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New research — which studied genomic changes in different types of brain cell — has yielded a potentially surprising result: many of the changes in Alzheimer’s disease are in brain cells other than neurons, the cells that actually die as the disease progresses. The cutting-edge research also revealed a number of new genes not previously implicated in dementia, which could be targets for future drug development.
The study, led by the University of Exeter and published in Nature Communications, is the largest of its kind to look at DNA methylation in Alzheimer’s disease. DNA methylation is the process by which the activity of genes is regulated, acting a bit like a dimmer-switch to turn genes on or off. Increasingly, this process is thought to have a key role in the development of diseases such as dementia.
So far, research on DNA methylation in the brain has only been able to look at “bulk” samples of post-mortem tissue. In other words, scientists have been limited to looking at average levels of DNA methylations across all the different cell types in a piece of brain tissue. Now, the Exeter team has developed a technique to “purify” the cell populations, meaning they can see DNA methylation activity in each distinct cell type for the first time.
Research lead Jonathan Mill, Professor of Epigenomics at the University of Exeter Medical School, said: “Our study has enabled us to explore the changes associated with the development of dementia across individual populations of cells. It’s often assumed that these changes primarily occur in neurons, but surprisingly we found much more dramatic shifts in non-neuronal cell-types. This means we can start to understand more about the mechanisms involved in disease and identify pathways that might be targetable by novel drugs.”
The research utilised 631 brain samples donated to the Brains for Dementia Research cohort, which included people who died with Alzheimer’s disease. From each person, the team dissected two distinct regions of the cortex that are affected differently in Alzheimer’s disease. Each donor had very comprehensive measures of the pathology of the brain taken at post-mortem, providing the team with very detailed information about the progression of the disease.
Professor Mill added: “Our study highlights the power of using multiple measures of neuropathology to identify epigenetic signatures of Alzheimer’s disease, as well as the importance of looking at the activity of different types of cell, and when and how they are activated in disease. The generosity of the people who donated their brains for research has allowed us to make these exciting discoveries and could hold the key to finding new treatments for Alzheimer’s disease.”
The study was funded by Alzheimer’s Research UK, Alzheimer’s Society and the Medical Research Council.
Dr Richard Oakley, Associate Director of Research, at Alzheimer’s Society, said: “We need to understand how the diseases that cause dementia develop to find the very best treatments. This Alzheimer’s Society funded study is a fantastic example of using a gold standard resource in understanding dementia, through brains generously donated by people who lived with dementia to Brains for Dementia Research, which we’re proud to co-fund.
“The results here form another piece of the puzzle — it’s not just the nerve cells which are affected in Alzheimer’s disease, but also the other types of cells in the brain which support them. We’ve known that changes to genes in these cells are involved, but this shows for the first time that changes to the ‘dimmer switches’ which turn these genes on and off in the brain’s support cells also play a key role in the development of Alzheimer’s disease. Through an exciting, cutting-edge technique, this was the first time researchers were able to examine these changes in specific groups of brain cells. Further research will enable researchers to pinpoint exactly what is going wrong inside brain cells to cause dementia, and will inform how we develop new targeted treatments for the different diseases of the brain that cause dementia, which are so desperately needed for people living with dementia today and in the future.”
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The presence of some fungal species in tumors predicts — and may even help drive — worse cancer outcomes, according to a study from Weill Cornell Medicine and Duke University researchers.
The study, which appears Sept. 29 in Cell, provides a scientific framework to develop tests that delineate specific fungal species in tumors that are relevant for prediction of cancer progression and therapy. The results also point to the possibility of using antifungal treatments to augment conventional cancer treatments in some cases.
“These findings open up a lot of exciting research directions, from the development of diagnostics and treatments to studies of the detailed biological mechanisms of fungal relationships to cancers,” said senior author Dr. Iliyan Iliev, associate professor of immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.
