̽��ֱ�� of Cambridge - smoking

Risk of premature birth from smoking while pregnant more than double previous estimates

cjb250 — Wed, 27 Sep 2023 23:01:31 +0000

̽��ֱ��study, published today in the International Journal of Epidemiology, also found that smoking meant that the baby was four times more likely to be small for its gestational age, putting it at risk of potentially serious complications including breathing difficulties and infections.

But the team found no evidence that caffeine intake was linked to adverse outcomes.

Women are currently recommended to stop smoking and limit their caffeine intake during pregnancy because of the risk of complications to the baby. For example, smoking during pregnancy is associated with an increased risk of fetal growth restriction, premature birth and low birthweight, though it has also been linked to a reduced risk of preeclampsia (high blood pressure during pregnancy).

High caffeine intake has also been shown to be associated with lower birthweights and possibly fetal growth restriction. Caffeine is more difficult to avoid than cigarette smoke as is found in coffee, tea, chocolate, energy drinks, soft drinks, and certain medications.

Studies looking at the links between smoking, caffeine and adverse pregnancy outcomes tend to rely on self-reported data to estimate exposure, which is not always reliable. A more objective measure is to look at levels of metabolites in the blood – chemical by-products created when substances such as tobacco and caffeine are processed in the body.

Researchers at the ̽��ֱ�� of Cambridge and the Rosie Hospital, part of Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust, recruited more than 4,200 women who attended the hospital between 2008 and 2012 as part of the Pregnancy Outcome Prediction (POP) study. ̽��ֱ��team analysed blood samples taken from a subset of these women four times during their pregnancies.

To assess exposure to cigarette smoke, the team looked at levels of the metabolite cotinine, which can be detected in blood, urine, and saliva. Only two out of three women with detectable levels of cotinine in every blood sample were self-reported smokers, showing that this measure is a more objective way of assessing smoking behaviour.

A total of 914 women were included in the smoking analysis. Of these, 78.6% were classified as having no exposure to smoking while pregnant, 11.7% as having some exposure and 9.7% as having consistent exposure.

Compared to women who were not exposed to smoking while pregnant, those with consistent exposure were 2.6 times more likely to experience spontaneous preterm birth – more than double the previous estimate of 1.27 from a meta-analysis of studies – and 4.1 times as likely to experience fetal growth restriction.

Babies born to smokers were found to be on average 387g lighter than babies born to non-smokers – that is, more than 10% smaller than the weight of an average newborn. This increases the risk that the baby will have a low birth weight (2.5kg or less), which in turn is linked to an increased risk of developmental problems as well as poorer health in later life.

Unlike in previous studies, however, the team found no evidence that smoking reduced the risk of pre-eclampsia.

Professor Gordon Smith, Head of the Department of Obstetrics and Gynaecology at the ̽��ֱ�� of Cambridge, said: “We’ve known for a long time that smoking during pregnancy is not good for the baby, but our study shows that it’s potentially much worse than previously thought. It puts the baby at risk of potentially serious complications from growing too slowly in the womb or from being born too soon.

“We hope this knowledge will help encourage pregnant mums and women planning pregnancy to access smoking-cessation services. Pregnancy is a key time when women quit and if they can remain tobacco free after the birth there are lifelong benefits for them and their child.”

Smoking cessation is offered routinely to all pregnant women and the NHS has local smoking cessation services for anyone, pregnant or not. Further information is available on the NHS website.

To assess caffeine intake, they researchers looked for the metabolite paraxanthine, which accounts for 80% of caffeine metabolism and is both less sensitive to recent intake and more stable throughout the day.

915 women were included in the caffeine analysis. Of these women, 12.8% had low levels of paraxanthine throughout pregnancy (suggesting low caffeine intake), 74.0% had moderate levels and 13.2% had high levels. There was little evidence of an association between caffeine intake and any of the adverse outcomes.

̽��ֱ��work was supported by the National Institute for Health and Care Research (NIHR) Cambridge Biomedical Research Centre and the Medical Research Council.

Reference
Selvaratnam, RJ et al. Objective measures of smoking and caffeine intake and the risk of adverse pregnancy outcome. International Journal of Epidemiology; 28 Sept 2023; DOI: 10.1093/ije/dyad123

Cambridge researchers have found that women who smoke during pregnancy are 2.6 times more likely to give birth prematurely compared to non-smokers – more than double the previous estimate.

