In a recent study published in Neurology, researchers found people whose scores on a dementia risk test indicated a less brain-healthy lifestyle, including smoking, high blood pressure, and a poor diet, may also have the following: lower scores on thinking skills tests, more changes on brain scans and a higher risk of cognitive impairment.
The study also found that in men, the test scores were linked to poor memory function and markers of brain shrinkage.
They also found that a substantial proportion of brain changes might be attributable to risk factors that can be modified.
The study is from Maastricht University. One author is Sebastian Köhler Ph.D.
In the study, the team examined 4,164 people with an average age of 59. All participants took a test called the “Lifestyle for Brain Health” (LIBRA). The total score reflects a person’s potential for developing dementia.
This study took into account 11 out of 12 lifestyle factors on the test, including high blood pressure, heart disease, smoking, diet, and physical activity.
Participants in the study took tests of memory and other thinking skills, such as information processing speed, executive function, and attention.
The team found that people who were in the high-risk group on the brain test, indicating a less brain-healthy lifestyle, had higher volumes of brain lesions.
The high-risk group also had lower scores on two tests of thinking: information processing speed and executive function and attention.
Only in men, however, did researchers find links between higher scores on the brain and lifestyle test and lower volumes of grey matter, as well as lower scores on tests of memory.
The team says more research is needed to confirm these findings and determine why there were differences between men and women.
It’s exciting that a simple test score may indeed be an index of brain health.
Scientists need to learn whether people can improve their scores by making changes in their diet, increasing physical activity, or limiting alcohol to low-to-moderate use.
Some people enjoy an occasional glass of wine with dinner. Others might grab a beer while watching a football game. Most people drink alcohol moderately, within their limits.
Others overdo it occasionally. But some people find they can’t control their drinking. How do you know when drinking is becoming a problem? And what can you do if it is?
About 18 million Americans have an alcohol use disorder. Drinking too much alcohol raises your risk of injury and accidents, disease, and other health problems.
Heavy drinking is one of the leading causes of preventable deaths in this country, contributing to nearly 88,000 deaths each year.
How much is too much? Men shouldn’t have more than 14 drinks per week and 4 drinks on any single day. Women shouldn’t have more than 7 drinks per week and no more than 3 drinks on any day.
But you might be surprised at what counts as a drink. A 5-ounce glass of table wine, a 12-ounce glass of regular beer, and 1½ ounces of hard liquor each contain the same amount of alcohol, and each counts as 1 drink.
You may need to adjust the amount you drink depending on how alcohol affects you. Some people—such as pregnant women or people taking certain medications—shouldn’t drink alcohol at all.
Alcohol problems come from drinking too much, too fast, or too often. People with alcohol dependence are addicted to alcohol, and they can’t control their drinking.
When alcohol-dependent people try to stop drinking, they may feel anxious and irritable—so they may drink some more, and it becomes a vicious cycle.
“Addiction has 3 major problems: You lose your ability to feel good, you get more stressed, and you have a hard time making proper decisions,” says Dr. George Koob, director of NIH’s National Institute on Alcohol Abuse and Alcoholism. “That’s a recipe for disaster.”
Signs of an alcohol problem include drinking more, or more often, than you intended, or making unsuccessful attempts to cut back or quit. People with alcohol problems often have trouble functioning at work, home, or school.
“A good indicator is that something is out of whack. Is your personal life deteriorating because of your drinking? Are people starting to shun you? If you’re feeling generally miserable, that’s a warning sign,” Koob says.
“You don’t have to hit bottom. You’ll save yourself a lot of damage socially, professionally, and probably in your own body if you attend to an alcohol problem a lot earlier.”
“People shouldn’t wait for a physical problem like liver disease,” says Dr. Lorenzo Leggio, an NIH researcher studying new alcoholism treatments.
“People develop an alcohol disorder before liver problems get bad. The goal is to identify an alcohol disorder sooner. The sooner you act can help prevent medical consequences.”
Studies show that most people with an alcohol use disorder can benefit from some form of treatment. If you or someone you care about may have an alcohol problem, help is available.
