Breath test for TB developed


Tuberculosis bacteria
Researchers have developed the first breath test for TB in the laboratory.

It provides rapid information on drug resistance that takes up to six weeks using standard methods, US scientists report in the journal, Nature Communications.

The bacteria emit a unique gas signature within 10 minutes of exposure to an inhaled antibiotic in rabbits.

TB infects 8.6m people each year worldwide and kills 1.3m, second only to HIV.

Early diagnosis and treatment are a priority in the global fight against TB, according to the World Health Organization.

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Optimally treating somebody the best you can at the time of that single encounter, so someone can go home with the right set of tablets, would be really, really useful”

Dr Graham TimminAssociate Professor at the University of New Mexico

The new research used an inhaled form of isoniazid – an antibiotic commonly used to treat the disease – which is activated by a TB enzyme.

The test exploits the fact that this enzyme is unique to TB, said Dr Graham Timmins, Associate Professor at the University of New Mexico, US, who led the research.

“We realised that we could actually look at the conversion of isoniazid to its active form by monitoring one of the labelled gases that’s given off during its activation,” he explained.

The researchers gave a special molecularly-labelled form of isoniazid to laboratory rabbits.

In the presence of TB, labelled nitrogen gas was released from the lungs and detected by a machine called a mass spectrometer.

A positive result indicates that TB bugs are present and suggests they are susceptible to isoniazid.

Treatment options

TB is very difficult to treat, requiring at least six months of treatment with multiple drugs.

Childhood TB can be harder to detect than the adult form of the disease
The test could be particularly useful in children where sputum samples are problematic

Failure to complete treatment has contributed to the rise of multidrug-resistant TB (MDR-TB), accounting for 30% of cases in some countries.

For many years diagnosis of TB relied on a lengthy wait for the bacteria to grow in a culture of the patient’s sputum.

“If you do it by culture, it can take a month to six weeks before you get a result,” said Dr Timmins.

In the last few years a new DNA detection technique called GeneXpert has been endorsed by the World Health Organization.

From a sample of sputum it can detect whether a sample contains TB and whether it is is resistant to one of the key drugs, rifampicin, in about three hours.

But for full drug resistance information the patient has to wait longer.

“Optimally treating somebody the best you can at the time of that single encounter, so someone can go home with the right set of tablets, would be really, really useful,” said Dr Timmins.

The new breath test samples the whole lung for what is hoped will be greater sensitivity, in a wider range of patients, with results available almost instantly.

‘Clever idea’

“It’s a clever idea,” said Dr Ruth McNerney, senior lecturer at the London School of Hygiene and Tropical Medicine.

The test could “add a bit more certainty” to the diagnosis of MDR-TB, and “it’s worth pursuing, definitely,” she said.

At present the breath test only detects isoniazid sensitivity. It will therefore need to be used in combination with other tests.

“This is just the start of the program we want to instigate,” said Dr Timmins.

The next step will be to show that the tests work in humans in a clinical setting.

“Lots of good ideas fail when you put them into the clinic,” conceded Dr Timmins.

Novel antibiotic class created


 

E. coli 0157
One of the bacteria targeted in the experiments was a strain of E. coli

Scientists have designed a new class of antibiotic which seeks and destroys resistance genes in bacteria.

The unique approach could be used to genetically engineer bacteria in our bodies to become less dangerous.

The technology might also lead to new treatments for metabolic diseases like obesity, the researchers claim.

Scientists and politicians have warned that we face a return to the medical “dark ages” if action is not taken against antibiotic resistance.

The human body houses ten times more bacterial cells than human ones. This community of bacteria is termed the microbiome and its importance in keeping us healthy is increasingly recognised.

One of the problems with current antibiotics is “they hit not only the bad bacteria but also the good bacteria,” explained Professor Timothy Lu of the Synthetic Biology Center at Massachusetts Institute of Technology, who led the team carrying out the new research.

“It allows the bad bacteria to flourish.”