We’ve known for a long time that smoking during pregnancy is not good for the baby, but our study shows that it’s potentially much worse than previously thought

Gordon Smith

Malte Mueller (Getty Images)

Pregnant woman smoking cigarette - stock illustration

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‘Fingerprint database’ could help scientists to identify new cancer culprits

cjb250 — Mon, 15 Apr 2019 23:19:27 +0000

Our DNA, the human genome, comprises of a string of molecules known as nucleotides. These are represented by the letters A, C, G and T. Sometimes, changes occur in the ‘spelling’ of our DNA – an A becomes a G, for example. These changes, known as mutations, can be caused by a number of factors, some environmental, such as exposure to tobacco smoke or to ultraviolet light.

As cells divide and multiply, they make copies of their DNA, so any spelling mistakes will be reproduced. Over time, the number of errors accumulates leading to uncontrolled cell growth – the development of tumours.

Previously, scientists have had only a limited number of tools for working out the cause of an individual’s tumour. As it is now possible to study the entire human genome very rapidly, scientists have been able to find all the mutations in a patient’s cancer, and see patterns – or ‘mutational signatures’ – in these tumours.

Now, in a study published in the journal Cell, a team of researchers from the ̽��ֱ�� of Cambridge and King’s College London have developed a comprehensive catalogue of the mutational signatures caused by 41 environmental agents linked to cancer. In future they hope to expand it further, using similar experimental techniques, to produce an encyclopaedia of mutation patterns caused by environmental agents.

“Mutational signatures are the fingerprints that carcinogens leave behind on our DNA, and just like fingerprints, each one is unique,” explains Dr Serena Nik-Zainal from the Department of Medical Genetics and MRC Cancer Unit at the ̽��ֱ�� of Cambridge, who led the Cambridge Team. “They allow us to treat tumours as a crime scene and, like forensic scientists, allow us to identify the culprit – and their accomplices – responsible for the tumour.”

̽��ֱ��researchers exposed induced pluripotent stem cells – skin cells that have been reprogrammed to return to their original, ‘master’ state – to 79 known or suspected environmental carcinogens. ̽��ֱ��team then used whole genome sequencing to look at the patterns of changes caused by the agents and found that 41 of the suspects left a characteristic fingerprint on the stem cells’ DNA.

“We’ve used this technique to create the most comprehensive catalogue to date of the patterns of DNA damage produced by environmental agents across the whole human genome,” explains Professor David Phillips, who led the King’s College London team. “It should allow us to examine a patient’s tumour and identify some of the carcinogens they have been exposed to that may have caused the cancer.”

Some of the environmental agents studied are known carcinogens, such as polycyclic hydrocarbons and sunlight. For the first time, the researchers also studied some of the individual chemicals found in tobacco smoke and identified which ones cause signatures similar to those found in smokers’ lung cancer.

They also identified the fingerprints left behind by common chemotherapy drugs, some dietary chemicals and some present in diesel exhaust fumes. This study shows how human DNA is vulnerable to many agents in our surroundings.

Image: Whole cancer genomes of six different patients: the plots show all the mutations that are present in whole cancer genomes.

Dr Nik-Zainal illustrates potential uses of the catalogue by referring to the case of Balkan endemic nephropathy (BEN), which is linked to dietary exposure to a plant chemical called aristolochic acid. ̽��ֱ��mutational signature of this chemical was verified in this study to be virtually identical to the signature found in the tumours of BEN patients. So, although this connection was first made prior to the current study, Dr Nik-Zainal says it is an example of how one might use their catalogue in future.

“Our reference library will allow doctors in future to identify those culprits responsible for causing cancer,” adds Dr Nik-Zainal. “Such information could be invaluable in helping inform measures to reduce people’s exposure to potentially dangerous carcinogens.”

̽��ֱ��research was funded by a Wellcome Strategic Award, with additional support from Cancer Research UK and the Medical Research Council.

Reference
Kucab, JE & Zou, X et al. A compendium of mutational signatures of environmental agents. Cell; 2 May 2019; DOI: 10.1016/j.cell.2019.03.001

Scientists in Cambridge and London have developed a catalogue of DNA mutation ‘fingerprints’ that could help doctors pinpoint the environmental culprit responsible for a patient’s tumour – including showing some of the fingerprints left in lung tumours by specific chemicals found in tobacco smoke.

