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Eating one avocado a day for six months was found to have no effect on belly fat, liver fat or waist circumference in people with overweight or obesity, according to a new study. However, it did lead to a slight decrease in unhealthy cholesterol levels.
In the randomized trial, the team — including Penn State researchers — also found that participants who ate avocados had better quality diets during the study period.
While prior, smaller studies have found a link between eating avocados and lower body weight, BMI, and waist circumferences, this was the largest, most extensive study to date on the health effects of avocados, including the large number of participants and length of the study period.
“While the avocados did not affect belly fat or weight gain, the study still provides evidence that avocados can be a beneficial addition to a well-balanced diet,” said Penny Kris-Etherton, Evan Pugh University Professor of Nutritional Sciences at Penn State. “Incorporating an avocado per day in this study did not cause weight gain and also caused a slight decrease in LDL cholesterol, which are all important findings for better health.”
Kristina Petersen, assistant professor of nutritional sciences at Texas Tech University, said the study also found that eating avocados daily improved the overall quality of the participants’ diets by eight points on a 100-point scale.
“Adherence to the Dietary Guidelines for Americans is generally poor in the U.S., and our findings suggest that eating an avocado per day can substantially increase overall diet quality,” Petersen said. “This is important because we know a higher diet quality is associated with lower risk of several diseases including heart disease, type 2 diabetes and some cancers.”
The research — recently published in the Journal of the American Heart Association — was conducted in conjunction with Loma Linda University, Tufts University, and UCLA, with coordinating support from Wake Forest University.

The gene defect underlying Krabbe disease causes degeneration of neurons directly, independent of its effects on other cell types, according to a new study publishing July 5 in the open-access journal PLOS Biology by Daesung Shin of the University at Buffalo, U.S. and colleagues. The discovery represents a new mechanism of action for the mutant gene, presenting a more accurate picture of the disease process that may help in the development of therapies.
Krabbe disease is a rare autosomal recessive neurodegenerative disorder caused by mutations in the galactosylceramidase (GALC) gene. GALC is an enzyme that is active in the lysosomes, and its absence leads to the buildup of the lipid psychosine. Accumulation of psychosine in the brain and elsewhere triggers destabilization of cell membranes, degeneration, and cell death. Loss of myelin insulation around the nerves is a major pathological feature of Krabbe disease, and oligodendrocytes, which make myelin, have naturally been thought of as the drivers of the disease process, with degeneration of neurons a secondary consequence of this loss of myelin.
Other, more recent evidence has suggested that neurons may be affected independently, but that hypothesis has been difficult to test, as GALC is expressed ubiquitously in the brain, and its disease-related loss occurs in all cell types. To overcome that barrier, the authors created a mouse model in which GALC expression was knocked out only in neurons, retaining activity of the normal gene elsewhere.
They found that psychosine accumulated in neurons, leading to abnormally shaped lysosomes, swollen axons, and increased neuronal death, along with neuroinflammation and deficits in motor ability and coordination in mice. While there was no loss of oligodendrocytes, lack of neuronal GALC expression did lead to a reduction in myelination, presumably through toxic effects on myelin sheaths from the accumulated psychosine.
“Our results indicate for the first time that neuronal expression of galactosylceramidase is essential to maintain and protect neuronal function, independent of its effects on myelin-producing oligodendrocytes,” Shin said. “These results suggest that lack of the enzyme in neurons may contribute directly to the pathogenesis in Krabbe disease, and that therapies for the disease may need to address the absence of neuronal expression of galactosylceramidase in order to be fully effective.”
Shin adds, “Our study is the first attempt in a preclinical live animal model to directly investigate the neuronal role of the Krabbe disease gene galactosylceramidase. In generating a neuron-specific mutant of Krabbe disease, we found an intrinsic neuronal role for this enzyme is particularly novel and exciting, suggesting that, independently of myelin and other brain cell types, neuronal galactosylceramidase has a primary role in neuronal homeostasis and thus galactosylceramidase-depleted neurons could primarily contribute to Krabbe disease. Since the protective role of neuronal galactosylceramidase is suggestive of a novel function unrelated to its canonical role in myelination, augmenting galactosylceramidase to neurons would likely improve the efficacy of therapeutic interventions for Krabbe disease.”
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New research by a scientist at the Milner Centre for Evolution at the University of Bath suggests that “selfish chromosomes” explain why most human embryos die very early on. The study, published in PLoS, Biology, explaining why fish embryos are fine but sadly humans’ embryos often don’t survive, has implications for the treatment of infertility.
About half of fertilised eggs die very early on, before a mother even knows she is pregnant. Tragically, many of those that survive to become a recognised pregnancy will be spontaneously aborted after a few weeks. Such miscarriages are both remarkably common and highly distressing.
Professor Laurence Hurst, Director of the Milner Centre for Evolution, investigated why, despite hundreds of thousands of years of evolution, it’s still so comparatively hard for humans to have a baby.
The immediate cause of much of these early deaths is that the embryos have the wrong number of chromosomes. Fertilised eggs should have 46 chromosomes, 23 from mum in the eggs, 23 from dad in the sperm.
Professor Hurst said: “Very many embryos have the wrong number of chromosomes, often 45 or 47, and nearly all of these die in the womb. Even in cases like Down syndrome with three copies of chromosome 21, about 80% sadly will not make it to term.”
Why then should gain or loss of one chromosome be so very common when it is also so lethal?

