Publisher Health

Since the 1960s, researchers have postulated that major depression stems from disruptions in the serotonin neurotransmitter system, but the evidence for that idea, though plentiful, was indirect. In fact, a recent comprehensive analysis of existing studies concluded that there was not strong evidence to support the “serotonin hypothesis.” In its wake, some in the field have called for a reexamination of the hypothesis. Not so fast, says a new study that provides direct evidence of disrupted serotonin release in the brains of individuals with depression.
The study appears in Biological Psychiatry, published by Elsevier.
Depression is among the most common mental illnesses and causes of disability worldwide. Despite the lack of direct evidence for disrupted serotonin signaling in the depressed brain, medications used to treat depression overwhelmingly target the serotonin signaling system to increase extracellular serotonin, also known as 5-hydroxytryptamine (5-HT). Only about half of patients respond to antidepressants, and fewer than 30% experience total remission. A better understanding of 5-HT dynamics in depression could help guide more effective therapies.
“Our thinking about the role of serotonin in depression has evolved significantly over the past decade. We once thought that serotonin changes could account for the entirety of depression. When this simple hypothesis could no longer be supported, some were inclined to dismiss any role for serotonin in depression,” said John Krystal, MD, editor-in-chief of Biological Psychiatry. “The current study provides important new support for further exploration of the role of serotonin in depression. This is particularly timely, as drugs targeting serotonin receptors, such as psychedelics, are being explored as potential new treatments for mood disorders.”
The study, conducted by Invicro, a global, imaging contract research organization, in collaboration with researchers from Imperial College London, King’s College London, Copenhagen University, and the University of Oxford, used a novel imaging technique to look directly at the magnitude of serotonin released from neurons in response to a pharmacological challenge. In previous work, these researchers pioneered the use of positron emission tomography (PET) with the radioligand [11C]Cimbi-36 to detect serotonin release. In the current study, the researchers applied this methodology to compare serotonin release in 17 patients with depression and 20 healthy individuals.
David Erritzoe, MRCPsych, PhD, lead author of the paper, said, “This study used a new and more direct method to measure serotonin in the living human brain, and the results suggest reduced serotonin (release) functioning in depression. This imaging method, in combination with similar methods for other brain systems, has the potential to help us to better understand the varying — sometimes limited or even lacking — treatment responses that people with depression have to antidepressant medication.”
Participants with depression and healthy controls underwent PET scanning with [11C]Cimbi-36 to measure 5-HT2A receptor availability in the frontal cortex; the two groups did not differ significantly at baseline. Both groups then received a dose of d-amphetamine, a stimulant drug that works to increase 5-HT concentration outside of neurons, where it interacts with 5-HT2A receptors and reduces the binding of [11C]Cimbi-36. In a second scanning session three hours after drug administration, healthy control participants had significantly reduced 5-HT2A receptor availability, indicating an increase in serotonin levels. Participants with depression, however, did not show a significant decrease in binding potential, suggesting they had a blunted serotonin release capacity in key brain regions.
The study found no relationship between the severity of depression and the extent of serotonin release capacity deficits. Of note, all patients were free of antidepressant medication, and 11 out of the 17 had never received antidepressant treatment, indicating that low serotonin release capacity is a feature of depression rather than a result of antidepressant treatment.
This first direct evaluation of serotonin levels in the brain of individuals with depression is a major step forward in laying to rest the speculations questioning the involvement of serotonergic neurotransmission in the pathology of depression. Depression is a multifaceted disorder that may have multiple causes, and different subtypes may involve multiple neurotransmitter systems. Serotonergic dysfunction is unlikely to explain all the clinical features encountered in this disorder. Nevertheless, this study demonstrates that serotonergic deficits are present in unmedicated depressed individuals.
Eugenii Rabiner, MBBCh, FCPsych SA, at Invicro and senior author of the paper said, “It has taken our field over 20 years to develop a method that enables the measurement of serotonin release in the living human brain. I am very pleased that we managed to develop this method and apply it to clarify this important aspect of the pathophysiology of depression. I hope that we can use this technique in future to explore the different symptoms of depression, as well as serotonergic deficits found in other conditions, such as Parkinson’s disease.”
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Drug overdoses in the United States have risen sharply in the last two decades. Nearly 92,000 people died from overdoses of illegal drugs and prescription opioids in 2020 — more than five times the number of deaths in the year 2000 — and synthetic opioids like fentanyl are one of the main culprits.