Mutational signatures ... allow us to treat tumours as a crime scene and, like forensic scientists, allow us to identify the culprit – and their accomplices – responsible for the tumour

Serena Nik-Zainal

geralt

Cigarettes

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Smoking and pre-eclampsia may cause fertility problems for offspring, study suggests

cjb250 — Fri, 29 Mar 2019 08:00:00 +0000

̽��ֱ��research, led by scientists at the ̽��ֱ�� of Cambridge, found that exposing fetuses to chronic hypoxia (low oxygen levels) during development led to them having advanced ageing of the ovaries and fewer eggs available.

Hypoxia in the womb can be caused by a number of factors, including smoking, pre-eclampsia, maternal obesity, and living at high altitude. ̽��ֱ��condition is already known to have potential long term effects on the health of offspring, including increased risk of heart disease. However, this study, published in ̽��ֱ��FASEB Journal, is the first time it has been shown to affect fertility.

To investigate the effects of hypoxia, researchers from the Metabolic Research Laboratories at the ̽��ֱ�� of Cambridge placed pregnant female rats in reduced levels of oxygen (13%, compared to the standard 21% found in air) from day six to day 20 of their pregnancy. They then examined the reproductive tract of their female pups at age four months.

Rats are a useful model for studying pregnancy. As a mammal, their bodies and underlying biology share some key similarities with those of humans. However, their gestation period and lifecycles are much shorter than those of humans, making them an ideal animal model in which to study pregnancy and fetal development.

When the team examined the pups, they found a decrease in the number of ovarian follicles in the reproductive tract. Females are born with fixed numbers of follicles, each with the potential of developing into an egg. In humans, women usually expend all their eggs around the age of fifty, at which point they will enter menopause.

̽��ֱ��researchers also looked at telomere length in the pups’ ovarian tissue. Telomeres are found at the end of chromosomes and prevent the chromosome from deteriorating – they are often compared to the plastic that seals the end of shoe laces. As we age, telomeres become shorter and shorter, and hence their length can be used as a proxy to measure ageing. ̽��ֱ��researchers found that telomeres in the ovarian tissue of pups exposed to hypoxia were shorter than in unexposed pups.

“It’s as if low levels of oxygen caused the female’s ovarian tissue to age faster,” says Dr Catherine Aiken from the ̽��ֱ�� of Cambridge. “Biologically, the tissue appears older and the female would run out of eggs – in other words, become infertile – at a younger age.”

Although the research was carried out in rats, Dr Aiken says there is every reason to expect that the findings could be translated to humans as previous studies looking at hypoxia during pregnancy in relation to other conditions such as heart disease have been shown to be relevant in humans.

While women are recommended not to smoke during pregnancy, other causes of hypoxia, such as pre-eclampsia and living in a high altitude, are beyond their control. However, says Dr Aiken, the findings of her team’s research may prove helpful to women who were exposed to low levels of oxygen during their mother’s pregnancy.

“Now that we’ve seen a link between hypoxia and fertility problems in rats, we know what to look for in women,” she says. “If the same turns out to be true for them, then women at risk will be able to take action: by having children earlier in life or looking to assisted reproduction, such as IVF, there should be no reason why these women cannot have children.”

Dr Aiken is also involved in research looking at whether anti-oxidant medication may help undo any damage caused by hypoxia.

Reference
Aiken, CE et al. Chronic gestational hypoxia accelerates ovarian ageing and lowers ovarian reserve in next-generation adult rats. FASEB; 27 March 2019; DOI: 10.1096/fj.201802772R

Low levels of oxygen in the womb – which can be caused by smoking or conditions such as pre-eclampsia – may cause problems with fertility later in life, a study carried out in rats suggests.

It’s as if low levels of oxygen caused the female’s ovarian tissue to age faster

Catherine Aiken

dife88

Hand Smoking Woman

Researcher profile: Dr Catherine Aiken

“ ̽��ֱ��very first time I delivered a baby, I was both terrified and thrilled – overwhelmed by the enormity of suddenly having a whole new human being in my hands,” says Dr Catherine Aiken. “That moment I knew I absolutely wanted to focus my research on understanding the problems that occur really early in development, and make sure that all children are born with the best start possible in life.”

Catherine grew up in Northern Ireland, but like many Cambridge researchers came to the ̽��ֱ�� as an undergraduate to study medicine, and “never really left”. For the last ten years, she has combined training in maternal and fetal medicine with parallel research projects.

