Publisher Health

The amount of nutrients people get from the crops that they eat is a type of ‘postcode lottery’, according to new research that has analysed thousands of cereal grains and soils as part of a project to tackle hidden hunger in Malawi and Ethiopia.
A global team led by the University of Nottingham and its Future Food Beacon including academics and researchers from Addis Ababa University (AAU) in Ethiopia and Lilongwe University of Agriculture and Natural Resources (LUANAR) in Malawi, working on the GeoNutrition project, have discovered more about the relation between soils, crops and micronutrient deficiencies among people living there. Their findings have been published today in the journal Nature.
The team analysed the grain of more than 3000 cereal crop samples from farmers’ fields in Ethiopia and Malawi. They found that the amount of the dietary micronutrients calcium, iron, selenium, and zinc in the cereal grain varied substantially with location, with some areas showing much lower levels of micronutrients than others. Some cereal types, such as millets, are more nutritious than others, such as maize. However, whether deficiencies are likely in an area also depends on its soils and landscapes.
Micronutrients include the vitamins and minerals which the body requires from the diet in small quantities, for a range of functions. Micronutrient deficiencies, also known as hidden hunger, are common globally, affecting more than half of children younger than 5 years of age, especially where access to sufficient food from plant and animal sources that are rich in micronutrients is limited for socioeconomic reasons. Micronutrient deficiencies pose a serious risk to human health, including the growth and cognitive development of children and susceptibility to infectious and non-communicable diseases.
This research shows that location is intrinsically linked to the nutritional quality of diets. Getting enough micronutrients is a type of ‘postcode lottery’ with nutritional value varying by location. This will particularly affect rural households who consume locally sourced food, including many smallholder farming communities where location may even be the largest influencing factor in determining the dietary intake of micronutrients.
The project was funded primarily by the Bill & Melinda Gates Foundation, led by Martin Broadley, Professor of Plant Nutrition in the School of Biosciences and a contributor to the Future Food Beacon. He said: “It is important to have good quality evidence on the nutritional quality of diets if we are going to support public health and agriculture policies to improve peoples’ health and wellbeing. Mapping the quality of diets is an important part of this evidence.”
The co-lead authors of the paper are Dr Dawd Gashu, working in the Centre for Food Science and Nutrition at AAU, and Dr Patson Nalivata, in the Department of Crop and Soil Science at LUANAR. Dr Gashu said, “Nutritional surveillance work on the quality of staple cereals is an important part of wider public health policies to address micronutrient deficiencies and we hope that this type of work is now adopted in more countries.” Dr Nalivata said, “By learning more about how the nutritional quality of cereal grains is linked to soil types and landscapes, as we have in this study, we are now better able to advise farmers how to choose and cultivate more nutritious crops.”
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Nearly a quarter of pregnant women say they’ve been around secondhand smoke — in their homes, at work, around a friend or relative — which, according to new research, is linked to epigenetic changes — meaning changes to how genes are regulated rather than changes to the genetic code itself — in babies that could raise the risk of developmental disorders and cancer.
The study, published today in Environmental Health Perspectives by researchers at Virginia Commonwealth University Massey Cancer Center, is the first to connect secondhand smoke during pregnancy with epigenetic modifications to disease-related genes, measured at birth, which supports the idea that many adult diseases have their origins in environmental exposures — such as stress, poor nutrition, pollution or tobacco smoke — during early development.
“What we recommend to mothers in general is that no level of smoke exposure is safe,” said study lead author Bernard Fuemmeler, Ph.D., M.P.H., associate director for population science and interim co-leader of the Cancer Prevention and Control program at VCU Massey Cancer Center. “Even low levels of smoke from secondhand exposure affect epigenetic marks in disease-related pathways. That doesn’t mean everyone who is exposed will have a child with some disease outcome, but it contributes to a heightened risk.”
Fuemmeler and colleagues analyzed data from 79 pregnant women enrolled in the Newborn Epigenetics Study (NEST) between 2005 and 2011. During the first trimester, all had a concentration of cotinine — a nicotine byproduct — in their blood consistent with low levels of smoke exposure, ranging from essentially none to levels consistent with secondhand smoke.
After these women gave birth, the researchers sampled the umbilical cord blood, which is the same blood that circulates through the fetus in utero, and performed what’s referred to as an epigenome-wide association study (EWAS) to search for correlations between blood cotinine levels of the mothers during pregnancy and epigenetic patterns in the babies at birth.
When cotinine levels were higher, the newborns were more likely to have epigenetic “marks” on genes that control the development of brain function, as well as genes related to diabetes and cancer.