Naloxone (an injectable medicine also marketed as the nasal spray Narcan) has saved countless lives, but it only works for opioid overdoses and has other limitations. Now, in an effort to identify a more universal treatment for drug overdose, a team of University of Maryland scientists tested a chemical compound — Pillar[6]MaxQ (P6AS) — as an antidote for methamphetamine and fentanyl. Their findings, published today in the journal Chem, were highly promising.
“Opioids already have a reversal agent in naloxone, but there are a variety of non-opioid drugs of abuse — like methamphetamine, PCP, mephedrone, ecstasy (MDMA) and cocaine — that do not have a specific antidote,” said the study’s lead author Lyle Isaacs, a professor in the Department of Chemistry and Biochemistry at UMD. “That’s one of the huge opportunities for our compound.”
In vitro and in vivo laboratory tests showed that P6AS successfully sequestered fentanyl and methamphetamine, a non-opioid stimulant, and mitigated their potentially deadly biological effects. Additional in vitro tests revealed that P6AS also binds strongly to other drugs, including PCP, ecstasy and mephedrone, which suggests that P6AS could someday be used to counteract a wide array of drugs.
The study was conducted by Isaacs’ lab in collaboration with researchers in UMD’s Department of Cell Biology and Molecular Genetics and Department of Psychology. Although the synthesis and chemical properties of P6AS were first documented in 2020 by Isaacs and Weijian Xue, a former post-doctoral associate in the Department of Chemistry and Biochemistry, this study reports its first in vivo applications.
P6AS works as a molecular container, which means that it binds and sequesters other compounds in its central cavity.

Thousands of nurses in England, Wales and Northern Ireland have begun the first of two day-long strikes over pay.We hear from three nurses who work for the NHS, explaining why they have walked out from their jobs for 12 hours.Live updates on this story here.

A large VA clinical trial found that the blood pressure drug chlorthalidone (CTD) was not superior to hydrochlorothiazide (HCTZ) for the prevention of cardiovascular disease or non-cancer death.
Both drugs are in a class of medications called thiazide diuretics, commonly known as water pills. They are used to help the body rid itself of excess fluid, which can lower blood pressure.
The study was a first-of-its-kind pragmatic trial that was embedded in usual clinical care. As part of VA’s clinical trials enterprise, it allowed participation from across the country with no additional staff. Also, all study procedures were done as part of routine clinical care. There was no additional burden placed on Veterans who participated in the study, including no extra visits.
“Because of the number of Veterans VA cares for and our systemwide electronic medical record, we were able to embed this massive clinical trial within day-to-day care without any additional burden to the thousands of Veterans who volunteered for this study,” said Rachel Ramoni, VA’s chief research and development officer. “The result is important evidence of how these widely-used medications work in the real world.”
Current clinical guidelines say that CTD may be more effective than HCTZ to lower blood pressure, but this recommendation is unsupported by direct evidence. Both medications have been used for more than 50 years and each is considered a first-line treatment for hypertension.
“In 2020, Medicare reported that approximately 1.5 million people were prescribed CTD compared to 11.5 million prescribed HCTZ, despite guideline recommendations,” said principal investigator Dr. Areef Ishani, director of the Minneapolis VA Health Care System’s Primary Care and Specialty Care Integrated Care Community. “This discrepancy between clinical guidelines and real-world usage is possibly related to the belief that CTD has a greater risk of adverse effects without clear evidence for differences in cardiovascular outcomes.”
The Diuretic Comparison Project (CSP 597) is a large pragmatic clinical trial that was conducted at 537 VA medical centers and community clinics in the U.S. The trial enrolled more than 4,000 providers and 13,500 Veterans with high blood pressure who were taking HCTZ at baseline. Study participants were randomized to stay on their current dose of HCTZ or take an equivalent dose of CTD. Ninety-five percent of study participants were taking a lower dose of HCTZ, so the main study comparison was 12.5 mg CTD to 25 mg HCTZ.
The team found no difference between the two drugs, at these lower doses, for the prevention of cardiovascular disease or non-cancer death, which included heart attack, stroke, heart failure, or lack of blood flow requiring medical intervention. There was a slight increase in the risk for low potassium in the CTD group, which quickly resolved with potassium supplements.
