Calling fast food "high fat" is true, but misleading. Image courtesy of avlxyz.

New research from UC Davis sheds light on how triglycerides induce atherosclerosis—the hardening of artery walls that causes heart disease—particularly in individuals with abdominal obesity. Unfortunately, however, the researchers credit the fat in the fast food meal they used to induce the triglyceride spike, while letting the more likely culprit, orange juice, completely off the hook.

In the study, researchers fed a fast food meal (two breakfast sandwiches, hash browns and orange juice, as noted in the press release) to people with either normal or elevated blood triglycerides. Triglycerides correlate strongly with risk of heart disease and are a better predictor of cardiovascular risk than total or LDL cholesterol.

After eating the horrible meal, triglycerides rose and LDL cholesterol was transported into cells in the artery wall, a process that leads to artery hardening and heart disease. This effect was worsened in the presence of cytokines, which are known to cause inflammation and correlate with a larger waist size.

The implication is that poor diet choices become more dangerous as a person's metabolic health declines, making good nutrition an even greater priority for people with abdominal obesity.

“The new study shows that eating a common fast food meal can affect inflammatory responses in the blood vessels," said the lead researcher, Anthony Passerini, and the effect seems to be worse in those with chronic inflammation and larger waists.

But why do they extrapolate and claim that this problem is caused by dietary fat?

The authors describe the fast food meal as “high-fat”, but neglect that it is also high in processed carbohydrates (two buns and hash browns) and fructose, the fruit sugar present in orange juice. Fructose is converted to triglycerides in the liver and is the most effective way to increase triglyceride levels.

Not only is fructose from the orange juice the most likely cause of the triglyceride effect, but it is particularly unlikely the fat had an impact. High-fat, low-carbohydrate diets have been used to treat high triglycerides since the 1960s, even at levels as high as 65% of calories from fat. In the current study the fat in the fast food meal represented only 47% of calories.

Though the fast food meal used by the researchers undoubtedly matches the “typical western diet,” it is unlikely that the fat content is responsible for elevating triglycerides and the risk of heart disease that comes with them.

A better message for people worried about triglycerides: watch your sugar.

38.5397702 -121.7554965

Shifting focus toward healthy habits and away from body size may be a more effective strategy for long-term health, but fat loss may still be a worthwhile target. Image courtesy of Kyle May.

The number one public health message today, as seen in the recent announcement of the new USDA Dietary Guidelines, is that we all need to lose weight. But a new review published in Nutrition Journal suggests that this message may be doing more harm than good.

Co-authors Linda Bacon, an associate nutritionist in the UC Davis Department of Nutrition, and Lucy Aphramor, an NHS specialist dietician and honorary research fellow at the Applied Research Center in Health and Lifestyle Interventions at Coventry University in England, argue that most of the assumptions made about the link between body fat and health are not substantiated, and that a more effective approach would be to emphasize healthy habits focused less on body weight.

“The weight-focused approach does not, in the long run, produce thinner, healthier bodies,” Bacon said in a press release. She suggests that while overweight and obesity are often linked to poor health outcomes, these ties are not as strong as most people assume and that the evidence suggests underlying bad habits cause both disease and weight gain. If this is the case, body fat itself may not be a cause but a symptom of poor health, and therefore targeting weight loss specifically may not be beneficial.

The authors note that evidence indicates that long-term weight loss is very difficult and often impossible to achieve for most people. They also point out that removing body fat without a change in lifestyle, as in cases of liposuction, create no measurable health benefits. Moreover, a focus on body weight instead of health changes can often lead to both physical and psychological problems.

“It's the unintended negative consequences that are particularly troubling, including guilt, anxiety, preoccupation with food and body shape, repeated cycles of weight loss and gain, reduced self esteem, eating disorders and weight discrimination,” says Aphramor.

The authors suggest that focusing on health instead of body weight does occasionally lead to a drop on the scale, but that health benefits are measurable even if no weight loss is achieved. They cite improvements in blood pressure, lipid profiles, self-esteem, body images and other markers of well-being. However there was no mention of diseases that are not tied to metabolism and cardiovascular health. Breast cancer, for example, is known to correlate with body size and is thought to be caused by the extra estrogen produced in fat cells.

