Scientists have discovered a cluster of cells in an unexpected area of the brain that could play a powerful role in regulating appetite and eating habits, says a report in the journal Nature.
In mouse experiments, destroying the cells caused the rodents to overeat and gain excessive weight. Activating the cells had the opposite effect: The mice lost their appetite and became almost anorexic.
The cells, called cholinergic neurons, were located in the basal forebrain at the front of the brain, in a region called the diagonal band of Broca. The neurons produce acetylcholine, a chemical that helps brain cells transmit information to one another, but its role in controlling appetite wasn’t previously known, researchers said.
The neurons use the same pathways in the brain as nicotine, a chemical in tobacco and an appetite suppressant, they noted.
“Targeting cholinergic neurons for either electrical, genetic or pharmacological manipulation may prove useful in treating detrimental eating habits or eating disorders—or aspects of addiction,” lead researcher Dr. Benjamin R. Arenkiel , associate professor in the departments of molecular and human genetics and neuroscience at Baylor College of Medicine in Houston, said in an email.
To assess acetylcholine’s effect on appetite, researchers used genetic-modification techniques to kill cholinergic neurons in mice without harming other brain cells. Mice without the neurons doubled in weight on an unrestricted diet and became increasingly inactive over two to three months. In contrast, control mice with intact neurons exhibited normal weight gain and activity levels.
Migraine sufferers have a different mix of gut bacteria that could make them more sensitive to certain foods, scientists have found.
The study offers a potential explanation for why some people are more susceptible to debilitating headaches and why some foods appear to act as triggers for migraines.
The research showed that migraine sufferers had higher levels of bacteria that are known to be involved in processing nitrates, which are typically found in processed meats, leafy vegetables and some wines.
The latest findings raise the possibility that migraines could be triggered when nitrates in food are broken down more efficiently, causing vessels in the brain and scalp to dilate.
Antonio Gonzalez, a programmer analyst at the University of California San Diego and the study’s first author, said: “There is this idea out there that certain foods trigger migraines - chocolate, wine and especially foods containing nitrates. We thought that perhaps there are connections between what people are eating, their microbiomes and their experiences with migraines.”
When nitrates in food are broken down by bacteria in the mouth and gut they are eventually converted into nitric oxide in the blood stream, a chemical that dilates blood vessels and can aid cardiovascular health by boosting circulation.
However, around four in five cardiac patients who take nitrate-containing drugs for chest pain or heart failure report severe headaches as a side effect.
Dr Brendan Davies, a consultant neurologist at the University Hospitals of North Midlands and a trustee of the Migraine Trust, said the idea of gut bacteria playing a role in migraine was medically plausible. “There’s something called a hot dog headache, where nitrates are suspected to be involved,” he said. “This is interesting work, but would need to be confirmed.”
The study, published on Tuesday in the journal mSystems, sequenced bacteria found in 172 oral samples and 1,996 faecal samples from healthy participants, who had also reported whether they were affected by migraines.
If you’re one of those people who puts tomatoes in the fridge, you are going to want to stop. Now.
Sure, chilling a tomato will keep it looking fresh for a longer period of time than if you left it on the counter, but it will also drain all that earthy, slightly grassy, distinctive tomato taste right out of the fruit. (And, yes, tomato is a fruit.)
Scientists and foodies have known for some time that cooling tomatoes is detrimental to their flavor, but they were not exactly sure why — until now.
According to new a study in the Proceedings of the National Academy of Sciences, when a tomato’s environment drops below 68 degrees, the genes responsible for making it taste like a tomato get turned off.
“Basically, the tomato gets cold and tells itself to stop making these aroma compounds,” said Denise Tieman, a research associate professor at the Plant Innovation Center at the University of Florida in Gainesville.
“The change is irreversible,” she added.
Tieman has been studying the science of tomato flavor for at least a decade. Previously she discovered that tomatoes taste the way they do because of a combination of sugars, acids and a collection of chemicals that scientists call volatile compounds or aroma compounds.
“Aroma compounds are what you smell, and they make up the wonderful part of the flavor,” Tieman said. “The sugars and acids are what you taste on the tongue, but there would be no excitement to the flavor without the aroma compounds.”
Scientists have for the first time shown that fully mature egg cells can be grown in the lab, raising hope for new infertility treatments.