The first step is to talk to a primary care doctor. In some cases, a brief intervention, or an honest conversation about drinking habits and risks, is all the person needs.
If the problem is more serious, the doctor can help create a treatment plan, prescribe medications, or refer the person to a specialist. In more severe cases, the doctor might recommend a treatment clinic or in-patient addiction center.
“Alcohol dependence is a complex, diverse disorder. There’s not one treatment that works for everybody,” says Dr. Raye Litten, an alcohol treatment and recovery expert at NIH.
“If one treatment doesn’t work, you can try another one. Sometimes a combination of these will work.”
Medications can help people stop or reduce their drinking. Three medications are approved by the U.S. Food and Drug Administration for treating alcohol use disorders.
One of these, disulfiram, causes unpleasant side effects such as nausea, vomiting, and a racing heart rate if you consume any alcohol while taking the drug. Understandably, some people don’t want to take this medication for that reason.
The 2 other drugs, naltrexone and acamprosate, also have been shown effective at reducing alcohol craving in many heavy drinkers.
Additional medications are under study as possible treatments for alcohol use disorders. These include a handful of medicines already approved to treat other medical conditions.
For example, the drug gabapentin is now used to treat pain and other conditions, but it also has shown promise for reducing heavy drinking in clinical research trials.
Gabapentin may reduce alcohol cravings as well as anxiety, trouble sleeping, and other symptoms associated with alcohol use disorders.
NIH researchers are working to develop other approaches as well. Some are exploring a possible connection between appetite and alcohol craving. Leggio is studying a hormone in the stomach called ghrelin.
His research suggests that when ghrelin is elevated, people feel hungry and also crave more alcohol. His lab is testing an experimental drug designed to block this hormone to help reduce alcohol craving. The drug is now being assessed in early trials at the NIH Clinical Center in Maryland.
“There’s not going to be a drug that cures you of alcoholism,” Koob says. “I think that drugs can help you along the way, so that some of the chemical changes in the brain can return to normal. Strengthen that with behavioral therapy to make recovery as permanent as you can.”
Behavioral therapy, such as counseling or support groups, can help people develop skills to avoid or overcome stress and other triggers that could lead to drinking.
The approach can help people set realistic goals, identify the feelings and situations that might lead to heavy drinking, and offer tips to manage stress. It also helps to build a strong social support network.
If the treatment plan created by your health care team is working, it’s important to stick to that plan. Many people repeatedly try to cut back or quit drinking, have a setback, then try to quit again.
Think of an alcohol relapse as a temporary setback and keep persisting toward full recovery.
“You always have to be aware there’s a possibility of relapse and temptation,” says Koob. “Any recovering alcoholic will tell you it’s a daily fight for a long time.”
Researchers have created a new hydrogel tablet that can rapidly purify contaminated water.
One tablet can disinfect a liter of river water and make it suitable for drinking in an hour or less.
As much as a third of the world’s population don’t have access to clean drinking water, according to some estimates, and half of the population could live in water-stressed areas by 2025.
Finding a solution to this problem could save and improve lives for millions of people, and is a high priority among scientists and engineers around the globe.
“Our multifunctional hydrogel can make a big difference in mitigating global water scarcity because it is easy to use, highly efficient, and potentially scalable up to mass production,” says Guihua Yu, an associate professor in the Cockrell School of Engineering’s Walker department of mechanical engineering and Texas Materials Institute at the University of Texas at Austin.
Today, the primary way to purify water is to boil or pasteurize it. But that takes energy, plus a lot of time and work.
That isn’t practical for people in parts of the world without the resources for these processes.
As reported in Advanced Materials, the special hydrogels generate hydrogen peroxide to neutralize bacteria at an efficiency rate of more than 99.999%.
The hydrogen peroxide works with activated carbon particles to attack essential cell components of bacteria and disrupt their metabolism.
The process requires zero energy input and doesn’t create harmful byproducts. The hydrogels can easily be removed, and they don’t leave any residue.
