Easy Recipe For Nasi Kuning (yellow rice) Anyone Can Try At Home

Cooking for family always caters the best feeling, don’t you think so? It really is a nice experience to see their happy expression when enjoying your food. Not to mention, but if you are now looking for some other recipe ideas for your family, how about you try recipe for nasi kuning (yellow rice)? Indeed, nasi kuning is commonly cooked for some special event, but it doesn’t mean that you can’t try nasi kuning for daily occasion, though it is not for everyday, but once a while it is worth cooking. Ready for the recipe? So to speak, the ingredients include; whole chicken, galangal, one package of Royco for fried chicken, rice, and coconut milk.

Another ingredients that should be there to cook nasi kuning, making sure you prepare turmeric, pandan leaf, bay leaf, shallot, lemon grass, lime juice, and pinch of slat. After the ingredients are prepared, you can do these following; for the chicken, boil the chicken with water after you cut the whole body based on your preference. When it is boiled, pour the Royco package altogether with the grated galangal. You need to wait until the water is reduced. If you want to the chicken more juicy, before the boiled water is totally drained, add some more water.

Once it’s done, you can directly fry the chicken or wait until some time by putting it into the fridge. When it comes to the nasi kuning, the preparation includes; first, you need to boiled the coconut milk with the mixture of salt, pandan leaf, bay leaf, lemon grass, and turmeric (that is already diluted with water), you need to keep stirring the coconut milk until it is boiled. Afterward, you can add rice and wait until it absorbs all of the liquid.

Move the half-cooked rice to the steamer and wait until it is cooked properly. Usually, it takes for about 45 minutes, but it depends on how much the rice that you use. Once it is cooked, you can serve nasi kuning with some sprinkles of fried shallot. Just like that nasi kuning is already delicious, but with the addition of chicken that you fry previously make nasi kuning taste even better. Guess what? If you want to, you can make it more personal by adding certain thing that is favored by your family. The idea is limitless, but if you unsure, the above recipe is enough.


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Does lack of sleep make you susceptible to common cold?


Using disposable tissues can help prevent spreading cold virusesHaving a cold can make you feel miserable

“Sleep longer to lower risk of catching cold,” says The Daily Telegraph of research on how sleep duration and quality could affect your risk of catching a cold.

In this small, research experiment, electronic sleep sensors and records of how much volunteers slept were used to determine sleep patterns before the volunteers were given a dose of a common cold virus. Researchers then looked at whether they developed cold symptoms over the following days.

Those who slept less than five hours were four-and-a-half times more likely to catch a cold than those sleeping more than seven hours a night. A similar result was found for those sleeping five to six hours. Those who slept between six and seven hours were at no greater risk of catching a cold.

These findings support the importance of a good night’s sleep in terms of health and wellbeing, but it doesn’t prove sleep to be the single direct cause of a cold.

Many factors will inevitably determine whether you catch a cold – and although the researchers tried to account for some of these factors they could together be influencing people’s susceptibility to the common cold.

Rather than worry about how long you’ve slept, simply try to keep your hands clean to reduce your chance of getting or spreading common cold viruses.

Where did the story come from?

The study was carried out by researchers from the University of California, Carnegie Mellon University and the University of Pittsburgh Medical Centre. Support for the study was provided by the National Center for Complementary and Alternative Medicine, the National Institute of Allergy and Infectious Diseases, National Institute of Health grants and the National Heart, Lung and Blood Institute.

The study was published in the peer-reviewed journal Sleep.

This has been reported widely and, for the most part, accurately in the UK media. However, the Daily Telegraph’s statement that “lack of sleep is the most important factor in determining whether someone will catch a cold” gives a misleading impression of the findings of this controlled experiment. It is likely that exposure to the cold viruses and lack of good hand hygiene are the most important factors in the spread of cold, but these were not examined in this study. Its headline assumption that you should “sleep longer to lower risk of catching cold” is also not necessarily supported by this evidence.

What kind of research was this?

This is a prospective study that looked at whether shorter sleep duration and interrupted sleep could predict susceptibility to the common cold. The study involved monitoring the sleeping habits of healthy, infection-free volunteers for a week before giving them nasal drops containing a common cold virus (rhinovirus 39). They were then monitored for the development of symptoms of the common cold.

This is a good way of observing how a particular exposure (in this case, sleep quality) may be associated with a subsequent outcome (in this case, the development of a common cold). However, it still can’t prove direct cause and effect, as other factors could be involved.

What did the research involve?

Researchers recruited 164 healthy volunteers, comprising 94 men and 70 women aged 18 to 55 years old. Volunteers were excluded if they:

  • had undergone nasal surgery
  • had a chronic illness, such as asthma or coronary heart disease
  • had obstructive sleep apnoea
  • had been hospitalised in the past five years
  • were currently taking medication for mental health conditions

The volunteers were enrolled two months before being given the rhinovirus dose. During that time they completed questionnaires, two weeks of daily interviews to assess emotions, and underwent a week of sleep behaviour monitoring using a combination of wrist actigraphy (by a kind of wrist-worn electronic motion-sensing device called an actiwatch) and sleep diary. Blood samples were taken before and after this two-month period to assess antibody levels.