In a series of laboratory experiments published in Nature Biotechnology, the researchers showed they could produce a molecular “conditional-lethality device” capable of highly targeted action against the “bad” bacteria in a consortium of different strains.

The new antibiotic uses an RNA-guided nuclease called a “Crispr” to hunt down and chop up target genes inside bacterial cells.

Infographic
  1. A Crispr is designed to target a specific bacterial DNA sequence
  2. The molecule is packaged into a bacteriophage carrier to enter the target cell
  3. The system finds the gene target, cuts the DNA strand at the specified location, and deletes the plasmid – with or without cell death
  4. Targeted cuts of chromosomal DNA always lead to cell death

“We designed Crispr systems that would go into bacteria and specifically kill only bacteria that contain antibiotic resistance genes or virulence genes,” explained Professor Lu.

The bacteria targeted in the experiments included a strain of E. coli which can cause severe diarrhoea and kidney failure.

But Professor Lu isn’t only interested in killing the deadly bacterium – he wants to rehabilitate it.

In separate experiments the researchers showed they could change the genetic makeup of bacteria without killing them.

“Inherently E. coli is not necessarily a bad organism,” Professor Lu explained. “They carry genes that make them bad.”

Targeting the bad genes, instead of killing the good and bad bacteria alike, is a new approach which “imposes direct evolutionary pressure at the gene level”.

Professor Lu is confident the new antibiotics could be ready for clinical trials in some infections “within a few years.”

Resistance is futile?

No new classes of antibiotic have been developed for more than 25 years.

The overuse of available antibiotics favours the survival of bacteria resistant to the drugs. These bacteria can then transmit their resistance genes to other bacteria using tiny circles of DNA called plasmids.

The process effectively speeds up evolution to produce bugs that cannot be killed when they cause disease.

The problem is huge and attracted the attention of Prime Minister David Cameron in July, when he announced a new interdisciplinary panel to address the issue.

“If we fail to act, we are looking at an almost unthinkable scenario where antibiotics no longer work and we are cast back into the dark ages of medicine where treatable infections and injuries will kill once again,” he said.

Professor Lu described the problem as “a technological arms race between us and the bacteria”.

The new system is “a new type of antimicrobial that really acts very differently to previous ones, and I think that’s why we’re particularly excited about it,” he explained.

Bacteriophages
Bacteriophages are natural virus predators of bacteria

The technology could eventually be given to healthy people to prevent antibiotic resistance developing.

“You might take probiotic bacteria while you are healthy, and that probiotic bacteria could distribute these Crispr constructs into your natural bacterial population, and kind of immunise them from being able to pick up bacterial resistance genes.

“So just like the antibiotic resistance plasmids naturally spread in a population, we could potentially design these Crispr constructs to also spread… like a parasite that hops from bacteria to bacteria.”

“Think about it like a vaccine – but it’s a vaccine for your bacteria, not for you.”

Introducing self-replicating gene treatments into the microbiome would not be without risk.

“This is admittedly a little bit radical but I think it’s an interesting thing to consider.”

‘An enabling toolkit’

“The use of antimicrobial agents based on DNA has exciting potential that has not yet been effectively harnessed,” said Lucinda Hall, professor of molecular microbiology at Queen Mary University of London.

“The greatest challenge is how to deliver a DNA-based agent into the bacteria to be targeted.”

The MIT team explored two approaches to this.

“One idea is that you can just piggy back off the same system that bacteria use to trade resistance genes,” Professor Lu explained. In this approach the target cell accepts a ‘Trojan horse’ plasmid of DNA from another bacteria, with the Crispr hidden inside.

But this would require live bacteria to be given to a patient – so “it is probably not the best solution for an acute infection,” he conceded.

Secondly, the team used bacteriophages – natural virus predators of bacteria which are highly adept at injecting DNA into host cells.

This approach is also not without difficulties. “You have to find the right type of phage to bind to each type of bacteria,” explained Professor Hall. “There is also a question about how easily phage can reach the site in the body where the bacteria are causing an infection, and whether they will be blocked by antibodies.”

