A latest research paper shows a diet low in nutrients might help increase the lifespan of humans.
The research conducted on laboratory animals argues that dietary restrictions can result in higher rates of cellular recycling and repair mechanisms in the body. But, according to them, this effect evolved to help organisms during famines.
The authors explain that animals need less food for survival as the stored nutrients in the cells can be recycled and reused.
“This is the most intriguing aspect, from a human health stand point. Although extended lifespan may simply be a side effect of dietary restriction, a better understanding of these cellular recycling mechanisms that drive the effect may hold the promise of longer, healthier lives for humans,” said lead study author, Dr Margo Adler, an evolutionary biologist at UNSW Australia in a press release.
“This effect has been demonstrated in laboratories around the world, in species ranging from yeast to flies to mice. There is also some evidence that it occurs in primates,” Adler said
“But we think that lifespan extension from dietary restriction is more likely to be a laboratory artifact,” said Adler. She further explained that the most commonly believed theory is that this effect evolved to enhance the survival chances during times of famine.
The authors explained why no extension in lifespan is seen in the wild. This is because restricted diets lower the ability of the immune system to fight diseases and reduce the muscle strength necessary to defend against predators.
“Unlike in the benign conditions of the lab, most animals in the wild are killed young by parasites or predators,” Adler explained
“Since dietary restriction appears to extend lifespan in the lab by reducing old-age diseases, it is unlikely to have the same effect on wild animals, which generally don’t live long enough to be affected by cancer and other late-life pathologies,” she added.
The paper is published in the journal ‘BioEssays.’
Scientists say two of the deadliest pandemics in history were caused by strains of the same plague and warn that new versions of the bacteria could spark future outbreaks.
Researchers found tiny bits of DNA in the teeth of two German victims killed by the Justinian plague about 1,500 years ago. With those fragments, they reconstructed the genome of the oldest bacteria known.
They concluded the Justinian plague was caused by a strain of Yersinia pestis, the same pathogen responsible for the Black Death that struck medieval Europe. The study was published online Tuesday in the journal, Lancet Infectious Diseases.
The two plagues packed quite a punch. The Justinian Plague is thought to have wiped out half the globe as it spread across Asia, North Africa, the Middle East and Europe. And the Black Death killed about 50 million Europeans in just four years during the 14th century.
“What this shows is that the plague jumped into humans on several different occasions and has gone on a rampage,” said Tom Gilbert, a professor at the Natural History Museum of Denmark who wrote an accompanying commentary. “That shows the jump is not that difficult to make and wasn’t a wild fluke.”
The plague is usually spread to humans by rodents whose fleas carry the bacteria.
“Humans are infringing on rodents’ territory, so it’s only a matter of time before we get more exposure to them,” Gilbert said.
Still, he and other experts doubted a modern plague epidemic would be as devastating.
“Plague is something that will continue to happen but modern-day antibiotics should be able to stop it,” said Hendrik Poinar, director of the Ancient DNA Centre at McMaster University in Canada, who led the new research. He said about 200 rodent species carry the plague and could potentially infect other animals or humans.
Poinar warned that if the plague transforms into an airborne version _ which can happen if the bacteria reaches the lungs and its droplets are spread by coughing _ it would be much harder to snuff out. That type of plague can kill people within 24 hours of being infected.
Poinar said scientists need to sharpen their surveillance of plague in rodent populations to try averting future human infections.
“If we happen to see a massive die-off of rodents somewhere with (the plague), then it would become alarming,” he said.
There are several thousand human cases of plague every year, most often in central and Eastern Europe, Africa, Asia and parts of the Americas.
Research published in the journal Nature has shown that vaccinated monkeys can clear Simian Immunodeficiency Virus (SIV) infection from their bodies.
It was effective in nine of the 16 monkeys that were inoculated.
The US scientists say they now want to use a similar approach to test a vaccine for HIV in humans.
Prof Louis Picker, from the Vaccine and Gene Therapy Institute at Oregon Health and Science University, said: “It’s always tough to claim eradication – there could always be a cell which we didn’t analyse that has the virus in it. But for the most part, with very stringent criteria… there was no virus left in the body of these monkeys.”
Search and destroy
The research team looked at an aggressive form of virus called SIVmac239, which is up to 100 times more deadly than HIV.
Infected monkeys usually die within two years, but in some inoculated primates the virus did not take hold.