Sleep measurements were taken using the actiwatch for seven nights. This measured total sleep time, used to estimate sleep duration, and fragmentation index, which is a measure of restlessness during sleep. The volunteers also filled in sleep diaries, reporting the time they went to sleep, what time they woke up and how long it took to fall asleep.

Volunteers were then given a dose of rhinovirus via a nasal dropper. They were considered to have a cold if they were infected and met illness criteria. To be infected, their virus-specific antibodies must have increased at least fourfold. Illness criteria were either:

  • a total adjusted mucus weight of 10 or more grams (assessed by collecting and weighing all their used tissues)
  • a total adjusted nasal clearance time of 35 minutes or longer (assessed by administering a coloured dye to the nasal passage)

The researchers looked for the association between sleep quality and the common cold, taking into account potential confounding factors, including:

  • age
  • sex
  • race
  • household income
  • season in which trial occurred
  • health habits – such as physical activity, smoking, alcohol consumption
  • psychological variables – perceived socioeconomic status, perceived stress, positive emotional state

What were the basic results?

Sleep duration was categorised as:

  • less than five hours
  • five to six hours
  • six to seven hours
  • more than seven hours

The study found that shorter sleep duration as recorded by the actiwatches was associated with increased risk of developing the common cold.

Participants who were recorded as having less than five hours’ sleep had an increase of four-and-a-half times the risk compared with those sleeping more than seven hours a night (odds ratio [OR] 4.5, 95% confidence interval [CI] 1.08 to 18.69). A similar result was found for those sleeping five to six hours a night (OR 4.24, 95% CI 1.08 to 16.71). Those who slept between six and seven hours were at no greater risk (OR 1.66, 95% CI 0.40 to 6.95).

Sleep fragmentation and self-reported sleep durations were not found to be significant predictors of cold susceptibility. These findings remained after adjusting for all measured confounding factors.

How did the researchers interpret the results

The researchers conclude that: “Shorter sleep duration, measured behaviourally using actigraphy prior to viral exposure, was associated with increased susceptibility to the common cold.”


This study assessed the effect of sleep duration and fragmentation on common cold susceptibility.

It demonstrated that those who had less than six hours’ sleep a night were at increased risk of catching a cold after direct exposure using the nasal dropper, compared with those having more than seven hours a night.

This finding matches previous work suggesting that poor sleep can lead to adverse health outcomes. However, the study cannot prove poor sleep as the single direct cause of susceptibility to infection.

The researchers took care to control for various possible confounders but may not have been able to capture all of the factors that could influence sleep time and quality, and also separately influence susceptibility to infection. These could include, for example, long working hours, family commitments, and physical or mental health problems.

Few people were included in the study, and as a result, the confidence intervals around the risk estimates are wide (for example, 1.08 to 18.69). This suggests uncertainty around the exact size of the risk, so we cannot be sure the risk is as greatly increased as it appears.

Some outcomes were self-reported and this is prone to bias. However, these outcomes were also objectively assessed using actigraphy, and this adds strength to the study.

It’s also worth noting that the study only recruited from one area and did not include children or older adults, so we do not know whether the results would be generalisable to other populations.

Overall, the results do support the importance of good sleep. However, this may be affected by many factors, such as stress levels, lifestyle and family life. There are a range of things you can do to help you get to sleep, such as:

  • avoiding caffeine later in the day
  • avoiding heavy meals late at night
  • setting regular times to wake up
  • using thick curtains or blinds, an eye mask and earplugs to stop you being woken up by light and noise

‘Antipsychotics used on people with no mental illness diagnosis’


Antipsychotic drugsDrugs are not the only way to control difficult behaviour

“‘Chemical cosh’ scandal: Thousands of patients with no history of mental illness needlessly given cocktail of antipsychotic drugs,” says the Mail Online. The emotive words “needlessly” and “cocktail” are the Mail’s imaginative inventions in its largely factually accurate report on a well-conducted and important piece of research.

The research in question looked at prescriptions of psychiatric drugs given to people with learning disabilities. It found – rather alarmingly and perhaps unexpectedly – that most people given antipsychotic drugs had never been diagnosed with a severe mental illness.

Antipsychotic drugs are usually used for conditions such as schizophrenia. They can help reduce hallucinations, ideas not based in reality, and extreme changes in mood. The story is in the news because of ongoing reports of the drugs’ overuse in care homes to keep people’s behaviour manageable – the so-called “chemical cosh”.

In this study, researchers crunched a large amount of data from the medical records of adults with learning difficulties. As well as finding that 71% of people with learning disabilities who had been prescribed antipsychotics had no diagnosis of severe mental illness, the researchers found that almost half the people who had been prescribed antipsychotics had a history of challenging behaviour.

Should people with learning disabilities be treated this way? The answer is “perhaps” and “sometimes”. The National Institute for Health and Care Excellence (NICE) says antipsychotics shouldn’t be used except in certain circumstances – for example, if other psychological treatments have not helped within an agreed amount of time.

