How a pregnant mother’s diet could change a child’s brain

Scientists have pursued every possible avenue to try to figure out why we keep getting fatter. They’ve explored our genes, our brains, our hormones and our gut bacteria, not to mention our fatty, sugary diets and sedentary lifestyles. Now, a recent study has come out blaming our expanding waistlines and poor health on our parents’ behaviors before we were born.

My newest article is up on The Atlantic, discussing recent research on the impact a mother’s diet has on her offspring’s health, affecting our brains and subsequently our bodies. This line of research isn’t new — other studies have shown links between a woman’s health during pregnancy and her child’s weight later in life — but this is one of the first to provide a potential explanation for this phenomenon by looking in the brain at some crucial hunger hormones.

However, you can’t blame all of your problems on your parents; what you eat still has a major impact on how these brain changes manifest:

Now, I’m all for shifting blame away from myself and onto my parents, but I feel that, like every possible explanation behind the obesity epidemic, this is only one piece of the puzzle. Genes undoubtedly play a role in body mass, fat percentage, and metabolism, but so does what you eat and how many calories you burn through physical activity…The problem of obesity, like so many health and social issues we face today, is that there isn’t just a single contributor to the problem. If there were, it would have been solved by now.

Check out the entire piece here.

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Fitter, happier

Have you ever heard that Radiohead song with the creepy computer voice telling you how to live a “fitter, happier, more productive” life? Regular exercise, not drinking too much, eating well, getting on better with your associates. Sardonic or not, it seems like we’re constantly inundated with recommendations for healthy living: eat five fruits and vegetables a day, get 150 minutes of exercise every week, don’t drink more than two glasses of wine a night.

The big question though, is, does anyone actually follow these guidelines?

Well apparently, we are. Two new studies have come out in the last week reporting that a recent leveling off in obesity rates around the country can be attributed to better eating habits, and that interventions among college freshman can actually reduce problem-drinking behaviors among students.

The first study, a survey of roughly 200,000 Americans on their grocery shopping habits and food and drink choices conducted between 2003-2011, revealed that we’ve reduced our average calorie intake by 34 calories per day in children and 14 calories in adults. Much of this improvement seems to stem from a reduction in sugary beverage consumption, which have taken a beating in public health campaigns over the last five years. Moreover, the researchers concluded that this change was not attributable to the economic recession or rising food prices. Instead, they believe that we are actually making better, more conscious decisions about what we put in our bodies; this was especially the case in households that had young children at home.

In the second study — a meta-analysis of 60 different intervention programs implemented on college campuses over the last ten years — researchers reported that students who had received some sort of alcohol education as freshmen had fewer problem-drinking behaviors and consumed less alcohol on average than those who hadn’t. While they acknowledge that no one intervention was perfect, they cite the “Prevention Paradox,” that a few small individual changes (i.e., getting students to reduce their drink intake by one on nights that they go out) can have larger overarching effects across the entire student body. One method that the researchers particularly recommended was providing individualized reports on each student’s drinking habits and how they measured up to their peers. Other general tips included alternating alcoholic beverages with water, being particularly mindful at fraternity parties, and setting goals or limits before going out.

All in all, this is encouraging news. It seems as if the barrage of public health campaigns that have papered our cities in recent years, admonishing us for our soda habits and encouraging better cooking and eating behaviors, have been effective. And apparently all those Alcohol EDU courses we had to take as freshmen were having a greater subliminal effect on us than we realized. Now, the only thing left to tackle is making us happier, more productive, comfortable…

Everyone poops: A weight loss story

It seems like we are always looking for a quick and easy weight loss solution. We spend millions of dollars every year on gym memberships, workout equipment, dietary supplements and self-help books in the vain attempt to lose those last 5 (or 10 or 20) pounds. Unfortunately, most of these attempts fail miserably and we end up right back where we started, if not worse. But what if there was an easier way? What if there was one simple solution to losing all that excess weight for good? What if all it took was a stool transplant. Would you do it?

Yes, fecal matter. That embarrassing brown lumpy bodily expulsion. We learned from an early age that Everyone Poops, and now a recent study has hinted that with the right transfer, somebody else’s poop could help you lose weight.

But let’s not get too far ahead of ourselves and take a look at the real science first. The concept of a personal microbiome, a unique bacterial make-up as individual as our DNA, has been gaining traction over the last few years. Gut bacteria, or ‘microbiota’, have been implicated in everything from food allergies to obesity, with some studies suggesting that these bacteria may account for up to 20% of our differences in body weight. Stool samples are teeming with these microbiota, and previous studies have used fecal transfers to replenish lost essential bacteria that help fight infections after they’ve been wiped out with antibiotics.

Research from scientists at Cedars-Sinai Medical Center in Los Angeles has recently confirmed that some strains of bacteria can contribute to weight gain, helping people to retain and store calories more easily by aiding in the digestion of nutrients. These bacteria appear to make the stomach and intestines more productive, breaking down food faster and more efficiently so that more nutrients and calories can be absorbed. While this may have been beneficial to our hunter-gatherer ancestors, when food was scarce and mostly consisted of difficult-to-digest plants and animals, today it may be contributing to our problems with over-nourishment and obesity. In the current study, people with greater levels of these bacteria, determined either through stool samples or breath tests measuring hydrogen and methane – by-products of this nutrient break-down – had higher BMIs and body fat percentages than those with lower trace products of the bacteria.

