Publisher Health

A team of researchers led by the National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN) and Osaka University established a new method to measure glomerular filtration rate (GFR), a primary kidney function, by calculating the clearance of D-serine.
The research group evaluated the clearance of D-serine when assessing GFR through the inulin clearance measurement in living kidney transplant donors and recipients. Consequently, they found that the D-serine clearance strongly correlated with GFR and was less biased than the creatinine clearance, a conventional marker for renal function.
Chronic kidney disease is a global problem, and its frequency is increasing with the aging population. Evaluation of GFR is essential for better clinical practice to reduce the number of dialysis patients; however, the current evaluation of GFR has several limitations, including a labor-intensive procedure for the inulin clearance, the gold standard of GFR, a major bias for the creatinine clearance, and imprecise estimation of estimated GFR (eGFR). Endogenous molecules potentiating the precise assessment of kidney function with low biases are still necessary for important clinical decisions, including drug administration design, transplant donor selection, and staging of kidney disease.
L- and D-amino acids are mirror-image enantiomers, and L-amino acids are exclusively present in the human body. “A trace amount of D-serine is present in human blood and reflects kidney function,” says study lead author Masataka Kawamura. He says “We are investigating the potential of D-serine for the precise assessment of kidney function.”
The research group evaluated the urinary excretion rate (clearance) of D-serine in living kidney transplant donors and recipients. The clearance of D-serine was calculated based on the D-serine levels in the blood and urine that, measured using a two-dimensional high performance liquid chromatography system, which is the most accurate and sensitive system for measuring D-amino acids.
Remarkably, the clearance of D-serine agreed well with GFR. The low bias as a measure of GFR was an advantage for the D-serine clearance. The degree of bias against GFR was smaller than that of the creatinine clearance. Additionally, the combinational analysis of clearances of D-serine and creatinine could measure GFR with high performance.
“D-Serine turned out to be of great clinical importance,” says the study senior author of the study, Tomonori Kimura. According to him, “D-Serine may solve the problem of kidney disease with more than 800 million patients in the world. Measuring D-serine is applicable in a wide range of clinical fields and for drug development.”
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For decades, psychiatrists routinely used both psychotherapy (talk therapy) and medication to treat patients. This is hardly the case anymore, according to a new study out of Columbia University.
The switch to medication management has swept psychiatric practices. Researchers analyzing 21 years of data across the U.S found that between 1996 and 2016 the percentage of psychiatrist visits involving psychotherapy had declined by half — dropping to only 21.6 % of patient visits.
By the mid-2010s, over half of U.S. psychiatrists no longer practiced any psychotherapy at all, and that number has likely fallen more since.
The study, published Dec. 8 in the American Journal of Psychiatry, finds that the decline in psychiatrists’ provision of psychotherapy did not affect all patient groups equally.
Older, white patients in the Northeast and the West who pay for treatment out of pocket were impacted less by these declines and still retained access to a small class of psychiatrists who saw fewer patients, saw them more often, and were more likely to provide them with psychotherapy. For other patient groups — and in particular for younger, rural, Black or Hispanic patients and those relying on public insurance to pay for care — receiving talk therapy from their psychiatrists has become exceedingly rare.
While declines in American psychiatrists’ practice of psychotherapy were first observed in the 1980s and tracked up to the mid-2000s, little was known about the phenomenon in the period since.