Where did the story come from?

The study was done by researchers at University College London, and was funded by the Baily Thomas Charitable Fund and the UK National Institute for Health Research.

It was published in the peer-reviewed British Medical Journal (BMJ). It has been made available on an open-access basis, so this research paper is free to read online.

The Mail asserted that, “Doctors are needlessly doling out powerful anti-psychotic drugs”, but the researchers said they did not know whether the drugs were being used inappropriately. The study produced genuinely concerning findings, but the colourful editorialising may cloud understanding of this important area of research.

The Guardian covered the study accurately, and reported how the prescription of such drugs in these groups had fallen from 1999 to 2013.

What kind of research was this?

This was a cohort study where researchers used diagnostic and prescription data collected by 571 UK general practices.

Cohort studies can show links between two factors. In this case, it showed people’s diagnosis of mental illness and their chances of being prescribed an antipsychotic drug. But it can’t show that the illness led to the drug being prescribed.

What did the research involve?

The researchers analysed GP data to find out how often people with learning disabilities were diagnosed with mental illness or had challenging behaviour recorded in their medical records. They also analysed how often people with learning disabilities were prescribed psychotropic drugs (drugs that affect how the brain works).

There were 33,016 adults identified as having a learning disability. For each of them, the researchers looked at their records to see whether they had a record of a mental illness. Where a diagnosis of mental illness had been recorded, the researchers looked into which type of illness, whether their GP had recorded challenging behaviour, and whether they had been prescribed psychotropic drugs at any time.

The researchers followed people’s records up to 2013 to see whether they were diagnosed with a mental illness, had been prescribed psychotropic drugs, or exhibited challenging behaviour. They looked at diagnoses of severe mental illness such as schizophrenia and bipolar disorder, as well as other types of mental illness, including depression, dementia and anxiety.

Challenging behaviour was defined as including aggression and self-harm, agitation, disruptive or destructive actions, withdrawn behaviour, and sexually inappropriate behaviour. The psychotropic drugs identified in this study included antidepressants, anti-anxiety drugs, mood stabilisers and antipsychotics.

Antipsychotics were studied in more depth, because they can have more serious side effects. They can cause movement disorders such as twitching and restlessness, sedation and weight gain, and lead to diabetes. Because of these side effects, antipsychotic drugs are usually only used to treat severe mental illnesses such as schizophrenia or bipolar disorder.

Finally, the researchers used statistical analysis to look at the relationship between people’s mental health, challenging behaviour and whether they were prescribed psychotropic drugs, especially antipsychotic drugs.

What were the basic results?

Of the more than 33,000 people studied, 9,135 people (28%) had been prescribed antipsychotic drugs by the end of the study. But of these people, 71% did not have any record of severe mental illness.

Many of the people in the study (36%) had a record of challenging behaviour. Almost half these people (47%) had been prescribed antipsychotic drugs, but only 12% of people with challenging behaviour had been diagnosed with severe mental illness.

The researchers calculated that people with challenging behaviour were more than twice as likely to be given a prescription of antipsychotic drugs compared with people without a record of challenging behaviour.

Over the course of the study, the use of antipsychotic drugs declined by about 4% a year. The diagnosis of new cases of severe mental illness also declined, by about 5% a year.

How did the researchers interpret the results?

The researchers said their results called into question why so many people without serious mental illness are being prescribed antipsychotic drugs. “We need to understand why most antipsychotics are prescribed to people without a record of severe mental illness, and why so many people with challenging behaviour receive antipsychotics,” they said.

They added: “We infer that … antipsychotics are used to manage behaviour, but this might not be the case.” They also said if antipsychotics were being used to manage behaviour, “investment in a skilled multidisciplinary team of professionals who can provide alternative evidence-based management strategies for challenging behaviour” would be needed.

The researchers also speculated that the drop in the number of prescriptions for antipsychotics might be the result of concerns raised about their use during the past 15 years.


This study presents a worrying impression of how people with learning disabilities are medically treated. The fact that more than a quarter of people with learning disabilities were given antipsychotics when the vast majority of them did not have a serious mental illness is hard to explain.

The study had several strengths. It is very large, and because it was based on GP records, it should represent a good cross-section of UK society. Computerised GP records in the UK have a good reputation for being reliable. However, it is always possible that some diagnoses or prescriptions were wrongly coded in the system, which would make the data less reliable.

The researchers’ definition of challenging behaviour and the way they collected records of challenging behaviour was new, which means it has not been tested in other studies.

Some GPs might not include diagnoses of severe mental illness – for example, they might just record the symptoms the people reported instead of the diagnosis. This would lead to fewer diagnoses of severe mental illness than you would expect and could skew the results.

Charities and campaign groups have long warned that elderly people – such as those with dementia – should not be treated with antipsychotic drugs unless they have a severe mental illness. This study showed that older people were also more likely to be prescribed an antipsychotic.

This study can’t tell us why people with learning disabilities were prescribed antipsychotic drugs when they didn’t have a severe mental illness. The authors suggest the drugs are being used to manage challenging behaviour.