“We were able to compare two commonly prescribed generic drugs using a low-cost methodology,” said Ishani. “This trial has shown that large, embedded trials are operationally feasible. They can be incorporated into the clinical workflow of providers by leveraging the electronic health record and other existing infrastructure.”
The study was funded by the VA Cooperative Studies Program. The study results were published online December 14, 2022, by the New England Journal of Medicine.
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Materials scientists at UNSW Sydney have shown that human pluripotent stem cells in a lab can initiate a process resembling the gastrulation phase — where cells begin differentiating into new cell types — much earlier than occurs in mother nature.
For an embryo developing in the womb, gastrulation occurs at day 14. But in a dish in a lab at UNSW’s Kensington campus, Scientia Associate Professor Kris Kilian oversaw an experiment where a gastrulation-like event was triggered within two days of culturing human stem cells in a unique biomaterial that, as it turned out, set the conditions to mimic this stage of embryo development.
“Gastrulation is the key step that leads to the human body plan,” says A/Prof. Kilian.
“It is the start of the process where a simple sheet of cells transforms to make up all the tissues of the body — nerves, cardiovascular and blood tissue and structural tissue like muscle and bone. But we haven’t really been able to study the process in humans because you can’t study this in the lab without taking developing embryonic tissue.”
“So it’s really exciting that we were able to see this happening in vitro.”
The achievement, which was reported today in the journal Advanced Science, has not only implications for our understanding of human embryonic development, but also new treatments in medicine including cell therapy, targeted drug development and CRISPR gene-editing technologies.

Dementia is a growing global public health concern currently affecting 50 million people and is expected to rise dramatically to more than 150 million cases worldwide by 2050. Obesity, commonly measured by body mass index (BMI), continues to be a global epidemic and earlier studies suggested that obesity at midlife may lead to increased risk for dementia. But the association between BMI and the risk of dementia remains unclear.
Now, researchers from Boston University Chobanian & Avedisian School of Medicine and Chinese Academy of Medical Sciences & Peking Union Medical College, have found that different patterns of BMI changes over one’s life course may be an indicator of a person’s risk for dementia.
“These findings are important because previous studies that looked at weight trajectories didn’t consider how patterns of weight gain/stability/loss might help signal that dementia is potentially imminent,” explained corresponding author Rhoda Au, PhD, professor of anatomy and neurobiology.
Through the Framingham Heart Study, a group of participants was followed for 39 years and their weight was measured approximately every 2-4 years. The researchers compared different weight patterns (stable, gain, loss) among those who did and did not become demented.
They found the overall trend of declining BMI was associated with a higher risk of developing dementia. However, after further exploration, they found a subgroup with a pattern of initial increasing BMI followed by declining BMI, both occurring within midlife, which appeared to be central to the declining BMI-dementia association.
Au points out that for individuals, family members, and primary care physicians, it is relatively easy to monitor weight. “If after a steady increase in weight that is common as one gets older, there is an unexpected shift to losing weight post midlife, it might be good to consult with one’s healthcare provider and pinpoint why. There are some potential treatments emerging where early detection might be critical in the effectiveness of any of these treatments as they are approved and become available,” she adds.
The researchers hope this study will illustrate that the seeds for dementia risk are being sowed across many years, likely even across the entire lifespan. “Dementia is not necessarily inevitable and monitoring risk indicators such as something as easy to notice as weight patterns, might offer opportunities for early intervention that can change the trajectory of disease onset and progression.”
These findings appear online in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
Funding for this study was provided by the Non-profit Central Research Institute Fund of Chinese Academic of Medical Science (2021-JKCS-023), the Framingham Heart Study’s National Heart, Lung, and Blood Institute contract (N01-HC-25195), the National Institute on Aging (AG016495, AG008122, AG033040, AG062109, AG049810, AG054156, AG062109, AG068753), National Institute of Neurological Disorders and Stroke (R01-NS017950) and VMF-14-318524 from the Alzheimer’s Association and Pfizer.
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For the longest time, clinicians have treated cardiovascular disease by focusing on diabetes and blood pressure control, reducing cholesterol using medications like aspirin and statins.
Despite these measures, heart disease remains the number one cause of death in the United States, with many patients having heart attacks even after their risk factors are controlled, says Salim Hayek, M.D., physician-scientist and medical director of the University of Michigan Health Frankel Cardiovascular Clinics.
