America's most widely consumed oil causes genetic changes in the brain
Soybean oil linked to metabolic and neurological changes in mice
January 17, 2020
Science Daily/University of California - Riverside
New UC Riverside research shows soybean oil not only leads to obesity and diabetes, but could also affect neurological conditions like autism, Alzheimer's disease, anxiety, and depression.
Used for fast food frying, added to packaged foods, and fed to livestock, soybean oil is by far the most widely produced and consumed edible oil in the U.S., according to the U.S. Department of Agriculture. In all likelihood, it is not healthy for humans.
It certainly is not good for mice. The new study, published this month in the journal Endocrinology, compared mice fed three different diets high in fat: soybean oil, soybean oil modified to be low in linoleic acid, and coconut oil.
The same UCR research team found in 2015 that soybean oil induces obesity, diabetes, insulin resistance, and fatty liver in mice. Then in a 2017 study, the same group learned that if soybean oil is engineered to be low in linoleic acid, it induces less obesity and insulin resistance.
However, in the study released this month, researchers did not find any difference between the modified and unmodified soybean oil's effects on the brain. Specifically, the scientists found pronounced effects of the oil on the hypothalamus, where a number of critical processes take place.
"The hypothalamus regulates body weight via your metabolism, maintains body temperature, is critical for reproduction and physical growth as well as your response to stress," said Margarita Curras-Collazo, a UCR associate professor of neuroscience and lead author on the study.
The team determined a number of genes in mice fed soybean oil were not functioning correctly. One such gene produces the "love" hormone, oxytocin. In soybean oil-fed mice, levels of oxytocin in the hypothalamus went down.
The research team discovered roughly 100 other genes also affected by the soybean oil diet. They believe this discovery could have ramifications not just for energy metabolism, but also for proper brain function and diseases such as autism or Parkinson's disease. However, it is important to note there is no proof the oil causes these diseases.
Additionally, the team notes the findings only apply to soybean oil -- not to other soy products or to other vegetable oils.
"Do not throw out your tofu, soymilk, edamame, or soy sauce," said Frances Sladek, a UCR toxicologist and professor of cell biology. "Many soy products only contain small amounts of the oil, and large amounts of healthful compounds such as essential fatty acids and proteins."
A caveat for readers concerned about their most recent meal is that this study was conducted on mice, and mouse studies do not always translate to the same results in humans.
Also, this study utilized male mice. Because oxytocin is so important for maternal health and promotes mother-child bonding, similar studies need to be performed using female mice.
One additional note on this study -- the research team has not yet isolated which chemicals in the oil are responsible for the changes they found in the hypothalamus. But they have ruled out two candidates. It is not linoleic acid, since the modified oil also produced genetic disruptions; nor is it stigmasterol, a cholesterol-like chemical found naturally in soybean oil.
Identifying the compounds responsible for the negative effects is an important area for the team's future research.
"This could help design healthier dietary oils in the future," said Poonamjot Deol, an assistant project scientist in Sladek's laboratory and first author on the study.
"The dogma is that saturated fat is bad and unsaturated fat is good. Soybean oil is a polyunsaturated fat, but the idea that it's good for you is just not proven," Sladek said.
Indeed, coconut oil, which contains saturated fats, produced very few changes in the hypothalamic genes.
"If there's one message I want people to take away, it's this: reduce consumption of soybean oil," Deol said about the most recent study.
https://www.sciencedaily.com/releases/2020/01/200117080827.htm
Researchers discover brain circuit linked to food impulsivity
This creates the possibility scientists can someday develop therapeutics to address overeating
December 11, 2019
Science Daily/University of Georgia
A team of researchers has now identified a specific circuit in the brain that alters food impulsivity.
You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.
Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.
Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.
A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.
The team's findings were published recently in the journal Nature Communications.
"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."
Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).
While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.
"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.
To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.
Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.
Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food. "Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."
https://www.sciencedaily.com/releases/2019/12/191211145630.htm
Brain activity intensity drives need for sleep
September 16, 2019
Science Daily/University College London
The intensity of brain activity during the day, notwithstanding how long we've been awake, appears to increase our need for sleep, according to a new UCL study in zebrafish.
The research, published in Neuron, found a gene that responds to brain activity in order to coordinate the need for sleep. It helps shed new light on how sleep is regulated in the brain.
"There are two systems regulating sleep: the circadian and homeostatic systems. We understand the circadian system pretty well -- our built-in 24-hour clock that times our biological rhythms, including sleep cycles, and we know where in the brain this rhythm is generated," explained lead author Dr Jason Rihel (UCL Cell & Developmental Biology).
"But the homeostatic system, which causes us to feel increasingly tired after a very long day or sleepless night, is not well understood. What we've found is that it appears to be driven not just by how long you've been awake for, but how intensive your brain activity has been since you last slept."
To understand what processes in the brain drive homeostatic sleep regulation -- independent of time of day -- the research team studied zebrafish larvae.