While this seems plausible, we can’t tell for sure from this study. Importantly, we don’t know what doses of medication were used and whether they were prescribed at a sedating level – the so-called “chemical cosh” depicted in the media.

The study also does not report how regularly the medications were used and whether or not the person with learning disability found them beneficial, which is, of course, the usual goal of prescribing medication. Why older people are more likely to receive antipsychotic drugs remains unexplained, even after taking account older people with dementia.

The study raises questions about the care of people with learning disabilities in society. Challenging behaviour is a rather vague and inclusive term, and can be used to encompass behaviour ranging from serious violence to making a lot of noise, or simply disrupting the routine of a care home. As the researchers note, simply cracking down on the inappropriate use of antipsychotic drugs may not solve the problem.

Radiotherapy – does it really do more harm than good?


Radiotherapy uses high-energy radiation to kill cancer cells In most cases, radiotherapy is a safe and effective treatment

“Could radiotherapy do more harm than good in some patients?” the Daily Mail asks.

The question is prompted by a new study looking at whether radiotherapy could lead to a type of cell, known as Langerhans cells, reducing the immune system’s ability to fight cancers, such as skin cancer.

They identified a protein which enabled these Langerhans cells to rapidly repair DNA damage caused by radiotherapy, and therefore survive. When mice were exposed to radiation, these cells also caused a suppression of their immune response to skin tumours, and greater tumour growth.

While the Mail’s headline might cause alarm to cancer patients and their families, it is important to remember that radiotherapy is a vital, and sometimes life-saving, aspect of many people’s treatments.

It should also be noted that this study was carried out on mice, and the radiation was given to the mice’s whole bodies shortly before they were injected with skin cancer cells. In humans, radiotherapy is directed specifically at an existing cancer site – therefore, the impact of these cells may not be exactly the same.

Researchers will now investigate further to see if these cells really contribute to radiation resistance in human cancer, and whether they can use this knowledge to improve the response of cancers to radiotherapy.

Where did the story come from?

The study was carried out by researchers from Icahn School of Medicine at Mount Sinai, New York. Funding was provided by the US National Institutes of Health, the American Medical Association, the National Institute of Arthritis, Musculoskeletal and Skin Diseases of the US National Institutes of Health, and the National Cancer Institute of the US National Institutes of Health. There were no conflicts of interest reported.

The study was published in the peer-reviewed medical journal Nature Immunology.

The headline in the Mail is bound to cause alarm, but readers should note the warning from an independent expert to “not throw the baby out with the bath water”, explaining that radiotherapy has an important part to play in the treatment of skin cancer.

What kind of research was this?

This was an animal study on mice assessing the effect of ionising irradiation (radiotherapy) on one type of immune system cells, called Langerhans cells. These are present in the outer layers of the skin and are known to be resistant to radiation.

Radiotherapy acts by damaging the DNA of cancer cells, killing them. While some research has suggested that radiotherapy may also help the immune system to attack cancers, other studies have suggested that it may also dampen some aspects of the immune response.

The researchers wanted to assess whether Langerhans cells might be contributing to this dampening, as it might then lead to cancer cells sometimes becoming resistant to radiotherapy. By understanding how radiotherapy resistance comes about, they hope to find ways to combat it and make radiotherapy more effective.

While the findings of animal studies may not be completely representative of what will be seen in humans, they do provide a starting point for further research.

What did the research involve?

The researchers exposed mice to radiotherapy to assess the resistance of Langerhans cells to apoptosis (cell death) after therapy. They then investigated whether the Langerhans cells were able to repair their DNA damage caused by the radiation, and which proteins in the cells might be helping them do this.

They then looked at what happened if they gave mice a whole-body dose of radiation, and then injected them with skin cancer cells. They compared this with what happened in mice not radiated before injecting them with skin cancer cells.

What were the basic results?

The study found that Langerhans cells did not undergo cell death after exposure to radiotherapy like normal cells; instead they managed to rapidly repair the radiation damage to their DNA. Langerhans cells were found to produce increased levels of proteins that could help them to survive, particularly one protein called cyclin-dependant kinase inhibitor (CDKN1A). Langerhans cells in mice genetically engineered to lack this protein were less resistant to radiation and not as able to repair radiation-induced DNA damage.

The researchers found that after radiation, Langerhans cells migrated to the lymph nodes and caused an increase in the number of another type of immune system cell, called Treg cells. These cells get into tumours and can reduce the immune system’s ability to fight the tumour.

Finally, the researchers showed that if they gave mice a whole-body dose of radiation and then injected them with skin cancer cells the next day, they grew larger tumours than non-irradiated mice.

The irradiated mice had more Treg cells in their tumours, and more Langerhans cells in their lymph nodes. This effect was short-lived, as mice injected with skin cancer cells five weeks after irradiation did not grow larger tumours.

How did the researchers interpret the results?