The first author of the study was Anders Dohlman, a doctoral student in biomedical engineering at Duke University.
The idea that viruses and bacteria can trigger or accelerate cancer development is now well established. However, little is known about the cancer-related roles of fungi — which, like bacteria and viruses, colonize the gut, lungs, skin and other barrier tissues, interact with the immune system, and sometimes cause disease.
In the new study, researchers catalogued fungal species and their associations with different cancers by analyzing The Cancer Genome Atlas, the largest well-annotated genomic database of human tumors.

You may not realize it, but each time you recall a memory — like your first time riding a bike or walking into your high school prom — your brain changes the memory ever so slightly. It’s almost like adding an Instagram filter, with details being filled in and information being updated or lost with each recall.
“We’re inadvertently applying filters to our past experiences,” says Steve Ramirez (CAS’10), a Boston University neuroscientist. Even though a filtered memory is different from the original, you can tell what that basic picture is for the most part, he says.
“Memory is less of a video recording of the past, and more reconstructive,” says Ramirez, a BU College of Arts & Sciences assistant professor of psychological and brain sciences. The malleable nature of memory is both a blessing and curse: it’s bad if we remember false details, but it’s good that our brains have the natural ability to mold and update memories to make them less potent, especially if it is something scary or traumatic.
So, what if it’s possible to use the malleable nature of our memories to our advantage, as a way to cure mental health disorders like depression and post-traumatic stress disorder (PTSD)? That is exactly what Ramirez and his research team are working to do. And after years of studying memory in mice, they’ve found not only where the brain stores positive and negative memories, but also how to turn the volume down on negative memories by artificially stimulating other, happier ones.
“Our million-dollar idea is, what if a solution for some of these mental disorders already exists in the brain? And what if memory is one way of getting there?” Ramirez says. In two new papers, he and his team demonstrate the power of our emotional memories and how our experiences — and the way we process them — leave actual physical footprints on the brain.
Mapping Positive and Negative Memories
One of the most important steps toward using memory to treat memory-related disorders is understanding where positive and negative memories exist in the brain, and how to distinguish between the two. Memories are stored in all different areas across the brain, and the individual memories themselves exist as networks of cells called engrams. Ramirez’s lab is particularly interested in the networks of memories located in the brain’s hippocampus, a cashew-shaped structure that stores sensory and emotional information important for forming and retrieving memories.

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A new study from the Garvan Institute of Medical Research shows how rises in core body temperature may trigger the inflammatory flares in people with a rare genetic autoinflammatory disease.
The recessive disorder, called mevalonate kinase deficiency (MKD), is caused by mutations in the gene for mevalonate kinase, an essential enzyme present in all cells in the body. Lack of this enzyme leads to a build-up of abnormal proteins, which causes cells of the immune system to malfunction and trigger inflammation.
The condition usually appears in early childhood, and patients experience regular episodes of high fever and skin rashes, ulcers, swollen lymph nodes and abdominal pain. Very severe disease also causes neurological and developmental problems and can be fatal.
“Our research provides exciting new insights into the underlying physiology of MKD and what may be triggering the inflammatory flares, opening up potential new ways of treating this devastating disorder,” says Professor Mike Rogers, Head of the Bone Therapeutics lab at Garvan.
The new study is published in the Journal of Clinical Investigation.
“There has been very little progress in understanding MKD, and in particular, what causes disease flares in MKD patients. One of the main reasons for this lack of knowledge is the absence of appropriate animal models to study the mechanisms of disease,” says Garvan’s Dr Marcia Munoz, lead author of the study.

New epigenetic biomarkers to predict more aggressive forms of prostate cancer have been discovered by scientists at the Garvan Institute of Medical Research.
The biomarkers can be used in combination with traditional clinical tools to predict if a man will go on to develop a more metastatic and lethal form of the disease and could help clinicians to develop a better treatment plan.