In addition to purifying water on their own, the hydrogels could also improve a process that has been around for thousands of years—solar distillation, the use of sunlight to separate water from harmful contaminants via vaporization.
Solar distillation systems often run into issues of biofouling, the accumulation of microorganisms on equipment that causes it to malfunction. The bacteria-killing hydrogels can prevent this from happening.
“A highly vigilant graduate student, Youhong Guo, discovered these hydrogels unexpectedly while doing something else, that is purification of water with sunlight,” says Keith Johnston, a professor in the chemical engineering department, who co-led the project.
The team is working to improve the hydrogels by increasing the different types of pathogens and viruses in water that they can neutralize. And the team is also in the process of commercializing several prototypes.
Scaling up the hydrogels would be straightforward, the researchers say. Materials for making them are inexpensive, and the synthesis processes are simple and remain that way at large scales. And they can easily control the shape and size of the hydrogels, making them flexible for different types of uses.
Guo, a graduate student in Yu’s lab, is the paper’s first author. Graduate students Christopher Dundas from chemical engineering and Xingyi Zhou from mechanical engineering were also part of the team. The Energy Institute at the University of Texas at Austin and the Dreyfus Foundation funded the work.
Artistic representation of an active galaxy jet. Credit: M. Kornmesser/ESO.
Astronomers have unveiled the nature of hundreds of gamma-ray emitting sources, discovering that most of them belong to the class of active galaxies known as blazars.
Their recent study was published in The Astronomical Journal.
One of the most intriguing challenges in modern gamma-ray astronomy is searching for low-energy counterparts of unidentified gamma-ray sources.
Unidentified sources constitute about 1/3 of all celestial objects detected by the Fermi satellite to date, the most recent gamma-ray mission with unprecedented capabilities for observing the high energy sky.
Since the largest population of known gamma-ray sources are blazars, astronomers believe they can also classify most unidentified gamma-ray sources as blazars.
However, they can completely understand their nature only by observing blazar candidates at visible frequencies.
Blazars are extremely rare, black hole-powered galaxies.
They host a supermassive black hole in their central regions that sweep out matter at almost the speed of light in the form of a powerful jet pointing towards the Earth.
Particles accelerated in these jets can emit light up to the most energetic gamma-rays, thus being visible by instruments onboard the Fermi satellite.
The team, led by Dr. Harold Peña Herazo from Mexico’s National Institute of Astrophysics, Optics, and Electronics (INAOE), analyzed hundreds of optical spectra collected by the Large Sky Area Multi-Object Fabre Spectroscopic Telescope (LAMOST) at the Xinglong Station in China.
LAMOST is hosted by National Astronomical Observatories of Chinese Academy of Sciences. It provided a unique opportunity to unveil the nature of blazar-like sources that can potentially be counterparts of unidentified gamma-ray sources.
From the list of sources discovered by the Fermi satellite, the researchers selected a sample of Blazar Candidates of Uncertain type (BCUs), which share several properties in common with blazars.
However, optical spectroscopic observations are necessary to determine their proper classification and confirm their nature.
Using spectroscopic data available in the LAMOST archive, the researchers were able to classify tens of BCUs as blazars. “LAMOST data also permitted verifying the nature of hundreds of additional blazars by searching for emission or absorption lines used to determine their cosmological distances,” said Prof. GU Minfeng from Shanghai Astronomical Observatory of Chinese Academy of Sciences.
The vast majority of sources belong to the blazar class known as BL Lac objects and have a completely featureless optical spectrum.
This makes measuring their cosmological distances an extremely challenging task. However, thanks to the LAMOST observations, a few more of them have luckily revealed visible signatures in their optical spectra.
“Our analysis showed great potential for the LAMOST survey and allowed us to discover a few changing-look blazars,” said Dr. Peña Herazo, currently a postdoctoral fellow at the East Asian Observatory.
“It is worth noting that the possibility of using LAMOST observations to estimate blazar cosmological distances is critical to studying this population, its cosmological evolution, the imprint in the extragalactic gamma-ray background light in the gamma-ray spectra, and the blazar contribution to the extragalactic gamma-ray background,” said Prof. Francesco Massaro from the University of Turin.