Researchers at the Department of Energy’s Oak Ridge National Laboratory have definitively linked the function of a specific domain of proteins important in plant-microbe biology to a cancer trigger in humans, knowledge that had eluded scientists for decades.
The team’s findings, published in Nature Communications Biology, open up a new avenue for the development of selective drug therapies to fight a variety of cancers such as those that begin in the breast and stomach.
ORNL scientists set out to prove experimentally what they first deduced with computational studies: that the plasminogen-apple-nematode, or PAN, domain is linked to the cell proliferation that drives tumor growth in humans and defense signaling during plant-microbe interactions in bioenergy crops. The association was first made as researchers explored the genomes of crops like poplar and willow.
In the latest study, the ORNL team pinpointed four core amino acids called cysteine residues in the HGF protein critical to the PAN domain’s function and studied their behavior in human cancer cell lines. They found that mutating any one of those amino acids turned off the signaling pathway known as HGF-c-MET that is abnormally heightened in cancer cells, causing them to rapidly multiply and spread.
Since cysteine residues are known to have many functions, the scientists also randomly tested other cysteines throughout the protein and found that none of them had the same impact on shutting down HGF-c-MET signaling. Mutating the four key cysteines had no effect on the overall structure of the protein, and merely inhibited the cancer signaling pathway, the team noted in the study.
Disrupting the right signal is one of the biggest challenges in developing new cancer therapies, said ORNL geneticist Wellington Muchero.

Artificial intelligence and machine learning are among the latest tools being used by cancer researchers to aid in detection and treatment of the disease.
One of the scientists working in this new frontier of cancer research is University of Colorado Cancer Center member Ryan Layer, PhD, who recently published a study detailing his research that uses big data to find cancerous mutations in cells.
“Identifying the genetic changes that cause healthy cells to become malignant can help doctors select therapies that specifically target the tumor,” says Layer, an assistant professor of computer science at CU Boulder. “For example, about 25% of breast cancers are HER2-positive, meaning the cells in this type of tumor have mutations that cause them to produce more of a protein called HER2 that helps them grow. Treatments that specifically target HER2 have dramatically increased survival rates for this type of breast cancer.”
Scientists can evaluate cell DNA to identify mutations, Layer says, but the challenge is that the human genome is massive, and mutations are a normal part of evolution.
“The human genome is long enough to fill a 1.2 million-page book, and any two people can have about 3 million genetic differences,” he says. “Finding one cancer-driving mutation in a tumor is like finding a needle in a stack of needles.”
Scanning the data
The ideal method of determining what type of cancer mutation a patient has is to compare two samples from the same patient, one from the tumor and one from healthy tissue. Such tests can be complicated and costly, however, so Layer hit upon another idea — using massive public DNA databases to look for common cell mutations that tend to be benign, so that researchers can identify rarer mutations that have the potential to be cancerous.