The researchers say they “found that [Langerhans cell] resisted apoptosis and rapidly repaired DNA damage after exposure to [ionising radiation]” and that the protein CDKN1A appears to help the cells do this. They say their findings might help them to develop a way of enhancing the response of cancers to radiotherapy.


This was an animal study looking at the effect of radiotherapy on a particular type of immune system cell found in the skin, called Langerhans cells. The high-energy radiation used in radiotherapy normally permanently damages the DNA of cancer cells, causing them to die. However, Langerhans seem able to repair this damage and survive.

The study found that a protein, CDKN1A, allows Langerhans cells to resist cell death and repair damage to DNA after exposure to radiotherapy. The cells also seemed capable of suppressing mice’s immune response to the tumours.

This study was on mice, so we cannot be sure the same effect would be seen in humans, particularly as these mice were given whole-body radiation before being injected with cancer cells. In human cancer, radiotherapy is directed specifically at an existing cancer.

The identification of this protein is of interest, as it may provide a route for further research to see if the effectiveness of radiotherapy can be improved for some patients. More laboratory and animal research will be needed before we know if this will become a reality.

The aim of radiotherapy is to give the highest chance of curing or shrinking the cancer, while reducing the risk of side effects. For many people it is an integral and effective part of their cancer treatment.

This study should not be seen as a warning against radiotherapy, but rather a possible means for further improving its outcomes in the future.

No conclusive evidence that e-cigs tempt teens to smoke

A 2015 evidence review estimated that e-cigarettes are 95% safer than smokingA recent survey estimated that 1 in 5 UK teens had tried vaping

“Young people who try e-cigarettes are much more likely to start smoking, scientists have concluded,” The Daily Telegraph reports. Though the conclusion, such as it is, is based on just 16 teenagers.

The study relies on results from two questionnaires, sent a year apart to about 700 young people in the US on whether they had ever smoked e-cigarettes or tobacco.

Just 16 of these youngsters had tried e-cigarettes at the start of the study, six of them had tried a cigarette by the next year and five thought they might in the future.

Importantly, the research did not ask people how often they had used e-cigarettes or smoked tobacco, so we have no idea whether they were “addicted” to nicotine.

This study leaves many unanswered questions, such as why young people tried e-cigarettes or tobacco.

Ultimately, this is a very small number to base such sweeping conclusions on.

E-cigarettes and young people

The UK will ban the sale of e-cigarettes to people under 18 from October 1 2015

Where did the story come from?

The researchers are from the University of Pittsburgh School of Medicine, Dartmouth University and the University of Oregon in the US.

The study was published in the peer-reviewed medical journal JAMA Pediatrics on an open-access basis, so it is free to read online.

It was funded by the National Cancer Institute and National Center for Advancing Translational Sciences.

The Telegraph and the Mail Online overplayed the fears about e-cigarettes being a gateway for teens into tobacco use.

The Telegraph wrongly stated that 68% of those who had tried e-cigarettes went on to smoke tobacco – the true figure was 37.5%. The Mail Online reported the percentages correctly, but did not say that these results were based on just 16 young people who had tried e-cigarettes.

Also, the reporting of the study could give the impression that the findings represented a consensus opinion, which is certainly not the case. The study has come in for harsh criticism from independent experts in public health.

For example, Professor Robert West, professor of health psychology at UCL, is quoted as saying: “This kind of propaganda by major medical journals brings public health science into disrepute and is grist to the mill of apologists for the tobacco industry who accuse us of ‘junk science’.”

What kind of research was this?

This was a longitudinal cohort study, which means the researchers followed a group of people over time to see what happened to them. These studies are good at finding links between things, but cannot show that one thing causes another.

What did the research involve?

Researchers reviewed the results of questionnaires sent to people aged 16 to 26, which asked them about whether they had ever smoked tobacco cigarettes (defined as just one puff) or ever tried e-cigarettes, and about their attitudes to smoking. They followed up with another questionnaire one year later, and asked them the same questions.

They then used statistical analysis to see whether people who said they had tried e-cigarettes, but did not smoke and would not accept a cigarette if offered one, had tried smoking tobacco or changed their attitudes to it.

Of the people surveyed, 728 said they had never smoked and would not accept a cigarette if offered one. Only 507 of these people responded to the survey again a year later, so the researchers used statistical techniques to estimate the likely responses of some of the people who dropped out, based on responses from people in similar circumstances. This gave them a total of 694 people to base the survey on.

The researchers looked to see whether some other factors were also associated with the chances of someone trying a tobacco cigarette during the year. These included people’s age, whether their parents smoked, whether their friends smoked, and how likely they were to try risky things.

What were the basic results?

Only 16 of the 694 people in the study had ever tried e-cigarettes at the start of the study. Of those, six (38%) tried a tobacco cigarette during the year of the study. Another five (31%) said they might try a tobacco cigarette if they were offered one, but had not done so yet.

Young people who had not tried an e-cigarette at the start of the study were less likely to say they had tried a tobacco cigarette at the end of it. The study found 65 of the 678 (10%) who had not tried an e-cigarette went on to try tobacco, and 63 (9%) said they might try a tobacco cigarette if offered one.