Scientists who injected idle mice with blood from athletic mice found improvements in learning and memory. The findings could have implications for Alzheimer’s research and beyond.What if something in the blood of an athlete could boost the brainpower of someone who doesn’t or can’t exercise? Could a protein that gets amplified when people exercise help stave off symptoms of Alzheimer’s and other memory disorders?That’s the tantalizing prospect raised by a new study in which researchers injected sedentary mice with blood from mice that ran for miles on exercise wheels, and found that the sedentary mice then did better on tests of learning and memory.The study, published Wednesday in the journal Nature, also found that the type of brain inflammation involved in Alzheimer’s and other neurological disorders was reduced in sedentary mice after they received their athletic counterparts’ blood.Scientific results with mice don’t necessarily translate to humans. Still, experts said the study supports a growing body of research.“We’re seeing an increasing number of studies where proteins from outside the brain that are made when you exercise get into the brain and are helpful for improving brain health, or even improving cognition and disease,” said Rudolph Tanzi, a professor of neurology at Massachusetts General Hospital and Harvard Medical School. He led a 2018 study that found that exercise helped the brains of mice engineered to have a version of Alzheimer’s.The most promising outcome would be if exercise-generated proteins can become the basis for treatments, experts said.“The demonstration that there are transferable factors in the blood that seemed to convey beneficial effects on the brain that improve learning and memory is by far the most interesting aspect of the work,” said Dr. Madhav Thambisetty, a neurologist and senior investigator at the National Institute on Aging, who was not involved in the new research.The study, led by researchers at Stanford School of Medicine, found that one protein — clusterin, produced in the liver and in heart muscle cells — seemed to account for most of the anti-inflammatory effects. But several experts noted that recent studies have found benefits from other proteins. They also said more needs to be learned about clusterin, which plays a role in many diseases, including cancer, and may have negative effects in early stages of Alzheimer’s before brain inflammation becomes dominant.“It’s far too premature to conclude that higher or lower levels of clusterin might be either beneficial or not,” said Dr. Thambisetty, who has studied clusterin. “I don’t think we’re at the stage yet where people can trade in their treadmills or cancel their gym memberships for a clusterin pill or a clusterin injection.”The study was led by Tony Wyss-Coray, a professor of neurology and neurological sciences at Stanford, who had previously done research finding that the blood of young mice can reverse age-related cognitive impairment in old mice.Dr. Wyss-Coray said he wanted to see “if exercise produced factors that would also accumulate in the blood and that you could then transfer them.”The study involved mice that were about three months old — roughly the equivalent of 25-to-30-years-old for humans. Some of the mice, nocturnal animals that love to run, could freely use exercise wheels in their cages and logged about four to six miles on the wheels each night. The wheels were locked for other mice that could scoot around their cages but could not get an extended cardio workout.After 28 days, the researchers took a third group of mice that also did not exercise and injected them with blood plasma, the liquid that surrounds blood cells, from either the runner mice or the non-runner mice. Mice receiving runner blood did better on two tests of learning and memory than those receiving blood from the non-runner mice.In one test, which measures how long a mouse will freeze in fear when it is returned to a cage where it previously received an electric foot shock, mice with runner blood froze 25 percent longer, indicating they had better memory of the stressful event, Dr. Wyss-Coray said. In the other test, mice with runner blood were twice as fast at finding a platform submerged in opaque water, he said.The team also found that the brains of mice with runner blood produced more of several types of brain cells, including those that generate new neurons in the hippocampus, a region involved in memory and spatial learning.A genetic analysis showed that about 1,950 genes had changed in response to the infusion of runner blood, becoming either more or less activated. Most of the 250 genes with the greatest activation changes were involved in inflammation and their changes suggested that brain inflammation was reduced.The team tested whether removing any of the four most significant proteins in the runner blood would matter, and found that if clusterin was removed, anti-inflammatory effects disappeared. And when mice engineered to have a type of brain inflammation or a version of Alzheimer’s were injected with clusterin, it lessened their brain inflammation.In the only part of the study involving humans, 20 military veterans with a pre-dementia condition called mild cognitive impairment who had participated in a six-month exercise program were found to have high levels of clusterin in their blood.Kaci Fairchild, associate director of the Department of Veterans Affairs Sierra Pacific Mental Illness Research, Education and Clinical Center, and an author of the new study, said the veterans, ranging in age from 50 to 89, exercised three times a week, combining cardio with weight training.Dr. Fairchild said that in results that have not yet been published, besides having elevated clusterin, the veterans did better on tests involving word memory and story recall.