But if your breath tastes especially methaney, don’t despair. According to recent research, there are now several ways to change your gut microbiota.

Physicians have long used gastric bypass surgery to aid in weight loss in cases of extreme obesity. The procedure involves removing up to 80% of an individual’s stomach and can result in weight loss of 75% of excess body weight. This dramatic success was initially thought to be driven by the reduction in stomach size, resulting in a lower capacity for consumption and absorption calories. Simply put, the smaller your stomach, the less food you can eat. However, new evidence suggests that a shift in gut bacteria may also aid in this change.

The microbiota of obese people is markedly different from those of lean individuals, contributing to and perpetuating weight problems. This bacterial profile is partly influenced by what we eat, and it turns out that changing the size of the stomach and intestines can also dramatically alter the make-up of these bacteria. A study published in Science Translational Medicine by researchers from Massachusetts General Hospital recently demonstrated this effect in mice, hinting that it also might apply to people.

In the study, animals who had undergone gastric bypass operations showed not only significant weight loss, but also a dramatic change in microbiota, potentially both resulting from and furthering their weight-loss. Notably, this change was larger and more stable in mice who had had the surgery than in those who lost a similar amount of weight through diet changes, but without the operation. The bypass mice also had greater fecal fat content (yes, we’re back to poop again), suggesting that the new gut bacteria make-up was limiting the break-down and digestion of fat, meaning more was passed through the body without being absorbed.

Previous research has suggested that body weight and fat can also be influenced by transferring lean animals’ intestinal bacteria into obese mice, and vice versa. To test this effect in the current study, gut bacteria from the bypass mice were inserted into new animals through intestinal content transfers – i.e. fecal matter transplants. Sure enough, these ‘donations’ from the bypass mice resulted in significant reductions in body weight and fat levels in the receiving animals, but interestingly did not affect food intake.

As fascinating as these results are, some important questions remain. Firstly, is this a long-lasting effect? Could stool bacterial transfers from lean individuals be a long-term solution to obesity, or would these effects fade away as the transferred super-bacteria die off and are replaced by the host’s natural ones? To date, no studies have followed up these effects long-term, so this remains to be seen. Also, like much innovative scientific research, these results come with ethical questions to consider. Does having a different type of gut bacteria change our responsibility for our own weight and healthy diet? And should we all receive an injection of lean bacteria to prevent future obesity and related health problems?

So what do you think, would you do it?

The second piece of chocolate

Imagine you have a piece of chocolate. Unwrap it, place it on your tongue. Savor its decadence as it melts in your mouth; relish the bitter and sweet coating your taste buds; indulge in its creamy texture. As the chocolate dissolves, signals are sent throughout your body. Chemicals are released, reinforcing its rewarding properties and preparing your body for the rush of sugar it is about to receive. You swallow. Immediately you want another piece.

The pleasure of eating is one of our most natural joys, be it savoring a perfectly cooked steak or delighting in that melt-in-your-mouth chocolate. But with the rise of obesity and related maladies – particularly cardiovascular disease, hypertension and type-II diabetes – such simple pleasures have been perverted, pathologized by experts and classed as a source of harm. With nearly 25% of English adults qualifying as obese, and with ensuing costs to the NHS reaching £5.1 billion each year, the UK is facing a self-induced public health pandemic. But how has this happened? And why can’t we all just put down that second piece of chocolate?

Added sugars have become the focus of widespread concern among doctors and researchers, their effects on our waistlines, livers, and even our brains, giving cause for alarm. Obesity specialist Dr. Robert Lustig has emerged as a crusader for the anti-sugar movement, contending that sugar, not fat, is behind the dramatic rise in ‘western diet’ conditions over the past 30 years. The problem stems from the way our bodies metabolize fructose – half of the refined sugar molecule, sucrose – as opposed to pure glucose, which makes up the other half and is found in foods like potatoes and white bread.

Glucose is metabolized by all cells in the body, whereas fructose is primarily processed by the liver. If the liver cannot adequately break down sugar into energy it is converted into fat, and the faster the body receives fructose, the more likely this is to happen. High fructose sugar solutions, like fizzy soft drinks, are particularly prone to this fat conversion, providing high volumes of fructose that reach the liver much more quickly. This inability to break down sugar and the subsequent rise in liver fat is believed to be at the root of insulin resistance, the main deficiency underlying type-II diabetes.

But regardless of doctors’ warnings and the evidence that increased sugar consumption leads to obesity, as well as liver and heart disease, our sugar intake continues to rise. This may be due to the seemingly addictive qualities of high-sugar foods themselves. For despite our best intentions to cut out the cake, doing so rivals quitting smoking in terms of difficulty. New research indicates that foods high in fat or sugar may qualify as addictive substances, causing similar neurochemical changes in the brain as drugs of abuse.

