Publisher Health

Adding additional salt to foods at a lower frequency is associated with a reduced risk of heart disease, heart failure and ischemic heart disease, according to a new study published today in the Journal of the American College of Cardiology. Even among those following a DASH-style diet, behavioral interventions to lessen salt consumption could further improve heart health.
There’s substantial evidence linking high sodium intake to high blood pressure, a major risk factor for cardiovascular disease. However, epidemiological studies investigating this link have produced conflicting results due to a lack of practical methods for assessing long-term dietary sodium intake. Recent studies suggest that the frequency at which an individual adds salt to their foods could be used to predict their individual sodium intake over time.
“Overall, we found that people who don’t shake on a little additional salt to their foods very often had a much lower risk of heart disease events, regardless of lifestyle factors and pre-existing disease,” said Lu Qi, MD, PhD, HCA Regents Distinguished Chair and professor at the School of Public Health and Tropical Medicine at Tulane University in New Orleans. “We also found that when patients combine a DASH diet with a low frequency of adding salt, they had the lowest heart disease risk. This is meaningful as reducing additional salt to food, not removing salt entirely, is an incredibly modifiable risk factor that we can hopefully encourage our patients to make without much sacrifice.”
In the current study, the authors evaluated whether the frequency of adding salt to foods was linked with incident heart disease risk in 176,570 participants from the UK Biobank. The study also examined the association between the frequency of adding salt to foods and the DASH diet as it relates to heart disease risk.
The study used a questionnaire at baseline to collect data on the frequency of adding salt to foods, not including salt used in cooking. Participants were also asked if they had made any major changes to their diet in the last 5 years, as well as complete 1-5 rounds of 24-hour dietary recalls over a three-year period.
The DASH-style diet was developed to prevent hypertension by limiting consumption of red and processed meats and focusing on vegetables, fruit, whole grains, low-fat dairy, nuts, and legumes. While the DASH diet has yielded benefits in relation to reducing cardiovascular disease risk, a recent clinical trial found that combining the DASH diet with sodium reduction was more beneficial for certain cardiac biomarkers, including cardiac injury, strain, and inflammation. The researchers calculated a modified DASH score that did not consider sodium intake based on seven foods and nutrients that were emphasized or deemphasized in the DASH-style diet.
Data on heart disease events was collected through medical history and data on hospital admissions, questionnaire and death register data.
Overall, study participants with a lower frequency of adding salt to foods were more likely to be women; white; have a lower body mass index; more likely to have moderate alcohol consumption; less likely to be current smokers; and more physically active. They also had a higher prevalence of high blood pressure and chronic kidney disease, but a lower prevalence of cancer. These participants were also more likely to adhere to a DASH-style diet and consumed more fruits, vegetables, nuts and legumes, whole grains, low-fat dietary but less sugar-sweetened drinks or red/processed meats than those with a higher frequency of adding salt to foods.
The researchers found the association of adding salt to foods with heart disease risk was stronger in participants of lower socioeconomic status, as well as in current smokers. A higher modified DASH diet score was associated with lower risk of heart disease events.
In a related editorial comment, Sara Ghoneim, MD, a gastroenterology fellow at the University of Nebraska Medical Center, wrote that the study is promising, builds on previous reports, and alludes to the potential impact of long-term salt preferences on total cardiovascular risk.
“A major limitation of the study is the self-reported frequency of adding salt to foods and the enrollment of participants only from the UK, limiting generalizability to other populations with different eating behaviors,” Ghoneim said. “The findings of the present study are encouraging and are poised to expand our understanding of salt-related behavioral interventions on cardiovascular health.”