These marks could mean either unusually many or unusually few molecules bound to the DNA strand, which affects how accessible a particular gene is. If a gene is bound up tightly by lots of marks, then it’s harder for molecular machinery to access and less likely to be expressed. On the other hand, if a gene is relatively unencumbered, then it might be expressed at higher levels than normal. Tipping the scale in either direction could lead to disease.
To solidify their results, the team repeated the analysis in a separate sample of 115 women and found changes to two of the same disease-related epigenetic regions — one that regulates genes involved in inflammation and diabetes and another that regulates cardiovascular and nervous system functions — are correlated with cotinine levels in mothers.
In all cases, the analyses controlled for race, ethnicity, age, prior number of children and maternal education.
“It highlights the importance of clean air,” said Fuemmeler, who is also a professor of health behavior and policy in the VCU School of Medicine and holds the Gordon D. Ginder, M.D., Chair in Cancer Research at Massey. “It’s important not only for our homes, but also in the environment. Clean air policies limit smoke in public, and for pregnant women that may have long-term effects on offspring.”
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The nerve cells, also called neurons, in our brain control all the basic processes of our body. For this reason, there are different types of neurons distributed over specific regions of the brain. Researchers at the Max Planck Institute for Metabolic Research and the CECAD Cluster of Excellence in Aging Research of the University of Cologne have developed an approach that allows them to show that neurons that are supposedly the same are actually very different: they not only sense different hormones for the body’s energy state, but also have a different influence on food intake. This can have a direct effect on our metabolism, for example by differentially restraining our appetite.
The brain processes our sensory perceptions, controls our behaviour and stores our memories. Because of these many functions, different types of nerve cells with specific tasks exist in different regions of our brain. One such type of nerve cells are the so-called POMC neurons, which play an important role in the metabolism of our body. “POMC neurons are critically involved in the control of appetite, energy expenditure and metabolism,” explains Nasim Biglari, a recently graduated PhD and first author of the study. “In recent years, it has been increasingly confirmed that POMC neurons are more diverse than previously thought.” Such differences result, for example, from a different response to hormones secreted by the body and are only noticeable when individual POMC neurons are compared with each other. In such a case, scientists refer to different subtypes of neurons. “Whether the different subtypes also play a different role in metabolism has not been clarified so far,” says Nasim Biglari.
Same nerve cell — different influence on food intake
“We have now succeeded in making different subtypes of neurons visible in mice at the genetic level and thus were able to subject them to more detailed investigation,” says Nasim Biglari. “Using this new, genetic approach, we were able to describe two different subtypes of POMC neurons in detail for the first time. For example, our results show a different distribution of the two subtypes within the same specific brain region. Moreover, they sense different hormones for the body’s energy state. The two subtypes even act differently on food intake, with one part of the POMC neurons suppressing appetite more potently than the other.” Because of the influence of POMC neurons on metabolism and food intake, these observations could also be relevant to diseases such as obesity and diabetes.
“We were able to show for the first time that the diversity of POMC neurons is important for their function in the control of metabolism. In further experiments, we would like to increasingly address the questions of how the two subtypes of POMC neurons influence metabolism in detail and which neuronal circuits in the brain they engage to carry out their effects,” Nasim Biglari is looking forward to future experiments. “More generally, however, the approach we have developed can also be used to identify cell subtypes in other organs and for other types of cells. This could lead to many more insights into the diversity of our body’s cells.”
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World-leading eye experts have made a breakthrough that could potentially change the way cataracts are treated — with potential for drug therapy to replace surgery.
Cataract is a clouding of the eye lens that develops over time and affects the quality of vision. It is caused by an accumulation of protein in the lens that reduce the transmission of light to the retina. Previous research led by ARU found that cataracts account for almost half of global cases of blindness.
A significantly developed cataract can only currently be treated by a surgical procedure to remove the cloudy lens and insert an artificial replacement.
A team of international scientists, led by Professor Barbara Pierscionek of Anglia Ruskin University (ARU), has published peer-reviewed research that shows the sophisticated optics of the lens develops much earlier in gestation than has previously been thought possible. They also found how a particular protein (aquaporin) responsible for water passage in the lens disrupts the optical development, leading to cataract formation.
The scientists have spent more than a decade conducting the most precise measurements on optics of the lens at SPring-8, the world’s largest and most powerful synchrotron, in Japan.
The synchrotron is a particle accelerator that produces powerful X-rays by accelerating electrons to the speed of light. The X-rays allow measurements to be taken with the highest accuracy yet on optical properties of the eye.