“I started working on this optical campaign and analyzing spectroscopic data in 2015, and nowadays, thanks to the observations available in LAMOST archive, we certainly made a significant step toward the identification of gamma-ray sources with blazars. Future perspectives achievable thanks to LAMOST datasets will definitively reveal the nature of hundreds of new blazars in the years to come,” commented Dr. Federica Ricci at Bologna University and INAF-OAS.
The group’s previous study was also published in The Astronomical Journal.
In a recent study from the University of Kentucky, researchers found that changes to mitochondria—the powerhouse of cells—drive chronic inflammation from cells exposed to certain types of fats.
This could be the real cause of inflammation in type 2 diabetes. The finding shatters the prevailing assumption that glucose was the culprit.
The study is published in Cell Metabolism. One author is Barbara Nikolajczyk.
To date, the underlying causes of inflammation in obesity and type 2 diabetes have been poorly understood.
This has hampered efforts to develop treatments to prevent complications from a disease that is the third leading cause of death in the United States.
Chronic inflammation fuels many of the devastating complications of type 2 diabetes, including cardiovascular, kidney, and periodontal diseases, and is thus one of the key targets for therapy development.
In the study, the team hypothesized that immune cells from patients with type 2 diabetes would produce energy by burning glucose.
But the finding showed that glycolysis wasn’t driving chronic inflammation. Instead, a combination of defects in mitochondria and elevated fat derivatives was responsible.
This new data may enlighten the conversation about tight glycemic control as the dominant treatment goal for people with diabetes.
The team says aggressive blood glucose control to lower the risk of diabetic complications has been the goal for most people with Type 2 Diabetes for decades.
The new data provide an explanation for why people with tight glucose control can nonetheless have disease progression.
If you’re looking to shed a few pounds, you might be tempted to try out popular new approaches like the keto diet or fasting.
But you might be unwittingly worsening a problem you don’t even know you have: a fatty liver.
Doctors are worried about an increasingly common condition called nonalcoholic fatty liver disease, or NAFLD, in which extra fat builds up in the liver.
It may lead to serious consequences like cirrhosis and liver cancer—just like liver problems caused by drinking too much alcohol.
“In clinic, I used to see mostly hepatitis C patients. Now most of the patients I see have fatty liver disease,” said Hugo Rosen, a liver disease specialist and chair of medicine at the Keck School of Medicine of USC.
“It’s a problem that closely tracks with the emergence of obesity and diabetes throughout the world.”
A quarter of the global population is estimated to have NAFLD—which doctors pronounce as “nah-fold” or “naffle-dee.”
Rosen said that figure may be even higher in the United States. The liver disease affects about 35 percent of Americans.
“It’s a really important issue to be aware of,” he said. “Patients with NAFLD have at least a twofold risk of dying of a coronary event or having a stroke.”
Scientists also believe the condition is linked to increased risk of liver cancer even in the absence of clear-cut cirrhosis, Rosen said.
He has seen results from a Mayo Clinic study that suggest NAFLD can increase susceptibility to other forms of cancer as well.
Many people don’t know they have a fatty liver, leading to its reputation as a “silent killer.” It usually causes no pain or other symptoms.
It’s often not until the disease has progressed to a more serious stage, like nonalcoholic steatohepatitis (NASH) or cirrhosis (serious scarring of the liver), that patients and doctors are alerted to the problem.
In NASH, the liver becomes inflamed and damaged, which can cause scarring and higher risk of cancer or liver failure.
Rosen said patients worried about NALFD or NASH should request liver blood tests and imaging tests like an MRI or ultrasound.
Concerning results could indicate the need for referral to a liver specialist and a liver biopsy.
Vitamin E and the diabetes drug pioglitazone have helped some patients, but results are inconsistent, he said. The FDA has approved no drugs for the disease yet.
Rosen said losing weight is the main strategy to combat the problem, because it helps reduce fat and inflammation in the liver.
