Study Shows How Herpes Viruses and Tumours Have Learned to Manipulate the Same Ancient RNA

Study Shows How Herpes Viruses and Tumours Have Learned to Manipulate the Same Ancient RNA
Findings Could Have Implications for Drugs and Insight Into Diseases Like Alzheimer's

Herpes viral infections use the ancient genetic material found in the human genome to proliferate, mimicking the same process tumours have been found to manipulate, Mount Sinai researchers have shown for the first time. These observations provide further insight about how herpes viruses can manipulate the immune system in ways that may drive neurodegenerative diseases like Alzheimer's, according to the study, published in Nature Communications in January.

The researchers found that herpes viruses appear to manipulate an ancient RNA species that originated several million years ago, called human satellite II RNA (HSATII RNA). HSATII RNA is normally inactive, but both herpes viruses and cancer cells have essentially learned to activate it, using this RNA to manipulate their environment to help them invade the body and grow.

The researchers believe that both viruses and cancer cells figured out how to use this RNA because they both rapidly evolve to test out different strategies to multiply and spread within the body over time. Researchers have yet to understand whether herpes and cancer came upon this strategy coincidentally or whether they work hand in hand in some cases. Several researchers involved in this work pioneered the study of how a different type of RNA affects tumor evolution.

"The evolution of tumours can teach us about viruses and vice versa, and understanding one system may help us treat the other," said one of the study's senior authors, Benjamin Greenbaum, PhD, Assistant Professor of Oncological Sciences, Pathology, and Medicine (Hematology and Medical Oncology) at The Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai. "The HSATII RNA induction seen in herpes infections and cancer cells suggests possible convergence upon common mechanisms in these seemingly disparate diseases."

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The study potentially gives further insight into how herpes viruses might play a role in developing colitis and neurodegenerative diseases like Alzheimer's. It is the first step toward potentially developing diagnostic tools that look for these types of RNAs in cancer and herpes patients and using the ancient RNAs as targets for drugs in the future, said Dr. Greenbaum.

The lead author of the study was Maciej Nogalski, PhD, Postdoctoral Research Fellow in the laboratory of co-senior author Thomas Shenk, PhD, James A. Elkins Professor of Life Sciences in the Department of Molecular Biology at Princeton University.

"Herpes viruses have been extensively studied for many years, but once again by investigating host-virus interactions at the cellular level we were privileged to get insights into novel regulatory mechanisms of human cells. Our virus-centered studies not only uncovered interesting aspects of viral infection, but also provided an inducible system that could accelerate investigations about possible roles HSATII RNA plays in other diseases," Dr. Nogalski says.

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Researchers Identify Multiple New Subtypes of Most Common Childhood Cancer

Researchers Identify Multiple New Subtypes of Most Common Childhood Cancer
Like cartographers completing a map, investigators have identified multiple new subtypes of the most common childhood cancer - research that will likely improve the diagnosis and treatment of high-risk patients. St. Jude Children's Research Hospital scientists led the study, which appears as an advance online publication today in the journal Nature Genetics.

Researchers used integrated genomic analysis, including RNA sequencing, to define the genomic landscape of B-cell acute lymphoblastic leukemia (B-ALL) in almost 2,000 children and adults. B-ALL is the most common form of ALL and the most common cancer in children. B-ALL remains the leading cause of pediatric cancer death.

Investigators identified 23 subtypes of B-ALL, including eight new subtypes, with distinct genomic and clinical features as well as outcomes. Subtype prevalence often varies with age. More than 90 percent of B-ALL cases can now be categorized by subtype compared with 70 percent a few years ago.

"B-ALL has remarkable molecular diversity, which we and others have used to refine classification and drive the development of precision medicines to improve B-ALL treatment and outcomes," said corresponding author Charles Mullighan, MBBS, M.D., a member of the St. Jude Department of Pathology. "Part of precision medicine is an accurate molecular diagnosis, which this study provides to more patients."

A novel subtype-defining alteration

Alterations of the transcription factor gene PAX5 defined two new subtypes, including PAX5 P80R, as the first lymphoblastic leukemia initiated by a point mutation. "While secondary mutations are necessary and often involve kinase signaling, we show this point mutation impairs development of B lymphoid cells and promotes development of B-ALL in mice," Mullighan said.