“Across the board, veterans had improvements in cognitive function, largely related to learning and memory,” Dr. Fairchild said. Noting that some people have disabilities or limitations that prevent them from exercising, she said she hoped that “the implications from this clusterin is that we can develop a medication targeting this protein for persons who weren’t able to engage in physical activity.”In the brain, clusterin binds to cells that line the blood vessels, cells that become inflamed in Alzheimer’s disease, Dr. Wyss-Coray said, suggesting that a potential drug might bind to those cells and “mimic the anti-inflammatory effects.”Still, experts who study Alzheimer’s disease and neuroinflammation said much more research is needed before therapies can be developed.“Not everything that works in mice works in humans, and we don’t know if there are other unexpected side effects that could make it untenable in humans,” said Mark Gluck, a professor of neuroscience and public health at Rutgers University in Newark, N.J., who was not involved in the study.Dr. Michael Heneka, the incoming director of the Luxembourg Centre for Systems Biomedicine who was not involved in the study, said the role of inflammation in diseases processes can change over time, being protective early on and detrimental later, so it is important to target inflammation at the appropriate time.It’s also unclear if clusterin is the optimal protein for a therapy.Other proteins linked to physical exercise have been shown in recent studies to improve cognition in mice. One, irisin, released by muscles, was found to reduce neuroinflammation and help mice perform better on memory and learning tests. Another, called Gpld1, an enzyme produced in the liver, was shown to increase after exercise and to correlate with better cognitive function in elderly mice.Whichever proteins end up being promising, it would be safer to develop a medication than to try to transfuse blood, which would contain other things beside the proteins, said Dr. Tanzi, who was not involved in the new study. “The big question,” he added, “is which proteins are the winners and how do we take advantage of them to provide new therapies?”

Among 52 incentives to exercise, giving people a 9-cent award if they returned to the gym after missing a workout helped the most.Receiving a tiny monetary reward at the right moment could play an outsize role in motivating us to exercise, according to a large-scale and innovative new study of how to nudge people to show up at the gym.The study, published today in Nature, involved 61,293 American gym members, 30 prominent scientists working at 15 universities, and more than 50 different motivational programs. In addition to reward points, incentives ranged from a free audiobook for gym use to cheery instructions from researchers to reframe exercise as fun. While some of the programs galvanized additional gym visits, others, including some the scientists had absolutely expected to inspire more exercise, did not.The study’s findings, positive and the reverse, offer timely insights into how the rest of us might better motivate ourselves to keep our upcoming New Year’s exercise resolutions. But just as important, the study, in its ambition, scope and structure, is meant to serve as a road map for future investigations into the mysteries of human behavior and why so many of us act as we do and sometimes, despite our best intentions, keep skipping that next spin class.The science of human behavior, including whether and why we exercise, can be squishy and rife with research hurdles. Many past studies have looked at how to build habits, for instance, or instill confidence or stick to an exercise routine. But the vast majority of those studies have been small-scale or homogeneous, recruiting only affluent, well-educated white people, for example, or healthy, young college students, or only men or only women.Those studies have also used a wide range of methods to track behavior change, making it difficult to compare data from one study to another. In addition, many have relied on subjective measures, such as asking people how they feel during and after a study, a topic on which we can be, intentionally or not, untrustworthy. The result has been a replication crisis in behavior science, with researchers unable to repeat the findings of many past studies, calling the original results into question.These issues naturally concerned Katy Milkman, a professor at the Wharton School of the University of Pennsylvania and author of the 2021 book “How to Change” (one of Well’s favorite health books of the year) and her colleague Angela Duckworth, also a professor at Wharton and author of the 2016 best seller “Grit.” Among the foremost behavioral scientists at work today, they were convinced their field could and should become more scientifically rigorous, which led them to begin noodling with the notion of megastudies.A megastudy, as they defined the concept, would