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Scientists Say They've Identified a Gene Linked to Anorexia

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People with anorexia nervosa have a distorted body image and severely restrict their food to the point of emaciation and sometimes death. It's long been treated as a psychological disorder, but that approach has had limited results; the condition has one of the highest mortality rates among psychiatric conditions. But recently, neuroscience researchers at the UC San Diego School of Medicine who study the genetic underpinnings of psychiatric disorders have identified a possible gene that appears to contribute to the onset of the disease, giving scientists a new tool in the effort to understand the molecular and cellular mechanisms of the illness.

The study, published in Translational Psychiatry, was led by UC San Diego's Alysson Muotri, a professor at the School of Medicine’s departments of pediatrics and cellular and molecular medicine and associate co-director of the UCSD Stem Cell Program. His team took skin cells known as fibroblasts from seven young women with anorexia nervosa who were receiving treatment at UCSD’s outpatient Eating Disorders Treatment and Research Center, as well as from four healthy young women (the study's controls). Then the team initiated the cells to become induced pluripotent stem cells (iPSCs). 

The technique, which won researcher Shinya Yamanaka the Nobel Prize in 2012, takes any nonreproductive cell in the body and reprograms it by activating genes on those cells. “You can push the cells back into the development stage by capturing the entire genome in a pluripotent stem cell state, similar to embryonic stem cells,” Muotri tells mental_floss. Like natural stem cells, iPSCs have the unique ability to develop into many different types of cells.

Once the fibroblasts were induced into stem cells, the team differentiated the stem cells to become neurons. This is the most effective way to study the genetics of any disorder without doing an invasive brain biopsy, according to Muotri. Also, studying animal brains for this kind of disorder wouldn’t have been as effective. “At the genetic level as well as the neural network, our brains are very different from any other animal. We don’t see chimpanzees, for example, with anorexia nervosa. These are human-specific disorders,” he says.

Once the iPSCs had become neurons, they began to form neural networks and communicate with one another in the dish similar to the way neurons work inside the brain. “Basically what we have is an avatar of the patient’s brain in the lab,” Muotri says.

His team then used genetic analysis processes known as whole transcriptome pathway analysis to identify which genes were activated, and which might be associated with the anorexia nervosa disorder specifically.

They found unusual activity in the neurons from the patients with anorexia nervosa, helping them identify a gene known as TACR1, which uses a neurotransmitter pathway called the tachykinin pathway. The pathway has been associated with other psychiatric conditions such as anxiety disorders, but more pertinent to their study, says Mutori, is that “tachykinin works on the communication between the brain and the gut, so it seems relevant for an eating disorder—but nobody has really explored that.” Prior research on the tachykinin system has shown that it is responsible for “the sensation of fat. So if there are misregulations in the fat system, it will inform your brain that your body has a lot of fat.”

Indeed, they found that the AN-derived neurons had a greater number of tachykinin receptors on them than the healthy control neurons. “This means they can receive more information from this neurotransmitter system than a normal neuron would,” Muotri explains. “We think this is at least partially one of the mechanisms that explains why [those with anorexia] have the wrong sensation that they have enough fat.”

In addition, among the misregulated genes, connective tissue growth factor (CTGF), which is crucial for normal ovarian follicle development and ovulation, was decreased in the AN samples. They speculate that this result may explain why many female anorexia patients stop menstruating.

Muotri next wants to understand what he calls “the downstream effect” of those neurons with too many TACR1 receptors. In other words, how does it affect the neurons at a molecular level, and what information do those neurons receive from the gut? “This link between the brain and the gut is unclear, so we want to follow up on that,” he says.

He also wants to look into the potential to design a drug that could compensate for the large amount of TACR1 receptors, and the over-regulation of that receptor in the brain—which would be a huge development for the notoriously difficult-to-treat disease.

While Muotri is excited about new avenues of research that can follow from this work, he doesn't see it as a panacea for the disease, but a way to begin to understand it more fully. He says, “It’s a good start, but arguably you have to understand what are the other environmental factors that contribute.”

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Medicine
Why Haven't We Cured Cancer Yet?
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Walkathons, fundraisers, and ribbon-shaped bumper stickers raise research dollars and boost spirits, but cancer—the dreaded disease that affects more than 14 million people and their families at any given time—still remains bereft of a cure.

Why? For starters, cancer isn't just one disease—it's more than 100 of them, with different causes. This makes it impossible to treat each one using a one-size-fits-all method. Secondly, scientists use lab-grown cell lines cultivated from human tumors to develop cancer therapies. Living masses are far more complex, so potential treatments that show promise in lab experiments often don't work on cancer patients. As for the tumors themselves, they're prone to tiny genetic mutations, so just one growth might contain multiple types of cancer cells, and even unique sub-clones of tumors. These distinct entities might not respond the same way, or at all, to the same drug.

These are just a few of the challenges that cancer researchers face—but the good news is that they're working to beat all of them, as this TED-Ed video explains below.

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Health
Skipping Breakfast Could Be Bad for Your Heart
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There are mountains of evidence supporting the claim that breakfast really is the most important meal of the day. Getting something in your stomach in the first hours of the morning can regulate your glucose levels, improve your cognition, and keep your hunger in check. Now new research published in the Journal of the American College of Cardiology points to another reason not to wait until lunchtime to break last night’s fast. As TIME reports, people who skip breakfast are at an increased risk for atherosclerosis, a disease caused by plaque buildup in the arteries.

Researchers surveyed over 4000 men and women between the ages of 40 and 54 living in Spain. After looking at the dietary habits of each participant, they broke them into three groups: people who consumed more than 20 percent of their daily calories in the morning; those who got 5 to 20 percent; and those who ate less than 5 percent.

The subjects who ate very little in the a.m. hours or skipped breakfast all together were 2.5 more likely to have generalized atherosclerosis. This meant that plaque was starting to collect on the walls of their arteries, hardening and narrowing them and increasing the risk for heart attack or stroke. People who fell into the 5 to 20 percent calorie category were also more likely to show early signs of the disease, while those who ate the most calories in the morning were the healthiest.

These results aren’t entirely surprising. Previous studies have shown a connection between skipping breakfast and health problems like high blood pressure, high cholesterol, diabetes, and unwanted weight gain. A possible explanation for this trend could be that waiting several hours after waking up to eat your first meal of the day could trigger hormonal imbalances. The time between getting into and out of bed is the longest most of us go without eating, and our bodies expect us to consume some calories to help kickstart our energy for the day (drinking straight coffee doesn’t cut it). Another theory is that people who don’t eat in the morning are so hungry by the time lunch rolls around that they overcompensate for those missing calories, which is why skipping breakfast doesn’t make sense as a diet strategy.

But of course there are many breakfast skippers who aren’t motivated by health reasons either way: They just don’t think they have the time or energy to feed themselves in the morning before walking out the door. If this describes you, here are some simple, protein-packed meals you can prepare the night before.

[h/t TIME]

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