The project team is the first in the world to have measured how the optics in the eye lens develop. Their research was presented earlier this month at the Association for Research in Vision and Ophthalmology (ARVO) annual meeting.
Professor Pierscionek, Deputy Dean (Research and Innovation) for the Faculty of Health, Education, Medicine and Social Care and member of the Medical Technology Research Centre at ARU, said: “Cataracts are one of the main causes of vision loss and blindness worldwide, yet for many people surgery is inaccessible for various reasons.
“Our findings indicate the role of the aquaporin proteins and the crucial importance of this for the lens to work correctly and the eye to see clearly.
“Further research in this area is planned, but this discovery, together with our research on nanotechnologies that indicate drug therapy for cataract is possible, could potentially revolutionise the way cataract is treated, opening up the field for drug-based therapy rather than surgery. This would have exciting implications for public health.”
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A pioneering new study led by UCL scientists has revealed, for the first time, a layer of genetic material involved in controlling the production of tau; a protein which plays a critical role in serious degenerative conditions, such as Parkinson’s and Alzheimer’s disease.
The international research, conducted in mice and cells, also revealed this material is part of a larger family of non-coding genes* which control and regulate other similar brain proteins, such as beta-amyloid associated with Alzheimer’s and alpha-synuclein implicated in Parkinson’s disease and Lewy body dementia.
Researchers say the breakthrough findings, published in Nature, shed an important new light on how proteins linked to neurological conditions are produced and controlled, and could pave the way for new treatments for a wide range of dementia related diseases.
Lead author, Dr Roberto Simone (UCL Queen Square Institute of Neurology), said: “Tau plays a vital role inside our brain cells: It helps to stabilise and maintain the cytoskeletal structures that allow different materials to be transported to where they need to be. We know that too much tau is detrimental — the excess unused tau converts into toxic species that may be responsible for damaging cells and driving the spread and progression of degenerative disease. However, despite the fact that tau has been studied for more than three decades, until now we did not know how tau protein production is controlled.”
For the laboratory-based study, researchers identified a section of genetic material known as ‘antisense long non-coding RNA’ (lncRNA). They discovered this material does not make tau directly but helps to regulate, fine-tune and repress the production of the protein inside brain cells. This precision provided by antisense lncRNA in tau regulation could be crucial for smooth functioning of the brain’s nerve cells.
Research group leader, Professor Rohan de Silva (UCL Queen Square Institute of Neurology) said: “Excitingly, we found that the lncRNA that controls tau is not unique. Other key proteins we know to be involved in neurological conditions, including alpha-synuclein in Parkinson’s disease and beta-amyloid in Alzheimer’s disease, are controlled by very similar lncRNAs. This means we may have found the key to regulating the production of a whole range of proteins involved in brain function and the development of these devastating conditions.

The latest findings show that with clever science, a single fingerprint left at a crime scene could be used to determine whether someone has touched or ingested class A drugs.
In a paper published in Royal Society of Chemistry’s Analyst journal, a team of researchers at the University of Surrey, in collaboration with the National Centre of Excellence in Mass Spectrometry Imaging at the National Physical Laboratory (NPL) and Ionoptika Ltd reveal how they have been able to identify the differences between the fingerprints of people who touched cocaine compared with those who have ingested the drug — even if the hands are not washed. The smart science behind the advance is the mass spectrometry imaging tools applied to the detection of cocaine and its metabolites in fingerprints.
This is a step up from research previously conducted by the University. In 2020 Surrey researchers were able to determine the difference between touch and ingestion if someone had washed their hands prior to giving a sample. Given that a suspect at a crime scene is unlikely to wash their hands before leaving fingerprints, these new findings are a significant advantage to crime forensics.
The Surrey team have continued to use their world-leading experimental fingerprint drug testing approach based on high resolution mass spectrometry. Cocaine and its primary metabolite — benzoylecgonine*, can be imaged in fingerprints produced after either ingestion or contact with cocaine using these techniques. By analysing the images of cocaine and its metabolite in a fingerprint, and exploring the relationship between these molecules and the fingerprint ridges, it is possible to tell the difference between a person who has ingested a drug, and someone who has only touched it.
Dr Melanie Bailey, Reader in Forensic and Analytical Science and EPSRC Fellow at the University of Surrey, said: “Over the decades, fingerprinting technology has provided forensics with a great deal of information about gender and medication. Now, these new findings will inform forensics further when it comes to determining the use of class A drugs.
“In forensic science being able to understand more about the circumstances under which a fingerprint was deposited at a crime scene is important. This gives us the opportunity to reconstruct more detailed information from crime scenes in the future. The new research demonstrates that this is possible for the first time using high resolution mass spectrometry techniques.”