be large in scale, involving thousands of participants, and not the dozens commonly used in behavioral research. It would also randomly expose large groups of volunteers to a range of behavior modifications or other interventions, employing objective measures to assess whether an intervention had actually worked.These ideas brought the research team to the 24 Hour Fitness chain. Already, they had decided that one of their first megastudies would concentrate on exercise behavior, in part because it is easy to measure increases or declines in workouts and visits to the gym, but also because encouraging people to exercise more can alter lives by boosting health.With its nationwide network of hundreds of gyms, 24 Hour Fitness offered the researchers millions of potential participants for their massive study. Then they invited dozens of other scientists to come up with interventions they felt would up people’s willingness to work out. They also created an umbrella program, called “Step Up,” which gym members could choose to join, earning Amazon reward points worth about $1.00 once they did. The “Step Up” program promised to provide them with new ways to motivate themselves to work out.Michelle V. Agins/The New York TimesMore than 61,000 members joined the “Step Up” program, after which the scientists divided them into 53 groups. One group, which served as a control, changed nothing about their lives or gym time. The others were then assigned to receive a basic package of motivational help that included advice to plan the exact day and time of each workout, a texted reminder from the research team about those plans, and a minuscule reward if they did work out, worth about 22 cents in reward points. These kinds of efforts can be key to increasing motivation, the researchers felt, and would serve as a baseline test of whether the study was inspiring people to exercise more.On top of this basic package of reminder texts and small rewards, the researchers then randomly assigned the gym members who were not in the control group to one of 52 different motivational programs developed by the researchers. In one, for example, the members earned reward points worth about $1.75 every time they visited the gym; in others, they shared their workouts with friends on social media, signed a fitness pledge to show up regularly or agreed to reflect after each workout on how it had affected them. Each group included at least 455 participants. Each intervention lasted a month.Before and during that month, the researchers tracked how often people turned up at their gym. They also asked outside exercise and behavior experts which interventions they expected would be most successful.The results surprised almost everyone. Dr. Duckworth, for one, told me she had thought encouraging people to view workouts as fun would get them to the gym more often, but that group showed only a minuscule increase in gym visits. (Almost everyone in the intervention groups worked out a bit more often than the people in the control group.)The most successful intervention, though, turned out to be giving people the equivalent of 9 cents’ worth of reward points if they returned to the gym after missing a planned workout. That program increased gym visits by about 16 percent, compared to the baseline package of planning and text reminders. Almost as effective was simply giving people a bigger reward, worth $1.75, every time they worked out. It increased exercise by about 14 percent, compared to the baseline package.Over all, the findings suggest that if we want to exercise regularly in 2022, we should, in general:Plan a reasonable workout schedule;Program reminders of that schedule into our phone or with an admonitory spouse or training buddy; andFind small ways to reward ourselves when we exercise as planned. Drop a dollar into a bowl for every workout, for instance, and let the proceeds mount.Perhaps most important, though, the study’s results show, we should “try not to miss more than one workout,” Dr. Milkman said. Getting ourselves back to the gym or pool or walking trail or cycling path after skipping one session might have special potency in helping us show up for the next workout, and the next after that.Of course, this study, large and complex as it is, involved only people interested enough in fitness to join a gym, so the results may not apply to everyone else. The interventions also lasted only a month, which could be too short to see behaviors change. Dr. Duckworth and Dr. Milkman, who now co-direct the Behavior Change for Good Initiative at Wharton, are planning other megastudies, related not only to encouraging exercise, but also other major health issues, such as vaccination hesitancy.

Older people taking a drug used to treat anxiety and insomnia — nitrazepam — as well as those on antidepressants, are twice as likely to suffer postoperative delirium after hip and knee surgery, a new Australian study has found.
The finding has prompted calls by University of South Australia (UniSA) researchers for older patients to temporarily cease these medications or change to safer alternatives prior to surgery.
In a study published in the international journal Drug Safety, UniSA scientists scanned data from 10,456 patients aged 65 years and older who had undergone knee or hip surgery in the past 20 years. A quarter of them (2614 people) had experienced delirium after surgery.