“It is something we have to take into consideration,” responded Professor Lu. “Other groups have found pretty interesting ways around this, for example coating the bacteriophages with chemicals that basically shield them from the immune system.”

Professor Hall was also critical of the bacterial kill rates reported, describing the numbers as “disappointing”.

“We need to continue to improve the efficacy,” conceded Professor Lu. “But even with [relatively modest] drops in bacterial count you can detect significantly increased survival of the waxworms we were using for testing.”

The benefits of manipulating the balance of “good” and “bad” bacteria in the body might extend beyond fighting infection.

“There are certain classes of bacteria in your gut that are known to be overrepresented in people who are obese or have metabolic diseases,” explained Professor Lu.

“We could design Crispr-based systems that would go into bacteria, targeted to certain subsets of bacteria, and only activate when they recognise genes that we know are correlated with human disease.”

“This is an enabling toolkit for the basic scientists to now start probing these systems a little bit better.”

Brazil releases ‘good’ mosquitoes


Brazilian researchers in Rio de Janeiro have released thousands of mosquitoes infected with bacteria that suppress dengue fever.

The hope is they will multiply, breed and become the majority of mosquitoes, thus reducing cases of the disease.

The initiative is part of a programme also taking place in Australia, Vietnam and Indonesia.

The intracellular bacteria, Wolbachia, being introduced cannot be transmitted to humans.

The programme started in 2012 says Luciano Moreira of the Brazilian research institute Fiocruz, who is leading the project in Brazil .

“Our teams performed weekly visits to the four neighbourhoods in Rio being targeted. Mosquitoes were analysed after collection in special traps.

“Transparency and proper information for the households is a priority. ”

Ten thousand mosquitoes will be released each month for four months with the first release in Tubiacanga, in the north of Rio.

‘Good’ bacteria

The bacterium Wolbachia is found in 60% of insects. It acts like a vaccine for the mosquito which carries dengue, Aedes aegypti, stopping the dengue virus multiplying in its body.

Wolbachia also has an effect on reproduction. If a contaminated male fertilises the eggs of a female without the bacteria, these eggs do not turn into larvae.

If the male and female are contaminated or if only a female has the bacteria, all future generations of mosquito will carry Wolbachia.

As a result, Aedes mosquitoes with Wolbachia become predominant without researchers having to constantly release more contaminated insects.

In Australia this happened within 10 weeks on average.

The research on Wolbachia began at the University of Monash in Australia in 2008. The researchers allowed the mosquitoes to feed on their own arms for five years because of concerns at the time Wolbachia could infect humans and domestic animals.

Three more neighbourhoods will be targeted next, and large scale studies to evaluate the effect of the strategy are planned for 2016.

Dengue re-emerged in Brazil in 1981 after an absence of more than 20 years.

Over the next 30 years, seven million cases were reported.

Brazil leads the world in the number of dengue cases, with 3.2 million cases and 800 deaths reported in the 2009-14 period.

Is it bad to wear a bra when going to bed?


This is one debate that will rage till eternity. While most ladies avoid wearing a bra when going to bed to avoid marks, the “constricted” feeling and even the fear of blocking the lymphatic glands leading to breast cancer, there are the religious nighttime-bra-wearers (like Marilyn Monroe) who strongly believe that it prevents their breasts from sagging. Scientifically both of these assumptions are myths at best.

11_Is-it-bad-to-wear-a-bra-when-going-to-bed-326x235

Lymph nodes in the underarms act as natural filters that drain the breast of lymph fluid, and are the body’s first defense against infection, foreign material, and cancer cells. Studies have not been able to prove that wearing a bra constricts the pathways of the lymph nodes.So get the breast cancer fear out of your mind.

Pregnancy and breastfeeding are the most common causes of breast sagging, and genetics and age determine the extent of sagging. If your breasts size is above C then choosing a soft-cup style, without much hardware or fasteners, should provide some support from sagging. For all others the bra isn’t preventing sagging in any way.