The other PAX5 subtype, PAX5-altered, was defined by diverse alterations in the gene, including sequence mutations or rearrangements with one of 24 other genes. Together the PAX5 subtypes accounted for almost 10 percent of the previously uncategorized cases of B-ALL.

The new subtypes include a high-risk variety of B-ALL that occurs primarily in adults. It is defined by rearrangement of the transcription factors BCL2 with MYC or BCL6. "This subtype has a dismal diagnosis," Mullighan said. "Recognition of this subtype-defining rearrangement may lead to alternative therapy for patients." In contrast, a subtype defined by rearrangement of the gene DUX4 was associated with a good prognosis in adults, as had previously been observed in children.

Tracking gene expression

The study demonstrated the capability of RNA sequencing to identify multiple types of genomic alterations, highlighting the utility of this technique for leukemia diagnosis, particularly when whole-genome sequencing is not available. Examples in this study included chromosomal rearrangements resulting in fusion genes, gene-expression profiles and other alterations.

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"Through this study, two-thirds of the previous uncharacterized B-ALL patients could be classified into different subtypes with distinct genetic alteration profiles and clinical features," said co-first author Zhaohui Gu, Ph.D., a postdoctoral fellow in the Mullighan laboratory. "That may substantially speed up the development of customized treatments for these patients.

"We also established a robust B-ALL classification pipeline based mainly on RNA sequencing data that may be integrated into clinical diagnosis of ALL," Gu said.

"As a clinician, these data describing the diversity of subtypes of B-ALL will allow us to refine our prognostic abilities for individual patients, and ultimately, will lead to the development of new targeted therapies that will more effectively treat the leukemia with fewer side effects," said co-author Mark Litzow, M.D., professor of medicine at the Mayo Clinic and chair of the Leukemia Committee, Eastern Cooperative Oncology Group and the American College of Radiology Imaging Network, which contributed to the study.

Additional subtypes revealed

The other newly identified subtypes include:

* NUTM1 gene rearrangement with different partner genes that researchers believe may be vulnerable to treatment
* HLF gene rearrangement to multiple genes, including TCF4 as well as the previously recognized partner TCF3.
* Three subtypes that share patterns of gene expression similar to those of established B-ALL subtypes. The classification suggests that the new subtypes, ETV6-RUNX1-like, KMT2A-like and ZNF384-like, have risk profiles and prognoses similar to the established subtype for which they are named.
* Additional subtypes driven by sequence mutations, including IKZF1 N159Y.

Previous work from St. Jude and the Children's Oncology Group TARGET initiative have shown IKZF1 (Ikaros) mutations to be a marker of high risk B-ALL.

The study included patients from St. Jude, the COG and adult cancer cooperative studies.

Patient samples of many of the B-ALL subtypes are available to the international scientific community through the St. Jude data portal PROPEL (Public Resource of Patient-derived and Expanded Leukemias). PROPEL makes patient-derived leukemia xenograft samples available free of charge to researchers with no obligation to collaborate.

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Overstretched 'Sandwich Carers' Trying to Help Parents and Children

Overstretched 'Sandwich Carers' Trying to Help Parents and Children
An exhausted, overstretched generation of carers, are in need of emotional support themselves, say researchers. A report from the Office for National Statistics (ONS) says more than a quarter of such "sandwich carers" are suffering from depression or stress.

"Sandwich carers" look after their elderly parents and their children.
There are 1.3 million people in the UK with such multi-generational caring responsibilities, say researchers, with many feeling ignored and undervalued.

The ONS says the numbers in this "sandwich" generation, often in their 40s and 50s, are being increased by a combination of longer life expectancy and women tending to have children later in life.

But the report warns of the hidden pressures being carried by these mid-life carers - with warnings that they can be worn down emotionally, physically and financially.
The majority of carers in this "sandwich generation" are women - and almost half of these women feel that they cannot work as many hours as they would like.

One in three sandwich carers say that financially they are "just about getting by".
For those with more than 20 hours per week of caring, the ONS says a third are experiencing some kind of mental health problems, which might be stretched out over many years.

They risk becoming isolated, running out of money and being constantly under pressure - while trying to juggle between responsibilities of care, work and their own relationships.