Apart from nitrazepam and antidepressants, five other benzodiazepine medications — commonly prescribed for anxiety, seizures and insomnia — were associated with delirium, although not to the same extent. They included sertraline, mirtazapine, venlafaxine, citalopram and fluvoxamine.
Lead researcher Dr Gizat Kassie says there was no link between pain-relieving opioids and delirium.
“Our findings show that different classes of medicine are riskier than others when it comes to causing delirium after surgery, and the older the patients are, the greater the risk,” he says.

Recent theoretical breakthroughs have settled two long-standing questions about the viability of simulating quantum systems on future quantum computers, overcoming challenges from complexity analyses to enable more advanced algorithms. Featured in two publications, the work by a quantum team at Los Alamos National Laboratory shows that physical properties of quantum systems allow for faster simulation techniques.
“Algorithms based on this work will be needed for the first full-scale demonstration of quantum simulations on quantum computers,” said Rolando Somma, a quantum theorist at Los Alamos and coauthor on the two papers.
Low-energy quantum states key to faster quantum simulation
The paper “Hamiltonian simulation in the low-energy subspace” demonstrates that the complexity of a quantum simulation algorithm depends on the relevant energy scale and not the full range of energies of the system, as previously thought. In fact, some quantum systems can have states of unbounded energies, hence simulations would prove intractable even on large quantum computers.
This new research found that, if a quantum system explores the low-energy states only, it could be simulated with low complexity on a quantum computer without errors crashing the simulation.
“Our work provides a path to a systematic study of quantum simulations at low energies, which will be required to push quantum simulations closer to reality,” said Burak Şahinoğlu, a theoretical physicist at Los Alamos and lead author on the paper, published in the journal Quantum Information, a Nature partner journal.

Researchers at the University of Virginia School of Medicine have made a discovery linking lupus, a potentially debilitating autoimmune disorder, and macular degeneration, a leading cause of blindness.
The two diseases share a common contributor to harmful inflammation, the scientists found. The insights could let researchers develop new treatments for those diseases and other conditions driven by the newly discovered inflammation source.
“We were quite surprised at the common link between lupus and macular degeneration,” said Jayakrishna Ambati, MD, of UVA’s Department of Ophthalmology and the founding director of UVA’s Center for Advanced Vision Science. “It appears that the new inflammatory pathway we identified could be therapeutically targeted for many chronic diseases.”
Macular Degeneration and Lupus
Ambati and his collaborators have discovered an unknown role for an inflammasome — an agent of the immune system — called NLRC4-NLRP3. Inflammasomes play an important role in marshaling the body’s defenses to protect it from invaders such as viruses and bacteria.
In lupus and atrophic macular degeneration, however, it appears that NLRC4-NLRP3 contributes to harmful inflammation, the UVA researchers found. In lupus, it helps drive the hyperactive immune response that leads to symptoms such as joint pain, rash, fever and more. In macular degeneration, meanwhile, NRC4-NLRP3 appears to contribute to inflammation that destroys the vital light-sensing cells in the eye’s retina.
Ambati’s new work helps explain why. The inflammasome, he found, is sent into action by a special class of genetic material called “short interspersed nuclear element RNAs,” or SINE RNAs. This type of RNA makes up more than 10% of our genomes, and it activates in response to cell stresses such as infection, genetic damage and aging. The resulting inflammation caused by SINE RNAs can be harmful in many chronic diseases.
SINE RNAs are elevated in both macular degeneration and lupus, Ambati found. In addition to discovering the role of SINE RNA in the two diseases, Ambati and his colleagues identified an unknown receptor for the SINE RNAs called DDX17. Scientists have been looking for this receptor for decades, and the new discovery helps them better understand the process that leads to the harmful inflammation.
“These findings indicate that blocking a single inflammasome might not be enough, and that targeting both the NLRC4 and NLRP3 inflammasomes would be a superior strategy,” Ambati said.