Published13 hours agoSharecloseShare pageCopy linkAbout sharingImage source, PA MediaBy Jasmine AnderssonBBC NewsMigrants with symptoms of diphtheria are to be put into isolation, as cases of the disease rise, ministers say.Those showing signs of infection will be separated for a “short period” at the Manston processing centre in Kent, or at a “designated isolation centre” while they are treated.The decision follows the death of a man at Manston, which may have been caused by diphtheria. Health secretary Steve Barclay said the risk to the public was “very low”. During a visit to the Royal Marsden Hospital in London, Mr Barclay said a “very high uptake” of diphtheria vaccinations within the British public meant many people were well protected. He stressed that the situation was being monitored “closely”.Diphtheria cases rising among asylum seekersManston migrant centre: What were the problems?Two councils lose asylum hotels legal fightDiphtheria is a highly contagious infection that affects the nose, throat and sometimes cause ulcers on the skin.According to the NHS website, it is spread by coughs and sneezes or through close contact with someone who is infected, and in serious cases can be fatal.It can also be spread by sharing items such as cups, cutlery, clothing or bedding with an infected person. The UK Health Security Agency (UKHSA) said there had been an “increase” in cases of diphtheria reported among migrants arriving in the UK.It has confirmed 50 cases were identified as of 25 November, including among children. The figure stood at 39 on November 10.Public health experts have raised concerns about the spread of the disease as migrants were moved to hotels.The latest UKHSA report said 38 of the cases have been reported in south-east England, with some cases also detected across London, the West Midlands and the north-east of England.The health body has also advised vaccines and antibiotics are offered to people on arrival at their new accommodation.Image source, ReutersImmigration minister Robert Jenrick said any asylum seekers who may have the infection but are already in hotels will be told to isolate in their rooms while they are treated. He later confirmed the isolation centres would be similar to those used to curb infections during the Covid-19 pandemic.Mr Jenrick told the Commons: “From today, no-one presenting with symptoms will progress into the asylum accommodation system.”They will either remain at Manston, isolating for a short period, or they will travel to a designated isolation centre in secure transport where they will be treated until deemed medically fit.”The treatment of migrants at the processing centre in Kent has triggered a wave of campaigns and concern from health professionals and campaigners. At one point, the facility designed to hold 1,600 people contained 4,000. Charity Detention Action launched a legal campaign to remove migrants housed in the facility for longer than 24 hours. Home Secretary Suella Braverman said the overcrowding was caused by a lack of suitable accommodation.She told MPs: “What I have refused to do is to prematurely release thousands of people into local communities without having anywhere for them to stay.”A post-mortem examination is being carried out to determine the cause of death of the man who died after being held at Manston. A test indicated “diphtheria may be the cause” of his illness, government officials have said.More on this storyDiphtheria cases rising among asylum seekers2 days agoMigrant death may have been caused by diphtheria2 days agoMigrant staying at Manston processing centre dies19 November

Researchers at The University of Texas at Dallas and Novartis Pharmaceuticals Corp. have devised a computer-based platform for drug discovery that could make the process more effective, more efficient and less costly.
Dr. Baris Coskunuzer, professor of mathematical sciences at UT Dallas, and his colleagues developed an approach based on topological data analysis to screen thousands of possible drug candidates virtually and narrow the compound candidates considerably to those that are most fit for laboratory and clinical testing.
The researchers will present their findings at the 36th Conference on Neural Information Processing Systems, which will be held Nov. 28 through Dec. 9 in New Orleans.
Typically, the early phases of drug discovery involve researchers identifying a biological target, such as a protein associated with a disease of interest. The next step is to screen libraries of thousands of potential chemical compounds that might be effective or could be modified to affect the target to alleviate the disease’s cause or symptoms. The most promising candidates move on to the lengthy and expensive process of laboratory and clinical testing and regulatory approval.
“The drug-discovery process can take 10 to 15 years and cost a billion dollars,” Coskunuzer said. “Drug companies want a more cost-effective way to do this. They want to find the most promising compounds at the beginning of the process so they’re not wasting time testing dead ends.
“We have provided a completely new method of virtual screening that is computationally efficient and ranks compounds based on how likely they are to work.”
While virtual screening of libraries of chemical compounds is not new, Coskunuzer said his group’s approach significantly outperforms other state-of-the-art methods on large data sets.

A Cornell-led collaboration used machine learning to pinpoint the most accurate means, and timelines, for anticipating the advancement of Alzheimer’s disease in people who are either cognitively normal or experiencing mild cognitive impairment.