Until now, researchers have only been able to produce cells that resemble sperm or eggs, but which can rarely produce live offspring because of abnormal organisation of their genetic material. But a team at Kyushu University, Japan, have now turned stem cells from mice into mature eggs than can be fertilised and develop into healthy, fertile adults. This could lead to a way for women who can’t naturally produce working eggs to have new ones made from their own cells.
Embryonic stem cells are living cells taken from an embryo that have the ability to develop into any other kind of cell. The researchers from Kyushu University team previously demonstrated that, under the right conditions, these cells could be turned into primordial germ cells, immature embryonic versions of sperm and eggs. But because they are immature, these germ cells can’t produce any offspring.
So the researchers adapted their methods to encase the stem cells in other cells taken from a mouse’s foetal gonad (the developing ovary or testis). This recreated an environment more like an ovary and, over a period of four to five weeks, the team saw the stem cells develop into cells resembling mature eggs.
Women are well aware that the number of eggs they're born with is all they'll ever have, and when they inevitably run out, they can no longer have children. Hence the pressure of the biological clock.
But a new study has found the first evidence that women's ovaries might actually be able to grow new eggs. If confirmed, it could mean that post-menopause women and those with fertility problems might be able to conceive naturally after all.
To be clear, this is very early evidence taken from a small study involving cancer patients, and it needs to be replicated and explored further before we can say for sure what's going on.
But the possibility that adult women could grow new eggs would overturn our current understanding of reproductive biology, and the results have scientists very interested.
Here's what we know so far: researchers studying a small group of cancer patients found that women taking a chemotherapy drug called ABVD had a higher density of eggs than healthy women of the same age - suggesting that the drug could actually be encouraging their ovaries to grow new eggs.
"This was something remarkable and completely unexpected for us. The tissue appeared to have formed new eggs," lead researcher Evelyn Telfer from the University of Edinburgh in Scotland told Hannah Devlin in an exclusive for The Guardian.
There are multiple answers to the question of where we come from: early hominins, monkeys, primordial goo, or the Big Bang, to name a few. Today’s answer, though, has probably, just a split second ago, popped into many readers’ minds. Today’s answer is sexual intercourse, a.k.a. “bleeping.” So let’s go back to the beginning, hundreds of millions of years before we invented euphemisms and censorship, and let’s ask: How in the evolutionary world did sex begin?
Algae, the green gunk that runs amok in our fish tanks, as well as the seaweed that stinks up our summer beaches, include some of the simplest sexually reproducing organisms on Earth. These lineages go back nearly 2 billion years. Algae do it. Plants do it. Insects do it. Even fungi do it. Much of this sex involves releasing sperm into the wind or the water so they can be carried to nearby eggs (as in mosses), relying on a different species to carry male gametes to female ones (many flowers), or maneuvering two bodies so that the openings to the internal reproductive organs are close enough together for fluid exchange (most insects and most birds).
During the most recent Ebola outbreak in West Africa, health-care workers treated some sick patients by injecting them with plasma—the translucent part of the blood—taken from individuals who had survived the disease. In the absence of an approved drug to treat patients, the hope was that protective proteins in the donor plasma would help recipients fight the disease and recover. A biotech company wants to use this same approach to treat a variety of infectious diseases, with one key difference: cows, not humans, will be the plasma donors.
SAB Biotherapeutics of South Dakota has genetically engineered cattle to produce large quantities of human antibodies—proteins that help remove harmful foreign pathogens from the body—in a rapid fashion that could be used to treat patients suffering from infectious diseases like Middle East respiratory syndrome (MERS), Ebola, and influenza. The World Health Organization recently recognized the company’s approach among six promising new technology platforms that could help respond to disease outbreaks worldwide. SAB Biotherapeutics of South Dakota has genetically engineered cattle to produce large quantities of human antibodies—proteins that help remove harmful foreign pathogens from the body—in a rapid fashion that could be used to treat patients suffering from infectious diseases like Middle East respiratory syndrome (MERS), Ebola, and influenza. The World Health Organization recently recognized the company’s approach among six promising new technology platforms that could help respond to disease outbreaks worldwide.
“The entire idea behind this is that human antibodies are the natural way that our bodies fight disease,” says Eddie Sullivan, president and CEO of SAB Biotherapeutics.
For the first time, scientists have edited DNA in healthy and viable human embryos using genetic tool CRIPR/Cas9.