“Currently I spend half of my time looking after mothers with high-risk pregnancies and delivering their babies, and the other half of my time leading studies looking into how pregnancy affects long-term health.”

Catherine’s clinical work takes place at the Rosie Hospital, part of Addenbrooke’s and Cambridge ̽��ֱ�� Hospital NHS Foundation Trust, where she holds clinics, carries out operations, and is on call for obstetric emergencies.

She loves the way the two sides of her work – the clinical and the academic – complement each other. “ ̽��ֱ��adrenaline of an obstetric emergency, where you have not one but two lives in your hands, and the incredible satisfaction of handing a mother a healthy baby after a complicated delivery, is something I could never give up. But I also know that in my clinical practice I am only helping one person at a time, whereas research findings can potentially affect the lives of millions.”

Catherine’s research sets out to explain how and why conditions in the womb have such a major impact on our health, even decades later. If we can understand how the very early environment shapes our likelihood of developing particular health problems, then these are the first steps towards putting protection in place to prevent them. Preventing diseases is so much more effective and economic than trying to treat them after the issues have taken hold.

“I want women experiencing pregnancy complications to get treatment that protects their baby’s health in the long-term as well as immediately. We’re getting better and better at improving the immediate outcomes (though there is still some way to go) but we need more focus on long-term and population health.”

Cambridge has a large community of researchers focused on health in early life, making it an ideal place for Catherine’s own work. “We even have an entire research centre devoted to the placenta!” she says, referring to the Centre for Trophoblast Research.

“Cambridge is full of researchers who are pushing the boundaries of what is possible in terms of state-of-the-art imaging and molecular biology techniques. There is almost no technical advance I can think of for my research, where there isn’t someone in Cambridge I can call who knows everything about it!”

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Young people exposed to vaping ads less likely to think occasional smoking is bad for health

cjb250 — Mon, 05 Sep 2016 21:21:41 +0000

Estimates suggest that among children who try smoking, between one third and one half are likely to become regular smokers within two to three years. However, young people are now more likely to experiment with e-cigarettes than they are with tobacco cigarettes. For example, a 2014 study found that 22% of children aged 11-15 in England had experimented with e-cigarettes, compared to 18% for tobacco cigarettes.

There is concern that the increasing exposure of children to e-cigarette adverts could be contributing to high rates of experimentation; in the US, adolescents’ exposure to e-cigarette adverts on TV more than trebled between 2011 to 2013. E-cigarette brands often market themselves as helping people quit smoking and as healthier and cheaper alternatives to tobacco cigarettes.

In this study from researchers at the Behaviour and Health Research Unit, ̽��ֱ�� of Cambridge, and the ̽��ֱ�� of North Carolina Gillings School of Global Public Health, and published today in the journal Tobacco Control, more than 400 English children aged 11-16 who had never smoked or ‘vaped’ previously were recruited and randomly allocated to one of three groups. One group was shown ten adverts that depicted e-cigarettes as glamorous, a second group was shown ten adverts that portrayed them as healthy, and a third control group was shown no adverts.

̽��ֱ��children were then asked a series of questions aimed at determining their attitudes towards smoking and vaping. Children shown the adverts were no more or less likely than the control group to perceive tobacco smoking as appealing and all three groups understood that smoking more than ten cigarettes a day was harmful. However, both groups of children exposed to the e-cigarette adverts, both healthy and glamorous, were less likely to believe that smoking one or two tobacco cigarettes occasionally was harmful.

Dr Milica Vasiljevic from the Department of Public Health and Primary Care at the ̽��ֱ�� of Cambridge says: “While we can be optimistic that the adverts don’t seem to make tobacco smoking more appealing to young people, they do appear to make occasional smoking seem less harmful. This is worrying, as we know that even occasional tobacco smoking is bad for your health, and young people who smoke occasionally believe they are somehow immune to its effects and do not feel the need to quit.”

̽��ֱ��group of children that were shown adverts depicting e-cigarettes as glamorous also believed e-cigarette vaping to be more prevalent than did the other two groups.

Professor Theresa Marteau, Director of the Behaviour and Health Research Unit and a Fellow of Christ’s College, ̽��ֱ�� of Cambridge, adds: “E-cigarette marketing across Europe is regulated under the new EU Tobacco Products Directive, which came into effect on the 20th May this year. ̽��ֱ��Directive limits the exposure of children to TV and newspaper e-cigarette adverts. However, it does not cover advertising in the form of posters, leaflets, and adverts at point of sale, nor does it cover the content of marketing materials depicting e-cigarettes as glamorous or healthy. ̽��ֱ��findings from our study suggest these omissions could present a threat to the health of children.”