To conclude, sleeping in a bra at night really is just a matter of the woman’s personal comfort. Some women have tender breasts, so need the bra support and for some who suffer from rashes below their breasts (moist skin-to-skin friction) wearing a bra can be painful. If you do wear it avoid an ill fitting one and choose a natural fiber (all-cotton wireless), soft cupped bra that will keep moisture away from the skin.

Dyslexic brain may solve some math problems in a roundabout way .


Children with the reading disorder rely heavily on right brain to do addition

solving math equations

ADDING IT UP  Children with dyslexia use their brains differently than other children to do certain kinds of math problems, a study suggests.

The brains of children with dyslexia rely on unusual strategies to solve certain kinds of math problems, researchers report in the Nov. 1 NeuroImage. The findings could explain why dyslexia, a disorder of reading, can bring math troubles too.

By revealing how the dyslexic brain tackles math, the research might eventually lead to better teaching methods, says study coauthor Guinevere Eden of Georgetown University Medical Center in Washington, D.C.

Usually, people use regions on the right side of the brain to solve math problems that require a step-by-step process, such as subtraction and division; regions on the left side of the brain typically handle more rote, fact-retrieval problems such as addition and multiplication.

 

Antidepressant medicines change brain architecture


A single dose of drugs used to treat depression can alter brain’s structure only within hours, German researchers have uncovered.

The study conducted by the scientists at the Max Planck Institute in Leipzig found that the most popular class of antidepressants, selective serotonin reuptake inhibitors (SSRIs) could impact brain can change connectivity.

Researchers used a magnetic resonance imaging machine to track brain connectivity in medication, according to the study report published the Cell Press journal Current Biology.

First they took data in free individuals whose minds wander for about 15 minutes in a brain scanner that measures the oxygenation of blood flow in the brain.

Next they gave the group a single dose of escitalopram, the SSRI antidepressant under the brand-name Lexapro, and then scanned the connections in the barin.

Comparing the brain connection 3-D maps indicated prominent changes in brain’s  architecture caused by taking the drug.

“A single dose reduced connectivity in most parts of the brain, but increased connectivity within the cerebellum and thalamus — the parts of the brain associated with motor control and signal regulation only within hours.”

“We were not expecting the SSRI to have such a prominent effect on such a short timescale or for the resulting signal to encompass the entire brain,” said the co author of the study Julia Sacher.

“The findings could be a first step toward figuring out whether a relatively simple brain scan might one day help psychiatrists distinguish between those who respond to such drugs and those who don’t, an area of mystery and controversy in depression treatment,” researchers say.

New analysis of human genetic history reveals female dominance


Female populations have been larger than male populations throughout human history, according to research published today in the open access journal Investigative Genetics. The research used a new technique to obtain higher quality paternal genetic information to analyse the demographic history of males and females in worldwide populations.

The study compared the paternally-inherited Y chromosome (NRY) with maternally inherited mitochondrial DNA (mtDNA) of 623 males from 51 populations. The analysis showed that female populations were larger before the out-of-Africa migration and remained so throughout almost all subsequent migrations. The main drivers of this trend are likely to be processes such as polygyny, where one male mates with many females, and the fact that in most societies, women tend to move to live with their husbands. This has resulted in females making a greater genetic contribution to the global population than males.

Previous research on genetic history has used different techniques to analyse NRY and mtDNA, which has led to an ascertainment bias in the results. In this study, researchers from the Max Planck Institute for Evolutionary Anthropology developed a high-resolution Y chromosome sequencing assay that allowed them to get paternal and maternal histories of similar quality and resolution, so they could make a direct comparison. The results confirmed previous findings that when comparing on a global scale, there are greater genetic differences in paternal NRY than in mtDNA. However, these differences are not as large as previously thought and the authors were surprised to see substantial variation in relative amounts of NRY vs. mtDNA differentiation at the regional level.

