The Daily Express has warned that a “few extra pounds ‘could be deadly’,” because of an increased risk of heart and circulation problems.
Most people’s weight fluctuates over time, and there is probably no need to panic if you’ve eaten a few extra biscuits this afternoon. However, this news, based on a large study of European adults, using a novel genetic technique, may be of concern for those who are a little overweight in the longer term.
Researchers used the new genetic technique to attempt to get round the fact that weight gain could both cause heart disease and be a result of it, and the issue is that it is difficult to prove that weight gain is causing heart disease.
The technique used in this study "Mendelian randomisation", focuses on genes rather than lifestyle factors. This, in theory, allows researchers to strip away outside influences and focus on the direct effect of obesity in causing cardiovascular diseases.
Based on the data the study revealed, researchers estimated that for each one unit rise in body mass index (BMI) the risk of experiencing heart failure increased by 17%.
It also found that being fatter increased the risk of developing other cardiovascular diseases such as type 2 diabetes.
The research has some limitations: the method used involves a range of assumptions that could introduce some degree of error and affect the results.
However, overall this study provides additional evidence that obesity has a causal influence on a number of different cardiovascular diseases.
The study was carried out by a collaboration of researchers from a range of European research institutions and was funded by national research councils and other national funding bodies. Some of the authors had potential competing interests as they were linked to or have received funding from biotechnology companies.
The media reporting was very bold, describing how this study proved being fat directly causes Britain’s biggest killer disease (cardiovascular disease), alongside diabetes and high blood pressure.
The Express quoted Tam Fry from the National Obesity Forum as saying this is “the final evidence” that being overweight causes heart failure. It seems this was a fair reflection of some people’s views, but others, including the editor of the journal the study was published in, reported that additional studies are needed to confirm and extend the findings of this study.
Finally, The Daily Telegraph’s headline stated how “piling on as little as 4lbs can raise risk of heart attack by 17%” when in fact the 17% figure related to heart failure. These are not the same thing.
Heart failure is a serious chronic (long term) condition whereby a damaged heart cannot pump enough blood around the body. A heart attack on the other hand is an acute medical emergency that happens when the supply of the blood to the heart is suddenly blocked.
This study took a genetic approach to looking at whether fatness (assessed through BMI) causes diseases of the heart and blood vessels (cardiovascular diseases) and related conditions such as type 2 diabetes.
Body mass index or BMI, is a commonly used measure of fatness (adiposity) and is calculated from your height and weight. A normal BMI is between 18.5 and 25. A BMI above 30 is categorised as obese.
The term “cardiometabolic traits” was used by the researchers to describe the cardiovascular diseases and risk factors associated with developing the diseases they were investigating.
The researchers used a relatively new genetic approach called "Mendelian Randomisation".
Typically, scientific studies observing and recording patterns of disease in populations (observational studies) struggle to establish cause and effect, (such as whether being overweight causes heart disease). This is because overweight people may tend to have other characteristics (confounders) that are the real cause of both their weight and cardiometabolic disease. ‘Reverse causation’ may muddy the picture further - for example, a person with heart problems may not be able to exercise as much and become obese.
The Mendelian randomisation method makes assumptions about a person’s underlying genetics and how this relates to disease risk. Instead of looking at a variable such as BMI, the method uses a genetic variation that influences this variable and looks at its association with the outcome that we are interested in (cardiometabolic traits in this case).
As genetic variations are assumed to be randomly distributed in the population, they are believed to be unaffected by confounding. Also, they are not susceptible to the possibility of reverse causation – for example, a person’s genetic variations would not be changed by their cardiometabolic traits.
Therefore, this method may help to eliminate the effects of these confounders and neutralise any chance of reverse causation.
However, there are limitations. For example, for Mendelian randomisation to work, the genetic variation has to only affect the outcome we are interested in. If it is linked to other factors that could also affect the outcome, then the findings could well be confounded.