̽��ֱ��study was funded by the Department of Health.

Reference
Petrescu, D, Vasiljevic, M, Pepper, JK, Ribisl, KM, Marteau, TM . What is the impact of e-cigarette adverts on children’s perceptions of tobacco smoking? An experimental study. Tobacco Control; 6 Sept 2016; DOI: 10.1136/tobaccocontrol-2016-052940

Exposure to advertisements for e-cigarettes may decrease the perceived health risks of occasional tobacco smoking, suggests new research from the ̽��ֱ�� of Cambridge, prompting concern that this may lead more young people to experiment with smoking.

While we can be optimistic that the adverts don’t seem to make tobacco smoking more appealing to young people, they do appear to make occasional smoking seem less harmful.

Milica Vasiljevic

Vaping360

E-cigarette

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‘Clogged-up’ immune cells help explain smoking risk for TB

cjb250 — Thu, 24 Mar 2016 16:00:00 +0000

TB is an infectious disease caused by Mycobacterium tuberculosis that primarily infects the lungs, but can also infect other organs. It is transmitted from person to person through the air. ̽��ֱ��disease can cause breathlessness, wasting, and eventual death. While treatments do exist, the drug regimen is one of the longest for any curable disease: a patient will typically need to take medication for six months.

For people exposed to TB, the biggest risk factor for infection is exposure to smoke, including active and passive cigarette smoking and smoke from burning fuels. This risk is even greater than co-infection with HIV. However, until now it has not been clear why smoke should increase this risk.

When TB enters the body, the first line of defence it encounters is a specialist immune cell known as a macrophage (Greek for ‘big eater’). This cell engulfs the bacterium and tries to break it down. In many cases, the macrophage is successful and kills the bacterium, preventing TB infection, but in some cases TB manages not just to avoid destruction, but to use macrophages as ‘taxi cabs’ and get deep into the host, spreading the infection. TB’s next step is to cause infected macrophages to form tightly-organised clusters known as tubercles, or granulomas. Once again here, the macrophages and bacteria fight a battle – if the macrophages lose, the bacteria use their advantage to spread from cell to cell within this structure.

An international team of researchers, led by the ̽��ֱ�� of Cambridge, and the ̽��ֱ�� of Washington, Seattle, studying genetic variants that increase susceptibility to TB in zebrafish – a ‘see-through’ animal model for studying the disease – identified a variant linked to ‘lysosomal deficiency disorders’. ̽��ֱ��lysosome is a key component of macrophages responsible for destroying bacteria. This particular variant caused a deficiency in an enzyme known as cathepsin, which acts within the lysosome like scissors to ‘chop up’ bacteria; however, this would not necessarily explain why the macrophages could not destroy the bacteria, as many additional enzymes could take cathepsin’s place.

̽��ֱ��key, the researchers found, lay in a second property of the macrophage: housekeeping. As well as destroying bacteria, the macrophage also recycles unwanted material from within the body for reuse, and these lysosomal deficiency disorders were preventing this essential operation.

Professor Lalita Ramakrishnan from the Department of Medicine at the ̽��ֱ�� of Cambridge, who led the research, explains: “Macrophages act a bit like vacuum cleaners, hoovering up debris and unwanted material within the body, including the billions of cells that die each day as part of natural turnover. But the defective macrophages are unable to recycle this debris and get clogged up, growing bigger and fatter and less able to move around and clear up other material.

“This can become a problem in TB because once the TB granuloma forms, the host’s best bet is to send in more macrophages at a slow steady pace to help the already infected macrophages.”

Image: Left - normal macrophages (green); Right - dysfunctional macrophages whose lysosomes (red) are clogged with cell debris. Credit: Steven Levitte

“When these distended macrophages can’t move into the TB granuloma,” adds co-author Steven Levitte from the ̽��ֱ�� of Washington, “the infected macrophages that are already in there burst, leaving a ‘soup’ in which the bacteria can grow and spread further, making the infection worse.”

̽��ֱ��researchers looked at whether the effect seen in the lysosomal deficiency disorders, where the clogged-up macrophage could no longer perform its work, would also be observed if the lysosome became clogged up with non-biological material. By ‘infecting’ the zebrafish with microscopic plastic beads, they were able to replicate this effect.

