"A brisk 30-minute walk five days a week is more effective than any other form of exercise for keeping weight down," The Times reports. That is the reported conclusion of two researchers who looked at data from the annual English Health Surveys from 1999 to 2012.
As expected, they found people who regularly walk briskly for half an hour five days a week were likely to have a lower body mass index (BMI) than people who are less active.
The study found women and those over the age of 50 were most likely to have a lower weight if they walked regularly. By walking, the researchers mean brisk walking that raises your heart rate and makes you sweat slightly, not a gentle stroll.
Walking was also linked to having a smaller waist size – although, for men, sport and other forms of exercise were more strongly linked to waist size than walking. Sport and exercise were also linked to a lower BMI, although the link was not as strong as it was for walking.
However, this study does not seem to have compared the effects of the two types of activity directly, so we cannot say for sure – as many in the UK media have done – that walking is more effective than other types of exercise.
Walking does have the obvious advantage of being free, as well as being an activity you can easily fit into your day-to-day life. Read more about walking for health and how the 10,000 steps a day challenge can help boost your fitness levels.Where did the story come from?
The study was carried out by researchers from the London School of Economics and the University of Queensland, and was funded by the Nuffield Trust. It was published in the peer-reviewed journal Risk Analysis.
Many UK media outlets covered the story. Most fell into the trap of assuming walking caused weight loss and, because the link was stronger for walking than for sport or exercise, walking was therefore better for losing weight.
However, the two types of activity were not directly compared, and on some of the analyses in the study, sport and exercise came out better, especially for men.What kind of research was this?
This data is compiled by the Health and Social Care Information Centre (HSCIC), the same organisation that operates Behind the Headlines and the rest of the NHS Choices website.
Cross-sectional studies can look at the links between factors, but cannot say whether one factor caused another, or vice versa.What did the research involve?
Researchers took data from seven separate years of the Health Survey for England to see what people said about how often they took part in specific activities. They compared this with people's recorded BMI and waist circumference. They wanted to find out whether people's weight and waist size could be predicted by how often they did specific types of physical activity.
The study is not clear about how many people were included in the analysis, although the researchers say they had more than 68,000 "observations" about the types of activity people did.
It's possible this means they used data from 68,000 people, although we can't be sure of this. The figures for BMI and waist measurements were based on 26,878 and 38,836 observations respectively.
The researchers put the data through a number of statistical models to work out the relationship between BMI and waist size and any type of physical activity, then looked specifically at brisk walking, heavy manual work, heavy housework, and sport or exercise, including gym workouts, cycling and running.
They adjusted their figures to take account of confounding factors, including people's age, gender, household size, marital status, ethnic background, where they lived, their level of education and employment.
Finally, they calculated the difference in BMI and waist circumference between people who regularly do each activity for more than 30 minutes five days a week (in line with UK government guidelines) and people not getting this kind of exercise.What were the basic results?
The first result, not surprisingly, was people who did the most activity, of any type, had the lowest BMIs and the lowest waist measurements. These effects were strongest in women and people over the age of 50.
Brisk walking was linked to the biggest difference in BMI for both men and women. The researchers found men who regularly walked briskly for more than 30 minutes five days a week had a BMI on average one unit less than those who did not, while for women the difference was 1.8 units.
The equivalent amount of sport and exercise was also linked to BMI, but the difference was smaller. Heavy manual work also showed a link, as did heavy housework for women, but not men.
The effect on waist measurement was similar, with one important difference: women who regularly walked briskly had a waist 4.3cm smaller than women who did not. The researchers say this was the biggest difference for any type of activity for women.
However, for men, sport and exercise had a stronger link to waist measurement than walking. Men who regularly took part in sport or exercise had a waist 3.3cm smaller than those who did not.How did the researchers interpret the results?
The researchers said: "The results suggest that those who do five days of any of these physical activities every week for a month could decrease their waist circumference on average by 4.3cm for women and 3.6cm for men."