“There’s a need for men with prostate cancer to have more personalised treatments guided by the nature of their tumours, and they can’t get that without new biomarkers that can better predict the risk of developing the lethal form the disease,” says Professor Susan Clark, Head of the Epigenetic Research lab at Garvan and lead researcher of the study.
Prostate cancer is, globally, the second most common cancer diagnosed in men. After diagnosis, about 50 percent of men will develop metastatic cancer during their lifetime. Typically, metastasis takes 15 or more years to develop, but a small percentage of men develop a fatal, metastatic form much earlier after diagnosis.
By identifying patients who might go on to develop this form of prostate cancer at the early stages, clinicians could begin more aggressive treatments earlier.
The new study is published in the journal, Clinical and Translational Medicine.
This is one of the most long-term and comprehensive molecular studies of prostate cancer progression. The slow progression of the disease makes studying its biology difficult.

An enzyme called Fic, whose biochemical role was discovered at UT Southwestern more than a dozen years ago, appears to play a crucial part in guiding the cellular response to stress, a new study suggests. The findings, published in PNAS, could eventually lead to new treatments for a variety of diseases.
“We think that Fic acts like a thermostat that adjusts a cell’s response to stressors. If we could gain control of that thermostat and set it how we want in different tissues, we might someday be able to slow or even stop progression of some diseases,” said Amanda Casey, Ph.D., Assistant Professor of Molecular Biology and former postdoctoral fellow in the Orth lab at UTSW. Dr. Casey co-led this study with Kim Orth, Ph.D., Professor of Molecular Biology and a Howard Hughes Medical Institute Investigator.
Originally discovered in the Vibrio parahaemolyticus bacteria known to cause food poisoning, Fic has been a longtime focus of the Orth lab. In 2009, Dr. Orth and her colleagues published the first paper showing that Fic is involved in a process called AMPylation, in which this enzyme facilitates transfer of a phosphate and adenosine group to other proteins, changing their activity. The researchers soon discovered that animals ranging from worms to humans also have a Fic enzyme.
Research in fruit flies suggested that Fic appeared to be important for stress resilience and recovery. A paper published in 2018 by Dr. Orth and Dr. Helmut Krämer, Ph.D., Professor of Neuroscience and Cell Biology at UTSW, and colleagues showed that flies constantly exposed to bright light, which damages their eyes, suffered permanent harm if their Fic gene was deleted through genetic engineering. However, the role of this enzyme in mammals was unclear.
To answer this question, the researchers engineered a mouse model without a Fic gene. These animals were initially indistinguishable from littermates with Fic and appeared healthy. However, when the researchers fasted the animals for 14 hours and then allowed them to eat as much as they wanted for two hours — a stressor for the pancreas, which controls blood sugar and produces key digestive enzymes — blood work on the Fic-deficient animals showed a much higher stress response than the animals with Fic. Further investigation showed that a molecular pathway called the unfolded protein response (UPR) — which becomes activated when stressed cells can’t keep up with folding newly generated proteins — was more strongly activated in the Fic-deficient animals.
The researchers made similar findings when the mouse models were dosed with a drug called caerulein, which acts on the pancreas to force an increased output of digestive enzymes. Although animals with Fic and those without developed pancreatitis, those without this enzyme had significantly worse disease, accompanied by a significantly stronger UPR.
Interestingly, although animals with Fic had a quick recovery, those without Fic developed permanent scarring in their pancreas — a sign of significantly lower resilience to stress, Dr. Casey said.
Dr. Orth added that an uncontrolled cellular stress response and UPR play a role in many diseases including cancer, metabolic syndrome, atherosclerosis, retinal degeneration, and various neurodegenerative disorders.
“If we can determine how the ‘stress thermostat’ is set, we could adjust it up or down in various diseases where stress response is a factor,” she said.