The modeling showed that predicting the future decline into dementia for individuals with mild cognitive impairment is easier and more accurate than it is for cognitively normal, or asymptomatic, individuals. At the same time, the researchers found that the predictions for cognitively normal subjects is less accurate for longer time horizons, but for individuals with mild cognitive impairment, the opposite is true.
The modeling also demonstrated that magnetic resonance imaging (MRI) is a useful prognostic tool for people in both stages, whereas tools that track molecular biomarkers, such as positron emission tomography (PET) scans, are more useful for people experiencing mild cognitive impairment.
The team’s paper, “Machine Learning Based Multi-Modal Prediction of Future Decline Toward Alzheimer’s Disease: An Empirical Study,” published Nov. 16 in PLOS ONE. The lead author is Batuhan Karaman, a doctoral student in the field of electrical and computer engineering.
Alzheimer’s disease can take years, sometimes decades, to progress before a person exhibits symptoms. Once diagnosed, some individuals decline rapidly but others can live with mild symptoms for years, which makes forecasting the rate of the disease’s advancement a challenge.
“When we can confidently say someone has dementia, it is too late. A lot of damage has already happened to the brain, and it’s irreversible damage,” said senior author Mert Sabuncu, associate professor of electrical and computer engineering in the College of Engineering and of electrical engineering in radiology at Weill Cornell Medicine.

A new study suggests a link between the large gatherings and a slightly higher number of transplants after traffic crashes.This summer, when half a million bikers clogged the streets of tiny Sturgis, S.D., for one of the country’s largest motorcycle rallies, there might have been a small unexpected benefit for nearby patients desperately awaiting organ transplants.Major motorcycle rallies are associated with increases in organ donors involved in motor vehicle crashes, according to a study published this week in JAMA Internal Medicine.The authors theorized this could be because of the numbers of motorcyclists attracted to the rallies, dangerously congested roads designed for far less traffic, or riskier behaviors such as riding while fatigued.Although they were careful to emphasize that policymakers should focus on reducing traffic deaths, the researchers wrote that they should also “anticipate and translate eligible deaths from these events into organ donations.”The lead author, Dr. David Cron, who is a surgery resident at Massachusetts General Hospital, said he got the idea for the study when a colleague described working at another facility near a major rally in New Hampshire. “They used to gear up for these events and increase staff in the emergency department and plan for an influx in motor vehicle-related trauma,” he recalled.Previous research has linked such rallies to increases in crashes and fatalities, but the new study found there were 21 percent more organ donors during major rallies than in the surrounding time periods, amounting to one additional donor for every two major motorcycle rallies.Dr. Cron and the article’s co-authors identified seven of the country’s largest annual motorcycle gatherings, including the one held in Sturgis, accounting for more than 100 separate rallies in a 16-year period. Then, the researchers analyzed data about organ donations and transplants from the Scientific Registry of Transplant Recipients, which divides the nation into eleven administrative regions.The researchers compared the number of people involved in motor-vehicle crashes who donated organs the week of a rally in one of those regions with the number of donors involved in crashes in four-week periods before and after the gathering.But the researchers were unable to determine whether the organ donors were people who died in motorcycle crashes or in other vehicles. Overall, motorcycle crash deaths account for a growing share of overall traffic deaths. According to the National Highway Traffic Safety Administration, there were 5,579 motorcycle fatalities in 2020, more than any previous year and nearly double the number from two decades ago.Laura Siminoff, a professor at Temple University and expert on organ donation who was not involved in the study, said it was “kind of obvious” that motorcycle rallies would be associated with greater numbers of fatal injuries. The more important implication, she said, was that hospitals and organ-procurement organizations were doing their jobs by facilitating donations from eligible patients.In the United States, motor vehicle crashes are among the most common circumstances leading to organ donations by deceased people, which can only take place under certain conditions. Deceased donors have typically suffered catastrophic brain injuries