Dr Allen Bellew, Applications & Marketing Manager at Ionoptika, commented: “To image these metabolites excreted through the skin requires very powerful analytical tools such as the unique Water Cluster Source that Ionoptika has been developing for over a decade. It’s clear that this new technique will be important for forensic science in the future, and as a small business in the UK it’s very exciting to see the role that our J105 SIMS instrument has played in its development.”
Dr Chelsea Nikula, Higher Research Scientist, NPL said: “This novel application of three different techniques illustrates the capabilities of mass spectrometry imaging to enable next generation forensics analyses. It is great to see that the work we do here at NPL and the facilities we have available to us at the National Centre of Excellence in Mass Spectrometry Imaging helped support this research.”
*Benzoylecgonine is a molecule produced in the body when cocaine is ingested, and it is essential in distinguishing those who have consumed the class A drug from those who have handled it.
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Base editing is a novel gene editing approach that can precisely change individual building blocks in a DNA sequence. By installing such a point mutation in a specific gene, an international research team led by the University of Zurich has succeeded in sustainably lowering high LDL cholesterol levels in the blood of mice and macaques. This opens up the possibility of curing patients with inherited metabolic liver diseases.
Lipoproteins are complex particles that deliver fat molecules to all tissues of the body through the blood system, supplying energy to the cells. One such lipoprotein, the low-density lipoprotein (LDL), can transport thousands of fat molecules, such as cholesterol, per particle. High levels of LDL in the blood are clinically associated with an increased risk of cardiovascular diseases. Since LDL can also carry cholesterol into smaller vessels and thus supply more distant tissues, it can increasingly block the artery lumen, which leads to atherosclerosis.
Introducing a single gene mutation blocks an enzyme
An international research team led by the University of Zurich (UZH) has now demonstrated that a novel precise gene editing approach can reduce high LDL cholesterol levels — substantially and sustainably. The scientists introduced a single point mutation in the gene encoding for an enzyme called PCSK9. This protein is involved in the uptake of LDL cholesterol from the blood into the cells. “The genetic change we induced in mice and macaques successfully blocked PCSK9, which led to a significant reduction of the LDL cholesterol concentrations in the blood. This provides a potential therapy for patients suffering from familial hypercholesterolemia, an inherited form of high cholesterol levels,” says study leader Gerald Schwank, professor at the Institute for Pharmacology and Toxicology of UZH.
Adaption of RNA technology used in COVID-19 vaccines
The gene editing technology applied by the researchers uses what are known as base editors. These proteins can change individual bases of the DNA molecule — a single “letter” of a genetic “text” — into another. Adenine base editors, for example, convert an adenine (A) into a guanine (G). And base editors do this much more precisely than previous CRISPR-Cas nucleases, which function as molecular scissors. To control the delivery of the base editor tool into the liver of animals, the researchers adapted the RNA technology used in COVID-19 vaccines. However, instead of encapsulating an RNA encoding the spike protein of SARS-CoV2 into lipid nanoparticles, they encapsulated an RNA encoding for the adenine base editor.
Accurate, efficient and safe
The RNA-lipid nanoparticles formulations were introduced into the animals intravenously, leading to liver-specific uptake and transient production of the base editor tool by the cell machinery. “Up to two-thirds of PCSK9 genes were edited in the mice and up to one-third in the non-human primates, leading to a significant reduction in LDL cholesterol levels,” says Schwank. In addition, the scientists carefully assessed whether unspecific editing at undesired locations occurred, but found no indications of such off-target events.
RNA-based therapies for metabolic liver diseases
“Our study shows the feasibility of installing single nucleotide base changes in the liver of non-human primates with high efficiency and accuracy. Approximately 30 percent of all disease-causing hereditary mutations are single base mutations that can, in principle, be corrected with base editors,” says Schwank. The new approach could therefore be used to treat a large number of patients suffering from inherited metabolic liver diseases, such as hypercholesterolemia, phenylketonuria or urea cycle disorders. Compared to conventional drugs, genome editing has the advantage that induced changes are sustainable. Thus, if a mutation is repaired in a sufficient number of cells, the patient will be permanently cured.
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Scientists have successfully treated flies displaying behavioural problems linked to newly discovered schizophrenia-associated genes in humans, using common anti-psychotics.
Schizophrenia is a severe long-term mental health condition that is historically poorly understood and treated. It is relatively common, affecting one to two per cent of the population, and is known to be up to 80 per cent genetic in origin.