Previous research indicated that a genetic variant (called rs9939609) within the FTO gene (which is known to be related to fat mass and obesity) was linked to a higher BMI.
This variation was selected by the researchers as it is not known to be linked to other traits that could influence the outcomes. By investigating the associations between this genetic variant and cardiometabolic traits, they aimed to establish whether a higher BMI might directly cause the traits.
Researchers collected health, genetic and BMI data on nearly 200,000 people of European descent from 36 different studies. They used this information to calculate the strength of the association between the genetic variant and the risk of developing cardiometabolic traits.
To validate their findings, they compared their genetic-disease risk associations with the links between BMI and risk of disease established in the original 36 studies.
The study confirmed the findings of previous research by first establishing that the genetic variant (rs9939609) was associated with higher BMI.
As a next step, the researchers also established that higher BMI was associated with many (but not all) cardiometabolic traits. They then looked at the association between the genetic variant and cardiometabolic traits directly. This found the genetic variant was associated with higher odds of:
The researchers then combined the results for the association of the genetic variant with BMI, and the association of the genetic variant with the outcomes. This meant they could estimate how strongly BMI increased the risk of developing the different cardiometabolic traits of interest.
They reported statistically significant causal links between higher BMI and heart failure, hypertension, type 2 diabetes, abnormal blood fat levels and metabolic syndrome. They also found a statistically significant increase in blood levels of liver enzymes (an indicator of liver damage, some metabolic disorders involve liver damage), and several other cardiometabolic traits.
For heart failure, the study estimated that for every one unit rise in BMI, the odds of experiencing heart failure increased by 17%.
Based on official figures on heart failure, the researchers estimated that a one-unit increase in BMI corresponds to roughly 220,000 additional heart failure cases in Europe (113,000 additional cases in the US).
So even a modest gain in weight (for a man who is 5'10", one BMI unit is equivalent to a seven pound or 3.2kg weight gain) can lead to extensive health costs at a population level.
The researchers concluded that their study provided “novel insights into the causal effect of obesity on heart failure and increased liver enzymes levels”. They went on to describe how “this study provides robust support for a causal relationship between obesity and a number of cardiometabolic traits reported previously. These results support global public prevention efforts for obesity in order to decrease costs and suffering from T2D [type 2 diabetes] and heart failure.”
This large study uses an interesting genetic approach (Mendelian randomisation) to suggest obesity increases the risk of heart failure and adverse changes in liver enzymes.
The combination of a very large sample, prospectively collected information, and a wide range of cardiometabolic measures lend credibility to the findings. The method the researchers used is also thought to reduce the chances of factors other than BMI influencing results, and the chance that the ‘outcome’ could be causing the ‘exposure’ (reverse causality).
The main limitation of this kind of research is that assumptions need to be made. The potentially weakest assumption is the reliability of the association between the FTO genetic variant and BMI. Although the researchers report that this link has been widely found in many other studies, they also note that the strength of the link is relatively weak – the variant is only thought to explain about 0.3% of the variation of BMI in the population.
Estimates of the effect of BMI would be more accurate if this link was stronger.
The researchers suggest that studies in the future might use more than one genetic variation to increase the strength of the link, leading to more precise estimates.
They also note that an effect of the variant on characteristics other than BMI cannot be ruled out.
Body mass index also has its limitations as a measure of fatness – you can be very muscular and have a high BMI. However, it is a widely used measure of obesity, and across the large number of people involved in the study, measuring BMI should give a reasonable measure of relative fatness.
Overall, this study provides additional evidence to suggest obesity (raised BMI) has a causal influence on a number of different cardiovascular diseases, including heart failure.
And this serves to re-emphasise the message that maintaining a healthy weight is beneficial to many aspects of health.
If you are concerned about your weight, try the free NHS Choices 12-week weight-loss guide – for an evidence-based method of working to achieve safe and sustainable weight loss.