“We saw that accumulation of material inside of macrophages by many different means, both genetic and acquired, led the same result: macrophages that could not respond to infection,” explains co-author Russell Berg.

This discovery then led the team to see whether the same phenomenon occurred in humans. Working with Professor Joe Keane and his colleagues from Trinity College Dublin, the researchers were able to show that the macrophages of smokers were similarly clogged up with smoke particles, helping explain why people exposed to smoke were at a greater risk of TB infection.

“Macrophages are our best shot at getting rid of TB, so if they are slowed down by smoke particles, their ability to fight infection is going to be greatly reduced,” says Professor Keane. “We know that exposure to cigarette smoke or smoke from burning wood and coal, for example, are major risk factors for developing TB, and our finding helps explain why this is the case. ̽��ֱ��good news is that stopping smoking reduces the risk – it allows the impaired macrophages to die away and be replaced by new, agile cells.”

Image: Smoke-clogged macrophages of cigarette smokers are unable to move to engulf infecting TB bacteria, which may explain why cigarette smokers are more susceptible to tuberculosis. Credit: Kevin Takaki and drawn by Paul Margiotta

̽��ֱ��research was supported by the National Institutes of Health, the Wellcome Trust, the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (BRC), the Health Research Board of Ireland and ̽��ֱ��Royal City of Dublin Hospital Trust.

Also contributing to this research were Professor David Tobin from Duke ̽��ֱ��, Dr Cecilia Moens from the Fred Hutchinson Cancer Research Institute, Drs C.J. Cambier and J. Cameron from ̽��ֱ�� of Washington, Dr Kevin Takaki from ̽��ֱ�� of Cambridge and Drs Seonadh O’Leary and Mary O’Sullivan from Trinity College Dublin.

Reference
Berg, RD, Levitte, S et al. Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration. Cell; 24 Mar 2016; 10.1016/j.cell.2016.02.034

Smoking increases an individual’s risk of developing tuberculosis (TB) – and makes the infection worse – because it causes vital immune cells to become clogged up, slowing their movement and impeding their ability to fight infection, according to new research published in the journal Cell.

Macrophages act a bit like vacuum cleaners, hoovering up debris and unwanted material within the body, including the billions of cells that die each day as part of natural turnover

Lalita Ramakrishnan

ZEISS Microscopy

Macrophage engulfing Tuberculosis bacteria

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No evidence that genetic tests change people’s behaviour

cjb250 — Tue, 15 Mar 2016 23:30:30 +0000

Researchers at the Behaviour and Health Research Unit analysed a number of studies that looked at whether testing an individual’s DNA for genetic variants that increased their risk of developing so-called ‘common complex diseases’ influenced their health-related behaviour. Complex diseases are those such as heart disease, most cancers and diabetes, where no single gene causes the disease, but rather it is the interaction of dozens – possibly hundreds – of genes together with an individual’s environment and behaviour that leads to the disease.

Genome sequencing – reading an individual’s entire DNA – has opened up the potential to provide individuals with information on whether or not they carry genes known to increase their risk of disease. Such tests are controversial – knowing that an individual carries these variants does not mean that individual will develop the disease; however, proponents argue that if an individual knows that he or she is at a greater risk of a particular disease, they can make an informed decision about whether or not to change their behaviour.

In the early 2000s, several companies launched direct-to-consumer tests for a range of common complex disorders, and these tests continue to be sold in Canada, the United Kingdom, and other European countries. In 2013 in the United States, the Food and Drug Administration ordered the company 23andMe to stop selling its health-related testing kits because of concerns about their accuracy and usefulness, but in October 2015 the company resumed selling some health-related services.

̽��ֱ��Cambridge researchers examined over 10,000 abstracts from relevant studies and identified from these 18 studies that matched their criteria for inclusion in their analysis. By compiling the data, they found that informing individuals of their genetic risk had little or no effect on their health-related behaviour, particularly for smoking cessation and physical activity.

Professor Theresa Marteau, who led the study, says: “Expectations have been high that giving people information about their genetic risk will empower them to change their behaviour – to eat more healthily or to stop smoking, for example – but we have found no evidence that this is the case. But nor does the evidence support concerns that such information might demotivate people and discourage them from changing their behaviour.”