Other UTSW researchers who contributed to this study include Hillery F. Gray, Suneeta Chimalapati, Genaro Hernandez, Andrew Moehlman, Nathan Stewart, Hazel A. Fields, Burak Gulen, Kelly A. Servage, Karoliina Stefanius, Aubrie Blevins, Bret Evers, and Helmut Kramer.
This research was funded by grants from The Welch Foundation (I-1561), the Once Upon a Time Foundation, the National Institutes of Health (R35 GM130305 and EY10199), and a Life Sciences Research Foundation Fellowship.
Dr. Orth holds the Earl A. Forsythe Chair in Biomedical Science and is a W.W. Caruth, Jr. Scholar in Biomedical Research. She is a member of the Harold C. Simmons Comprehensive Cancer Center.

Despite decades of medical advances, children who develop the pediatric eye cancer retinoblastoma often lose their vision or an eye due to a lack of specific, targeted therapies and a poor molecular understanding of the cancer. Now researchers at UT Southwestern and the University of Miami have discovered that a molecule — estrogen-related receptor gamma, or ESRRG — becomes hyperactive and promotes tumor cell survival in retinoblastoma. Blocking ESRRG, the team reported in Science Advances, kills retinoblastoma cells.
“Our discovery could lead to innovative new treatments for this cancer that take advantage of this dependence of retinoblastoma on ESRRG,” said study leader J. William Harbour, M.D., Chair and Professor of Ophthalmology at UT Southwestern. Before joining UTSW last year, Dr. Harbour served as Vice Chair for Translational Research at the Bascom Palmer Eye Institute at the University of Miami.
Retinoblastoma is a rare cancer affecting the retina — the tissue in the back of the eye that receives light and converts it into signals to the brain. It is most often diagnosed in children under 2 and has been associated with mutations in the RB1 gene. However, there are currently no specific, targeted therapies; doctors rely on broad-acting chemotherapy drugs that carry numerous side effects and toxicities.
In the new study, Dr. Harbour and his colleagues analyzed genes and proteins in tumor cells from 103 retinoblastoma patients, representing the largest sequencing analysis of retinoblastoma reported to date. While 94% of the tumors contained RB1 mutations, many also contained other altered genes. When the scientists analyzed these other mutations, they discovered that many were involved in the same signaling pathway inside cells: a molecular network that regulates ESRRG. ESRRG is known to play a role in the early development of the retina and other components of the nervous system but had never been linked to retinoblastoma before.
The team went on to show that RB1 normally puts the brakes on ESRRG in normal retinal cells. However, in retinal cells that have transformed into retinoblastoma, ESRRG becomes activated and helps keep cells alive and proliferating, even as oxygen levels drop — normally a signal that kills healthy cells. Blocking ESRRG causes cells to die under these low-oxygen conditions that are common in rapidly growing tumors and inside the eye.
“We found that when cells lose RB1, ESRRG is unleashed to allow continued tumor growth despite low-oxygen conditions,” said Dr. Harbour, a member of the Harold C. Simmons Comprehensive Cancer Center.
The researchers noted that more studies are needed to prove that drugs targeting ESRRG could be used in humans to treat retinoblastoma. But their results are encouraging.
“Retinoblastoma is the most common eye cancer in children, and it is incredibly exciting to finally have a potential drug target,” said Dr. Harbour.
This work was supported by the Alex’s Lemonade Stand/Tap Cancer Out Innovation Grant, University of Miami Sheila and David Fuente Graduate Program in Cancer Biology, University of Miami Center for Computational Science Fellowship, University of Miami Lois Pope LIFE Fellowship Award, Alcon Research Award, NIH/NCI (R01CA248890 and P30CA240139), NIH/NEI (P30EY014801), Research to Prevent Blindness Unrestricted Grant, and a philanthropic gift from M. J. Daily.
Dr. Harbour holds The David Bruton, Jr. Chair in Ophthalmology.