Using this new information, scientists may be able to target the source of harmful inflammation in lupus, macular degeneration and other diseases driven by SINE RNAs. That could lead to new treatments to benefit patients, the UVA researchers say.
“We’re excited to have developed drugs called Kamuvudines that block this dual inflammasome, which we anticipate will be in clinical trials next year,” Ambati said.
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A combination of vaccination and naturally acquired infection appears to boost the production of maximally potent antibodies against the COVID-19 virus, new UCLA research finds.
The findings, published in the peer-reviewed journal mBio, raise the possibility that vaccine boosters may be equally effective in improving antibodies’ ability to target multiple variants of the virus, including the delta variant, which is now the predominant strain, and the recently detected omicron variant. (The study was conducted prior to the emergence of delta and omicron, but Dr. Otto Yang, the study’s senior author, said the results could potentially apply to those and other new variants.)
“The main message from our research is that someone who has had COVID and then gets vaccinated develops not only a boost in antibody amount, but also improved antibody quality — enhancing the ability of antibodies to act against variants,” said Yang, a professor of medicine in the division of infectious diseases and of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA. “This suggests that having repeated exposures to the spike protein allows the immune system to continue improving the antibodies if someone had COVID then been vaccinated.”
(The spike protein is the part of the virus that binds to cells, resulting in infection.)
Yang said it is not yet known whether the same benefits would be realized for people who have repeated vaccinations but who have not contracted COVID-19.
The researchers compared blood antibodies in 15 vaccinated people who had not been previously infected with SARS-CoV-2, the virus that causes COVID-19, with infection-induced antibodies in 10 people who were recently infected with SARS-CoV-2 but not yet vaccinated. Several months later, the 10 participants in the latter group were vaccinated, and the researchers then reanalyzed their antibodies. Most people in both of the groups had received the Pfizer-BioNTech or Moderna two-dose vaccines.
The scientists evaluated how antibodies acted against a panel of spike proteins with various common mutations in the receptor-binding domain, which is the target for antibodies that help neutralize the virus by blocking it from binding to cells.
They found that the receptor-binding domain mutations reduced the potency of antibodies acquired both by either natural infection or vaccination alone, to about the same degree in both groups of people. When previously infected people were vaccinated about a year after natural infection, however, their antibodies’ potency was maximized to a point that they recognized all of the COVID-19 variants the scientists tested.
“Overall, our findings raise the possibility that resistance of SARS-CoV-2 variants to antibodies can be overcome by driving further maturation through continued antigenic exposure by vaccination, even if the vaccine does not deliver variant sequences,” the researchers write. They suggest that repeated vaccinations may have the capacity to accomplish the same thing as getting vaccinated after having had COVID-19, although further research will be required to address that possibility.
The study’s other authors are F. Javier Ibarrondo, Christian Hofmann, Ayub Ali, Paul Ayoub and Dr. Donald Kohn, all of UCLA.
The study was funded by the AIDS Healthcare Foundation and various private donors.
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Materials provided by University of California – Los Angeles Health Sciences. Original written by Enrique Rivero. Note: Content may be edited for style and length.

New research suggests early warning signals (EWSs) could help in the monitoring of disease outbreaks, such as COVID-19. The study, led by the University of Bristol, found warnings could be detected weeks earlier than any rapid increase in cases. The findings could help governments and policy makers improve the accuracy of their decisions and allow timely interventions if needed.
Using a novel, sequential analysis combined with daily COVID-19 case data across 24 countries, the research, published today [8 December] in Biology Letters, suggests EWSs can predict COVID-19 waves. The researchers found that warnings were regularly detectable prior to exponential cases changes. but the reliability of these signals depended on the amount of time between successive waves of infection and the mathematical likelihood of a critical transition, Consequently, EWSs showed highest accuracy for waves that experienced a suppressed R number over a long period before the outbreak.
As the ongoing COVID-19 pandemic has shown, being able to identify rapid increases in cases before they occur is important for people to modify their behaviours, and to inform government actions.