This is a surprising claim, as the study did not show a change in waist circumference over time, or establish that exercise caused a drop in waist size.
They went on to say: "Overall, we find that brisk walking has the highest association with these measures of weight, with sports/exercise being the runner up in this regard."
They admitted: "We cannot interpret our findings here as causal," but they called for a public health campaign to encourage walking as an "easy policy option" to combat the obesity epidemic.Conclusion
Walking has long been advocated as a good way to keep fit. It is easy to fit into everyday activities, doesn't need special equipment, and most people can do it.
This study shows people who regularly took brisk walks for at least half an hour five days a week – fast enough to get you out of breath and sweat slightly – were likely to have a lower BMI and smaller waist size than other people.
The results don't mean other types of exercise, such as swimming, cycling, playing sport or going to the gym, are worthless. People who regularly did these activities were also likely to have a lower BMI and waist circumference.
The study does not seem to have directly compared the effect of sport and exercise versus brisk walking. We don't know whether the differences in BMI the researchers found would have stood up as statistically significant in a head to head comparison.
It is interesting that men who did regular sport or exercise had a lower waist measurement than men who walked instead. Waist measurement is important as it shows how much fat you carry around vital organs, which has been linked to heart attacks.
It may be that exercise and sport are less strongly linked to BMI than walking because men who work out gain muscle, which weighs more than fat, so will result in a higher BMI.
The main limitation of the study is it cannot prove people's weight is a result of their activity levels. We know diet is also important in determining weight, as well as other factors such as genetic make-up.
It is possible people are more likely to walk or take part in sport and exercise if they have a lower BMI as slimmer people find physical activity easier and more comfortable. We cannot tell whether the people in this study with a higher BMI would have lost weight by walking or exercising more regularly.
However, this study does add to the evidence that walking is a healthy form of exercise linked to keeping to a healthy weight, especially for women and in later life.
Links To The Headlines
Half an hour of walking better than gym for losing weight. The Times, November 4 2015
Good news! Brisk walks are BETTER at keeping weight off than going to the gym. Mail Online, November 3 2015
Want to lose weight but hate the gym? We have some VERY good news. Daily Mirror, November 3 2015
Forget the gym - just 30 minutes of WALKING a day will keep you slim. Daily Express, November 4 2015
Fitness is a walk in the park. The Sun, November 4 2015
You're better off going for a brisk walk than going to the gym if you want to keep weight off. Metro, November 4 2015
Links To Science
Lordan G, Pakrashi D. Do All Activities "Weigh" Equally? How Different Physical Activities Differ as Predictors of Weight. Risk Analysis. Published online May 20 2015
"Just two sweetened drinks a day can dramatically raise heart risk," The Sun reports. A Swedish study found that men who consumed two or more sugary drinks a day had, on average, a 23% increase in the risk of heart failure.
The study included more than 42,000 Swedish men aged 45 to 79 and data on their estimated daily or weekly intake of sweetened drinks from a food frequency questionnaire completed in 1997.
After a follow-up period of nearly 12 years, men who reported consuming two or more glasses (two 200ml portions) of sweetened beverages a day were 23% more likely to experience heart failure compared to individuals who did not consume any sweetened drinks.
However, the study has a number of limitations – for example, there was no adjustment for salt intake, which is known to raise blood pressure and contribute to the development of heart failure.
In addition, the study only included middle-aged and elderly men, so the results cannot be generalised to the overall population and both genders.
That said, most nutritionists would agree that sugary drinks have an adverse impact on public health, and so-called "sports drinks" are often the worst offenders. A standard 500ml bottle of Lucozade contains 4.8 teaspoons (17.5g) of sugar.
When it comes to hydration, tap water is by far the healthiest, and the cheapest, option.
Where did the story come from?
The study was carried out by researchers from the Institute of Environmental Medicine in Stockholm, Sweden. It was funded by the Swedish Research Council Committee for Medicine and the Swedish Research Council Committee for Infrastructure.