That’s why poor eating habits and fad diets that boost fat intake are particularly worrisome, he said.
The keto diet, which emphasizes eating lots of fats and restricting carbohydrates, can lead to NAFLD, according to research done in mouse models.
Keto is attractive to many people because “you can eat a lot of tasty stuff—butter, red meat, cheese,” he said.
“But you’re basically consuming 80 percent of your caloric intake from fat. It certainly makes sense why in rodents, we’re seeing that this causes NAFLD.”
Don’t overdo it on fats, Rosen recommends, especially from processed foods. Fructose and other sugars are a major concern as well, especially in sodas, candy, sugary cereals, sweetened juices and fast food.
Those kinds of refined foods can increase cholesterol and cause inflammation in the liver.
Instead, he suggests eating a well-balanced diet that features high-fiber foods, vegetables, fruits, fish, lean meats, nuts, eggs, seeds and unrefined oils.
It’s a menu familiar to those following other popular diet trends: the paleo and Mediterranean diets.
“Some data have shown that a paleo diet has a significant and persistent effect on lowering liver fat compared to a low-fat diet, simply because a low-fat diet isn’t palatable to a lot of people,” he said.
That’s one problem with fad diets, Rosen said—they can be difficult to stick with, especially if they cut out tasty items entirely. Fasting is another approach that can have dramatic weight-loss effects but is hard to maintain.
“Rapid weight loss is not recommended because it’s rarely sustainable,” he said. “I would favor a gradual weight loss of 5 percent to 10 percent.”
Beyond consulting with a doctor or nutritionist about their dietary habits, Rosen said people with NAFLD or NASH should consider moderate exercise to avoid a condition called sarcopenia, or low muscle mass and strength.
When combined with obesity, sarcopenia can further increase the risk of liver inflammation.
Another concern is alcohol. Although by definition, NAFLD is unrelated to alcohol use, people with poor liver health should be careful about how much they drink.
Rosen said even moderate alcohol consumption (10 to 20 grams for women and 10 to 30 grams for men per day) can cause issues, citing a recent study that followed 60,000 Koreans with NAFLD. A typical drink has 10 to 14 grams of alcohol.
“It turns out that if a patient has NAFLD and they drink this moderate amount, they have a much higher rate of developing worsening fibrosis over time,” Rosen said.
Over the past year, discussions—sometimes heated ones—about ending the COVID-19 pandemic have largely focused on the availability, effectiveness, and safety of vaccines.
But in early October, Merck reported on a promising new drug treatment that could be given as a pill in the days after COVID-19 symptoms arise to prevent severe disease.
This news, which many are hailing as a potential game-changer, is already starting to change the conversation.
Merck has applied to the Food and Drug Administration (FDA) for emergency use authorization (EUA) of the pill, called molnupiravir. While an authorization could become available in a matter of weeks, it’s not yet clear who would get it.
But what we do know is that the company says it performed so well in a clinical trial that it halted the trial early, so it could move quickly to apply for the EUA.
A company press release reports that the drug cut the risk of hospitalization and death by half in patients who had mild-to-moderate disease.
“It certainly has the potential to be a really important advance,” says Albert Shaw, MD, Ph.D., a Yale Medicine infectious diseases specialist.
“Other COVID-19 treatments, such as remdesivir or monoclonal antibodies against the SARS-CoV-2 virus causing COVID-19, are given intravenously. This is a pill your physician could write a prescription for, that you could pick up in a drugstore.”
We asked Dr. Shaw and other infectious disease experts to answer commonly asked questions about Merck’s new COVID pill.
How does the COVID-19 pill (molnupiravir) work?
It’s important to note that the pill is meant to be taken after you’ve experienced COVID-19 symptoms.
In the clinical trial, molnupiravir was given to study participants in four capsules twice a day for five days—starting within five days after patients experienced the first symptoms of COVID-19.
When the drug enters your bloodstream, it blocks the ability of the SARS-CoV-2 virus to replicate, Dr. Shaw explains.