But a study led by Michigan Medicine has uncovered a protein produced by the immune system that causes atherosclerosis — the hardening of arteries that affects over a billion people worldwide — which offers the promise of new treatments.
“Targeting the immune component central to the development of atherosclerosis is the Holy Grail for the treatment of heart disease,” said Hayek, senior author of the study “This is the first time that a component of the immune system is identified that meets all the requirements for being a promising treatment target for atherosclerosis.”
This protein, called soluble urokinase plasminogen activator receptor, or suPAR, is produced by the bone marrow. It acts as a regulator, essentially a thermostat for the activity of the immune system, or “immunostat.”
Past studies have shown suPAR to be a marker of cardiovascular disease. But this study, published in the Journal of Clinical Investigation, is the first evidence showing that the protein actually causes atherosclerosis when at high levels.

Millions of people across the globe regularly consume arsenic-contaminated water. Exposure to arsenic has previously been associated with the development of various cancers including skin cancer. Research on the underlying molecular mechanisms regulating arsenic-mediated carcinogenesis remains sparse. Using in vitro studies, researchers from Japan demonstrate how calcitriol, or activated vitamin D3, inhibits arsenic-mediated carcinogenesis in certain types of skin cells known as “keratinocytes.”
According to recent estimates, over 140 million people from 50 countries regularly get exposed to arsenic through drinking water. The exposure level significantly exceeds the guideline value (10 μg/L) stipulated by the World Health Organization. It is an established fact that chronic arsenic exposure from drinking water causes a variety of cancers including skin cancer. Unfortunately, there is a general paucity of data on the underlying biological mechanisms that regulate arsenic-mediated carcinogenesis. Moreover, methods for the prevention and treatment of arsenic-mediated carcinogenesis have remained elusive thus far.
Researchers at the Shibaura Institute of Technology (SIT) and Nagoya University have recently been able to identify the underlying biological mechanisms of carcinogenesis inhibition. Using in vitro studies, the research team has been able to demonstrate how calcitriol, or activated vitamin D3, inhibits arsenic-mediated carcinogenesis in certain types of skin cells known as “keratinocytes.” These cells are primarily found in the epidermis, the outermost layer of the skin. It is a scientifically established fact that certain signaling molecules — kinase proteins (e.g., MEK or “AKT”) that control the fate of various biological processes — are strongly associated with tumor development.
Professor Ichiro Yajima from the Unit of Molecular and Cellular Toxicology, Department of Bioscience and Engineering, SIT, who led the research team, says, “Our in vitro study in human nontumorigenic HaCaT skin keratinocytes showed that calcitriol, which is also known as activated vitamin D3 or 1,25-dihydroxy-vitamin D3, inhibited arsenic-mediated anchorage-independent growth with downregulations of cancer-related activation of several signaling pathways, including MEK, ERK1/2, and AKT, as well as activity of cell cycle.”
To elucidate the relationship between arsenic uptake and calcitriol treatment, the researchers measured arsenic levels in HaCaT cells — long-lived, spontaneously immortalized human epidermal keratinocytes — treated with calcitriol using an inductively coupled plasma-mass spectrophotometer. Quite interestingly, arsenic levels in HaCaT cells cultured with arsenic significantly decreased when these cells were treated with increasing doses of calcitriol. The findings from their study have been published in the American Journal of Cancer Research.
Dr. Masashi Kato, who serves as a Professor at the Department of Occupational and Environmental Health, Nagoya University, Japan, and is a collaborator on the study, adds, “Calcitriol significantly repressed arsenic uptake in HaCaT cells with the regulation of expressions of aquaporin genes (AQP7, 9, and 10), which were modified by arsenic exposure. Vitamin D receptor expression was significantly increased by arsenic exposure whereas calcitriol had no effect on the expression of the receptor.”
The researchers then sought to understand whether calcitriol had an inhibitory effect on arsenic-induced tumorigenesis in cells other than skin keratinocytes. To this end, they performed anchorage-independent growth assays using a human normal lung epithelial cell line called “Beas-2b.” The results of these assays were equally astonishing: arsenic-mediated anchorage-independent growth of Beas-2b cells treated with calcitriol was suppressed by 21.4-70.0%, suggesting that calcitriol’s potential to suppress arsenic-induced tumorigenesis is not restricted to keratinocytes.
