Obesity may be passed on through the father’s sperm

During pregnancy – and maybe even whilst trying for a baby – most sensible women will usually decide to stop drinking and quit cigarettes in a boosted attempted to conceive, and then protect the health of the baby whilst in the womb.

However, new research has suggested that men may also need to watch what they eat and drink, following advice usually reserved for women, for an obesity risk may be passed on to children through the father’s sperm.

The Danish scientists involved in the new study discovered a series of genetic markers in the sperm of obese men, which have the chance of altering brain development and appetite control. It is interesting to note that these same changes were not present within the sperm of lean males.
Although more research is clearly needed in order to confirm such a theory is definitive, the tentative finding – if confirmed in much bigger studies – could lead to pressure on overweight men to lose weight and get in shape prior to starting a family, which may boost the chances of a healthier child.
“We don’t yet know if this is important. But if what we’ve found is transmitted to children and is doing something negative, it raises new questions about what do we need to do, and how long we need to do it before we conceive,” said Romain Barrès who led the study at the University of Copenhagen.

Past studies have demonstrated that obesity risk is strongly linked to both their inherited genes and their surrounding environment. The combination of factors leads to childhood BMI increasing line with parental weight, whilst previous analysis of twins found that as much of 70% of the differences between people’s fat mass can be attributed to DNA.

Researchers in the Danish study decide to look at the ‘epigenetic information’ found in the sperm of 10 obese men and 13 lean men. This information isn’t encoded in DNA, but is contained within other chemicals that work with DNA. One such example is the methyl molecules that can attach to specific genes and silence them.

Epigenetics can function in different ways, by changing the the protein that wraps DNA (adding or removing chemical “tags” that alter the structure of DNA), or via genetic molecules called small RNAs.

Reporting their findings in the journal Cell Metabolism, the researchers analysed the epigenetic marks on sperm from the two groups of men, formulating what they argue is a “distinct epigenome that characterises human obesity.” A few of the changes found change behavioural genes and eating “and could participate in predisposing the offspring to obesity”.

The researchers next decided to study the epigenetic information contained in the sperm of 6 morbidly obese men both prior to, and after undergoing gastric bypass surgery. A week after surgery, the epigenetic markers on 1509 genes had found to be changed in the sperm, increasing to 3,910 after a year. Over half also differed between obese and lean men.

It is uncertain if the epigenetic markers discovered are passed onto offspring, in addition to the extent of the effects if they indeed are passed on. Although a small proportion survives, the majority of such epigenetic information transmitted by sperm is eradicated during fertilisation. Barrès said added that the next step will be to conduct studies to investigate the sperm from obese fathers and IVF embryos they have donated after completing their families.

Wolf Reik, head of epigenetics at the Babraham Institute in Cambridge said that studies in animals have shown that changes in nutrition can alter the epigenetic markers carried by sperm. “It’s totally unknown what happens to these marks after fertilisation. In some ways the signals need to survive the global wipeout system, which is why it’s even more remarkable,” he said. “How strong the effects are in human populations is totally unknown. It’s impossible to tell at this point. That’s why the study is provocative, but much more needs to be done.”

Allan Pacey, professor of andrology at Sheffield University, commnted although the study was intriguing and could warrant further investigation, it is too early to say what the observations meant for human health. “Until we know more, would-be parents should just aim to be as healthy as possible at the time of conception and not be drawn to faddy diets or other activities in order to try and influence the health of their children in ways we don’t properly understand.”

How an obese sibling can leave the other at risk

Contrary to popular belief that a child’s obesity risk is more determined by their parent’s weight, it could be true that siblings have more of an impact on their brother’s or sister’s chance of becoming obese. This is according to the findings of a new study carried out in the US.

The research analysed information extracted from the national Family Habits Survey, finding that kids with obese siblings were five times more likely to be obese themselves, whereas children with obese parents were only twice as likely to also be obese.

“When you look at a two-child family, a child’s obesity status was more strongly related with their sibling than with their parent,” commented Mark Pachucki, a researcher with the Mongan Institute for Health Policy at Massachusetts General Hospital in Boston, and leader of the research.

According to the NHS, you are considered obese if you have a body mass index (BMI) reading of between 30 and 39.9. Becoming obese is basically the result of a calorie imbalance; gaining a large amount of weight from taking in more calories through your diet than you are burning from physical activity. However, the risk can increase through a combination of different factors such as genetics, the environment and lifestyle choices.

Previous research has found links between parent’s obesity and their children’s weight, but there has been little in the way of assessing the role of the weight of one sibling effecting the other’s obesity risk.

“This is really the first project to come out the bigger study, in which we are actually merging about 10 years of families’ food purchases with information about their health,” Pachucki said.

The research comprised of 1,948 families – 807 families with two children and 1,141 with just a single child. Eating and exercising were looked at, in addition to height and weight data to determine who was obese.

Around 12% of the only children could be classified as obese, with nearly a fifth not being physically active and over a third consuming fast food on two or more occasions each week.

A similar pattern emerged for those households with two children, but only 8% of the elder children could be classified as obese, in comparison to 12% of their younger brother or sister.

“We looked at one-child and two-child households, and in one-child households having an obese parent made a child more than twice as likely to be obese themselves,” Pachucki said.

Unsurprisingly, if the parents of an only child had a large intake of junk food, this led to a higher chance that the child would be obese, with a lesser risk if those children were involved in vigorous physical activity.
 
For two-child families, having an obese sibling led to a risk that was in excess of fives time of that than if the brother or sister wasn’t obese.

It was also found that if both children in a two-child family were the same gender, the elder sibling being obese resulted in an even heavier likelihood of the younger child being obese.

Girls with an older sister who was obese were 8 times more at risk of being obese themselves compared to girls with an older sister of a healthy weight, whilst boys with an older obese brother were a staggering 11 times more at risk.

“Parents are often very explicit models of behaviour; they do the food purchasing, and they control a lot of aspects of their children’s lives,” Pachucki said. “I was expecting there to be a stronger correlation with parents’ obesity, but I was surprised that the siblings were stronger.”