Zebrafish are commonly used in biomedical research, partly due to their near-transparent bodies that facilitate imaging, in addition to similarities to humans such as sleeping every night.
The researchers facilitated an increase in brain activity of the zebrafish using various stimulants including caffeine.
Those zebrafish which had drug-induced increased brain activity slept for longer after the drugs had worn off, confirming that the increase in brain activity contributed to a greater need for sleep.
The researchers found that one specific area of the zebrafish brain was central to the effect on sleep pressure: a brain area that is comparable to a human brain area found in the hypothalamus, known to be active during sleep. In the zebrafish brain area, one specific brain signalling molecule called galanin was particularly active during recovery sleep, but did not play as big a role in regular overnight sleep.
To confirm that the drug-induced findings were relevant to actual sleep deprivation, the researchers conducted a test where they kept the young zebrafish awake all night on a 'treadmill' where the fish were shown moving stripes -- by imitating fast-flowing water, this gives the fish the impression that they need to keep swimming. The zebrafish that were kept awake slept more the next day, and their brains showed an increase in galanin activity during recovery sleep.
The findings suggest that galanin neurons may be tracking total brain activity, but further research is needed to clarify how they detect what's going on across the whole brain.
The researchers say their finding that excess brain activity can increase the need for sleep might explain why people often feel exhausted after a seizure.
"Our findings may also shed light on how some animals can avoid sleep under certain conditions such as starvation or mating season -- it may be that their brains are able to minimise brain activity to limit the need for sleep," said the study's first author, Dr Sabine Reichert (UCL Cell & Developmental Biology).
The researchers say that by discovering a gene that plays a central role in homeostatic sleep regulation, their findings may help to understand sleep disorders and conditions that impair sleep, such as Alzheimer's disease.
"We may have identified a good drug target for sleep disorders, as it may be possible to develop therapies that act on galanin," added Dr Reichert.
https://www.sciencedaily.com/releases/2019/09/190916110556.htm
Brain circuit connects feeding and mood in response to stress
September 4, 2019
Science Daily/Baylor College of Medicine
An international team has looked into the possibility of crosstalk between eating and mood and discovered a brain circuit in mouse models that connects the feeding and the mood centers of the brain.
Many people have experienced stressful situations that trigger a particular mood and also change certain feelings toward food. An international team led by researchers at Baylor College of Medicine looked into the possibility of crosstalk between eating and mood and discovered a brain circuit in mouse models that connects the feeding and the mood centers of the brain. Published in the journal Molecular Psychiatry, these findings may help explain some of the observations between changes in mood and metabolism and provide insights into future solutions to these problems by targeting this circuit.
"This study was initiated by first author Dr. Na Qu, a psychiatrist of Wuhan Mental Health Center, China, when she was visiting my lab," said corresponding author Dr. Yong Xu, associate professor of pediatrics and of molecular and cellular biology at Baylor College of Medicine.
Qu, a practicing psychiatrist who also conducts basic brain research, was interested in investigating whether there was a neurological basis for the association between depression and other psychiatric disorders and alterations in metabolism, such as obesity or lack of appetite, she had observed in a number of her patients.
Xu, Qu and their colleagues worked with a mouse model of depression induced by chronic stress and observed that depressed animals ate less and lost weight. Then, they applied a number of experimental techniques to identify the neuronal circuits that changed activity when the animals were depressed.
"We found that POMC neurons in the hypothalamus, which are essential for regulating body weight and feeding behavior, extend physical connections into another region of the brain that has numerous dopamine neurons that are implicated in the regulation of mood," said Xu, who also is a researcher at the USDA/ARS Children's Nutrition Research Center at Baylor and Texas Children's Hospital. "We know that a decrease in dopamine may trigger depression."
In addition to the physical connection between the feeding and the mood centers of the brain, the researchers also discovered that when they triggered depression in mice, the POMC neurons were activated and this led to inhibition of the dopamine neurons. Interestingly, when the researchers inhibited the neuronal circuit connecting the feeding and the mood centers, the animals ate more, gained weight and looked less depressed.
"We have discovered that a form of chronic stress triggered a neuronal circuit that starts in a population of cells that are known to regulate metabolism and feeding behavior and ends in a group of neurons that are famous for their regulation of mood," Xu said. "Stress-triggered activation of the feeding center led to inhibition of dopamine-producing neurons in the mood center."
Although more research is needed, Xu, Qu and their colleagues propose that their findings provide a new biological basis that may explain some of the connections between mood alterations and changes in metabolism observed in people, and may provide solutions in the future.
"Our findings only explain one scenario, when depression is associated with poor appetite. But in other cases depression has been linked to overeating. We are interested in investigating this second association between mood and eating behavior to identify the neuronal circuits that may explain that response," Xu said.
https://www.sciencedaily.com/releases/2019/09/190904213722.htm