Normally, fat cells store energy. In brown fat cells, however, energy is dissipated as heat — brown fat thus serves as a biological heater. Most mammals therefore have this mechanism. In humans it keeps newborns warm, in human adults, brown fat activation positively correlates with cardio-metabolic health.
“Nowadays, however, we’re toasty warm even in winter,” explains Prof. Dr. Alexander Pfeifer from the Institute of Pharmacology and Toxicology at the University of Bonn. “So our body’s own furnaces are hardly needed anymore.” At the same time, we are eating an increasingly energy-dense diet and are also moving far less than our ancestors. These three factors are poison for brown fat cells: They gradually cease to function and eventually even die. On the other hand, the number of severely overweight people worldwide continues to increase. “Research groups around the world are therefore looking for substances that stimulate brown fat and thus increase fat burning,” says Pfeifer.
Dying fat cells boost energy combustion of their neighbors
Together with a group of colleagues, the team at the University of Bonn has now identified a key molecule named inosine that is capable of burning fat. “It is known that dying cells release a mix of messenger molecules that influence the function of their neighbors,” explains Dr. Birte Niemann from Pfeifer’s research group. Together with her colleague Dr. Saskia Haufs-Brusberg, she planned and conducted the central experiments of the study. “We wanted to know if this mechanism also exists in brown fat.”
The researchers therefore studied brown fat cells subjected to severe stress, so that the cells were virtually dying. “We found that they secrete the purine inosine in large quantities,” Niemann says. More interesting, however, was how intact brown fat cells responded to the molecular call for help: They were activated by inosine (or simply by dying cells in their vicinity). Inosine thus fanned the furnace inside them. White fat cells also converted to their brown siblings. Mice fed a high-energy diet and treated with inosine at the same time remained leaner compared to control animals and were protected from diabetes.
The inosine transporter seems to play an important role in this context: This protein in the cell membrane transports inosine into the cell, thus lowering the extracellular concentration. Therefore, inosine can no longer exert its combustion-promoting effect.
Drug inhibits the inosine transporter
“There is a drug that was actually developed for coagulation disorders, but also inhibits the inosine transporter,” says Pfeifer, who is also a member of the Transdisciplinary Research Areas “Life and Health” and “Sustainable Futures” at the University of Bonn. “We gave this drug to mice, and as a result they burned more energy.” Humans also have an inosine transporter. In two to four percent of all people, it is less active due to a genetic variation. “Our colleagues at the University of Leipzig have genetically analyzed 900 individuals,” Pfeifer explains. “Those subjects with the less active transporter were significantly leaner on average.”
These results suggest that inosine also regulates thermogenesis in human brown fat cells. Substances that interfere with the activity of the transporter could therefore potentially be suitable for the treatment of obesity. The drug already approved for coagulation disorders could serve as a starting point. “However, further studies in humans are needed to clarify the pharmacological potential of this mechanism,” Pfeifer says. Neither does he believe that a pill alone will be the solution to the world’s rampant obesity pandemic. “But the available therapies are not effective enough at the moment,” he stresses. “We therefore desperately need medications to normalize energy balance in obese patients.”
The key role played by the body’s own heating system is also demonstrated by a major new joined research consortium: The German Research Foundation (DFG) recently approved a Transregional Collaborative Research Center in which the Universities of Bonn, Hamburg and Munich conduct targeted research on brown adipose tissue.
The University of Bonn as well as the University Hospital Bonn, the University Medical Center Hamburg-Eppendorf, the University as well as the University Hospital Leipzig, the Helmholtz Center Munich and the University of Texas were involved in the study.
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Published1 hour agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesA big burst of exercise at the weekend is as good as spreading activity out across the week, according to a study.US researchers tracked 350,000 people over 10 years to see how well so-called weekend warriors fared. The findings, in the JAMA Internal Medicine journal, suggest the type and total amount of exercise count, rather than how many sessions.At least 150 minutes a week of moderate intensity exercise is recommended. Going for a brisk walk, a light effort cycle on a bike or playing doubles in tennis would count towards this.Or you could do 75 minutes of vigorous activity – something like running, swimming or playing a game of football – say health experts in guidance published by the NHS. Many of the participants in the US study clocked up this amount in a week. But some crammed it into one or two sessions rather than spacing it out. Those who reached their recommended level of activity, whether during the week or the weekend, had lower a death risk than those who did less than the recommend amount.Image source, Getty ImagesThe NHS also says people should do some form of physical activity everyday including strength exercises and try not to stay seated for extended periods of time.Strength exercises include yoga, pilates and heavy gardening. Very vigorous activity that can help achieve recommended physical activity levels and can be done in shorter, sharper bursts, includes:high-intensity interval trainingspinning classeslifting heavy weights hill sprintingBreathe harderBritish Heart Foundation senior cardiac nurse Joanne Whitmore said: “This large study suggests that, when it comes to exercise, it doesn’t matter when you do it. “The most important thing is that physical activity is undertaken in the first place.”Whether you cram your exercise in on the weekend or spread it across the week, aim for 150 minutes of moderate-intensity activity each week. “Exercise can improve your health, reducing your risk of heart and circulatory diseases like heart attack and stroke.”Moderate-intensity activities make you breathe harder and make your heartbeat faster than usual but you should still be able to have a conversation whilst doing them.”The NHS also recommends:toddlers are active for at least 180 minutes a daychildren and young people are active for about an hour a day More on this storyWeekend exercise ‘warriors’ boost health10 January 2017Could music festivals be good for your health?5 August 2019Related Internet LinksJAMA Internal MedicineThe BBC is not responsible for the content of external sites.