After adjusting their figures to take account of other factors, the researchers calculated that people were eight times as likely to try tobacco in the following year if they had tried an e-cigarette (adjusted odds ratio (AOR) 8.3, 95% confidence interval (CI) 1.2 to 58.6).

Looking at other factors that were linked to the chances of smoking tobacco, the study found young people who said they were open to trying risky things were more than twice as likely to try tobacco (AOR 2.6, 95% CI 1.3 to 5.2), and those who had more friends who smoked were almost twice as likely to try tobacco (AOR 1.8, 95% CI 1.2 to 2.9).

Not surprisingly, people who had tried e-cigarettes were more likely than those who had not tried them to say they were open to trying new or risky things.

How did the researchers interpret the results?

The researchers said their findings showed that e-cigarettes might make young people more likely to try smoking tobacco. They said: “Because e-cigarettes deliver nicotine more slowly than traditional cigarettes, they may serve as a ‘nicotine starter’ allowing a new user to advance to cigarette smoking,” as they get used to the effects.

They also say that using e-cigarettes might lead people to get used to the habit of smoking. They say the results of their study “support regulations to limit sales and decrease the appeal of e-cigarettes to adolescents and young adults”.


On the face of it, this study seems to support the idea that young people progress to smoking tobacco via e-cigarettes. However, there are many limitations, which means we cannot draw such a conclusion from the study findings.

The first serious limitation is that only 16 of the 694 young people in the study had actually tried e-cigarettes. With numbers so small, we cannot be sure the results are reliable. There is a high chance that another group of 16 young people who had tried e-cigarettes might have given different answers.

Also, this type of study can never prove that one thing (in this case trying e-cigarettes) causes another (trying tobacco cigarettes). Young people try lots of things while they grow up, and some people are more likely than others to take risks. It is perhaps not surprising that those who try e-cigarettes are also more likely to try tobacco.

The language in the study could be misleading. For example, it describes people who had ever tried an e-cigarette as “e-cigarette users” and people who have taken even one puff of a cigarette as “smokers”. Teenagers may try something once and then never try it again.

It also talks about young people’s “progression to smoking”, which you might think means the numbers who had actually started to smoke. However, the definition of progression includes those who moved from saying they would definitely not accept a cigarette if offered one, to saying that they were not likely to accept one but could not rule it out completely.

This may be why The Daily Telegraph got its figures wrong – it combined the young people who had tried smoking with the young people who had not ruled it out completely.

It is important to know whether e-cigarettes encourage people to start smoking tobacco. Tobacco is much more harmful than e-cigarettes, because of the toxins created when tobacco is burned. A recent evidence review carried out by Public Health England stated that e-cigarettes were probably 95% safer than smoking tobacco.

This study does not add much to our knowledge about whether e-cigarettes encourage young people to start smoking tobacco. We would need to see bigger, more detailed studies over time that look at how often people use e-cigarettes and tobacco, to get closer to answering that question.

Tiny ‘cancer trap’ could stop cancer spread


Current technology is unable to detect when cancer starts spreadingThe trap could pull in circulating cancer cells

“A small sponge-like implant that can mop up cancer cells as they move through the body has been developed,” BBC News reports. The implant has only been used in mice, but it could be used in humans to detect and warn about spreading cancer cells.

The problem is cancer spread from one part of the body to another (metastasis) usually only becomes apparent after it has happened, and when it is often too late to do much about it.

In this latest study, researchers injected mice with breast cancer cells and then put a tiny biological implant or “scaffold” into their abdomen to see if it could catch the cells before they spread to other organs.

The results were promising. Subsequent tests confirmed the scaffold became infiltrated with cancer cells soon after the cancer had developed, and also reduced the spread of cancer to other organs, such as the lungs and liver.

This could have two potential uses. It could provide an “early warning system”, alerting clinicians the cancer is beginning to spread, and it could also possibly slow the spread.

However, many questions remain, including whether it would work the same way in humans and for what cancers, how it would be used and, most importantly, if it would be safe.

The new technology has not yet been tested on people.

Where did the story come from?

The study was carried out by researchers from the University of Minnesota and other institutions in the US, and was funded by the National Institutes of Health and the Northwestern H Foundation Cancer Research Award.

It was published in the peer-reviewed scientific journal, Nature Communications.

BBC News gives reliable coverage of the study, making it clear the tests have so far been carried out in mice, and we do not know if the technology is similarly safe and effective in humans.

According to the BBC, the study lead confirmed they were soon planning the first clinical trials in people.

What kind of research was this?

This laboratory and animal study investigated the potential use of an implant to capture cancer cells spreading through the body to cause metastases – cancer in body sites distant from the original.

Metastases are generally associated with poor prognosis. The researchers consider that if it was possible to identify circulating cancer cells before they have taken hold in other organs, and employ strategies to stop them, this could halt disease progression. So far, several technologies have been investigated to capture and count the number of circulating cancer cells in blood samples.

However, as the researchers say, some cancer cells can be shed into the circulation early on in the course of a cancer, and remain in the circulation for long periods of time before colonising a distant site. Therefore, they aimed to develop a method that would detect and capture these cells.