Prof. Yajima muses, “These results suggest that calcitriol suppresses arsenic-induced tumorigenesis not only in keratinocytes, but also in other target cells including lung epithelial cells. Furthermore, the expression pattern of aquaporin genes involved in arsenic uptake, a critical step in arsenic-induced carcinogenesis, is significantly altered by calcitriol treatment. We therefore believe that activated vitamin D3, or calcitriol, may contribute to the prevention and therapy for arsenic-mediated diseases including cancer.”
Environmental toxins such as arsenic contribute significantly to the development of life-threatening diseases such as cancer. However, it may take years, even decades, for cancer to develop from drinking arsenic-contaminated water. The current research clearly indicates that calcitriol could be used as a test compound for validating the safety and efficacy of activated vitamin D3 and/or its analogs in preventing or treating arsenic-triggered cancer. Taking vitamin D3 beforehand in arsenic-contaminated areas may reduce the risk of cancer development 5 or 10 years later and help people maintain good health for a long time. This is certainly welcome news for millions of people forced to survive on polluted water worldwide.

Published2 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Madeline HalpertBBC News, WashingtonUS households are once again able to order free at-home Covid-19 tests, as the government attempts to limit the spread of the virus this winter.The White House said up to four rapid tests could be ordered from the government website CovidTests.gov.It announced that the test programme, which was paused in September, would be restarted on Thursday with deliveries beginning the week of 19 December.The decision comes as Covid infections rise ahead of the winter holidays. The Biden administration began sending free at-home tests in January, but stopped in September after more than 600 million tests were distributed because Congress did not approve the extra funding needed for the programme to continue.But the government is now using funding left over from the American Rescue Plan, the Covid relief bill that was passed last year, to pay for the tests, a US official told the BBC’s US partner CBS. “We feel confident that we are going to have enough tests to get through this round, four per household, in the coming weeks,” a senior administration official told reporters on Wednesday,It is part of a broader White House plan to prepare for Covid this winter, when some Americans are at an increased risk of catching the virus as they gather indoors for the holidays. Three reasons Biden’s Covid bill was a big dealDoctors urge holiday caution as RSV and flu riseSurging viruses stretch US children’s hospitalsThe White House said it hoped to encourage Americans to take at-home tests when they are symptomatic, before and after travelling for the holidays and when visiting vulnerable individuals.Covid cases, hospital visits and deaths have all begun to rise in recent weeks. Some cities are calling on Americans to wear masks again in indoor spaces to prevent the spread of respiratory illnesses, while White House officials have urged Americans to get the latest Covid and flu jabs.Only 13.5% of those aged five and older in the US have received the updated coronavirus shot targeting the omicron variant, according to the CDC. Highly contagious omicron subvariants – which are now the dominant coronavirus strains in the US – are contributing to the uptick in cases.You might also be interested in: This video can not be playedTo play this video you need to enable JavaScript in your browser.More on this storyDoctors urge holiday caution as RSV and flu rise30 NovemberCovid-19 pandemic is over in the US – Joe Biden20 SeptemberBiden buys 500m test kits to tackle Omicron surge21 December 2021

Doctors fail to recognize serious conditions like stroke and sepsis in tens of thousands of patients each year, according to a new study.As many as 250,000 people die every year because they are misdiagnosed in the emergency room, with doctors failing to identify serious medical conditions like stroke, sepsis and pneumonia, according to a new analysis from the federal government.The study, released Thursday by the Agency for Healthcare Research and Quality, estimates roughly 7.4 million people are inaccurately diagnosed of the 130 million annual visits to hospital emergency departments in the United States. Some 370,000 patients may suffer serious harm as a result.Researchers from Johns Hopkins University, under a contract with the agency, analyzed data from two decades’ worth of studies to quantify the rate of diagnostic errors in the emergency room and identify serious conditions where doctors are most likely to make a mistake. Many of the studies were based on incidents in European countries and Canada, leading some officials of U.S. medical organizations to criticize the researchers’ conclusions.While these errors remain relatively rare, they are most likely to occur when someone presents with symptoms that are not typical, like stroke patients complaining the room is spinning.A doctor may not immediately think that a young woman with shortness of breath is having a heart attack or that someone who has back pain could have a spinal abscess.