The study was widely covered by the UK media both accurately and responsibly.
The Daily Telegraph reported a statement from the researchers at the Karolinska Institute in Stockholm, who said the study findings: "suggest that sweetened beverage consumption could contribute to heart failure development. These findings could have implications for heart failure prevention strategies."
They also quoted Francesco Cappuccio, professor of cardiovascular medicine at the University of Warwick, who said: "high-sugar drinks can contribute to heart failure by increasing weight gain and diabetes". He added: "an alternative explanation (not discussed in the paper) is that high salt intake (salt intake is higher in low socio-economic groups) increases thirst, hence increased drinking, including sweetened drinks. The increase in heart failure could therefore be a consequence of higher salt intake, higher blood pressure and higher heart failure risk."
The Sun and the Mail Online carried a quote from the British Soft Drinks Association chief Gavin Partington, who said, unsurprisingly, that the study was "limited" and that "no definitive conclusions can be drawn about cause and effect".
What kind of research was this?
This was an observational study that aimed to investigate whether drinking sweetened beverages was associated with risk of heart failure in a large cohort of Swedish men. The study was carried out over a period of nearly 12 years to capture the long-term associations of this exposure (1998 to 2010).
Researchers say that more than 23 million people are affected by heart diseases worldwide and the prevalence is increasing among elderly and males. The World Health Organization (WHO) says that more than 80% of premature heart disease and stroke cases are preventable. According to their research predictions, deaths from heart diseases in the UK could be halved by small changes in the risk factors (such as cholesterol) that are associated with these conditions.
Observational studies such as this one, which includes a large population with a long follow-up period, can show us if there is any association between an exposure and an outcome. However, we cannot establish causality from such study designs, as more than one factor may be responsible for the observed outcome.
What did the research involve?
This research included 42,400 Swedish men aged 45 to 79. These individuals were residents of Västmanland counties in Sweden.
All the study participants were asked to complete a food frequency questionnaire (FFQ) designed to assess the Swedish diet in 1997. In this questionnaire, individuals were asked to report their average consumption of 96 different foods and beverages over the past year.
To gather information on sweetened drink consumption, study subjects were asked "How many soft drinks or sweetened juice drinks do you drink per day or per week?". They were also separately asked how much coffee, alcohol, fruit, vegetables, processed meat and fish they consume.
The researchers then recorded heart failure incidence from 1998 to 2010 through the Swedish National Patient Register and the Cause of Death Register, which included the details of diagnosis and treatment.
The participants were also asked about the following commonly known confounding factors that may have influenced the outcome measured:
- history of angina or stroke
- physical activity
- body mass index (BMI)
- educational attainment
- family history of heart attack
What were the basic results?
Over a period of nearly 12 years, 4,113 people were diagnosed with heart failure. Among these, 3,604 were first events of heart failure that required hospitalisation, and there were 509 deaths due to heart failure.
After adjusting the results for all of the potential confounding factors measured, individuals who consumed two or more glasses (two 200ml portions) of sweetened beverages per day were 23% more likely to experience heart failure compared to individuals who did not consume any sweetened drinks (hazard ratio (HR) 1.23, 95% confidence interval (CI) 1.12 to 1.35).
The researchers also observed a strong trend between the lower education level of an individual and higher consumption of sweetened beverages.
How did the researchers interpret the results?
Researchers concluded by saying the "study findings suggest that sweetened beverage consumption could contribute to HF [heart failure] development. These findings could have implications for HF prevention strategies. Further prospective studies examining this relationship are therefore necessitated. Moreover, possible biological mechanisms linking sweetened beverage consumption with HF risk need to be studied carefully."
This observational study found an association between the consumption of sweetened drinks and risk of heart failure.
The study has some strengths, such as the large population size and long follow-up period. However, it has several limitations, which are acknowledged by the researchers. These include the following:
- The study included middle-aged and elderly men, so the results cannot be generalised to all age groups and genders.