What's it like?

Sarah, a 52-year-old mother of five children, lives in London, where she looks after her mother-in-law, who has dementia.

The work of carers is "completely undervalued," she says.

In fact, she says it makes her angry when in questionnaires carers are categorised as "not working", when they never stop working, often to the detriment of their own health.

Even though this affects a "massive number of people", Sarah says much of this huge and unrelenting responsibility goes by without being recognised.
"There is no spare time at all and you can get very tired," she says.

Sarah says she has a good network of support around her, but there is still a residual sense of guilt about whether she is spending enough time with her children or her mother-in-law, as she tries to stretch herself across helping all of them.

'Lose touch with friends'

The people who are often most neglected are the carers themselves, and she says it would be easy for someone to get "unwell".

"You can lose touch with friends, when it's hard to see people," she says.

Going out together as a family becomes difficult and holidays become limited, at a time in life when people might be expecting to enjoy some travelling.

Sarah says it is important to resist the "feeling of horizons being limited".

"You could easily feel that your life is getting narrower."

Her mother-in-law had previously lived alone in Dorset, and Sarah says that created another set of pressures, needing hours of travel, sometimes at short notice.
But she says it is worth it and feels that it is the right thing to do - but Sarah says that there needs to be much more openness about the stress and struggles facing so many people in her generation.

'So exhausted'

Catherine, aged 61, living in Cheshire, helps her 89-year-old mother at the same time as caring for her daughter, who has cerebral palsy.

The emotions can be a "roller coaster", she says, with some very low dips, such as if there are problems with navigating the care system.

A big practical problem, she says, is the shortage of reliable carers and the difficulties created when there are interruptions and gaps in staff available.

Catherine says she has sometimes spent a fortnight as the sole carer, through nights and days.

"I couldn't speak in full sentences, I was so exhausted," she said.

She says that other people are not "heartless", but they fail to see the extent to which carers can be trapped and unable even to get out of their house.

Even simple things like going for a walk have to be planned, Catherine says.

Carers find their own release from stress, she says, and in her own case she says that she "knits, knits, knits", as a hobby.

"Good friendships" have been very important to her, she says, otherwise people can become very isolated and feel all the weight on their shoulders.

But she warns that carers can sometimes feel excluded and neglected by neighbours who might be "afraid of saying the wrong thing".

She says that caring has its own lessons - and she has learned to "live in the moment" and enjoy what she can.

"How many other people get pleasure from getting out to the supermarket?" says Catherine.

'Time-poor and stressed'

This is a growing problem for a "time-poor and stressed" generation, says Helen Walker, chief executive of the Carers UK charity.

As well putting pressure on health and wellbeing, it is also tough on those balancing being a carer with their own jobs.

The charity estimates that about two million people have left work as a result, with consequences for their finances and careers.

Both Sarah and Catherine spoke of the difficulties in having to negotiate the care and health support system for their relatives, and Carers UK says getting the right care for the elderly is often tougher than getting childcare.

"With the social care system under extreme pressure, additional stress is being placed on families who are trying to juggle children, work and older relatives," says Ms Walker.

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New Findings Bring About Better Understanding Of Many Cancers' Metabolic Needs

New Findings Bring About Better Understanding Of Many Cancers' Metabolic Needs
Scientists at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have discovered that squamous cell skin cancers do not require increased glucose to power their development and growth, contrary to a long-held belief about cancer metabolism.

The findings could bring about a better understanding of many cancers' metabolic needs and lead to the development of more effective therapies for squamous cell skin cancer and other forms of epithelial cancer.

The research, led by senior authors Heather Christofk and Bill Lowry, was published in the journal Nature Communications.

A fundamental doctrine of cancer metabolism theory is that cancer cells are glycolytic, meaning they consume more glucose and produce more lactate than normal cells. This metabolic shift, called aerobic glycolysis, or the Warburg effect, has been observed in thousands of experiments and inspired treatments that aim to stop tumor growth by preventing cancer cells from increasing their glucose consumption. To date, this treatment approach has not proven successful in clinical trials.

Considering these clinical limitations, Christofk and Lowry set out to examine if increased glucose consumption is truly indispensable to cancer formation and growth.