The researchers, led by developmental biologist Fredrik Lanner from the Karolinska Institutet in Sweden, hope the research will lead to new ways to treat infertility and prevent miscarriage.
"Having children is one of the major drives for a lot of people," Lanner told Rob Stein at NPR. "For people who do struggle with this, it can tend to become an extremely important part of your life."
Although Chinese scientists made headlines back in April for genetically modifying human embryos, those embryos were unusable for IVF, and would never have been able to develop into healthy infants.
But two-day-old embryos Lanner is using are still viable, and were all donated by couples at an IVF clinic in Sweden.
The researchers are attempting to edit genes in these embryos to regulate certain aspects of their development. If the genes are removed and the embryo no longer functions, it signals that a particular gene is essential for embryotic growth.
However, Lanner says these embryos are only being studied for the first seven days of growth, and will be destroyed after 14 days.
Treatments for symptoms of spinal cord injuries may be a step closer, as researchers at University of California San Francisco (UCSF) have transplanted human neurons into mice with these injuries, and found that over time they made new connections in the spine, reducing chronic pain and helping the mice regain some bladder control.
Difficulties with walking may seem like the most obvious symptom of spinal cord injury, but according to a 2004 study, bladder control was ranked as the top priority for treatment by almost 20 percent of paraplegics, and 10 percent of quadriplegics. Like chronic pain, loss of bladder control is a symptom of inflammation following spinal injury, which damages inhibitory spinal circuits that use the neurotransmitter, gamma-Aminobutyric acid (GABA). When GABA is lessened, the spine's ability to inhibit pain and control bladder function decreases.
The UCSF team wanted to test whether implanting human cells that produce GABA into mice with spinal cord injuries could reroute the damaged circuits, and whether that could help address pain and improve bladder control. To do so, they transplanted immature human GABA-producing cells into mice two weeks after they sustained an injury to the thoracic spinal cord, with the injection site being below the inflamed area caused by the injury.
When they checked in after six months, they found the cells had migrated towards the injured area, matured into inhibitory neurons and had actually formed new connections with the spinal cord, effectively restoring some function below the injury site. The mice showed significantly less signs of neuropathic pain and had much better bladder control when compared to injured mice that didn't receive the treatment.
A new study increases and strengthens the links that have led scientists to propose the “transposon theory of aging.”
Transposons are rogue elements of DNA that break free in aging cells and rewrite themselves elsewhere in the genome, potentially creating lifespan-shortening chaos in the genetic makeups of tissues.
As cells get older, prior studies have shown, tightly wound heterochromatin wrapping that typically imprisons transposons becomes looser, allowing them to slip out of their positions in chromosomes and move to new ones, disrupting normal cell function. Meanwhile, scientists have shown that potentially related interventions, such as restricting calories or manipulating certain genes, can demonstrably lengthen lifespans in laboratory animals.
“In this report the big step forward is towards the possibility of a true causal relationship,” says Stephen Helfand, a professor of biology at Brown University and senior author of a new study in the Proceedings of the National Academy of Sciences.
This month, pupils across France will be able to use the first full-size anatomical model of a clitoris in their sex education classes. Considering all the technological, medical and scientific achievements humans have made, this seems to have taken a long time. The distribution of this model has been possible due to 3D printing technology; but even three-dimensional MRI scans, which previously produced the most accurate representations of the clitoris, only became available in 2009.
But it was worth the wait. The truth is, you might struggle to gain pleasure from a tool you don’t even know you have. In 2016, women finally know without speculation what the whole of their sexual organ looks like; and for many it won’t be quite what they imagined.
You may be wondering, what’s the big deal? Is the clitoris not the “small, sensitive, erectile part of the female genitals at the anterior end of the vulva”, as Oxford Dictionaries defines it? And isn’t the real issue simply whether it brings a woman sexual gratification?
Well, decide for yourself. The popular opinion seems to be that the 3D printed clitoris resembles a wishbone. To my eyes, it also (fittingly) resembles a fleur-de-lys, or, to use a more contemporary example, a tulip emoji.