- The men were all from Sweden, where there is a different typical diet to that of the UK.
- Researchers collected data on the daily and weekly intake of sweetened drinks in the past year just once in 1997. This introduces two limitations. Firstly, since the participants were asked to report their intake in the past year, there may be some recall bias. Secondly, the dietary habits of these individuals might have changed in the 12-year follow-up period.
- Sweetened drinks included artificially sweetened drinks such as low-calorie fizzy drinks, yet fruit juice was not included in the dietary questionnaire. These factors limit any conclusions we can make about which type of drink may be having a negative effect.
- There was no adjustment for salt intake, which is known to raise blood pressure and contribute to the development of heart failure.
- The study design itself, although helping to establish an association, cannot confirm a causal link.
- The researchers have accounted for a number of commonly noted confounding factors.
- However, there may be some other factors that are not considered in the analysis that may have influenced the observed outcome.
It is no secret that a healthy diet including lots of vegetables, whole fruits and food low in salt, along with an active physical lifestyle, help to prevent a number of ailments. Losing weight (if you are overweight), quitting smoking, lowering cholesterol and reducing alcohol intake also have a positive impact on overall health and in reducing the risk of heart failure.
Most nutritionists would recommend that you and your family should drink sugary drinks as an occasional treat and not as a daily dietary staple.
Links To The Headlines
Diet Coke heart risk. The Sun, November 3 2015
Just ONE can of fizzy drink a day could raise heart failure risk by 23%. Daily Mirror, November 3 2015
How even ONE can of Coke a day can increase the risk of heart failure by 20%. Mail Online, November 3 2015
Fizzy drinks linked to increased risk of heart failure. The Daily Telegraph, November 3 2015
Heart risk in sweet drinks: How just TWO glasses a day can be DEADLY. Daily Express, November 3 2015
Links To Science
Rahman I, Wolk A, Larsson SC. The relationship between sweetened beverage consumption and risk of heart failure in men. Heart. November 2 2015
"Children who grow up with a pet dog in the family home have a lower risk of developing asthma," The Times reports.
A large Swedish study found an association between pet ownership and reduced risk of asthma. Living on a farm was also found to reduce this risk.
The study found exposure to dogs reduced the risk of both preschool (by 10%) and school-age children having asthma by 13%. And living on a farm as a child – not just visiting one – also appeared to reduce asthma risk by an estimated 31% for preschool children and 52% for school-age children.
Some commentators have argued these results add weight to what is known as the hygiene hypothesis. This is the idea that children who grow up in sterile environments have reduced exposure to infectious agents, such as those carried by dogs, so they have an underdeveloped immune system. This may then make them more vulnerable to allergic conditions such as asthma.
However, one of this study's limitations is the findings can only highlight a potential link: it cannot categorically prove living with or around animals reduces the risk of childhood asthma.
The research has attempted to adjust for various potential confounders, including parental asthma, but other factors may still have had an influence.
One proven way to reduce the risk of childhood asthma is to never expose your children to tobacco smoke (secondhand smoke) both during pregnancy and when they are growing up.
Where did the story come from?
The study was carried out by researchers from Uppsala University in Sweden.
It was funded by the Swedish Research Council, Stockholm County Council, the Strategic Research Program in Epidemiology at Karolinska Institutet, and the Swedish Heart Lung Foundation. There were no significant conflicts of interest.
The study was published in the peer-reviewed JAMA Pediatrics.
The UK media has generally reported the findings accurately. The Independent quoted one of the authors of the study, who said: "These kinds of epidemiological studies look for associations in large populations, but do not provide answers on whether and how animals could protect children from developing asthma.
"We know that children with established allergy to cats or dogs should avoid them, but our results also indicate that children who grow up with dogs have reduced risks of asthma later in life."What kind of research was this?
This cohort study aimed to investigate the association between exposure to dogs and farm animals during the first year of life – as in living with or around them – and having asthma as a preschool (around three years old) or school-age child (around six years old).