but their other organs are sufficiently healthy to transplant. About one in 30 people who die in motor vehicle crashes ultimately becomes an organ donor. (Last year, about 6,500 living people donated a kidney or part of their liver, too.)The researchers showed that the motorcycle rallies were not associated with upticks in the number of organ donors who died of strokes or drug overdoses, other circumstances that commonly allow for donations. During the weeks of the rallies, there were no observable changes in organ donation in non-neighboring regions, which made it less likely to be some unknown factor causing an increase in organ donation.Kevin Myer, president of LifeGift Organ Donation Center based in Houston, said most victims of fatal motorcycle crashes suffered significant injuries that rendered their organs unusable, which he suggested might have reduced the number of donations that otherwise would have been possible at the time of the rallies.Most states that previously required all motorcyclists to wear helmets have relaxed those laws. Of the states where the major motorcycle rallies in the study occurred, none have universal helmet laws, according to the Governor’s Highway Safety Association.“While I respect folks who love motorcycles and stuff like that, they really should wear their helmets,” Mr. Myer said.Although the apparent effect the rallies had on the number of transplants was small, there are scores of motorcycle rallies held across the county each year.Still, Dr. Cron said, “it’s just scratching the surface of the massive organ shortage.”Over 105,000 people are on the national waiting list for an organ transplant, and 17 die each day. Although over 90 percent of people have voiced support for organ donation, just half the population has registered to be an organ donor.

A research team led by the University of California, Riverside, has discovered important details about how therapeutically relevant human monoclonal antibodies can protect against Crimean Congo Hemorrhagic Fever virus, or CCHFV. Their work, which appears online in the journal Nature Communications, could lead to the development of targeted therapeutics for infected patients.
An emerging zoonotic disease with a propensity to spread, CCHF is considered a priority pathogen by the World Health Organization, or WHO. CCHF outbreaks have a mortality rate of up to 40%. Originally described in Crimea in 1944-1945, and decades later in the Congo, the virus has recently spread to Western Europe through ticks carried by migratory birds. The disease is already endemic in Africa, the Balkans, the Middle East, and some Asian countries. CCHFV is designated as a biosafety level 4 pathogen (the highest level of biocontainment) and is a Category A bioterrorism/biological warfare agent. There is no vaccine to help prevent infection and therapeutics are lacking.
Scott D. Pegan, a professor of biomedical sciences in the UCR School of Medicine, collaborated on this study with the United States Army Medical Research Institute of Infectious Diseases, or USAMRIID, which studies CCHFV because of the threat it poses to military personnel around the world. They examined monoclonal antibodies, or mAbs, which are proteins that bind to antigens — foreign substances that enter the body and cause the immune system to mount a protective response.
In a previous publication, USAMRIID scientists Joseph W. Golden and Aura R. Garrison reported that an antibody called 13G8 protected mice from lethal CCHFV when administered post-infection. They provided Pegan with the sequence information for that antibody, clearing the way for UCR to “humanize” it and conduct further research.
“The USAMRIID study showed that the mouse mAb, 13G8, helps the immune system clear the infection,” Pegan said. “We knew 13G8 binds to a viral glycoprotein called GP38, but it wasn’t clear where that binding took place. So we analyzed the structure to gain an understanding of how it works and pinpoint exactly where the binding occurs. This knowledge sheds light on the potential of these mAbs to be effective against a broad range of CCHF viral strains.”
Members of Pegan’s research team were also able to obtain serum from patients who contracted CCHF in Turkey. The researchers isolated seven mAbs from a CCHFV survivor and identified two new antigenic sites on GP38. They then solved the structure of GP38 bound to one of the seven non-neutralizing human antibodies, in addition to 13G8. Knowledge of the structure of this complex can confer a clinical benefit as well, according to the authors.
“This structural information further characterizes GP38 as an antigen of interest for vaccination studies, while also advancing mAb development toward CCHFV,” Garrison said. “The therapeutic role for non-neutralizing antibodies in preventing disease is becoming more evident for high-risk pathogens such as Ebola, Lassa, and Nipah virus.”