But the important thing is that it debunks myths that have repressed female sexuality for centuries. For one, it refutes the dictionary/textbook education that wrongly asserts the clitoris is the size of “a fingertip”, a “pea” or that it is small. We can now clearly see that the clitoris includes two shafts (crura) which are actually about 10cm long. Not only can we visualise that the clitoris is more than what the eye perceives; with the visual model we can also now get a mental image of how it encircles the vagina, making penetrative sex potentially orgasmic. This means that a demystified discussion about the female orgasm is possible at long last.
Our eyes are designed to flush out any contaminants that get into them. While this is generally a good thing, it's not so helpful when it comes to administering medication in the form of eye drops – up to 95 percent of the medicine is typically flushed out before it's able to work. Now, however, a Canadian scientist is developing what could be a solution to the problem.
Working with a team of graduate students, McMaster University's Prof. Heather Sheardown has created microscopic packets of medicine that are suspended in a carrier liquid.
She tells us that when applied in the form of eye drops, these "molecular packets" adhere to the mucus layer of the tear film that covers the eye. This causes them to remain on the cornea instead of being washed away. Over the next several days, they gradually dissolve and release their payload into the eye.
Conceivably, this means that people currently needing to use eye drops on a daily basis could instead apply them once a week. Additionally, of course, it would result in less wasted medication.
According to Sheardown, there has been interest in developing the technology commercially. She will be presenting her research to the Tear Film and Ocular Surface Society in France, later this month.
A new study, done by pooling data from most of those studies, throws cold water on the idea that extra pounds may stem from an imbalance of the bacteria inside us.
In fact, the study published in the journal mBio finds, there’s no clear common characteristic of the microbe populations, or microbiomes, in the digestive systems of obese people that makes them different from the microbiomes of those with a healthy weight.
This lack of a clear “signature” across more than 1,000 volunteers in 10 of the largest studies done to date may not please overweight people. It may also disappoint the companies that sell them products aimed at altering the gut’s microscopic population through fiber, nutrients, and “good” bacteria.
Still, according to the researchers from the University of Michigan Medical School, this finding’s actually exciting. It means that there’s much more complexity—and therefore much more to learn—when it comes to the relationship between our microbiome and our health.
The researchers have created an open online site where other researchers can see how they did what they did, and add more data from gut microbiome studies in obese and non-obese people to continue the search for any links.
As more data gets added, the trustworthiness of the findings will only grow. And perhaps specific linkages and signatures will be found in future.
The region of the brain that serves as the physical source of feelings of depression has been identified, with new MRI data being the latest evidence to show that depression isn't just a 'frame of mind'.
Scientists have scanned the brains of more than 900 people, and the results suggest that feelings of loss and low self-esteem are tied to the functioning of the orbitofrontal cortex – a region of the brain associated with sensory integration, expectation, and decision-making.
"Our finding, with the combination of big data we collected around the world and our novel methods, enables us to locate the roots of depression, which should open up new avenues for better therapeutic treatments in the near future for this horrible disease," says computational psychiatrist Jianfeng Feng from the University of Warwick in the UK and Fudan University in China.
To isolate the brain mechanisms involved in depression, Feng's team recruited 909 people in China to take part in MRI brain scans. Of this group, 421 of the participants had been diagnosed with major depressive disorder (aka depression). The remaining 488 participants – who didn't have depression – acted as a control group.
The scans showed that depression is related to the neural activity of two different portions of the orbitofrontal cortex (OFC): the medial OFC and lateral OFC.
In a small weight-loss study, women on a high-protein diet did lose weight but didn’t see improvements in insulin sensitivity, which can help lower diabetes risk.
The women who ate less protein lost weight, too, but they also had a 25 to 30 percent improvement in their sensitivity to insulin.
“That’s important because in many overweight and obese people, insulin does not effectively control blood-sugar levels, and eventually the result is type 2 diabetes,” says principal investigator Bettina Mittendorfer, professor of medicine at Washington University School of Medicine in St. Louis. 65 vs. 100 grams of protein
Mittendorfer and her colleagues studied 34 women with obesity who were 50 to 65 years of age. Although all of the women had body mass indices (BMI) of at least 30, none had diabetes.
The women were randomly placed into one of three groups for the 28-week study. In the control group, women were asked to maintain their weight. In another group, the women ate a weight-loss diet that included the recommended daily allowance (RDA) of protein: 0.8 grams per kilogram of body weight. For a 55-year-old woman who weighs 180 pounds, that would come to about 65 grams of protein per day.