It used the infectious power of CMV to sweep throughout the body. But instead of causing disease, it has been modified to spur the immune system into action to fight off the SIV molecules.
“It maintains an armed force, that patrols all the tissues of the body, all the time, indefinitely,” explained Prof Picker.
The researchers gave rhesus macaque monkeys the vaccine, and then exposed them to SIV.
They found that at first the infection began to establish and spread. But then the monkeys’ bodies started to respond, searching out and destroying all signs of the virus.
Of the monkeys that successfully responded to the vaccine, they were still clear of infection between one-and-a-half and three years later.
Prof Picker said his team was still trying to work out why the vaccination worked in only about half of the monkeys.
“It could be the fact that SIV is so pathogenic that this is the best you are ever going to get.
“There is a battle going on, and half the time the vaccine wins and half the time it doesn’t,” he said.
The researchers are now testing the vaccine to see if it can be used after SIV exposure to treat and potentially cure infected monkeys.
They also want to see if the technique could work in humans.
Prof Picker said: “In order to make a human version we have to make sure it is absolutely safe.
“We have now engineered a CMV virus which generates the same immune response but has been attenuated [modified to lose its virulence] to the point where we think it is unequivocally safe.”
This would first have to pass through the regulatory authorities, but if it does, he said he hoped to start the first clinical trials in humans in the next two years.
Commenting on the research, Dr Andrew Freedman, from Cardiff University School of Medicine, said: “This suggests that prophylactic vaccines – vaccines designed to prevent infection – using CMV vectors may be a promising approach for HIV.
“While they may not prevent the initial infection, they might lead to subsequent clearance, rather than the establishment of chronic infection.”
How a lack of money could make you less intelligent: Financial worries ‘reduce IQ by up to 13 points’
The drop in intelligence means these people are more likely to make bad decisions, such as taking on too much debt, which perpetuate financial woes
But when they had their financial burdens removed, their intelligence returned to the same levels as higher earners
Researchers say that far from low intellect resulting in reduced pay, it is our financial woes that render us less clever
The size of your pay packet dictates more than just your holiday choice or the size of your car – it also influences your intelligence. Financial worries tax the brain of those on low incomes, reducing their IQ by up to 13 points, scientists have found. As a result, those with limited means are more likely to make bad decisions, such as taking on too much debt, which perpetuate their financial woes.
But researchers discovered when low-income individuals had their financial burdens removed, their intelligence returned to the same levels as higher earners.
The findings suggests that far from low intellect resulting in reduced pay, it is our financial woes that render us less clever.
‘Our results suggest that when you’re poor, money is not the only thing in short supply. Cognitive capacity is also stretched thin,’ said Harvard economist Sendhil Mullainathan.
‘That’s not to say that poor people are less intelligent than others. What we show is that the same person experiencing poverty suffers a cognitive deficit as opposed to when they’re not experiencing poverty.
‘It’s also wrong to suggest that someone’s cognitive capacity has gotten smaller because they’re poor. In fact, what happens is that your effective capacity gets smaller, because you have all these other things on your mind, you have less mind to give to everything else.’ He said individuals with financial worries are like a computer that has slowed down because it is carrying out more than one function.
‘It’s not that the computer is slow, it’s that it’s doing something else, so it seems slow to you. I think that’s the heart of what we’re trying to say,’ he added.
In the study, published in the journal Science, the team from US and British universities carried out a series of experiments in a US shopping mall.
Researchers selected 400 people at random and divided them into a ‘poor’ or ‘rich’ group based on their income, before subjecting them intelligence testing.
Prior to the experiment, half of the participants were asked to think about how they would pay for $1,500 of urgent repairs on their car if it had broken down. The aim was to get participants to focus on their own financial worries.
The study found poor participants performed much worse in the IQ test if they first considered their economic circumstances, but the better off were unaffected.
However, the group that was not primed to think about their finances scored similarly in the intelligence tests irrespective of their income.
‘For the poor, because these monetary concerns are just below the surface, the question brings them to the top,’ said Professor Mullainathan. ‘The result was, for that group, the gap between the rich and the poor goes up, in both IQ and impulse control. There was no gap in the other group, but ask them anything that makes them think about money and you see this result.’
In a second set of tests, the scientists travelled to rural India, where sugar cane farmers are paid the majority of their income once a year.