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The 21st Century Cures Act gave patients easy access to their health information. Now, some diagnoses delivered without context are causing high anxiety.Late last fall I suffered a second-trimester pregnancy loss. The experience was devastating, and the weeks after were a blur of grief, anger and physical turmoil. About a month later, on a day when I was feeling more like myself than I had in a while, I was folding clothes in my 3-year-old son’s room when I received an alert from MyChart, an app that gives patients access to their records and doctors’ messages, with a new test result to view.But I was not prepared for what I saw on the screen — a fetal autopsy report.Later, my OB-GYN explained that I had received the alert without hearing from her first because of a provision in the 21st Century Cures Act, a federal law that requires all medical testing centers to release results to patients “without delay.” In practice, this means that doctors and patients often receive results simultaneously — and some patients are seeing them before their doctors have a chance to look.President Barack Obama signed the Cures Act, which also provided billions of dollars for medical research, in December 2016. But the provision governing access to patient records didn’t take effect until April 2021, when the U.S. Department of Health and Human Services began enforcing a rule declaring that “blocking” patients from their own health information was against the law and could result in fines for hospitals and doctors.Its intention was to bring health care into the modern era. And the provision has successfully given patients easy access to their medical records, empowering them to play a more active role in their care by eliminating the doctor as gatekeeper.But it has also led to experiences like mine, in which patients are confronted with material they never wanted to see. Some have learned about life-altering diagnoses and developments — from cancer to chronic illness to miscarriage — through emails and online portals, left to process the information alone.Most doctors support the Cures Act as a whole. “We’re big supporters of the move in this direction” in general, said Dr. Jack Resneck, president of the American Medical Association and a dermatologist in San Francisco. But this provision, he said, is leading to “emotional and mental harm.”Nicki Swann, 38, a professor in Eugene, Ore., was shocked and confused when she learned through an app that she had colon cancer after having polyps removed. She was home alone — her husband had taken their infant daughter on a walk — when she received an email letting her know that results were ready. “I couldn’t imagine that anything but good news would be shared in that way,” she said.She immediately called her doctor’s office. But it was a Friday afternoon, and the physician was unavailable. They didn’t speak until the following week. “Any cancer diagnosis is going to cause trauma,” she said. “But I think it was much worse to receive it in that way.”“When information is just given in black-and-white type on MyChart, that’s not the full expression of compassionate care,” said Dr. Elizabeth Comen, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. “Yes, it is immediate care, but it’s care out of context.”How did we get here?Before the Cures Act provision, doctors had different approaches to giving patients their test results. Some offices would contact patients within hours or days; others sent paper results via mail. Some would take a “no news is good news” approach, sharing results only if they revealed something worrisome; others waited to share results in person.Lawmakers hoped to standardize the way we get results and increase transparency, said Micky Tripathi, the national coordinator for health information technology at the U.S. Department of Health and Human Services. With the Cures Act’s provision on releasing medical records, there was to be no more wondering, waiting or spending time trying to track down answers.“We should be adopting modern internet conventions,” Dr. Tripathi said, which includes making information accessible to consumers as soon as it is available.“I think that is the normal internet expectation all of us have.”Genevieve Morris, a senior director at the health technology company Change Healthcare who, in a previous role, helped draft the Cures Act, said she thought patients had become used to not having access to personal data. “We now have to adjust to a world where we are going to have all of our data at our fingertips,” she said.Many patients I spoke with appreciated having direct access to their health information. “I feel more in control,” said Yasi Noori-Bushehri, 32, an engineer in San Diego who has Graves’ disease, an autoimmune disorder that requires her to closely monitor her thyroid hormone levels. Having access to her medical information has given Ms. Noori-Bushehri confidence to ask for changes in her treatment plan: When her doctor suggested tweaking her thyroid medication, she pointed to previous lab reports suggesting that the change might throw her hormones out of whack. After talking it through, the doctor agreed.Some patients said receiving test results — even difficult ones — before speaking with their doctor had allowed them to feel more prepared when they did connect. “You can go into the next appointment having done your homework,” said Teresa Christopherson, 59, who regularly gets updates on the status of her breast cancer via an online portal. She said that gave her the opportunity to “ask the right questions” about next steps. “Everyone has