They decided to approach this problem using squamous cell skin cancer as a model, as they had made two key discoveries about the nature of this cancer in recent years.

In 2011, they determined that squamous cell skin cancer, which forms in the thin, flat cells found on the surface of the skin - can originate from hair follicle stem cells. Hair follicle stem cells produce hair throughout a person's lifetime and remain mostly inactive, but spring to action during a new hair cycle, which is when new hair growth occurs. In 2017, the pair found that hair follicle stem cells are glycolytic and ramp up their glucose consumption to quickly activate and produce hair follicles.

"These findings led us to question: Are squamous cell skin cancer cells glycolytic because they are cancer cells that altered their metabolism to fuel their rapid growth, or because the cells they originated from - hair follicle stem cells - were glycolytic?" said Lowry, a professor of molecular, cell and developmental biology.

To answer this question, the team studied the progression of squamous cell skin cancer in animal models whose hair follicle stem cells had been genetically modified to limit their glucose consumption. Specifically, they de-activated a gene called lactate dehydrogenase-a, which catalyzes the final step in a cell's process of converting glucose to lactate. Deactivating this gene prevented this final step from taking place, which in turn caused the cells to dramatically reduce their glucose consumption.

The change had no effect on cancer incidence or progression. When faced with insufficient glucose for their increased needs, the cancer cells in this model simply altered their metabolism to derive energy from the amino acid glutamine.

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"These findings suggest that tumors are metabolically flexible and can use nutrients other than glucose to fuel growth," said Christofk, an associate professor of biological chemistry and molecular and medical pharmacology. "Understanding all of the nutrients cancers use for growth is critical to developing drugs that can successfully target cancer's metabolism".

The team double-checked their findings by conducting a converse experiment using hair follicle stem cells that had been genetically modified to increase glucose consumption. If their initial finding was incorrect, stimulating glucose consumption would make the tumors grow faster - it did not.

"The cells still formed cancer, but they didn't do so any faster and it wasn't any more serious," said Aimee Flores, a postdoctoral fellow in Lowry's lab and a first author of the study. "The behavior and progression of the disease was quite similar to the disease observed in the model with reduced glucose consumption".

As a next step, the team will conduct experiments to determine if reducing the consumption of both glucose and glutamine can stop the growth of squamous cell skin cancers.

"If limiting cancer's intake of both of these nutrients is shown to be effective, then that points to a path toward the clinic in the form of a combination therapy," said Lowry.
There is already some evidence that a combination therapy of this kind could treat squamous cell lung cancer. David Shackelford, an associate professor in the division of pulmonary and critical care medicine and a colleague of Christofk and Lowry's at the UCLA Jonsson Comprehensive Cancer Center, found that squamous cell lung cancers metabolize glutamine when unable to increase their glucose consumption.

Shackelford and his collaborators - including Christofk -  also identified two drug candidates that, when used in combination, may stop the growth of squamous cell lung cancers by reducing the uptake of both of these nutrients.

Despite these encouraging findings, the road to bringing combination therapies for squamous cell cancers to humans is a long one, cautioned Lowry. "Every drug you add to a potential treatment carries its own risks and side effects, so identifying and testing combination therapies that will be both safe and effective in humans is a long and arduous process," he said.

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Air Pollution On The London Underground Is 30 Times Higher Than A Busy Road

Air Pollution On The London Underground Is 30 Times Higher Than A Busy Road
A new report by the Committee on the Medical Effects of Air Pollutants has revealed that the air within the London Underground (or 'the Tube') is 30 times more polluted than the air surrounding London's busiest roads.

The report suggested that traveling the same by bus would expose passengers to only around one-third of the particulate matter (PM) present within the London Underground.

Researchers found that in general, the London Underground is the most polluted underground railway system in the world when compared to other subways. The reasons attributed for this include the age of the system and the extensive use of deep tunnels with inadequate air circulation.

The health effects of such high exposures are not clear at present, according to Committee Chairman Frank Kelly.

The report followed ten days of testing for PM performed at the deepest station in the LU, namely, Hampstead Station on the Northern Line.

The Committee's attitude towards the results was that further study was required to understand the implications, but implied that they were unlikely to be dangerous for commuters.