They found they performed significantly better at intelligence tests in the month after being paid – the equivalent of 10 IQ points – than just before, when their savings had dwindled.
‘The month after the harvest, they’re pretty rich, but the month before – when the money has run out – they’re pretty poor,’ Professor Mullainathan said. ‘What we did is look at the same people the month before and the month after the harvest, and what we see is that IQ goes up, cognitive control, or errors, goes way down, and response times go way down.’
The University of East Anglia team is starting human trials following on from successful lab studies.
Tests on cells and mice showed that a broccoli compound – which humans can also get from Brussels sprouts and cabbage – blocked a key destructive enzyme that damages cartilage.
They are asking 20 patients to eat a daily dose of “super-charged” broccoli.
This special cruciferous vegetable has been bred to be extra rich in nutrients – it is a cross between standard broccoli and a wild relative from Sicily.
Our body takes this glucoraphanin compound and turns it into another, called sulforaphane, which appears to protect the joints.
The volunteers will have two weeks on the diet before going under the knife to have their badly arthritic knees repaired by surgeons.
Dr Rose Davidson and her team will look at the tissue that has been removed to see what impact, if any, the broccoli has had.
She said: “We’re asking patients to eat 100g (3.5oz) every day for two weeks. That’s a normal, good-sized serving – about a handful – and it’s an amount that most people should be happy to eat every day.”
While two weeks is highly unlikely to be enough to cause any big change, Dr Davidson hopes it will be enough to offer some evidence that “super” broccoli could benefit humans.
“I can’t imagine it would repair or reverse arthritis… but it might be a way to prevent it,” she said.
Her team will be looking for proof that sulforaphane has travelled to where it is needed in the joint and that it is causing beneficial changes at the cellular level.
Another 20 knee replacement patients who have not been on the diet will be used as a comparison group.
Prof Alan Silman, of Arthritis Research UK, which is funding Dr Davidson’s work, said: “Until now research has failed to show that food or diet can play any part in reducing the progression of osteoarthritis, so if these findings can be replicated in humans, it would be quite a breakthrough.
“We know that exercise and keeping to a healthy weight can improve people’s symptoms and reduce the chances of the disease progressing, but this adds another layer in our understanding of how diet could play its part.”
The results of Dr Davidson’s animal trials are published in the journal Arthritis & Rheumatism.
The special broccoli, known as Beneforte, was developed from publicly funded research at the UK’s Institute of Food Research and the John Innes Centre.
More than 8.5 million people in the UK have osteoarthritis, a degenerative disease affecting in particular the hands, feet, spine, hips and knees.
The US Food and Drug Administration (FDA) has approved a new clinical trial of a groundbreaking strategy using stem cells for the treatment of MS (multiple sclerosis).
Researchers from the Tisch MS Research Center of New York say the FDA has granted approval to begin early clinical investigation (phase 1 trial) of autologous neural stem cells in the treatment of MS.
Multiple sclerosis is a chronic disease that attacks the central nervous system (the spinal cord, optic nerves and brain). Common symptoms are numbness of the limbs, but more severe cases can lead to paralysis and blindness.
According to the Multiple Sclerosis Foundation, there are currently between 350,000 to 500,000 people in the US who have been diagnosed with MS, and 200 people are diagnosed with the disease every week.
The new regenerative strategy will involve using autologous, mesenchymal stem cell-derived neural progenitor cells (MSC-NPs), which will be harvested from the bone marrow of 20 MS patients who meet the criteria for the trial.
Spinal injections of stem cells
The stem cells will then be injected into the cerebrospinal fluid that surrounds the spinal cords of the patients.
The main objective of the clinical trial, the researchers say, is to determine the safety of the treatment, while the secondary objective is to measure the effectiveness.
The injections will be repeated at 3-month intervals, with their safety and efficacy frequently monitored through follow-up visits. After the final injection, patients will be monitored for up to 27 months.
Preclinical testing of this procedure showed that after injecting the stem cells, brain inflammation was reduced in seven MS patients, myelin was repaired (an insulating layer that forms around nerves), and protection of the neuronal structure and function of the brain was improved.
Dr. Saud Sadiq, senior research scientist at Tisch MS Research Center of New York, says: “This study provides a hope that established disability may be reversed in MS.”