The authors argue that using this new technique, greater analysis can be undertaken at a regional level to create a clearer picture of the paternal and maternal influences on specific populations. In the African populations they studied, they saw lower paternal genetic diversity, which may be a direct result of the Bantu expansion into eastern and southern Africa beginning about three thousand years ago. In samples taken from the Americas, initial results suggest higher maternal genetic diversity, indicating that there were fewer males than females among the original colonisers.

Dr. Mark Stoneking, Department of Evolutionary Genetics, Max Planck Institute, an author on the paper, said: “Our new sequencing technique removes previous biases, giving us a richer source of information about our genetic history. It allows us to take a closer look at the regional differences in populations, providing insights into the impact of sex-biased processes on .”

Polyethylene Glycol for Hepatic Encephalopathy:A New Solution to Purge


Hepatic encephalopathy is a well-known neuropsychiatric complication of cirrhosis with symptoms ranging from mild confusion and sleep disturbance to obtundation. It is highly associated with increased mortality and health care costs.1 As the population of patients with cirrhosis grows, so do these burdens on the health care system. Lactulose treatment has long been the standard of care,2thought to be effective by acidifying stool and eradicating toxic metabolites created by gut flora that the cirrhotic liver is unable to clear. This therapy is widely available and inexpensive. However, with reported 20% to 30% nonresponse rate and refractory encephalopathy, additional therapies have been sought. Nonabsorbable antibiotics have been explored, with the goal of altering the gut microbiome and decreasing ammonia levels and other toxins implicated in hepatic encephalopathy. A randomized, double-blinded controlled trial from 20133 demonstrated the greater efficacy of lactulose with rifaximin compared with lactulose alone.

Antifreeze proteins in Antarctic fishes prevent freezing … and melting .


Antarctic fishes that manufacture their own ‘antifreeze’ proteins to survive in the icy Southern Ocean also suffer an unfortunate side effect, researchers report: The protein-bound ice crystals that accumulate inside their bodies resist melting even when temperatures warm.
Special ‘antifreeze’ proteins in the blood of several Antarctic fish species bind to ice crystals and prevent the creatures from freezing. A new study finds that the proteins also allow the internal ice crystals to persist at temperatures that normally would melt them.
Credit: Paul Cziko

Antarctic fishes that manufacture their own “antifreeze” proteins to survive in the icy Southern Ocean also suffer an unfortunate side effect, researchers report: The protein-bound ice crystals that accumulate inside their bodies resist melting even when temperatures warm.

The finding is reported in the Proceedings of the National Academy of Sciences.

“We discovered what appears to be an undesirable consequence of the evolution of antifreeze proteins in Antarctic notothenioid fishes,” said University of Oregon doctoral student Paul Cziko, who led the research with University of Illinois animal biology professors Chi-Hing “Christina” Cheng and Arthur DeVries. “What we found is that the antifreeze proteins also stop internal ice crystals from melting. That is, they are anti-melt proteins as well.”

Five families of notothenioid fishes inhabit the Southern Ocean, the frigid sea that encircles Antarctica. Their ability to live in the icy seawater is so extraordinary that they make up more than 90 percent of the fish biomass of the region.

DeVries discovered antifreeze proteins in Antarctic notothenioid fishes in the late 1960s, and was the first to describe how the proteins bind to ice crystals in the blood to prevent the fishes from freezing.

In the new study, the team investigated whether the antifreeze protein-bound ice crystals inside these fishes would melt as expected when temperatures warmed. When researchers warmed the fishes to temperatures above the expected melting point, some internal ice crystals failed to melt. Ice that doesn’t melt at its normal melting point is referred to as “superheated.”

The researchers also found ice crystals in wild notothenioid fishes swimming in relatively warmer Antarctic summer waters, at temperatures where they would be expected to be free of ice. By testing the antifreeze proteins in the lab, the team found that these proteins also were responsible for preventing the internal ice crystals from melting.

“Our discovery may be the first example of ice superheating in nature,” Cheng said.