The coronavirus uses RNA as its genetic material. The structure of molnupiravir resembles the nucleosides (or chemical building blocks) used to make the virus’s RNA. The drug works by incorporating itself into the RNA as it’s being synthesized.
“This results in many mutations, or changes in the RNA genetic code, introduced into the viral RNA,” says Dr. Shaw. “And when this RNA is translated into viral proteins, these proteins contain too many mutations for the virus to function.”
Does molnupiravir have any side effects?
Based on the data in the company’s release, the drug appears to have a clean safety profile, meaning there were no serious side effects in trial volunteers.
Because molnupiravir works by disrupting how the coronavirus replicates RNA, there could be a concern of a similar effect on human DNA or RNA.
Merck reportedly has data from laboratory studies indicating that molnupiravir does not cause mutations in humans, but “the FDA will obviously need to see and evaluate this safety data in the approval process,” Dr. Shaw says.
Dr. Shaw notes that several approved antiviral drugs already in wide clinical use—such as acyclovir and related drugs for herpesvirus infections, and reverse-transcriptase inhibitors for HIV infection—also work (via different mechanisms) in interfering with the replication of viral DNA or RNA.
Yale Medicine infectious diseases specialist Jaimie Meyer, MD, MS, noted that in its clinical trial, Merck didn’t test the drug on pregnant women.
“In the trial, not only did they exclude women who were pregnant, breastfeeding, or anticipating becoming pregnant, but they also told the men enrolled in the trial that they couldn’t have unprotected sex with women for a week after they were done with their medication,” she says.
The concern might be that this drug would interfere with RNA replication needed for fetus development and cause birth defects. This will be important to tease out as this drug moves from clinical trials to the market, she adds.
Is molnupiravir similar to Tamiflu?
Yes, this new pill is similar—in function, ease of use, and availability—to Tamiflu, the antiviral medication that is used to prevent serious symptoms of flu.
There is a key difference, though, says Dr. Shaw. “Tamiflu works through a different mechanism—by interfering with the entry of influenza virus into cells—instead of targeting the reproduction of viral RNA,” he says.
Interestingly, Tamiflu also can be given in a single dose to prevent infection with the flu, “like a post-exposure prophylaxis [PEP],” says Dr. Meyer, explaining how some people may be prescribed antiviral medications after a potential exposure to a disease, like HIV, to prevent infection.
“Molnupiravir has not yet been tested as a PEP against COVID-19,” she says, “but that would be a hope for the future.”
Does molnupiravir prevent infection or severe illness and death?
The goal of the Merck pill is to keep people out of the hospital, explains Dr. Meyer. “We want to prevent severe illness and death in people who are infected with mild-to-moderate COVID, but who are not yet hospitalized,” says Dr. Meyer.
The Merck study suggested that molnupiravir would help patients who have at least one risk factor for severe COVID-19 to avoid hospitalization.
Who is molnupiravir recommended for?
Merck is seeking an EUA for its pill for high-risk adults. In the clinical trial, molnupiravir was mostly given to people who were over 60 or those who were younger but had other conditions that put them at high risk of bad outcomes from COVID-19, such as diabetes, heart disease, or obesity.
The FDA will also decide whether it should be given to vaccinated people—only unvaccinated individuals were included in the trial.
Will molnupiravir work on virus variants, including Delta?
Yes, in what may come as a relief to many.
The research, which was conducted in the U.S. and other countries, also suggests the drug would be effective against mutations of the virus that the Centers for Disease Control & Prevention (CDC) classifies as “variants of concern,” including the Delta, Gamma, and Mu mutations.
Could molnupiravir be a turning point for other COVID-19 treatments?
So far, treatments for COVID-19 have been hard to deliver or not very effective. “We don’t have a lot of COVID medications in our arsenal,” Dr. Shaw says. Remdesivir, the only COVID-19 drug treatment fully approved by the FDA, can only be administered intravenously in the hospital.
It’s also only for those ages 12 and older, regardless of how severe their symptoms are, and studies suggest it may provide only modest benefit.