This study design is able to suggest links for further investigation, but is unable to prove cause and effect. There may be a number of other factors influencing risk, such as parental asthma, other allergies, air pollution, or other environmental exposures.
The only way to establish a causal link would be to run a randomised controlled trial (RCT), but realistically such a trial would be both expensive and impracticable – it would be difficult to convince thousands of families to adopt a dog at random or move to a farm, for example.What did the research involve?
The researchers included all children born in Sweden over a 10-year period from 2001-10, who were identified through the Swedish Register of the Total Population and the Medical Birth Register.
The need for informed consent and parental permission was waived by the regional ethical board in Stockholm.
The study population was split into two groups:
- children born between January 1 2001 and December 31 2004 (school-age children)
- children born between July 1 2005 and December 31 2010 (preschool-age children)
Children were excluded if their parents moved to Sweden after the child was 15 years of age or if there was incomplete information on parental identity or migration.
For school-age children, their asthma status was assessed during the seventh year of life. For preschoolers, this was assessed from the age of one and then throughout the study period.
Four different asthma definitions were explored:
- an asthma diagnosis obtained only from the National Patient Register (NPR)
- asthma medications noted in the Swedish Prescribed Drug Register (SPDR)
- having both the NPR diagnosis and asthma medications noted in the SPDR
- having either one or both NPR diagnosis and asthma medications noted in the SPDR
The researchers selected having either one or both NPR diagnosis and asthma medications noted in the SPDR as the most appropriate outcome measure.
Exposure to dogs was defined as having a parent registered as a dog owner during the child's whole first year of life. Exposure to farm animals was defined as parents who were animal producers and related workers in the child's first year of life.
A number of statistical analyses were performed to assess different levels of exposure to dogs and farm animals. The analyses were adjusted for potential confounders, including parental age, educational level, country of birth, and asthma status.What were the basic results?
During the 10-year study period, there were 1,011,051 children born in Sweden. Researchers included 376,638 preschool-age children, of whom 53,460 (14.2%) were exposed to dogs and 1,729 (0.5%) were exposed to farm animals. They included 276,298 school-age children, where 22,629 (8.2%) of whom were exposed to dogs and 958 (0.3%) were exposed to farm animals.
After controlling for potential confounders, having a dog during the first year of life was associated with a decreased risk of asthma:
- of 13% in school-age children (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.81 to 0.93)
- of 10% in preschool children aged three years or older (hazard ratio [HR] 0.90, 95% CI 0.83 to 0.99)
When analysed by parental asthma status, school-age children had a reduced risk regardless of whether their parent had asthma or not. However, when dividing up preschool children, exposure to dogs no longer had any effect on asthma risk, either for those with parental asthma or without.
Living with or around farm animals was also associated with a reduced risk of asthma in both school-age children (OR 0.48, 95% CI 0.31 to 0.76) and preschool-age children (HR 0.69, 95% CI 0.56 to 0.84) after adjusting for confounders.
However, again, the results changed when divided by parental asthma status. For both school-age and preschool children, those who had a parent free from asthma had a reduced risk, but those with a parent with asthma did not.
Dog or farm animal exposure had no significant effect on risk of asthma in children under the age of three.How did the researchers interpret the results?
The researchers concluded that: "The data support the hypothesis that exposure to dogs and farm animals during the first year of life reduces the risk of asthma in children at age six years.
"This information might be helpful in decision making for families and physicians on the appropriateness and timing of early animal exposure."Conclusion
This cohort study aimed to study the association between living with or around dogs or farm animals during the first year of life and the risk of asthma in preschool children and school-aged children. The results suggest early exposure to dogs and farm animals may reduce the risk of childhood asthma.
However, there are a number of limitations and caveats to consider. This study type can suggest an association, but it cannot prove cause and effect. The researchers adjusted their analysis for various potential confounders, including parental age, education level and country of birth. But it was not possible to account for all confounding factors, and other factors could have had an influence.