A diver himself, Cziko worked with other divers to place and maintain a temperature-logging device in McMurdo Sound, Antarctica, one of the coldest marine environments on the planet. The device recorded ocean temperatures there for 11 years, a substantial portion of notothenioids’ lifespan. Not once in that time did temperatures increase enough to overcome the antifreeze proteins’ anti-melting effect to completely rid the fishes of their internal ice, the researchers report.

The researchers suspect that the accumulation of ice inside the fishes could have adverse physiological consequences, but none have yet been discovered.

If the fishes are destined to carry ice crystals around all their lives, Cheng said, it is conceivable that ice particles could obstruct small capillaries or trigger undesired inflammatory responses. Cziko likens the potential threat to dangers posed by asbestos in the lungs or blood clots in the brain.

“Since much of the ice accumulates in the fishes’ spleens, we think there may be a mechanism to clear the ice from the circulation,” he said.

“This is just one more piece in the puzzle of how notothenioids came to dominate the ocean around Antarctica,” he said. “It also tells us something about evolution. That is, adaptation is a story of trade-offs and compromise. Every good evolutionary innovation probably comes with some bad, unintended effects.”

The long-term temperature record of McMurdo Sound produced in the study also “will prove to be of great importance and utility to the polar research community that is addressing organismal responses to climate change in this coldest of all marine environments,” Cheng said.


Story Source:

The above story is based on materials provided by University of Illinois at Urbana-Champaign. Note: Materials may be edited for content and length.


Journal Reference:

  1. Paul A. Cziko, Arthur L. DeVries, Clive W. Evans, and Chi-Hing Christina Cheng.Antifreeze protein-induced superheating of ice inside Antarctic notothenioid fishes inhibits melting during summer warming. PNAS, September 22, 2014 DOI: 10.1073/pnas.1410256111

Often go to bed late? It could leave you with a chronic sleep disorder


It could leave you with a chronic sleep disorder: Millions think they’re just night owls. In fact, they could be wreaking havoc on their body clocks

  • Niamh Spence, 23, from Manchester, has survived on little sleep for 4 years
  • Now doesn’t feel tired before 3am and she can’t sleep before 3.30am
  • She is one of an increasing number of people suffering from DSPS
  • Long-standing sleep deprivation is associated with increased heart rate, blood pressure and higher levels of chemicals linked with inflammation

When her alarm goes off at 7am, Niamh Spence aches so much that she wonders momentarily if she is ill. At best, she will have had four hours’ sleep, but usually it’s nearer three.

Niamh, 23, has survived on this little sleep for the past four years. As a child and teenager, she got at least eight hours’ sleep a night. But her sleep patterns shifted at university when juggling two waitressing jobs, as she’d start her university work after coming home at midnight.

Now she doesn’t feel tired before 3am and she can’t sleep before 3.30am.

Scroll down for video  

Niamh has survived on this little sleep for the past four years

Niamh has survived on this little sleep for the past four years

‘No matter what I do, I can’t change my body clock back,’ says Niamh, who lives in Manchester.

Every so often she tries sleeping from 11pm, but ends up tossing and turning for two hours, before giving up to do some work on her laptop instead.

So, normally, she doesn’t bother trying to sleep before 3am. She stays up doing laundry, cleaning or working until she’s tired, despite having to be at work by 9.30am. ‘I take work home and if I’m not asleep, I’ll reply to emails and check news feeds on my phone. It’s as if I can’t switch off.’

Niamh’s habits might sound unusual, but she is one of an increasing number of people suffering from delayed sleep phase syndrome (DSPS), a disorder affecting the body clock, or circadian rhythm.

What it means for sufferers is that their natural sleep patterns are pushed back – so they don’t feel sleepy until the early hours of the next morning. However, unlike insomniacs, once they do fall asleep, they sleep well.

Yet because they have problems getting to sleep at a decent time they can become chronically sleep deprived, so their physical and mental health can suffer as a result.

She is one of an increasing number of people suffering from delayed sleep phase syndrome

She is one of an increasing number of people suffering from delayed sleep phase syndrome

‘Delayed sleep phase syndrome is an extreme version of being a night owl – someone who sleeps late and gets up late – and it became a recognised condition in the Eighties,’ says sleep expert Dr Neil Stanley.