Researchers at Princeton University have demonstrated this phenomenon by intermittently exposing rats to a sucrose solution in addition to their regular food. After a month, rats began to show binge, craving and withdrawal-like behaviors for sucrose, self-administering extremely large quantities when it was available. Adaptations similar to those seen in cocaine-addicted animals emerged in the rats’ brains, with surges of dopamine released during a binge – a process linked to feelings of reward and novelty, and a key facet of drug addiction. An increase in craving was also seen in the test animals, demonstrated by greater sucrose-seeking when deprived of the solution, even in the face of punishment. Additionally, rats experienced withdrawal-like symptoms when the sugar was removed, exhibiting tremors, head-shakes and signs of anxiety and aggression. Such behavior is typically seen in animals going through opiate withdrawal, and is caused by the release of endogenous opioids in the brain by high-sugar foods, reinforcing their hedonic characteristics and creating a withdrawal effect when removed.

Given sugar’s apparently addictive properties, one proposed response to the obesity epidemic is to regulate its availability in much the same way as tobacco and alcohol. Labeling foods high in sugar and fat as ‘addictive’ could potentially remove the stigma attached to being overweight, re-characterising it as a complex medical condition rather than simply one of personal weakness and poor self-control. Furthermore, tougher regulations on the advertising and availability of junk food might help to reduce the proliferation of cheap high-fat/high-sugar snacks that has made diet control increasingly difficult. However, taking responsibility for diet out of the hands of individuals also diminishes personal accountability and the imperative for each of us to make positive food choices. The fast food industry certainly isn’t helping us to lose weight, but it’s also not forcing the food down our throats. Should we be trusted to control what we put into our bodies, or do we need someone to stop us from taking that second piece of chocolate?

*So this post is a bit cheeky. I originally wrote this as a submission for a writing competition, but seeing as how it was never published, I figured it made an apt piece in honor of New Year’s resolutions!

(Thanks to Paul Sagar for help in editing the original piece.)

That Diet Coke isn’t so diet anymore

While everyone is working on their New Year’s resolutions for 2012, either making them or not breaking them, I thought it would be a good time to write about a trio of articles on sugar and artificial sweeteners and their respective health consequences.

A piece published in New York Times magazine several months ago raised the alarm on the extreme health detriments of our sugar habits. Author Gary Taubes cited Dr. Robert Lustig, a researcher in pediatric obesity and hormone deficiencies, as promoting the idea that sugar, not fat, is the main cause for the dramatic rise in type 2 diabetes, hypertension and other “western diet” diseases seen in the last 30 years. These particular detriments stem from the way our bodies metabolize fructose (which makes up half of the refined sugar molecule sucrose), as opposed to pure glucose, which makes up the other half and is found in foods such as potatoes and white bread.

Glucose is metabolized by all cells in the body, whereas fructose is primarily processed by the liver. If the liver cannot adequately break down the sugar (both fructose and glucose) it receives into energy, it is converted into fat. This is more likely to occur if the liver becomes overloaded by the fructose in sucrose solutions, such as in high fructose corn syrup which has a greater concentration of fructose to glucose. The more and faster the body receives the fructose the more likely this is to happen. Therefore, drinking a sugary beverage, such as soda or even fruit juice, results in an even greater spike in fructose as it reaches the liver much more quickly. These drinks place a greater strain on the body than a raw piece of fruit, a “pure” form of fructose, which contains fiber and is digested much more slowly. This failure to break down sugar and the subsequent rise in liver fat is believed to be at the root of insulin resistance, the main underlying deficiency in metabolic disorders such as type 2 diabetes and heart disease.

It is undeniable that as our sugar consumption increases, so do our rates of obesity, diabetes and heart disease. Currently the average American consumes roughly 90 pounds of added sugar a year, and recently non-sugar sweeteners have been proposed as an alternative to sugar and high-fructose corn syrup to help reduce these rates. However two studies from the University of Texas: San Antonio presented at the American Diabetes Association’s Scientific Sessions suggest that these changes might not provide any real benefit.

The first, a longitudinal health study, measured participants’ waist circumference over a ten-year period. They discovered that diet soda drinkers had an almost 70% increase in waist circumference over this time, and those who reported drinking more than two diet soft drinks every day had waist circumference increases 500% greater than individuals who did not consume any diet drinks. These results remained even after controlling for variables such as starting circumference, diabetes, age, sex, smoking status, physical activity levels, and neighborhood of residence.

The second study assessed the effect of aspartame on a high fat diet in mice. One group received food chow with added corn oil and aspartame, the other just the additional corn oil. The group that consumed the extra aspartame had significantly higher glucose levels, but similar insulin levels than the mice who only received the high fat diet. This signifies severe consequences of a fake sweetener diet on diabetes, as blood sugar levels were elevated but insulin (which lowers blood sugar) was not compensatorily raised. This suggests that diet sodas and other foods made with fake sugar could actually lead to an increased risk for developing type 2 diabetes compared to a high fat diet alone.

So if anyone is still looking for a resolution this New Year, perhaps try cutting back on your soda consumption, both regular and diet. Your liver will thank you.