Importantly, the researchers did take parental asthma status into account, but adjusting for this gave inconsistent results, with some links remaining significant, while others did not. For example, school-age children with early dog exposure had a reduced risk regardless of whether their parent had asthma.
But when the two groups were divided in two according to parental asthma status, no risk reduction was found for either. When it came to farm animal exposure, risk was reduced in children of parents without asthma, but not in those who had parental asthma, for both groups.
This slightly clouds the picture and makes it difficult to give a clear, consistent message on whether animal exposure has a direct effect on risk, or whether it is influenced by other factors, such as parental or child eczema, hay fever, or dust mite or animal fur allergies. These things may influence both the decision to live with an animal and the child's risk of developing asthma.
That said, the study has strengths: it included a large sample, followed participants for a number of years, and also used medical registers to identify child asthma, rather than relying on parental report.
However, as the researchers used official registers, there may be a problem with missing data for dog ownership or parental asthma status, for example. The study was also unable to account for exposure to other animals, particularly at close family members' homes, where there may be high levels of exposure that would not have been linked.
It is not exactly clear what causes asthma, although it is thought to be a combination of factors, including genetic and environmental. Modern hygiene standards are often considered to be one of these factors, and the researchers suggest this may be why exposure to animals could have a protective effect.
However, this cannot be confirmed at this stage. More research is needed before we can consider giving any official advice to parents about the benefits – or otherwise – of having a pet.
Links To The Headlines
Family dogs reduce risk of asthma in children. The Times, November 3 2015
Pet dogs 'may help children avoid asthma'. BBC News, November 2 2015
Children 'less likely to suffer' asthma if they grow up around dogs. The Independent, November 2 2015
Farm-ocology: why a visit to the farmyard protects kids against asthma. The Daily Telegraph, November 2 2015
Living with a dog cuts child's risk of asthma by 15%, study shows. The Guardian, November 2 2015
Having a pet dog reduces risk of children developing asthma and allergies, new study claims. Daily Mirror, November 3 2015
Why having a dog is good for a child's health: Being exposed to a pet at a young age 'cuts risk of asthma by 15%'. Daily Mail, November 2 2015
Links To Science
Fall T, Lundholm C, Örtqvist AK, et al. Early Exposure to Dogs and Farm Animals and the Risk of Childhood Asthma. JAMA Pediatrics. Published online November 2 2015
"A single gene mutation may be all it takes to determine if a person is prone to becoming obese," the Mail Online reports.
A particular genetic variant may disrupt the normal workings of a protein – brain-derived neurotrophic factor (BDNF) – that helps regulate appetite after eating.
Researchers have examined brain tissue samples to see whether variations in the DNA sequence of the gene that "codes" for the BDNF protein influenced how much of the protein was produced.
It then followed up the findings in cohorts of adults and children to see whether this sequence was linked to people's body mass index (BMI).
The findings suggested that one particular variation in the DNA sequence of the gene was associated with lower levels of this protein. Those inheriting two copies of the BDNF gene with this variation were more prone to obesity.
The suggestion is that lower levels of BDNF protein may mean that a person is still hungry even if they have eaten enough food to satisfy the body's energy requirements, leading to weight gain.
The researchers suggest that increasing BDNF protein levels may be a possible therapeutic target to treat obesity. However, it is difficult to say at this stage whether such a treatment could be developed or be effective.
Where did the story come from?
The study was carried out by researchers from the National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health (NIMH), Bethesda, Maryland, and several other institutions in the US and Belgium, and was published in the peer-reviewed scientific journal Cell Reports.
Funding was provided by the Intramural Research Program of NICHD and NIMH, the National Institute of Health, and the National Institute of Minority Health and Health Disparities.
The Mail Online's headline "Being obese IS in your genes!" is misleading; it seems to suggest that being obese definitely is all in the genes, and that one precise "mutation" provides the whole answer to obesity, which is not the case. Even in this study, some people who did not carry this genetic variation were overweight or obese.