Similar trials but with larger number of patients (phase 2) have already been under way in the UK. In 2011, UK scientists received £1 million from the MS Society and the UK Stem Cell Foundation (UKCSF) towards research investigating whether stem cells can slow, stop or reverse brain and spinal cord damage in MS patients.
Dr. Sadiq says of this most recent trial in the US: “To my knowledge, this is the first FDA-approved stem cell trial in the United States to investigate direct injection of stem cells into the cerebrospinal fluid of MS patients, and represents an exciting advance in MS research and treatment.”
The clinical trial will begin enrolling patients once ethical approval has been granted and funding secured.
Pregnant women who don’t produce enough thyroid hormone are nearly four times likelier to give birth to autistic children than their healthy peers, a new study has claimed. Scientists from the Houston Methodist Neurological Institute in US and Erasmus Medical Centre in Rotterdam, Netherlands studied more than 4,000 Dutch mothers and their children. Their results support the growing view that autism spectrum disorders can be caused by a lack of maternal thyroid hormone, which past studies have shown is crucial to the migration of foetal brain cells during embryo development.
“It is increasingly apparent to us that autism is caused by environmental factors in most cases, not by genetics. That gives me hope that prevention is possible,” said lead author Gustavo Roman, a neurologist and neuroepidemiologist who directs the Nantz National Alzheimer Center. The researchers also found that autistic children had more pronounced symptoms if their mothers were severely deficient for T4, also called thyroxine. Mild T4 deficiencies in mothers produced an insignificant increase in autistic children’s symptoms. The most common cause of thyroid hormone deficiency is a lack of dietary iodine – because both the thyroid hormones, T3 and T4, contain that element.
The present work was based on the Generation R Study, conducted by Erasmus Medical Centre doctors and social scientists, in which thousands of pregnant women were voluntarily enrolled between 2002 and 2006. Researchers identified 80 “probable autistic children” from a population of 4,039. Around 159 mothers were identified as being severely T4 deficient (defined as having 5 per cent or less of normal T4, but producing a normal amount of thyroid stimulating hormone), and 136 were identified as mildly T4 deficient.
The researchers found a weak association between mild T4 deficiency and the likelihood of producing an autistic child, but a strong association between severe T4 deficiency and autism (3.89 more likely, as compared with mothers with normal thyroid hormone). The study presents a troubling correlation, but it does not prove that the thyroid function of expecting mothers causes autism in their children, researchers said. The study will be published in the journal Annals of Neurology.
US scientists say they have moved a step closer to being able to grow a complete human ear from a patient’s cells. In a new development in tissue engineering, they have grown a human-like ear from animal tissue. The ear has the flexibility of a real ear, say researchers at Massachusetts General Hospital in Boston. The technique may one day be used to help people with missing or deformed outer ears, they believe.
Tissue engineering is a growing field in medical science, where substitute organs are made in the laboratory in the hope of using them to replace damaged ones.
The US research team is working on artificial living ears to help people born with malformed ears or who have lost them in accidents or trauma. Previously the researchers had grown an artificial ear, the size of a baby’s, on a mouse. In the latest development, published in the Journal of the Royal Society Interface, they took living tissues from cows and sheep and grew them on a flexible wire frame that has the 3D shape of a real human ear. This was then implanted into a rat whose immune system they had suppressed enabling the ear to grow. “We’ve demonstrated the first full-sized adult human ear on the rat model,” Dr Thomas Cervantes, who led the study, told BBC News.
It was significant for several reasons, he said.
“One – we were able to keep the shape of the ear, after 12 weeks of growth in the rat. And then secondly we were also able to keep the natural flexibility of the cartilage.”
Titanium scaffold. The cells were grown on a titanium wire scaffold that is modelled on the dimensions of a real human ear, taken from CT scans. The new work shows that in theory it is possible to grow up enough cells – at least in animals – to make a full-size human ear.
“In a clinical model, what we would do is harvest a small sample of cartilage, that the patient has, and then expand that so we could go ahead and do the same process,” said Dr Cervantes.
“This research is a significant step forward in preparing the tissue-engineered ear for human clinical trials.”
He said he expected that the process could move into human clinical trials in about five years. Other research into bioengineered organs is progressing fast. About a dozen patients have received transplants of artificial wind pipes coated with stem cells taken from either the patient or a donor. Meanwhile, a kidney grown in the laboratory has been transplanted into a rat, where it started to produce urine.