Recent advances in sequencing genomes of people with schizophrenia have identified a list of novel genes and mutations associated with the disease. Many are expressed in the brain and are involved in how neurons communicate with each other by electrical and chemical signals released at synapses.
The research was performed by the first student, Dr Sergio Hidalgo, on the dual PhD program from the Universities of Bristol (UK) and the Pontificia Universidad Catolica de Chile. He studied the role of two schizophrenia associated genes on behaviours associated with the disease, using the genetics of the fruit fly, Drosophila.
“We studied two of these schizophrenia-associated genes — one called Rim, which is involved in neurotransmitter release at synapses, and another called CACNA1A and CACNA1B in humans and cacophony in flies, voltage-sensitive calcium channels involved in electrical and chemical signalling in and between neurons. We found that fly Rim mutants showed several behavioural changes seen in people with schizophrenia who may have Rim mutations. These included preferring larger social distances between individuals when in a group and changes in smell or olfaction. We also found the circadian (24-hour body clock) deficits reported in schizophrenia were also present in Rim mutant flies,” said Dr James Hodge, who supervised the research at School of Physiology, Pharmacology and Neuroscience at the University of Bristol.
Strikingly, treatment with the commonly used antipsychotic, haloperidol, rescued some of the Rim mutant’s behavioural problems.

While the APP protein is well-known for its key role in Alzheimer’s disease, its contribution to healthy brain function, by contrast, has remained largely unknown until now. Recently, an international research team, led by molecular biologist Prof. Dr Ulrike Müller from Heidelberg University, gained new insights on the physiological functions of the APP protein family by using a mouse model lacking APP. The absence of APP during brain development was shown to result in the malformation of important brain regions implicated in learning and memory. Consequently, these mice were severely impaired in their learning abilities and exhibited autistic-like behaviour.
Alzheimer’s disease is triggered by insoluble protein deposits in the brain, which aggregate around nerve cells to form plaques. These plaques consist mainly of small ?-amyloid peptides (A?), which are a cleavage product of the amyloid precursor protein (APP). A? peptides inflict damage on nerve cells and ultimately lead them to their death. While the detrimental effect of A? peptides on neurons has been recognised for many years, little is known about the natural physiological functions of APP. According to the researchers, this non-pathological perspective is worthy of investigation considering the fact that APP, as well as two other closely-related proteins, is produced by most nerve cells in the brain — particularly in critical regions for learning and memory formation.
To investigate the role of the APP protein family in the development and functionality of the nervous system, Prof. Müller’s research group used mice as a model organism, which had been genetically engineered to block the production of all APP family proteins. Close examination of their brains revealed that the loss of APP during brain development led to malformations in the layered structure of the hippocampus — an essential brain region for memory formation. “We observed that the absence of APP led to impaired neuronal wiring and a decrease in the number of synaptic connections. It also greatly reduced communication between nerve cells and severely affected the animal’s performance in behaviour tests that assess learning,” says Ulrike Müller, who heads the department of Functional Genomics at the Institute of Pharmacy and Molecular Biotechnology of Heidelberg University.
According to Prof. Müller, the team was surprised to discover that these disruptions in brain development also gave rise to behavioural changes that resembled those occurring in autism spectrum disorder. The mice displayed the characteristic recurring movement patterns and lack of interest in social interactions with other mice. “Our findings suggest that the APP family plays a crucial role in the normal development of the nervous system, learning, memory formation and social communication,” explains the scientist. “In the future, these understandings may aid the development of novel therapeutics for Alzheimer’s disease.”
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A new study from Columbia University and an international team of researchers identifies multiple ways to achieve the same health benefits from exercise — as long as the exercise “cocktail” includes plenty of light physical activity.
“For decades, we’ve been telling people that the way to stay healthy is to get at least 30 minutes of exercise five days a week,” says Keith Diaz, PhD, assistant professor of behavioral medicine and director of the exercise testing laboratory at the Center for Behavioral Cardiovascular Health at Columbia University Vagelos College of Physicians and Surgeons.
“But even if you’re one of the few adults who can stick to this advice, 30 minutes represents just 2% of your entire day,” says Diaz. “Is it really possible that our activity habits for just 2% of the day is all that matters when it comes to health?”
Diaz says that the recommendation about how much exercise to do may be insufficient depending on how individuals spend the rest of their waking day.
Previous studies tended to look at the impact of one type of activity or another in isolation. But each activity has either harmful or beneficial effects on health. “What we don’t know is the best combination, or cocktail, of ingredients needed to prolong life,” Diaz says.
Only through recent cheap and easy-to-use activity monitors, which can be worn by study participants throughout the day, have researchers been able to address the question.