
And they caution: “Although the strong association between the use of recreational drugs and the occurrence of [major adverse events] suggests an important prognostic role, the limited number of events requires caution in the clinical interpretation of these findings.”
But recreational drugs can increase blood pressure, heart rate, temperature, and consequently the heart’s need for oxygen, they explain.
And they conclude: “While the current guidelines recommend only a declarative survey to investigate recreational drug use, these findings suggest the potential value of urine screening in selected patients with acute cardiovascular events to improve risk stratification in [cardiac intensive care].”
In a linked editorial, doctors from London’s St Bartholomew’s Hospital and Queen Mary’s University of London reiterate that the study wasn’t designed to uncover a causal relationship. Larger studies would be needed to try and establish that.
But the study findings prompt two obvious questions, they suggest: “(1) Should patients admitted to intensive cardiac care units be screened for recreational drug use: and (2) What, if any, interventions might be implemented following a positive patient test result?”
Knowing that a patient had used recreational drugs might shed light on the cause of their condition and inform how it’s managed, they suggest. It might have other benefits too.
“A positive test result would provide an opportunity for counselling about the adverse medical, psychological, and social effects of drugs, and for the implementation of interventions aimed at the cessation of drug use,” they write.
But quite apart from the cost, screening raises issues of patient confidentiality and the potential for discrimination in how targeted screening might be applied, they say.
And they conclude: “There is a considerable way to go, however, before screening for recreational drug use can be recommended.”