Convalescent plasma, widely given to severely ill patients hospitalized with COVID-19 during the pandemic, does not improve their ability to survive or recover, according to a national clinical trial led by Vanderbilt University Medical Center and published in the journal CHEST.
The multicenter blinded, randomized placebo-controlled, Passive Immunity Trial for our Nation (PassITON), looked at the efficacy and safety of COVID-19 convalescent plasma therapy for adults hospitalized with moderate to severe COVID-19 within 14 days of the onset of symptoms.
The rationale for using convalescent plasma for acute viral infections like COVID-19 has been that transfusing the plasma component of blood from a patient who has recently recovered from the same disease to a patient early in the stage of infection might provide the currently infected patient with antibodies against the infecting virus, helping them recover more quickly.
“During this trial, we were fortunate to have tremendous collaboration among thousands of people across the country, including patients, families, clinicians, study personnel at 25 hospitals and a wonderful team at VUMC,” said Wesley Self, MD, MPH, associate professor of Emergency Medicine, vice president for Clinical Research Networks and Strategy at VUMC and lead author of the study. “We asked a very specific question in this study: At time of hospital admission when a patient is severely ill with COVID, does the transfusion of convalescent plasma available to clinicians in the U.S. improve the ability to recover and survive? The answer is clearly no.”
“Providing passive immunity with convalescent plasma does not appear to benefit patients once their illness has progressed to the point of needing treatment in the hospital. Despite receiving convalescent plasma with a higher titer of neutralizing antibodies, the therapy did not help hospitalized patients,” said Todd Rice, MD, MSc, associate professor of Medicine, vice president for Clinical Trial Innovations and Operations at VUMC, and senior author of the study.
In the study 960 adults hospitalized with COVID-19 were randomized into two groups — those receiving one unit of convalescent therapy and those receiving placebo. The results showed that the two groups had nearly identical clinical outcomes; at 28 days following treatment, 18.5% of patients in the convalescent plasma group and 17.2% of patients in the placebo group had died.

A new type of vaccine provides protection against a variety of SARS-like betacoronaviruses, including SARS-CoV-2 variants, in mice and monkeys, according to a study led by researchers in the laboratory of Caltech’s Pamela Bjorkman, the David Baltimore Professor of Biology and Bioengineering.
Betacoronaviruses, including those that caused the SARS, MERS, and COVID-19 pandemics, are a subset of coronaviruses that infect humans and animals. The vaccine works by presenting the immune system with pieces of the spike proteins from SARS-CoV-2 and seven other SARS-like betacoronaviruses, attached to a protein nanoparticle structure, to induce the production of a broad spectrum of cross-reactive antibodies. Notably, when vaccinated with this so-called mosaic nanoparticle, animal models were protected from an additional coronavirus, SARS-CoV, that was not one of the eight represented on the nanoparticle vaccine.
“Animals vaccinated with the mosaic-8 nanoparticles elicited antibodies that recognized virtually every SARS-like betacoronavirus strain we evaluated,” says Caltech postdoctoral scholar Alexander Cohen (PhD ’21), co-first author on the new study. “Some of these viruses could be related to the strain that causes the next SARS-like betacoronavirus outbreak, so what we really want would be something that targets this entre group of viruses. We believe we have that.”
The research appears in a paper in the journal Science on July 5.
“SARS-CoV-2 has proven itself capable of making new variants that could prolong the global COVID-19 pandemic,” says Bjorkman, who is also a Merkin Institute Professor and executive officer for Biology and Biological Engineering. “In addition, the fact that three betacoronaviruses — SARS-CoV, MERS-CoV, and SARS-CoV-2 — have spilled over into humans from animal hosts in the last 20 years illustrates the need for making broadly protective vaccines.”
Such broad protection is needed, Bjorkman says, “because we can’t predict which virus or viruses among the vast numbers in animals will evolve in the future to infect humans to cause another epidemic or pandemic. What we’re trying to do is make an all-in-one vaccine protective against SARS-like betacoronaviruses regardless of which animal viruses might evolve to allow human infection and spread. This sort of vaccine would also protect against current and future SARS-CoV-2 variants without the need for updating.”
How it works: A vaccine composed of spike domains from eight different SARS-like coronaviruses

If carbon emissions are limited to slow temperature rise, up to an estimated 6,000 child deaths could be prevented in Africa each year, according to new research.
A team of international scientists, led by the University of Leeds in collaboration with researchers at the London School of Hygiene & Tropical Medicine (LSHTM), have shown that thousands of heat-related child deaths could be prevented if temperature increases are limited to the Paris Agreement’s 1.5ºC target through to 2050.
However, heat-related child deaths could double in sub-Saharan Africa by mid-century if high emissions continue.
Their workpublished in the journal Environmental Research Letters, estimated the impact of climate change on annual heat-related deaths of children under five years old in sub-Saharan Africa, from 1995 — 2050.
The findings show that since roughly 2009, heat-related child mortality has been at least double what it would have been without climate change.
The heat mortality increase from climate change caused by human activities and population growth outweighed reductions in heat-related death due to improvements associated with development, such as improved healthcare and sanitation measures.