The study was conducted in mice, and though animal studies can inform how treatments or technologies may work in humans, this is very early-stage research.

What did the research involve?

This study involved an implant or “scaffold” that could capture metastatic cancer cells, combined with an imaging system to detect them.

The researchers injected cancer cells into the breast tissue of female mice. The cancer cells they chose to inject were a variant known to be highly metastatic. One week after injecting the cancer, the scaffold was implanted into the abdominal fat or beneath the skin.

The scaffold was made of a porous biological material called poly(lactide-co-glycolide) or PLG, which has been approved by the Food and Drug Administration for a number of uses.

When this scaffold is implanted, it triggers an immune response and is colonised by various immune cells. The theory is that these immune cells then “recruit” and capture cancer cells in the scaffold.

Optical imaging (using a system called inverse spectroscopic optical coherence tomography, or ISOCT) was used to detect the arrival of the cancer cells at the implant.

About one month later, the implant and mouse organs were removed and examined in the laboratory.

What were the basic results?

Both the optical imaging and subsequent examination of the implant/scaffold in the laboratory demonstrated it had captured metastatic cancer cells.

Laboratory examination showed cancer cells were not present elsewhere in the abdominal fat tissue, where the implant had not been placed. Monitoring the initial cancer site also showed implanting the scaffold did not influence growth of the primary tumour in the mammary glands.

Examination of other organs showed the implant reduced the tumour burden of other organs, such as the liver and lung. For example, in the lung of mice who received the implant, the ratio was 1 cancerous cell to 5,400 healthy lung cells. Comparatively, in mice who did not receive the implant, the ratio was 1 to 645. Therefore, the implant reduced the metastatic tumour burden by about 88%.

Other tests showed the implants were recruiting the cancer cells at a much earlier stage than when they arrived in the distant organs. Two weeks after injecting the initial cancer cells, most implants contained cancer cells, compared with minimal tumour burden in other organs until one month.

Further study also confirmed, as expected, immune cells were playing a role in recruiting the cancer cells to the implant.

How did the researchers interpret the results?

The researchers concluded that, “This study demonstrates a platform technology for the capture and detection of cancer cells early in the metastatic process”.

They go on to say that, “For patients at risk of recurrence, scaffold implantation following completion of primary therapy has the potential to identify metastatic disease at the earliest stage, enabling initiation of therapy while the disease burden is low”.


This animal study offers early promise of a new technology that may be able to halt metastatic cancer spread to other sites in the body, which is associated with notoriously poor prognosis.

The study suggested the implant could capture cancer cells shed from the tumour, even in its earliest stages of development, and reduce the eventual spread to other organs.

However, the investigation of this new technology is in its earliest stages. It has so far only been tested in mice injected with a highly metastatic strain of breast cancer, which caused very rapid tumour spread and development in these animals.

Animal studies can give a good indication of how a technology may work in people. But the two are not identical and many questions surround the research at this early stage.

Though the implant showed potential, we don’t know it would work the same way in people. Even in mice, the implant didn’t actually prevent metastases. The cancer still spread to other organs – the tumour burden was just less than when the implant was used.

This may mean disease progression would be slower, but indicates it couldn’t completely stop it. The researchers say this could provide earlier detection of metastases so further treatment could be started, such as adjuvant chemotherapy.

We don’t know whether the implant may have different effects on cancer spread by different routes. For example, the implant may have some effect in halting cancer spread through the bloodstream, but it may not prevent spread through the lymphatic system.

The researchers suggest the technology has the potential to be applicable to many types of cancer. But we don’t know at this stage whether there may be certain cancers the implant would be more or less suitable for.

Practically, it is not yet known how the implant would be used in humans – for example, when they would be implanted, where in the body, and how long they would remain there. Importantly, it is also unknown whether there could be any adverse effects of using the implant, such as cancer spread.

Hopefully, the results of the upcoming clinical trials in people will shed light on these uncertainties.

Eight tips for healthy eating

Eating a healthy, balanced diet is an important part of maintaining good health, and can help you feel your best. It doesn’t have to be difficult either. Just follow these eight tips to get started.

The key to a healthy diet is to do the following:

  • Eat the right amount of calories for how active you are, so that you balance the energy you consume with the energy you use. If you eat or drink too much, you’ll put on weight. If you eat and drink too little, you’ll lose weight. It is recommended that men have around 2,500 calories a day (10,500 kilojoules). Women should have around 2,000 calories a day (8,400 kilojoules). Most adults are eating more calories than they need, and should eat fewer calories.
  • Eat a wide range of foods to ensure that you’re getting a balanced diet and that your body is receiving all the nutrients it needs.

Get started

These practical tips cover the basics of healthy eating, and can help you make healthier choices:

Base your meals on starchy foods

Starchy foods should make up around one third of the foods you eat. Starchy foods include potatoes, cereals, pasta, rice and bread. Choose wholegrain varieties (or eat potatoes with their skins on) when you can: they contain more fibre, and can help you feel full.