Pegan explained that CCHFV has a tri-segmented RNA genome, consisting of a large, medium, and small segment. In 2006, GP38 was identified as a component of the medium fragment by the Special Pathogens Branch at the Centers for Disease Control and Prevention, or CDC, which also contributed to the Nature Communications study. The function of GP38 and its role in CCHFV infection remain unclear.
“We know that targeting GP38 stops CCHFV’s progression, but no one is fully certain about how it works,” Pegan said. “We would like to know more about its mechanism of action so that specific and effective therapeutics can be developed.”
The research was funded by grants to Pegan and his CDC partner, Éric Bergeron, from the National Institutes of Health and the Department of Defense. Golden and Garrison were supported by the Military Infectious Diseases Research Program.
Pegan, Garrison, and Bergeron were joined in the study by Elif Karaaslan, Jack McGuire, and David Gonzalez of UC Riverside; Ian A. Durie, Suzanne Enos, and Jarrod J. Mousa of the University of Georgia; Zahra R. Tehrani and Mohammad M. Sajadi of the University of Maryland School of Medicine; Teresa E. Sorvillo, Stephen R. Welch, Markus H. Kainulainen, Jessica R. Harmon, Jessica R. Spengler, and Christina F. Spiropoulou of the CDC’s Special Pathogens Branch; Joseph W. Golden of USAMRIID; Iftihar Koksal of Acibadem University Atakent Hospital, Turkey; Gurdal Yilmaz, Sanaz Hamidi, and Cansu Albay of Karasdeniz Technical University School of Medicine, Turkey; and Hanife Nur Karakoc of Bitlis State Hospital, Turkey.

More than half of all women in the United States are overweight or obese when they become pregnant. While being or becoming overweight during pregnancy can have potential health risks for moms, there are also hints that it may tip the scales for their kids to develop psychiatric disorders like autism or depression, which often affects one gender more than the other.
What hasn’t been understood however is how the accumulation of fat tissue in mom might signal through the placenta in a sex-specific way and rearrange the developing offspring’s brain.
To fill this gap, Duke postdoctoral researcher Alexis Ceasrine, Ph.D., and her team in the lab of Duke psychology & neuroscience professor Staci Bilbo, Ph.D., studied pregnant mice on a high-fat diet. In findings appearing November 28 in the journal Nature Metabolism, they found that mom’s high-fat diet triggers immune cells in the developing brains of male but not female mouse pups to overconsume the mood-influencing brain chemical serotonin, leading to depressed-like behavior.
The researchers said a similar thing may be happening in humans, too.
People with mood disorders like depression often lose interest in pleasurable activities. For mice, one innately pleasurable activity is drinking sugar water. Since mice preferentially sip sugar water over plain tap when given the choice, Ceasrine measured their drink preference as an estimate for depression. Males, but not females, born by moms on a high-fat diet lacked a preference for simple syrup over tap water. This rodent-like depression suggested to Ceasrine that mom’s nutrition while pregnant must have changed their male offspring’s brain during development.
One immediate suspect was serotonin. Often called the “happy” chemical, serotonin is a molecular brain messenger that’s typically reduced in people with depression.

Gene variants associated with leukaemia can produce ‘rogue’ immune cells that drive autoimmune diseases, according to a new study from the Garvan Institute of Medical Research.
Scientists had previously noticed that leukaemia patients were also likely to develop an autoimmune disease, such as rheumatoid arthritis or aplastic anaemia. Research into this link revealed that immune cells called killer T cells — responsible for destroying harmful cells and pathogens — were a key player.
This new research provides insight into the role these killer T cells play in leukaemia and autoimmune disease. Gene variations affecting a protein that controls the growth of killer T cells can turn them rogue, the researchers found.
“We showed that these rogue killer T cells are driving the autoimmunity. They’re probably one of the cell types most directly contributing to autoimmune disease,” says Dr Etienne Masle-Farquhar, a postdoctoral researcher in the Immunogenomics and Genomic Medicine Labs at Garvan.
“Our research also narrows down a few pathways that might be helpful in targeting these cells for future treatments,” he says.
The findings are published in the journal, Immunity.