But there are other drugs in the pipeline for the treatment of COVID-19, says Dr. Shaw.
Pfizer, which produced the first COVID-19 vaccine to be authorized—and later fully approved—in the U.S., is expected to report results on a promising protease inhibitor that would also be given in pill form.
“Hopefully, there will be more tools to help us better treat our COVID patients,” he says.
Why was the trial stopped early?
The trial was halted on the recommendation of a data and safety monitoring board, an independent committee charged with evaluating progress of the study at specified intervals.
“This is not uncommon in clinical trials,” Dr. Shaw says. “In consultations with statisticians, and without input from Merck, the board concluded that the results showing efficacy were clear and would not be affected by continuation of the trial—and, that the best thing would be to stop the trial and make the results known, so we can move forward.”
It’s important to note that at the time the study was stopped, they were 70% fully enrolled, “so they had data on nearly 800 individuals randomized to receive either the study drug or the placebo,” adds Dr. Meyer.
If molnupiravir is authorized, do we still need vaccines?
Both doctors emphasized that if and when molnupiravir is authorized—and even if it is as successful in real-world scenarios as it was in the study—vaccination will remain essential for preventing SARS-CoV-2 infection—and for slowing its spread.
People who are vaccinated have a much lower chance of getting sick and needing any treatment, they say.
“The vaccine is our first-line tool for preventing hospitalization, and I’m a little concerned that the attention on molnupiravir will draw attention away from vaccination,” says Dr. Meyer.
“Some people might say, “I’m not getting vaccinated because I’ll have access to these medications’—to this pill or to remdesivir or other treatments. But you can’t trade one for the other. If you haven’t done so already, the most important thing is still to get the vaccine.”
In a new study from Monash University, researchers found moderate carbohydrate intake and not saturated fat could provide a heart health benefits to women.
Cardiovascular disease (CVD) is the leading cause of death in women.
Poor diet is recognized as both an independent CVD risk factor and a contributor to other CVD risk factors, such as obesity, diabetes and high blood pressure.
The research found that in middle-aged women, increasing the percentage of carbohydrate intake was strongly linked to reduced odds of CVD, high blood pressure, diabetes and obesity.
Furthermore, a moderate carbohydrate intake between 41%—44.3% of total energy intake was linked to the lowest risk of CVD compared to women who consumed less than 37% energy as carbohydrates.
In addition, increasing proportional saturated fat intake was not linked to heart disease or mortality in women.
Rather, increasing saturated fat intake is linked to lower odds of developing diabetes s, high blood pressure, and obesity.
The results contradict much of the historical epidemiological research that supported a link between saturated fat and CVD.
While the cause of this inconsistency in the literature is unclear, it has been suggested that historical studies neglected to adjust for fiber, which is known to help prevent plaque from forming in the arteries.
Researchers say that quality carbohydrate foods such as vegetables and whole grains—including whole grain bread, cereals, and pasta—are beneficial for heart health, whereas poor quality carbohydrates such as white bread, biscuits, cakes, and pastries can increase risk.
Similarly, different fats have different effects on heart health.
That is why the Heart Foundation focuses on healthy eating patterns—that is, a combination of foods, chosen regularly over time—rather than a single nutrient or food.
Include plenty of vegetables, fruit, and whole grains, and heart-healthy fat choices such as nuts, seeds, avocados, olives and their oils for cooking and a variety of healthy proteins especially seafood, beans and lentils, eggs and dairy.
In a new study from the University of Melbourne and elsewhere, researchers found individuals who are diagnosed with high blood pressure at ages 35-44 had smaller brain size and were more likely to develop dementia compared to people who had normal blood pressure.
The results raise the possibility that taking steps in young adulthood to control or delay the onset of high blood pressure may reduce the risk of dementia.
In the study, the team analyzed data from participants in the UK Biobank, a large database containing detailed anonymous health information of about half a million volunteer participants in the United Kingdom.
To determine brain changes, they compared magnetic resonance imaging (MRI) measurements of brain volume between two large groups of adults in the database: 11,399 people with high blood pressure diagnosed at different ages (younger than age 35; 35-44 years; and 45-54 years), and 11,399 participants who did not have high blood pressure.