In the third group, the women ate a diet designed to help lose weight, but they consumed more protein, taking in 1.2 grams per kilogram of body weight, or almost 100 grams for that same 180-pound woman.
“We provided all of the meals, and all the women ate the same base diet,” Mittendorfer says. “The only thing we modified was protein content, with very minimal changes in the amount of fat or carbohydrates. We wanted to home in on the effects of protein in weight loss.”
In 1959, Peter Tripp, a popular New York DJ, pledged to stay awake for 200 hours for charity while continuing to host his radio show.
Studies into sleep deprivation were rare at the time so no one knew what to expect. This made it a major event, not only for Tripp’s millions of listeners, but also for the scientific community.
The subsequent impact of the “wakeathon” on Tripp’s mind was far more dramatic than anyone had expected. The personality of a man normally described as cheerful and upbeat appeared to significantly change as time went by. By the third day he had become highly irritable, cursing and insulting even his closest friends. Towards the end of his endeavour, he began to hallucinate and exhibit paranoid behaviours.
But despite the concerns of the doctors monitoring him (and with the help of the stimulants they gave him), he persisted and finally went to bed after 201 hours of continuous wake time.
Modern laboratory studies have replicated some of the behaviours seen in Tripp as a consequence of sleep loss. Sleep deprivation or prolonged restricted sleep results in increasing irritability, worsening mood, and feelings of depression, anger, and anxiety. Some argue that sleep loss leads to heightened emotional reactivity.
While the zika virus might be grabbing all the headlines these days, malaria continues to hold the dubious honor of being the most deadly vector-borne disease, claiming the lives of more than 400,000 people each year. No cure has been found yet, though scientists have been attempting everything from altering the mosquitoes' sense of smell to rendering them infertile. That said, a recent study by researchers at Johns Hopkins University School of Medicine has identified a new approach: changing how humans smell and taste.
In order to find a human host, mosquitoes have to rely on their sense of smell. Female Anopheles gambiae mosquitoes, in particular, have a strong preference for humans and use olfactory cues to locate and distinguish us from other mammals. But what if scientists could figure out what smells turn them off so that we could change our "flavor" to something less mouthwatering?
To head down that path, the researchers decided to find out what makes mosquitoes' sensory neurons tick. "All mosquitoes, including the one that transmits malaria, use their sense of smell to find a host for a blood meal. Our goal is to let the mosquitoes tell us what smells they find repulsive and use those to keep them from biting us," says Dr. Christopher Potter, an assistant professor of neuroscience at the Johns Hopkins University School of Medicine.
The technique shows that using donor stem cells might one day be a viable way to regenerate the organs of human heart attack patients – an approach that could dramatically reduce the time and expense of developing individualised stem cell treatments.
While using stem cell therapy to treat conditions like heart problems isn't new, the technique usually involves cultivating stem cells taken from the patient themselves – which can be very expensive.
Alternatively, stem cells can be harvested from human embryos, but that procedure is controversial, since the embryo is destroyed in the process.
If the new technique demonstrated by researchers at Shinshu University can be replicated in humans, we could avoid these difficulties in future stem cell therapies by enabling scientists to develop a resource of ready-made, donor-based treatments to help any number of patients.
"They strengthen the case that a bank of pre-prepared matched [cells] could be used to treat patients, without relying on the long process of reprogramming and differentiating the patient's own cells," cardiac researcher Sian Harding from Imperial College London in the UK, who wasn't involved with the study, told Ian Sample at The Guardian.
Scientists have held an all-you-can-eat buffet to test how a rare gene mutation affects people's appetites – and found that those who were born with this mutation were significantly more likely to crave fatty food, but less likely to eat sugary food.
While lots of us enjoy foods that are high in fat, the research shows that people with a mutation in their melanocortin–4 receptor (MCR4) gene seem to prefer it more than others – and tend to eat more high-fat foods, even when the fat content is totally hidden.
"Our work shows that even if you tightly control the appearance and taste of food, our brains can detect the nutrient content," says lead researcher Sadaf Farooqi from the University of Cambridge in the UK.
Farooqi and her team recruited 54 people to take part in their chicken korma buffet – a popular, creamy curry dish. Of this group, 20 participants were lean, 20 were obese, and 14 were obese and had a mutation in their MCR4 gene.