Most of us should eat more starchy foods: try to include at least one starchy food with each main meal. Some people think starchy foods are fattening, but gram for gram the carbohydrate they contain provides fewer than half the calories of fat.

Eat lots of fruit and veg

It’s recommended that we eat at least five portions of different types of fruit and veg a day. It’s easier than it sounds. A glass of unsweetened 100% fruit juice (150ml) can count as one portion, and vegetables cooked into dishes also count. Why not chop a banana over your breakfast cereal, or swap your usual mid-morning snack for a piece of fresh fruit?

Eat more fish

Fish is a good source of protein and contains many vitamins and minerals. Aim to eat at least two portions of fish a week, including at least one portion of oily fish. Oily fish contains omega-3 fats, which may help to prevent heart disease. You can choose from fresh, frozen and canned: but remember that canned and smoked fish can be high in salt.

Oily fish include salmon, mackerel, trout, herring, fresh tuna, sardines and pilchards. Non-oily fish include haddock, plaice, coley, cod, tinned tuna, skate and hake. If you regularly eat a lot of fish, try to choose as wide a variety as possible.

Cut down on saturated fat and sugar

We all need some fat in our diet. But it’s important to pay attention to the amount and type of fat we’re eating. There are two main types of fat: saturated and unsaturated. Too much saturated fat can increase the amount of cholesterol in the blood, which increases your risk of developing heart disease.

Saturated fat is found in many foods, such as hard cheese, cakes, biscuits, sausages, cream, butter, lard and pies. Try to cut down on your saturated fat intake, and choose foods that contain unsaturated fats instead, such as vegetable oils, oily fish and avocados.

For a healthier choice, use just a small amount of vegetable oil or reduced-fat spread instead of butter, lard or ghee. When you’re having meat, choose lean cuts and cut off any visible fat.

Most people in the UK eat and drink too much sugar. Sugary foods and drinks, including alcoholic drinks, are often high in energy (measured in kilojoules or calories), and if eaten too often, can contribute to weight gain. They can also cause tooth decay, especially if eaten between meals.

Cut down on sugary fizzy drinks, alcoholic drinks, sugary breakfast cereals, cakes, biscuits and pastries, which contain added sugars: this is the kind of sugar we should be cutting down on, rather than sugars that are found in things such as fruit and milk.

Food labels can help: use them to check how much sugar foods contain. More than 22.5g of total sugars per 100g means that the food is high in sugar, while 5g of total sugars or less per 100g means that the food is low in sugar.

Eat less salt

Even if you don’t add salt to your food, you may still be eating too much. About three-quarters of the salt we eat is already in the food we buy, such as breakfast cereals, soups, breads and sauces. Eating too much salt can raise your blood pressure. People with high blood pressure are more likely to develop heart disease or have a stroke.

Use food labels to help you cut down. More than 1.5g of salt per 100g means the food is high in salt. Adults and children over 11 should eat no more than 6g of salt a day. Younger children should have even less.

Get active and be a healthy weight

Eating a healthy, balanced diet plays an essential role in maintaining a healthy weight, which is an important part of overall good health. Being overweight or obese can lead to health conditions such as type 2 diabetes, certain cancers, heart disease and stroke. Being underweight could also affect your health. Check whether you’re a healthy weight by using our Healthy weight calculator.

Most adults need to lose weight, and need to eat fewer calories to do this. If you’re trying to lose weight, aim to eat less and be more active. Eating a healthy, balanced diet will help: aim to cut down on foods that are high in fat and sugar, and eat plenty of fruit and vegetables.

Don’t forget that alcohol is also high in calories, so cutting down can help you to control your weight.

Physical activity can help you to maintain weight loss or be a healthy weight. Being active doesn’t have to mean hours at the gym: you can find ways to fit more activity into your daily life. For example, try getting off the bus one stop early on the way home from work, and walking. Being physically active may help reduce the risk of heart disease, stroke and type 2 diabetes. For more ideas, see Get active your way.

After getting active, remember not to reward yourself with a treat that is high in energy. If you feel hungry after activity, choose foods or drinks that are lower in calories, but still filling.

If you’re underweight, see our page on underweight adults. If you’re worried about your weight, ask your GP or a dietitian for advice.

Don’t get thirsty

We need to drink about 1.6 to 2 litres of fluid every day to stop us getting dehydrated. This is in addition to the fluid we get from the food we eat. All non-alcoholic drinks count, but water and lower-fat milk are healthier choices.

Try to avoid sugary soft and fizzy drinks that are high in added sugars and calories, and are also bad for teeth. Even unsweetened fruit juice is sugary, so try to limit how much you drink to no more than one glass (about 150ml) of fruit juice each day.

When the weather is warm, or when we get active, we may need more fluids.

Don’t skip breakfast

Some people skip breakfast because they think it will help them lose weight. In fact, research shows that eating breakfast can help people control their weight. A healthy breakfast is an important part of a balanced diet, and provides some of the vitamins and minerals we need for good health. A wholegrain, lower-sugar cereal with fruit sliced over the top is a