From the MRI scans, the team found in each diagnostic age category (from 35 to 54), the total brain volume was smaller in people diagnosed with high blood pressure, and the brain volume of several regions were also smaller compared to the participants who did not have high blood pressure.
Hypertension diagnosed before age 35 was associated with the largest reductions in brain volume compared with controls.
Analyzing the occurrence of dementia in relation to blood pressure diagnosis, the researchers found:
The risk of dementia from any cause was significantly higher (61%) in people diagnosed with high blood pressure between the ages of 35 and 44 compared to participants who did not have high blood pressure.
The risk of vascular dementia (a common form of dementia resulting from impaired blood flow to parts of the brain, as might happen after one or more small strokes) was 45% higher in the adults diagnosed with hypertension between ages 45-54 and 69% higher in those diagnosed between ages 35-44, compared to participants of the same age without high blood pressure.
Although vascular dementia risk was 80% higher in those diagnosed with high blood pressure before age 35, there were fewer cases of dementia among the younger participants, and the association with high blood pressure was not statistically significant, whereas the risk association was meaningful for individuals ages 45-54 with high blood pressure.
These results provide evidence to suggest an early age at onset of hypertension is associated with the occurrence of dementia and, more importantly, this association is supported by structural changes in brain volume.
The findings raise the possibility that better prevention and control of high blood pressure in early adulthood could help prevent dementia.
Kelly Naab was waiting in a drive-thru lane with her two young boys in the back seat when her body suddenly felt strange. Her face began drooping. She couldn’t move her right arm or speak.
She tried, unsuccessfully, to call for help. Naab – then a 35-year-old pediatric nurse practitioner – recognized she was experiencing common symptoms of a stroke.
“I can’t die,” she thought. “This can’t be happening.”
As quickly as the symptoms came on, they went away. Naab drove away, took a deep breath and went for tests that showed she had experienced a TIA, short for transient ischemic attack, also called a mini-stroke.
A few days later, she learned the likely cause: a hole in her heart that was supposed to close shortly after birth but didn’t.
About 25% of people have this congenital heart defect, called patent foramen ovale or PFO, and often don’t realize it until it causes a problem, such as a stroke.
After her mini-stroke in December 2013, doctors opted not to surgically repair Naab’s PFO. Instead, they prescribed medication to reduce the risk of blood clots that could cause a future stroke.
Naab, shaken by the experience, gradually returned to her routine.
“You always live your life with a little fear because in the back of your mind, you know it could happen again,” she said. “But the farther I got from it, the more confident I felt I was going to be OK.”
A lifelong athlete living near Buffalo, New York, Naab returned to running. She completed half-marathons in 2016, 2017 and 2018, her times improving each year. She felt like she was in the best shape of her life after turning 40.
But while training at the gym in July 2018, Naab had a concussion on the left side of her brain, the same side as the mini-stroke.
When her symptoms – headaches, fatigue, vertigo and nausea – seemed to worsen six weeks after the injury, Naab underwent additional testing. It revealed she had experienced an acute ischemic stroke within the five days preceding the scan.
“I can’t pinpoint a time when it would have happened,” she said.
A few weeks later, she had surgery to close the PFO.
Naab’s husband, Tim, a physical therapist, said the two strokes have left them wary.
“Whenever Kelly has a headache, you always think, ‘Could it be another TIA?’” he said.
After recovering from surgery, Naab didn’t feel ready to run her usual half-marathon.
Instead, this past May, she formed a team of family and friends to compete in the Kaleida Health Heart to Heart Relay, supporting cardiac health research and programs at the hospital where she was treated, Buffalo General Medical Center/Gates Vascular Institute.
In September, she formed a team for CycleNation, a fundraiser for the American Stroke Association.
“It is sometimes hard to believe that I’ve had two stroke events and a heart surgery and am here today,” Naab said. “I’m so grateful for the care I have received and the latest research and procedures.”