These particles are of a different nature from the ones above ground so we are uncertain about their health effects." - Professor Frank Kelly, Committee Chairman

The committee was appointed by Transport for London (TfL), which claims that dust levels within the Tube are carefully monitored.

We closely monitor dust levels on the Tube and, through a wide range of measures, ensure that particle levels are well within Health & Safety Executive guidelines."
Peter McNaught, TfL Director of Asset Operations.

McNaught pointed out that though the report found high PM levels in the tube, no guidelines were violated, making their effects uncertain.

McNaught finished by saying that TfL was determined to achieve the highest possible standards of air quality.

Tube particle pollution '30 times higher than by roads'.

Statement on the evidence for health effects in the travelling public associated with exposure to particulate matter in the london underground.

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Study Raises Hopes For New Approaches To Treat Osteoporosis

Study Raises Hopes For New Approaches To Treat Osteoporosis
A handful of brain cells deep in the brain may play a surprising role in controlling women's bone density, according to new research by UC San Francisco and UCLA scientists.

In a study published January 11, 2019 in Nature Communications, researchers showed that blocking a particular set of signals from these cells causes female (but not male) mice to build extraordinarily strong bones and maintain them into old age, raising hopes for new approaches to preventing or treating osteoporosis in older women.

"Our collaborators who study bone for a living said they'd never seen bone this strong," said study senior author Holly Ingraham, PhD. "Our current understanding of how the body controls bone growth can't explain this, which suggests we may have uncovered a completely new pathway that could be used to improve bone strength in older women and others with fragile bones".

More than 200 million people worldwide suffer from osteoporosis, a weakening of the bones to the point where falls or even minor stresses like bending over or coughing can trigger fractures. In healthy individuals, bone tissue is constantly being recycled -- old bone tissue is broken down and replaced by new bone. As we age, this cycle tilts in favor of bone loss, causing our bones to become increasingly porous and fragile.

Women are at particularly high risk of osteoporosis after menopause (nearly one in three post-menopausal women in the U.S. and Europe suffer from weakened bones) because of declining levels of the sex hormone estrogen, which normally promotes bone growth.

Estrogen plays many roles in the female body, particularly in the regulation of reproduction, but its function in the brain is still poorly understood. The Ingraham lab has long sought to understand how oestrogen's signaling in the brain impacts the female metabolism at different life stages, including how estrogen-sensitive neurons in a brain region called the hypothalamus balance energetic demands needed for survival or reproduction.

Their new study began when Stephanie Correa, PhD, then an Ingraham lab postdoctoral researcher and now an assistant professor at UCLA, found that genetically deleting the estrogen receptor protein in hypothalamic neurons caused mutant animals to gain a little weight, and also to become less active. Correa expected to find that the animals had put on extra fat or gained lean muscle, but these did not explain the difference. To find the source of the extra weight, she decided to use an extra-sensitive laboratory technique that could also reveal changes in bone density. To her surprise, she discovered that her heavy mice were truly just big-boned: the animals' bone mass had increased by as much as 800 percent.

"I was immediately struck by the size of the effect. The two groups didn't overlap at all, which I had never seen," Correa said. "We knew right away it was a game changer and a new, exciting direction with potential applications for improving women's health".

The mutant animals' extra-dense bones also proved to be super-strong. When collaborators such as UCSF's Aaron Fields, PhD, an assistant professor in the Department of Orthopedic Surgery, tested the mechanical strength of these bones by crushing them, his equipment almost failed, Ingraham says.

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After Correa moved to UCLA, Ingraham lab postdoctoral fellows Candice Herber, PhD, and William Krause, PhD, spearheaded a series of experiments that zeroed in on a specific population of just a few hundred estrogen-sensitive brain cells - located in a region of the hypothalamus called the arcuate nucleus - which appeared to be responsible for these dramatic increases in bone density. The authors hypothesized that estrogen must normally signal these neurons to shift energy away from bone growth, but that deleting the estrogen receptors had reversed that shift.

Notably, interfering with arcuate estrogen signaling in male mice appeared to have no effect. "Most neuroscientists limit studies to male mice, and few study estrogen, which may explain why this had never been seen before," Ingraham said. "I've always been interested in how sex hormones make male and female brains different, and this is a really wonderful example of how dramatic those differences can be".