According to the researchers, about 1 in 100 obese people have this defect in the MC4R gene, which makes them more likely to put on weight. The defect disrupts the melanocortin–4 receptor, which means that satiety signals in the brain don't get processed properly.
In the experiment, the three groups of participants were each given a taste test of three different chicken korma preparations. The three curries were manipulated to look and taste the same, but were in fact low, medium, and high-fat versions of the same dish. In other words the fat content provided 20 percent, 40 percent, or 60 percent of calories respectively.
After sampling each curry, the participants were free to serve themselves and eat as much of any version of the dish as they liked.
While each group ended up eating approximately the same amount of food overall, the researchers found that the participants with the MC4R gene mutation ate almost twice as much of the high-fat korma as the lean participants (95 percent more), and 65 percent more than the obese group.
Doctors use brain stimulation to treat epilepsy, depression, pain, and other conditions, but it’s not exactly clear how it works or even which areas to target.
New research suggests stimulating a single region of the brain can activate other regions and even alter global brain dynamics.
“We don’t have a good understanding of the effects of brain stimulation,” says Sarah Muldoon, an assistant professor of mathematics at the University at Buffalo. “When a clinician has a patient with a certain disorder, how can they decide which parts of the brain to stimulate? Our study is a step toward better understanding how brain connectivity can better inform these decisions.”
Danielle S. Bassett, associate professor of bioengineering in the University of Pennsylvania, says if you look at the architecture of the brain, “it appears to be a network of interconnected regions that interact with each other in complicated ways. The question we asked in this study was how much of the brain is activated by stimulating a single region.
“We found that some regions have the ability to steer the brain into a variety of states very easily when stimulated, while other regions have less of an effect.”
A new material made of graphene nanoribbons and a common polymer might help knit damaged or even severed spinal cords.
The nanoribbons are highly soluble in polyethylene glycol (PEG), a biocompatible polymer gel used in surgeries, pharmaceutical products, and in other biological applications. When the nanoribbons have their edges functionalized with PEG chains and are then further mixed with PEG, they form an electrically active network that helps the severed ends of a spinal cord reconnect.
“Neurons grow nicely on graphene because it’s a conductive surface and it stimulates neuronal growth,” says James Tour, a chemist at Rice University.
Earlier experiments have suggested that neurons will grow along graphene.
“We’re not the only lab that has demonstrated neurons growing on graphene in a petri dish,” he says. “The difference is other labs are commonly experimenting with water-soluble graphene oxide, which is far less conductive than graphene, or nonribbonized structures of graphene.
“We’ve developed a way to add water-solubilizing polymer chains to the edges of our nanoribbons that preserves their conductivity while rendering them soluble, and we’re just now starting to see the potential for this in biomedical applications,” Tour says.
Motherless babies could be on the horizon after scientists discovered a method of creating offspring without the need for a female egg.
The landmark experiment by the University of Bath rewrites 200 years of biology teaching and could pave the way for a baby to be born from the DNA of two men.
It was always thought that only a female egg could spark the changes in a sperm required to make a baby, because an egg forms from a special kind of cell division in which just half the number of chromosomes are carried over.
Sperm cells form in the same way, so that when a sperm and egg meet they form a full genetic quota, with half our DNA coming from our mother and half from our father.
But now scientists have shown embryos could be created from cells which carry all their chromosomes which means that, in theory, any cell in the human body could be fertilised by a sperm.
Three generations of mice have already been created using the technique and are fit and healthy and now researchers are planning to test out the theory using skin cells.
The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show.
The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry.
“They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA Internal Medicine paper.
The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat.
Even though the influence-peddling revealed in the documents dates back nearly 50 years, more recent reports show that the food industry has continued to influence nutrition science.
Apple cider vinegar is a traditional folk remedy that has been around for many centuries. But is it beneficial for our health, asks Michael Mosley.
Apple cider vinegar is made by mixing chopped-up apples with water and sugar, then allowing the mixture to ferment, turning some of it into acetic acid.
Despite being acidic and definitely something of an acquired taste, in recent years apple cider vinegar has become incredibly popular. At least a part of that is because of claims that it can help with everything from obesity to split ends and arthritis.
But which, if any, of the many different health claims made on its behalf stand up to scientific scrutiny? For Trust Me, I'm A Doctor we teamed up with Dr James Brown from Aston University to find out.
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