It makes intuitive sense that shifting focus toward healthy habits and away from body size would be a more effective strategy for long-term health, but fat loss (rather than weight loss) may still be a worthwhile target.

38.552848 -121.734745

You read that right. In a new study out in Nature Neuroscience, scientists tinkered with a single gene in a mouse and made it less likely to get fat. Finally I can eat as many Double Stufs as I want without worrying about gaining weight. If scientists can turn what they've learned into a pill, that is.

How'd the researchers do it? By changing one part of the mouse's brain, the hypothalamus. One of the hypothalamus' many jobs is body weight regulation. So it was a logical place to start.

The scientists couldn't go in with a wrecking ball and tear the hypothalamus apart. It is an important part of the brain with lots of different duties. They needed to something pretty subtle so the mice would survive but be thinner.

What they did was to keep certain cells in the hypothalamus from being able to release a neurotransmitter called GABA. This was enough to make a mouse better able to maintain a lower weight.

This study suggests that GABA's normal job in the hypothalamus is to keep mice (and probably us) from burning too much energy. Makes sense in the wild. But is quite a pain in my cubicle.

Now, we can't go changing human genes (at least not yet). But perhaps scientists can come up with a pill that will do the same thing. A pill that keeps AgRP neurons from releasing GABA in the hypothalamus.

This is as hard as it sounds. But now that scientists know what to do, pharmaceutical companies will be able to apply all of their firepower to solving this problem. Given the potential market, if anyone can find a medicine for restricting weight gain using this finding, they will.

Before I get too excited, though, I want to see what happens to these mice as they age. Burning calories makes free radicals which damages DNA which causes aging and can cause cancer. Perhaps burning more calories this way might generate more free radicals.

Of course even if it does, maybe we could just take the pills with cranberries or some other anti-oxidant. Or maybe Nabisco can make an Oreo laced with antioxidants…

37.332 -121.903

Given today's environment, it is surprising that there are still thin people around.

The origins of this epidemic are pretty easy to spot– lots of food and less opportunity for exercise. And yet, not everyone in the U.S. is overweight. So why is one person fat and the next thin?

One big reason is genetics. A number of twin, family and adoption studies have found that somewhere between 45-60% of body mass index (BMI) comes from the genes we inherit. In other words, some people are more likely to be sucked into a Super-Sized meal because of their genes.

So how might genes affect someone’s chances of succumbing to the mountain of food now available? Lots of ways.

Some people burn energy more slowly than other people. These folks need to eat less to maintain their weight. Not an easy thing to do!

Some people take longer to realize they are full. Others get hungrier more quickly after eating. Still others need more sweets and fat to get enjoyment from their food.

The last example was <a href="http://psycnet.apa.org/index.cfm?fa=main.showContent&id=2007-13974-007&view=fulltext&format=html
">addressed by a study last year. One of the reasons people eat is that they get a hit of dopamine when they do. The dopamine makes us feel good and once we get it, we feel less inclined to keep eating.

The study found that people with a certain version of the DRD2 gene needed more food to get enough dopamine to stop eating. So they ate more on average.

There are more and more studies finding gene variations just like this one. Finding these gene variations might be useful in creating new medicines to help people eat less by decreasing hunger, burning calories faster, etc.

Knowing about these gene variations might also help doctors identify who is at a greater risk for obesity. These folks can get early help in maintaining their optimal body weight.

Now none of this is an excuse for getting fat (although I wish it was). For the most part, genes that affect our BMI make maintaining a healthy weight harder, not impossible.

But what it also means is that the thin should be a bit nicer to the overweight. Recognize that it might be easier for the thin person to not overeat.

This is not to take away from the thin person's accomplishment. In a world awash in high calorie foods and with work and play involving a lot of sitting, it takes will power not to become overweight. Just remember that it is easier for some people to be thin.

http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm

37.332 -121.903