Cancers can grow when tumour cells are not identified or destroyed by the immune system. Autoimmune diseases occur when the immune system attacks the body’s own cells, mistaking them for harmful or foreign cells.

Researchers at Tohoku University have shown that astrocytes in the mouse brain exhibit an acid response with intensified epileptic seizures. The astrocytes’ acid response could lead to the amplification of excitatory neuronal signals and be the underlying drive for generating plasticity for epileptogenesis.
The findings were detailed in the journal Brain on November 25, 2022.
Cells in the brain can be divided into neurons and glia. Astrocytes are a major subtype of glia, controlling the local ionic and metabotropic environment in the brain.
To better understand astrocytes and the brain environment, fluorescent sensor proteins were genetically expressed in the astrocytes of mice. The researchers then implanted an optical fiber into the lateral hypothalamus of the mouse brain, to send excitation light and record fluorescence signals. By analyzing the signals recorded with this newly devised fiber photometry method, astrocytes’ activity was evaluated and critical components of local brain environmental changes were dissected.
Utilizing optical signals to gain insights into the living brain of experimental animals has been widely used in recent neuroscience studies. Despite occupying nearly half of the brain, astrocytes do not generate electrical signals, meaning traditional electroencephalogram studies, where electrical activity in the brain is measured with electrodes attached to the scalp, cannot be applied to study the function of astrocytes. Hence why the researchers turned to fiber photometry technology.
“Glia’s participation in the brain’s information processing, plasticity, and health has long been an enigma,” says Professor Ko Matsui of the Super-network Brain Physiology lab at Tohoku University, who led the research. “Our newly created fiber photometry method provides a gateway for understanding the physiology of glia in healthy and diseased living brains.”
The researchers were not the first to employ fiber photometry technology, but most previous studies have neglected the effects of local blood volume and cytosolic pH changes on the detected fluorescence signals. Lead study investigator Dr. Yoko Ikoma, Matsui, and their team, however, broadened the analysis of detected fluorescence signals to extract as much of the local environmental parameters as possible.
“This study could equal the feat of Hodgkin and Huxley in the 1970s,” adds Matsui. “They dissected the time course of Na+ and K+ channel activation from a single action potential waveform; whilst we were able to dissect the Ca2+, pH, and local brain blood volume changes from the detected fluorescence signals. The general goal of physiology is to untangle the detected signals and to unveil the essential truth behind what we can observe.”
Ikoma says that their technological breakthrough could be harnessed to understand the role of local brain environmental changes in many brain pathologies. “A therapeutic strategy designed to control astrocytes’ pH could potentially be used not only for treating epilepsy but also stroke or trauma-induced brain injury — even for memory enhancement in dementia treatment.”
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Many human diseases can be detected and diagnosed using biomarkers in blood or other body fluids. Parkinson’s disease is different: to date, there is no such biomarker being used in the clinicto indicate this neurodegenerative disease.
A team led by ETH Zurich Professor Paola Picotti could now help to close this gap. In a study just published in the journal Nature Structural and Molecular Biology, the researchers present 76 proteins that might serve as biomarkers for the detection of Parkinson’s disease.
Different protein structure
What makes this study special is that while the potential biomarker proteins are found in both healthy and diseased individuals, their molecules are present in different shapes (or structures) in each of the two groups. It is not the presence of certain proteins that indicates the disease, but rather the shape they have assumed. This is the first time that scientists have shown that an analysis of the structures of all proteins in a body fluid can identify potential biomarkers for disease.
The next step will be to thoroughly test the markers found and verify them using larger groups of patients. That means these candidates are not yet available for clinical diagnoses. “But from what we’ve seen so far, they’re actually a very strong indicator for the disease. So I’m confident that this idea of structural biomarkers will bear out,” says Natalie de Souza, senior scientist in Paola Picotti’s group and one of the study’s co-authors.
Measuring structural changes
In their study, the ETH Zurich researchers examined the cerebrospinal fluid of 50 healthy individuals and 50 Parkinson’s patients. The sample material was provided to them by Dutch clinicians.