‘It could be genetic, behaviour you’ve learned from your parents or that you’ve slipped into from going to bed later than normal and your body has got used to it. This can happen over up to three months.’

Research suggest about 0.15 per cent of the population – 96,000 Britons – suffer from the disorder yet this may be the tip of the iceberg, says Dr Stanley, who runs The Sleep Consultancy.

He says that the number of sufferers is probably rising thanks to a stressful work culture and increased use of technology, with the light emitted by devices such as TV, computers and mobile phones confusing the body clock.

‘People suffer in silence,’ he says. ‘We don’t go to our GP with sleep problems and, if we did, most of our GPs don’t know enough about sleep illnesses to make an accurate diagnosis. Most GPs will never have heard of delayed sleep phase syndrome and might misdiagnose it as depression.’

When you sleep and how long you sleep for is not a problem unless it affects your daytime behaviour, says Dr Stanley.

‘If you’re at university and you go to bed at 3am and get up at 10am, yet you still attend all your lectures, it’s not a problem, but because of our nine-to-five society it is a problem for anyone who has to be at work at 9am.’

People with this problem will go to bed at least two or three hours later than most people and so often end up chronically tired.

Niamh has tried various remedies to help her drop off earlier, including lavender oils (lavender may help to lower the heart rate and blood pressure, aiding relaxation), drinking warm milk (which contains tryptophan, an amino acid that helps produce the sleep-inducing chemicals serotonin and melatonin) and chamomile tea (thought to work as a mild tranquiliser). But nothing has helped.

‘My lack of sleep has affected my health,’ she says. ‘I’m run down and get ill more often now. It takes weeks to shake off a cold or a bug.

‘I look tired most of the time. I have dark circles under my eyes, and I’m getting paler through lack of sleep.

‘My social life has been affected because I’m so shattered physically. There are times I feel I can’t take on any more – it’s hard to cope on so little sleep.’

 I look tired most of the time. I have dark circles under my eyes, and I’m getting paler through lack of sleep

Long-standing sleep deprivation is associated with increased heart rate, blood pressure and higher levels of chemicals linked with inflammation, which may put extra strain on the heart.

It has been suggested that missing out on deep sleep may also change the way the body processes glucose, the high-energy carbohydrate that cells use for fuel, leading to type 2 diabetes. But that’s not the only risk to those with delayed sleep phase syndrome, says Dr Stanley.

‘If you’ve been awake for 16 hours, your performance driving a car can be as impaired as if you’re over the drink-driving limit because without sleep, your brain is like a battery that has run out of charge, so judgment will be poor.’

Little sleep also means that the body hasn’t had the repair and renewal process that takes place through the night.

This affects concentration and mood by destroying the balance of neurotransmitters (chemical messengers) and hormones. Skin loses its tone, giving dark circles and bags under the eyes.

‘It can make people gain weight because lack of sleep affects appetite hormones,’ says Dr Stanley. ‘This puts them at higher risk of diabetes and heart disease. Lack of sleep also weakens the immune system, so people get ill more often.’

The CIRCADIAN rhythm, the natural cycle that guides when we fall asleep and wake up, is governed by light. One thing that can muddle sleeping patterns is that artificial light at night can signal to the brain that it needs to stay awake.

Dr Stanley says blue wavelengths – given out by televisions, computers, tablets, mobile phones and laptops – can also cause problems, as the eye (and therefore the brain) responds to this light as a signal of daylight.

People with delayed sleep phase syndrome should avoid technology and bright light

People with delayed sleep phase syndrome should avoid technology and bright light

Light plays a key role in the production of melatonin, the so-called sleep hormone, produced by the pineal gland in the brain.

Our melatonin levels vary in 24-hour cycles and they’re controlled by our body clock. Normally, melatonin levels increase at night to ensure we sleep and they’re reduced in bright light to ensure we are alert.