the right to their own medical information in real time, not on the doctor’s time,” she said.Many doctors said they supported instant access, too, in most cases. “If your cholesterol has gone up, that might not be good news, but it’s not the same as finding out that you have a lung nodule in a chest X-ray,” Dr. Resneck said.But when difficult, life-changing information is delivered in this way, “it cuts off any opportunity for doctors to get ahead of things,” said Dr. Emily Porter, an emergency room and sexual health physician in Austin, Texas, who has criticized the policy on social media.The Cures Act does offer a “preventing harm exception” to its provision requiring the swift release of test results. But the bar for what counts as harm is high: The provider must be able to anticipate that the test results could lead a patient to harm himself or herself.This exception also doesn’t account for cases in which a routine test reveals an unexpected finding. A weekend spent searching online for medical information with knots in your stomach — or, in my case, seeing an upsetting report — does not qualify as harm.The emotional cost of instant accessLast month, the A.M.A. released the results of a survey of 1,000 people about the Cures Act’s provision on test results. Roughly 42 percent of the patients surveyed wanted test results as soon as they were available, while about 43 percent preferred to hear from their doctors first. But among those who wanted instant access, more than half said that, in the case of a “debilitating, life-limiting or terminal illness,” they would like to speak with a doctor first.Since the provision took effect, Dr. David Gerber, a lung cancer specialist at the University of Texas Southwestern Medical Center in Dallas, has met with many patients and caregivers who have shared their emotional distress over receiving results without context. In an editorial he wrote for an oncology medical journal last year, he described the experience of trying to get to a patient before the patient could receive results through an app as if it were a race. “I still remember the first time we lost,” he wrote, referring to a time when a patient’s wife was convinced that her husband’s cancer had returned after she misinterpreted a technical report delivered via email.In an interview, Dr. Gerber said that he had previously provided results to patients within 72 hours — that was enough time to review them, confer with other physicians and come up with a treatment plan. “Things seemed a little bit smoother and less turbulent,” he said, “but not necessarily slower in a way that was clinically meaningful.” He would also release full medical reports to patients, but only after discussing the results with them. Dr. Comen also acknowledged that previous systems had been imperfect. “We have to honor the reality that waiting can feel impossibly hard,” she said. “But I don’t think anything replaces a doctor holding your hand and looking you in the eye and saying: ‘I’m going to go through every aspect of this with you in real time. You can ask me your questions. I will read your body language. I will give you tissues. I will be there with you.’”What’s next for patient care?For the past several months, the A.M.A. has been urging the Department of Health and Human Services to make what Dr. Resneck calls “common sense” exceptions to the current rule. Last month, the group published a statement laying out its concerns and requesting language to “explicitly allow physicians, using their professional judgment, to withhold some information if immediate or proactive release could cause a patient mental or emotional harm.”While such exceptions are allowed currently, they must be requested beforehand by a patient or caregiver. And with the existing technology, few providers have the practical ability to prevent a patient’s results from being automatically released electronicallyDr. Tripathi of Health and Human Services said, “We recognize this is a really big transition for all of us.” But he added that department officials hoped the Cures Act would encourage patients to become more engaged with their own care and talk with their doctors about how they want to receive information. They would also like to see health care apps introduce more flexibility — including options for physicians to indicate a patient’s preferences on a case-by-case basis and ways for patients to opt out of receiving certain results in real time.So what can patients do right now?If you are undergoing a medical test, ask your doctor for expectations around timing, doctors said — both in terms of when results might be released electronically and when you can expect to hear from the doctor’s office, so you can prepare mentally and emotionally.For Ashley Collins, 39, a breast cancer survivor in Durham, N.C., this kind of conversation was crucial to easing her emotional distress after a mastectomy.After the surgery, Ms. Collins was eager to learn the results of biopsies that would reveal whether chemotherapy had eliminated her breast cancer. But before leaving the hospital, she spoke with her surgeon about timing, and her doctor told her that she would call her as soon as possible after the results were posted online. Knowing that she would be hearing from her doctor within a certain time frame, Ms. Collins opted not even to look at the MyChart report and waited for her call.“From the time that you get the ding on your Apple Watch that says, ‘New results are in your chart,’ it’s a sort of Pavlovian response of anxiety that kicks in,” Ms. Collins said. “Mercifully, my surgeon called me very soon after the result was posted.”