Duncan O’Brien in Bristol’s School of Biological Sciences said: “We’ve always been aware that any technique that’s able to predict the appearance of disease would be useful in protecting human health. This has never been more apparent with the global COVID-19 pandemic and the many discussions around when governments should put interventions in place.
“Our research found that hotly debated early warning signals were most reliable before the second COVID-19 wave that was experienced by many, and whilst these signals performed less well for the first and third waves, any rapid increase in cases could be identified well in advance.
“There is a lot of conflicting evidence surrounding EWS use in epidemiology and ecological monitoring in general, so we hope some the methodological points we raise in this work helps others disentangle the complicated behaviour of these warnings.”
EWSs’ interpretation can be difficult when using real world data due to their need for specific mathematical conditions. However, recent conceptual work relaxing some of these requirements is supported in this study but has generally been discounted during the use of EWSs in epidemiology. The next steps for research are therefore to explore how the methodological differences published today improve generic assessments of disease dynamics.
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International guidelines developed to help doctors diagnose cow’s milk allergy may lead to over-diagnosis, according to University of Bristol-led research published in the journal Clinical and Experimental Allergy today [8 December]. The study found that three-quarters of infants have two or more symptoms at some point in the first year of life which guidelines say may be caused by cow’s milk allergy, yet the condition only affects one in 100.
Cow’s milk allergy can present with either acute or delayed symptoms. Delayed symptoms are more varied and include gut and skin symptoms, such as posseting (bringing up milk) and vomiting, colic, loose stools or constipation, and flaring of eczema. Many of these symptoms are already known to be common in infants, making delayed cow’s milk allergy difficult to diagnose.
Researchers found that one in four parents reported two or more possible “mild to moderate” symptoms every month. Symptoms were most numerous at three months of age, when all children were fully breastfed and not directly consuming cow’s milk. At six months of age, there was no difference in the number of children with two or more symptoms between those consuming and not consuming cow’s milk. Together, these findings suggest that the majority of symptoms listed in cow’s milk allergy guidelines are common, normal and not caused by cow’s milk allergy.
Dr Rosie Vincent, Honorary Clinical Research Fellow at the Centre for Academic Primary Care, University of Bristol who led the research, said: “Guidelines, designed to help the non-specialist to diagnose cow’s milk allergy in infants may unintentionally medicalise normal infant symptoms and promote over-diagnosis of cow’s milk allergy.”
Senior co-researcher and children’s allergy doctor, Dr Michael Perkin, from the Population Health Research Institute at St George’s, University of London, added: “Our findings come against a background of rising prescription rates for specialist formula for children with cow’s milk allergy, which is completely out of proportion to how common we know the condition is. Parents of young infants are often seen in clinics, worried about a medical cause for their infant’s symptoms such as colic, bringing up milk or loose stools. However, our research confirms that these symptoms are extremely common. In an otherwise healthy infant, an underlying cause is unlikely. Incorrectly attributing these symptoms to cow’s milk allergy is not only unhelpful, but it may also cause harm by discouraging breastfeeding.”
The researchers (from the University of Bristol, St George’s, University of London, Imperial College London, King’s College London, and St John’s Institute of Dermatology), used data from the Enquiring About Tolerance study of 1,303 infants aged between three and twelve months, in which parents were asked to record any symptoms their child experienced on a monthly basis. They counted how many infants had cow’s milk allergy symptoms each month, as defined in the international Milk Allergy in Primary Care (iMAP) guideline.
Professor Matthew Ridd, a GP and senior co-researcher at the Centre for Academic Primary Care, University of Bristol, said: “Our study was based on iMAP but our results are likely to apply to other cow’s milk allergy guidelines. Well-meaning guidelines need to be supported by robust data to avoid the harms from over-diagnosis, which may be greater than the damage of delayed diagnoses that they seek to prevent.”
The research was funded by the International Society of Atopic Dermatitis (ISAD) and supported by the National Institute for Health Research. The EAT study was funded by the UK Food Standards Agency.
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