Dr Stanley says that people with delayed sleep phase syndrome should avoid technology and bright light and use only a dim light for an hour before bed. ‘They should also try shifting their bedtime by 15 minutes at a time gradually to train themselves to sleep at a normal time.’

He believes a 10,000 lux blue light box used on waking for 30 minutes can help too by encouraging wakefulness in the morning. These are about the size of an iPad, with several high-powered blue LED lightbulbs instead of a screen.

‘This gives the brain the signal it is day time. Once you’re used to this box, you can experiment with waking up a bit earlier to try to shift your sleep pattern.’

Dr Nerina Ramlakhan, a London-based sleep and energy coach and author of Tired But Wired, says finding ways to tackle stress can also help. Stress causes production of adrenaline, the hormone that prepares the body for a fight or flight response and keeps us alert.

Signs to watch out for

Feeling tired later and later at night, with bedtime shifting to the early hours.

UNLIKE with insomnia, you sleep well once you drift off.

Struggling when you get up at a normal time.

Feeling sleepy through the day.

Suffering from low mood, exhaustion and poor concentration.

‘We’re in a state of high alert all the time, especially if we sleep with our phones switched on and on our pillow,’ says Dr Ramlakhan. ‘The brain is almost over-wired. It’s getting harder to calm the brain down and get into deep levels of sleep.’

She believes that getting the body clock into the right rhythm starts with breakfast. ‘Eating well, including having a good breakfast, keeps the blood sugar levels stable and gives us the resources to make melatonin.’ However, many sufferers often skip breakfast either because they’re too tired or are running late, and opt for a shot of caffeine instead.

‘I’m not hungry in the morning,’ says Niamh. ‘Caffeine is my reassurance that my body can get me through the next 19 hours. I have three or four lattes and four cans of Diet Coke a day.’

Because caffeine increases heart rate, a safe limit is around 400mg daily, but Niamh, a senior account executive for a public relations company, has up to 760mg. But she says it is the only thing keeping her going. ‘I think I’m stuck in this pattern.’

Long-standing sleep deprivation is associated with increased heart rate and blood pressure

Long-standing sleep deprivation is associated with increased heart rate and blood pressure

Dr Ramlakhan also advises making ‘to do’ lists before bed to get the day’s pressures out of your head and onto paper, and calm the mind with yoga or meditation.

10,000 lux light boxes such as the Sad Light Therapy Daylight Sunlight Box Lamp, £69.99, are available from Tesco.com and Amazon.

Gadgets to help you drift off without pills

Many of us think we get less sleep than we do, and it’s worrying about it that causes problems, says Professor Jim Horne of the Sleep Research Centre at Loughborough University. Talking therapies can help, but what about gadgets that promise to help you sleep? Here, he gives his verdict.

Sound Asleep Original Speaker Pillow

£10.99, soundasleeppillow.co.uk

THIS contains speakers inside the pillow which connect to a music source, such as an MP3 player, radio or TV.

EXPERT VERDICT: Won’t break the bank and music can encourage sleep.

Lumie Bodyclock Active 250, £99.95, lumie.com

Lumie Bodyclock Active 250, £99.95, lumie.com

Lumie Bodyclock Active 250

£99.95, lumie.com

A ‘sunset’ light (pictured) signals your body to produce sleep hormones such as melatonin.

EXPERT VERDICT: If dimming light helps you sleep this may be worth buying, but I’d like more evidence showing this works.

The Alpha Stim AID

£449, alpha-stim.co.uk

This small portable device uses microcurrents delivered through ear clip electrodes which manufacturers claim change your brain waves to boost relaxation.

EXPERT VERDICT: I haven’t seen solid evidence it works. Surely there are cheaper and simpler ways to encourage sleep?

Marsona DSI-600A

£94.99, whitenoisemachine.co.uk

Gives out a constant ‘white noise’ but comes with other sounds, such as rain and crickets. The theory is these shut out other noise and help sleep.

EXPERT VERDICT: If you find listening to these noises relaxing it may help, but this isn’t cheap.

How a lack of sleep can lead to changes in your body (related)