In one of the first studies to examine the relationship between different types of grain intake and premature coronary artery disease in the Middle East, researchers found a higher intake of refined grain was associated with an increased risk of premature coronary artery disease in an Iranian population, while eating whole grains was associated with reduced risk. The study will be presented at the American College of Cardiology (ACC) Middle East 2022 Together with the 13th Emirates Cardiac Society Congress, taking place in Dubai, United Arab Emirates, October 7-9, 2022.
According to the researchers, previous epidemiological studies have reported an association between different types of grain intake with the risk of coronary artery disease. The current study evaluated the association between refined and whole grains consumption and risk of PCAD in an Iranian population.
Premature coronary artery disease (PCAD) refers to atherosclerotic narrowing of coronary arteries in males under 55 years old or in females under 65 years old. It is often asymptomatic early in the course of the disease but may lead to chest pain (angina) and/or heart attack with progressive development of narrowing (stenosis) or plaque rupture of the arterial wall. Risk factors for PCAD include smoking, high cholesterol, high blood pressure and diabetes.
“There are many factors involved in why people may be consuming more refined grains as opposed to whole grains and these cases differ between people, but some of the most important factors to consider include the economy and income, job, education, culture, age and other similar factors,” said Mohammad Amin Khajavi Gaskarei, MD, of the Isfahan Cardiovascular Research Center and Cardiovascular Research Institute at Isfahan University of Medical Sciences in Isfahan, Iran, and the study’s lead author. “A diet that includes consuming a high amount of unhealthy and refined grains can be considered similar to consuming a diet containing a lot of unhealthy sugars and oils.”
Whole grains are defined as containing the entire grain, while refined grains have been milled — ground into flour or meal — to improve shelf life but they lose important nutrients in the process. The 2019 ACC/American Heart Association Guideline on the Primary Prevention of Cardiovascular Disease recommends a diet that emphasizes the intake of vegetables, fruits, legumes, whole grains and fish to decrease heart disease risk factors.
The study recruited 2099 individuals with PCAD from hospitals with catheterization labs in different cities and ethnicities throughout Iran who underwent coronary angiography (women aged ≤ 70 and men ≤ 60). In total, 1,168 patients with normal coronary arteries were included in the control group, while 1,369 patients with CAD with obstruction equal or above 75% in at least a single coronary artery or ≥ 50% in the left main coronary artery made up the case group.
Participants were given a food frequency questionnaire for dietary assessments to evaluate dietary behaviors and evaluate the association between whole grain and refined grain intake and the risk of PCAD in individuals without a prior diagnoses of heart disease. After adjusting for confounders, a higher intake of refined grains was associated with an increased risk of PCAD, while whole grain intake was inversely related to reduced risk of PCAD.
“As more studies demonstrate an increase in refined grains consumption globally, as well as the impact on overall health, it is important that we find ways to encourage and educate people on the benefits of whole grain consumption,” Khajavi Gaskarei said. “Tactics to consider include teaching improved dietary choices in schools and other public places in simple language the general population can understand, as well as on television programs and by continuing to do high level research that is presented at medical conferences and published in medical journals. Clinicians must also be having these conversations with each other and their patients.”
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