“This is the elephant in the room no one is paying attention to,” said Dr. David E. Newman-Toker, a neurologist at Johns Hopkins University and director of its Armstrong Institute Center for Diagnostic Excellence, and one of the study’s authors.The findings underscore the need to look harder at where errors are being made and the medical training, technology and support that could help doctors avoid them, Dr. Newman-Toker said. “It’s not about laying the blame on the feet of emergency room physicians,” he said.In reviewing the studies, the researchers also found that women and people of color had a roughly 20 to 30 percent higher risk of being misdiagnosed. While these results are not surprising, they point to the need to address how different patients are assessed in the emergency room as part of the effort to improve care, said Jennie Ward-Robinson, the chief executive of the Society to Improve Diagnosis in Medicine. “Equity must be core and must be fundamental,” she said.Medical societies representing emergency room doctors strongly criticized the study. “In addition to making misleading, incomplete and erroneous conclusions from the literature reviewed, the report conveys a tone that inaccurately characterizes and unnecessarily disparages the practice of emergency medicine in the United States,” Dr. Christopher S. Kang, the president of the American College of Emergency Physicians, said in a statement.“As with all medical specialties, there is room for improvement in the diagnostic accuracy of emergency care,” Dr. Kang added. “All of us who practice emergency medicine are committed to improving care and reducing diagnostic error.”Doctors say addressing diagnostic errors is challenging. While the National Academy of Medicine identified medical errors as a critical issue more than 20 years ago, most of the efforts to improve patient safety have focused on mistakes that are easier to identify, like when a patient gets the wrong medicine or develops an infection while in the hospital, said Dr. Robert Wachter, the chairman of medicine at the University of California, San Francisco, who had not seen the full report. “Diagnostic errors are a huge part of the problem,” he said.The deaths that the report suggests occur every year “is a very concerning number,” Dr. Wachter said. The study’s findings are higher than previous estimates, he noted.The researchers largely relied on studies conducted outside the United States, in countries like Canada, Spain and Switzerland, to come with up with their overall estimate of error and harm rates. But Dr. Kang argued the reliance on these studies may have distorted the findings and led the researchers to overestimate the number of mistakes. “While most medical specialties have similar training in Western nations, emergency medicine does not,” he said.The study’s authors acknowledged the need to do more research looking specifically at emergency rooms in the United States. “We need studies done in the United States,” said Dr. Susan M. Peterson, a Johns Hopkins emergency medicine physician who is also one of the study’s authors. “It’s a huge gap in the literature.”But she also emphasized the benefit of paying more attention when doctors tend to miss a crucial diagnosis. In recent years, she said, doctors have become much better at detecting heart attacks because of a concerted effort involving public health campaigns, better diagnostic testing, and collaboration between cardiologists and emergency medicine doctors to address the issue.Experts also emphasized that while the study focused on those mistakes made in emergency rooms, where a harried doctor, dealing with overcrowding, must make a quick decision about what is wrong with a patient, the issue of misdiagnosis is a common problem among all doctors.“The bottom line is diagnosis is hard,” said Dr. Doug Salvador, an infectious disease specialist who is the board president of the Society to Improve Diagnosis in Medicine and the chief quality officer at Baystate Health in Springfield, Mass.The researchers found that teaching hospitals were less prone to errors. Emergency room doctors working at an academic medical center may be able to consult with a specialist who is familiar with patients who have atypical symptoms, and they may have more resources to offer a wider range of tests or to keep patients longer while they figure out what’s wrong.The study also suggested that doctors were more likely to miss specific diseases. A patient with a spinal abscess, for example, is more frequently misdiagnosed than someone having a heart attack.Some doctors warn that the answer is not simply to do more testing. “This is a really complicated calibration problem,” Dr. Wachter said. “The answer can’t be let’s test everybody for all this stuff all the time,” he said.The Johns Hopkins researchers say there needs to be more effort to understand how to avoid the most deadly errors, including thinking about how doctors are trained and what kinds of technology could help alert them to a possible missed diagnosis. “This is going to have to be a sustained effort, and that requires resources and support,” Dr. Newman-Toker said.Not enough money is being spent on how to improve diagnosis despite its role in improving care, Dr. Peterson said. “A lot of research dollars are focused on treatment,” she said. “That’s a little more sexy than diagnosis.”