However, the researchers recognise that DNA testing may still play a role in improving people’s health. “DNA testing, alone or in combination with other assessments of disease risk, may help clinicians identify individuals at greatest risk and allow them to target interventions such as screening tests, surgery, and drug treatments,” explains co-author Dr Gareth Hollands.

̽��ֱ��team argue that these results are consistent with other evidence that risk communication typically has at best only a small effect on health behaviour.

̽��ֱ��study was funded by the Medical Research Council and the National Institute for Health Research.

Reference
Hollands, GJ et al. ̽��ֱ��impact of communicating genetic risks of disease on risk-reducing health behaviour: systematic review with meta-analysis. BMJ; 15 March 2016; DOI: 10.1136/bmj.i1102

Genetic tests that provide an estimate of an individual’s risk of developing diseases such as lung cancer and heart disease do not appear to motivate a change in behaviour to reduce the risk, according to a study led by the ̽��ֱ�� of Cambridge and published in ̽��ֱ��BMJ today.

Expectations have been high that giving people information about their genetic risk will empower them to change their behaviour, but we have found no evidence that this is the case

Theresa Marteau

Shaury Nash

Alineando secuencias (cropped)

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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Old before your time: Study suggests that ageing begins in the womb

cjb250 — Tue, 01 Mar 2016 15:11:52 +0000

However, the offspring of mothers with lower levels of oxygen in the womb – which, in humans, can be a consequence of smoking during pregnancy or of pregnancy at high altitude – aged more quickly in adulthood.

Our DNA is ‘written’ onto chromosomes, of which humans carry 23 pairs. ̽��ֱ��ends of each chromosome are known as telomeres and act in a similar way to the plastic that binds the ends of shoelaces, preventing the chromosomes from fraying. As we age, these telomeres become shorter and shorter, and hence their length can be used as a proxy to measure ageing.

In a study funded in the UK by the British Heart Foundation and published today in ̽��ֱ��FASEB Journal, scientists report a study that involved measuring the length of telomeres in blood vessels of adult laboratory rats born from mothers who were or were not fed antioxidants during normal or complicated pregnancy.

̽��ֱ��most common complication in pregnancy is a reduction in the amount of oxygen that the baby receives – this can be due to a number of causes, including expectant mothers who smoke or who experience preeclampsia. To simulate this complication, the researchers placed a group of pregnant laboratory rats in a room containing 7% less oxygen than normal.

̽��ֱ��researchers found that adult rats born from mothers who had less oxygen during pregnancy had shorter telomeres than rats born from uncomplicated pregnancies, and experienced problems with the inner lining of their blood vessels – signs that they had aged more quickly and were predisposed to developing heart disease earlier than normal. However, when pregnant mothers in this group were given antioxidant supplements, this lowered the risk among their offspring of developing heart disease.

Even the offspring born from uncomplicated pregnancies – when the fetus had received appropriate levels of oxygen – benefited from a maternal diet of antioxidants, with longer telomeres than those rats whose mothers did not receive the antioxidant supplements during pregnancy.

Professor Dino Giussani from the Department of Physiology Development & Neuroscience at the ̽��ֱ�� of Cambridge, the study’s senior author, says: “Our study in rats suggests that the ageing clock begins ticking even before we are born and enter this world, which may surprise many people.

“We already know that our genes interact with environmental risk factors, such as smoking, obesity and lack of exercise to increase our risk of heart disease, but here we’ve shown that the environment we’re exposed to in the womb may be just as, if not more, important in programming a risk of adult-onset cardiovascular disease.”

First author Dr Beth Allison adds: “Antioxidants are known to reduce ageing, but here, we show for the first time that giving them to pregnant mothers can slow down the ageing clock of their offspring. This appears to be particularly important when there are complications with the pregnancy and the fetus is deprived of oxygen. Although this discovery was found using rats, it suggests a way that we may treat similar problems in humans.”

Professor Jeremy Pearson, Associate Medical Director at the BHF, said: “Previous research funded by the BHF has shown that sub-optimal conditions within the mother’s womb can lead to an increased risk of cardiovascular disease in later life. However, the mechanisms involved are poorly understood. Although conducted in rats, this research emphasises the need for pregnant mothers to maintain a healthy lifestyle for the sake of their baby’s future heart health.”

Reference
Allison, BJ et al. Divergence of mechanistic pathways mediating cardiovascular aging and developmental programming of cardiovascular disease. FASEB; 1 March 2016

̽��ֱ��process of ageing begins even before we are born, according to an international team of researchers led by the ̽��ֱ�� of Cambridge. In a study using rats to model pregnancy and fetal development, the researchers also found that providing mothers with antioxidants during pregnancy meant that their offspring aged more slowly in adulthood.