Further experiments showed that Ingraham and Correa's mutant animals maintained their enhanced bone density well into old age. Normal female mice begin to lose significant bone mass by 20 weeks of age, but mutant animals maintained elevated bone mass well into their second year of life, quite an old age by mouse standards.

Remarkably, Herber and Krause were even able to reverse existing bone degeneration in an experimental model of osteoporosis. In female mice that had already lost more than 70 percent of their bone density due to experimentally lowered blood estrogen, deletion of arcuate estrogen receptors caused bone density to rebound by 50 percent in a matter of weeks.

These results highlight the opposite roles played by estrogen in the blood, where it promotes bone stability, and in the hypothalamus, where it appears to restrain bone formation, Ingraham said. "We hypothesize that after puberty the estrogen system in the female brain actively shifts resources away from bone growth and towards things like reproduction, which could contribute to women's higher risk of weakened bones as we age".

The dramatic pattern of enhanced bone growth seen in the current study is unlike anything in the scientific literature, the researchers say, suggesting that Correa's fortuitous discovery may have uncovered a totally novel biological pathway by which the brain regulates bone density. Ingraham and colleagues are now investigating exactly how this brain-bone communication happens, and whether drugs could be developed to boost bone strength in post-menopausal women without potentially dangerous effects of estrogen replacement therapy.

"This new pathway holds great promise because it allows the body to shift new bone formation into overdrive," Correa said.

"I'm in the clouds about this result," Ingraham added. "If our next experiments show that the brain releases a novel circulating factor that triggers enhanced bone growth, we might have a real chance of developing a drug that counteracts osteoporosis".

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Excess Belly Fat May Lead To A Reduction In Gray Matter

Excess Belly Fat May Lead To A Reduction In Gray Matter
A study conducted by researchers at Loughborough University has found that excess abdominal fat is associated with a lower volume of gray matter in the brain.

Professor of exercise, Mark Hamer, and colleagues found that a higher body mass index (BMI), together with a higher waist-to-hip ratio, was linked to a lower gray matter volume, when compared to leaner individuals.

Interestingly, a higher BMI, together with an average waist-to-hip ratio, was not associated with any significant reduction in gray matter volume.

BMI is a general measurement of body weight compared to height, meaning taller individuals or those with more muscle mass may have a high BMI, even if they are lean. Abdominal fat, on the other hand, indicates how much visceral fat may be surrounding abdominal organs such as the liver and intestines. This visceral fat can have toxic effects by triggering inflammation that can drive conditions such as arthritis and heart disease.

As reported in the journal Neurology, Hamer and team studied brain images available for 9,652 people (aged an average of 55 years) who had their BMI and waist-to-hip ratios measured between 2006 and 2010. The subjects were enrolled in the UK Biobank study, which includes information from volunteers who regularly update their medical information.

A healthy BMI is defined as a score between 18.5 and 24.9, while a score of 30 or higher is defined as obese. The waist-to-hip ratio score is considered high and indicative of central obesity if it is above 0.90 for men and above 0.85 for women.

The researchers found that people who had a higher BMI combined with a higher waist-to-hip ratio had a lower grey matter volume (average of 785cm3) than individuals with a healthy BMI and waist-to hip ratio (average of 798 cm3). This effect was observed after adjustment for factors such as age, smoking history, physical activity, education level and a history of poor mental health.

However, people who had a higher BMI, but a healthy waist-to-hip ratio, had a similar gray matter volume to those with both a healthy BMI and waist-to hip ratio, at an average of 793cm3.

"The reductions in brain size increase in a linear fashion as fat around the middle grew larger", writes Hamer.

The results support the evidence that staying lean has beneficial health effects, not just by decreasing the risk of heart-related problems, but possibly by maintaining a healthy brain as well.

Hamer points to recently published research demonstrating how exercise can increase gray matter volume and may represent a way of counteracting some of the negative impacts obesity may have on the brain and body:

The take-home message is that being overweight and obese has a multitude of effects on health, so it's unsurprising that obesity is also going to have an effect on our brain health".

Professor Mark Hamer, Lead Researcher, Hamer, M., Batty D. G. 2019. Association of body mass index and waist-to-hip ratio with brain structure. Neurology. Jan 2019.

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