Also, the main body of the article is contradictory, saying first that the variant in question is rare and then saying that it was common.
What kind of research was this?
This was laboratory research that aimed to look into the possible genetic determinants of obesity. The research centres on a particular protein called BDNF, which is thought to play a role in energy balance, influencing our body weight and how much we eat.
The researchers say how population-based studies have linked obesity to single "letter" changes in the DNA sequence (single nucleotide polymorphisms or SNPs) of the BDNF gene, which carry the instructions (codes) for making the protein.
This study aimed to look at a variety of SNPs in the BDNF gene to see what influence they had on activity of the BDNF protein in a brain region that has a role in telling us that we feel full (the ventromedial hypothalamus).
What did the research involve?
The laboratory study involved donated human brain tissue obtained at autopsy and data collected from people participating in different cohort studies.
The researchers examined the ventromedial hypothalamus in the autopsy samples from 84 people, looking at 44 target SNPs in the BDNF gene.
The SNP that was found to be most significantly associated with BDNF gene activity in the ventromedial hypothalamus was then further investigated in the data from the cohort studies. The ventromedial hypothalamus is an area of the brain associated with some of the most primal human emotions, such as sexual attraction, fear and appetite.
Four cohorts were subsequently examined: two cohorts of African-Americans (almost 30,000 people), and two cohorts of healthy children and adolescents (almost 2,000) – one of which included only Hispanic individuals. In these populations they examined the association of the SNP with body composition.
What were the basic results?
Of the 44 SNPs examined in the BDNF gene, one called rs12291063 was significantly associated with BDNF protein production and activity in the ventromedial hypothalamus, and with BMI.
The four "letters" called bases, which make up our DNA, are called A, C, T and G. The researchers found that having a T base at this rs12291063 location on both copies of the BDNF gene (called having a TT genotype) was required for normal BDNF gene activity.
Instead, inheriting two gene copies with a C base at this location was associated with reduced gene activity of the protein. Children and adults with a CC genotype had a higher BMI than those with either TT or CT genotypes.
How did the researchers interpret the results?
The researchers conclude that their findings "provide a rationale for [increasing BDNF levels] as a targeted treatment for obesity in individuals who have the rs12291063 CC genotype."
This research aimed to look into possible genetic influences on obesity – an area that has been frequently studied in the past.
This study focused on the brain protein BDNF, which is known to play a role in controlling energy balance and how much we eat, and the gene coding for it.
The findings suggested that a particular base letter in the DNA sequence of the gene was associated with levels of this protein and with BMI. It appears that those with two copies of the BDNF gene carrying a C base in one particular location were more prone to obesity.
The researchers suggest that increasing levels of BDNF may be a possible therapeutic target in people who carry two C variants. However, it is difficult to say at this stage whether such a treatment could be developed or be effective.
What it is possible to say is that even if this single substitution on the BDNF gene is one genetic factor that has an influence on our appetite, satiety and BMI, it is does not provide the whole answer to the obesity epidemic. To show this, even some people with no C variants in this study were overweight or obese.
Though including a large overall sample size in the cohorts, it was predominantly African-American and Hispanic populations that were studied. The same observations may not have held true in other population samples. There are likely to be other genes which affect a person's predisposition to being overweight or obese.
Regardless of any genetic influence there may be on BMI – and whether or not treatments could be developed to target our genetics – one way that will tackle overweight and obesity is to follow a healthy, balanced diet combined with regular exercise.
The NHS Weight Loss plan uses both to help you achieve sustainable weight loss.
Links To The Headlines
Being obese IS in your genes! Well, just one to be precise: Mutation 'triggers weight gain by stopping you feeling full'. Mail Online, October 30 2015
Links To Science
Mou Z, Hyde TM, Lipska BK, et al. Human Obesity Associated with an Intronic SNP in the Brain-Derived Neurotrophic Factor Locus. Cell Reports. Published online October 29 2015