Our study in rats suggests that the ageing clock begins ticking even before we are born and enter this world, which may surprise many people

Dino Giussani

Valentin Ottone

Portrait #122 - Coline - While she was smoking (cropped)

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Ads for candy-flavoured e-cigarettes could encourage vaping among school children

cjb250 — Mon, 18 Jan 2016 00:00:03 +0000

E-cigarettes are now the most commonly consumed nicotine product amongst children in countries with strong tobacco control policies. In the USA, the 2014 National Youth Tobacco Survey found that e-cigarette use tripled from 2013 to 2014 amongst high schoolers, rising from 4.5% to over 13%, and amongst middle school students increasing from 1% to 4%. These figures are mirrored in England, where e-cigarette use has risen from 5% in 2013 to 8% in 2014 amongst 11-18 year olds.

As e-cigarette use, rises amongst children and adolescents, there are concerns that their use could lead to tobacco smoking, say researchers from the Behaviour and Health Research Unit at the ̽��ֱ�� of Cambridge. ̽��ֱ��Behaviour and Health Research Unit (BHRU) is based in the Department of Public Health and Primary Care and funded by the UK Department of Health Policy Research Programme.

E-cigarettes are currently marketed in around 8,000 different flavours. Internal tobacco industry documents show that young people find tobacco products with candy-like flavours more appealing than those without. Candy- and liqueur-flavoured tobacco products were heavily marketed to young people from the 1970s until 2009, when regulations were imposed.

In a study funded by the Department of Health, researchers at Cambridge assigned 598 school children to one of three groups: one group was shown adverts for candy-like flavoured e-cigarettes; a second group adverts for non-flavoured e-cigarettes; and a third, control group, in which the children saw no adverts.

̽��ֱ��school children were then asked questions to gauge issues such as the appeal of using e-cigarettes and tobacco smoking (did the children think e-cigarettes or tobacco were ‘attractive’, ‘fun’ or ‘cool’?), the perceived harm of smoking, how much they liked the ads and how interested they might be in buying and trying e-cigarettes.

̽��ֱ��children shown the ads for candy-flavoured e-cigarettes liked these ads more and expressed a greater interest in buying and trying e-cigarettes than their peers. However, showing the ads made no significant difference to the overall appeal of tobacco smoking or of using e-cigarettes – in other words, how attractive, fun or cool they considered the activities.

“We’re cautiously optimistic from our results that e-cigarette ads don’t make tobacco smoking more attractive, but we’re concerned that ads for e-cigarettes with flavours that might appeal to school children could encourage them to try the products,” says Dr Milica Vasiljevic from the Department of Public Health and Primary Care at the ̽��ֱ�� of Cambridge.

Currently across Europe and the USA, marketing and advertising of e-cigarettes is virtually unregulated. For example, in the UK the Committee on Advertising Practice has issued rules for the advertising of e-cigarettes. A key aspect of these rules is that e-cigarette adverts must not be likely to appeal to people under 18, and those who are non-smokers or non-nicotine users as well as not allowing the models in these adverts to appear younger than 25; however, the rules do not provide any explicit prohibitions regarding the advertising of candy-like flavours designed to appeal to children.

̽��ֱ��results of the current study support the imminent changes in EU regulations surrounding the marketing of e-cigarettes, but raise questions about the need for further regulation regarding the content of products with high appeal to children. More research is needed to examine both the short- and long-term impact of e-cigarette advertising, as well as the link between e-cigarette use and tobacco smoking.

Reference
Vasiljevic, M, Petrescu, DC, Marteau, TM. Impact of advertisements promoting candy-like flavoured e-cigarettes on appeal of tobacco smoking amongst children: an experimental study. Tobacco Control; 18 Jan 2016

Advertisements featuring e-cigarettes with flavours such as chocolate and bubble gum are more likely to attract school children to buy and try e-cigarettes than those featuring non-flavoured e-cigarettes, according to new research published in the journal Tobacco Control.

We’re cautiously optimistic from our results that e-cigarette ads don’t make tobacco smoking more attractive, but we’re concerned that ads for e-cigarettes with flavours that might appeal to school children could encourage them to try the products

Milica Vasiljevic

sarahjohnson1

E-Cigarette

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