Medical News Today: New research may explain why evolution made humans ‘fat’

Scientists have compared fat samples from humans and other primates and found that changes in DNA packaging affected how the human body processes fat.
close up of hand drawing evolution of humans from primates
Evolution made humans the ‘fat primate,’ researchers suggest.

Our bodies need fat to store energy and protect vital organs.

Fat also helps the body absorb some nutrients and produce important hormones.

Dietary fats include saturated fats, trans fats, monounsaturated fats, and polyunsaturated fats, all of which have different properties.

People should try to avoid or only consume saturated and trans fats in moderation because they raise low-density lipoprotein (LDL), or “bad,” cholesterol levels. Monounsaturated and polyunsaturated fats, however, can lower LDL cholesterol levels.

Triglycerides are the most common type of fat in the body. They store excess energy from the food we eat. During digestion, our bodies break these down and transfer them to the cells via the bloodstream. Our bodies use some of this fat as energy and store the rest inside the cells.

Fat metabolism is key to human survival, and any imbalances in the process can lead to obesity, diabetes, and cardiovascular disease.

Cardiovascular disease is the number one cause of death worldwide. The World Health Organization (WHO) estimate that almost 18 million people died from the condition in 2016.

How humans became the ‘fat’ primate

Modern eating habits and a lack of exercise have contributed to the obesity “epidemic,” but new research highlights the role that evolution played in the increasing formation of human body fat.

The scientists found that changes to how DNA is packaged inside fat cells reduced the human body’s ability to turn “bad” fat into “good” fat. The results of the research now appear in the journal Genome Biology and Evolution.

“We’re the fat primates,” says study co-author Devi Swain-Lenz, a postdoctoral associate in biology at Duke University in Durham, NC.

The researchers — who Swain-Lenz and Duke biologist Greg Wray led — compared fat samples from humans, chimps, and other primates using a technique called ATAC-seq. This analyzes how fat cell DNA is packaged in the bodies of different species.

The findings revealed that humans have anywhere from 14% to 31% body fat, while other primates have less than 9%. Also, DNA regions in humans are more condensed, thereby limiting accessibility to the genes involved in fat metabolism.

The researchers also found that around 780 DNA regions were more accessible in chimps and macaques compared with humans. This means that the human body has a reduced capacity to transform bad fat into good fat.

Not all fat is the same

Swain-Lenz explains that most fat is made up of “calorie-storing white fat.” This is the type of fat that accumulates on our bellies and around our waistlines. Other fat cells, called beige and brown fat, help burn calories.

The results of this new study revealed that one of the reasons humans carry more fat is because the DNA regions that should help convert white fat into brown fat are compressed and do not allow this transformation to take place.

“It’s still possible to activate the body’s limited brown fat by doing things like exposing people to cold temperatures, but we need to work for it,” Swain-Lenz adds.

The team believes that early humans may have needed to accumulate fat not just to protect vital organs and warm up, but also to nurture their growing brains. In fact, the human brain tripled in size during evolution, and it now uses more energy than any other organ.

Scientists have been working to understand if promoting the body’s ability to convert white fat to brown fat could reduce obesity, but more research is necessary.

“Maybe we could figure out a group of genes that we need to turn on or off, but we’re still very far from that,” Swain-Lenz concludes.

Medical News Today: Could this chemical help explain anxiety?

A recent study on anxiety examined the role of glutamate, which is a neurotransmitter. The findings could help scientists develop more effective interventions.
Anxious young woman
A new study digs into the neuroscience of anxiety.

Almost everybody experiences anxiety in one of its forms.

Over time, evolution honed anxiety as a survival mechanism; it forms part of our “fight-or-flight” response.

The heart pumps a little faster, and there might be a sensation of nausea as the body prepares for action.

Although anxiety is a natural response, it can spiral out of control for some people.

Rather than being a protective force that helps us navigate everyday life, it becomes a burden that impacts well-being. Also, being more prone to anxiety increases the risk of developing an anxiety disorder and depression.

Beyond mental health, anxiety might also have physical effects; the authors of the new study write that sustained high levels of anxiety “may increase the risk of developing cardiovascular disease.”

The Anxiety and Depression Association of America say that anxiety disorders impact almost 1 in 5 adults in the United States each year.

Anxiety disorders are as common as depression, but until relatively recently, they received much less attention.

Because of its growing prevalence, the neurological mechanisms that are involved are receiving increased attention. The latest study, which now appears in The Journal of Neuroscience, investigates the role of glutamate in the hippocampus.

What is glutamate?

Glutamate is an amino acid and the primary excitatory neurotransmitter in the brain. In recent years, studies have hinted that glutamate might be involved in anxiety.

Reductions in glutamate activity seem to increase anxious behavior, and glutamate levels within the hippocampus — which is the part of the brain primarily involved in regulating emotions and memory — seem particularly important.

Earlier studies have also concluded that two other regions of the brain work with the hippocampus to modulate anxiety; called area 25 and area 32, these regions form part of the prefrontal cortex.

However, our understanding of glutamate’s role in anxiety is not fully formed — other studies have produced conflicting results.

As an example, a study using nonanxious rats found that a reduction of activity at some glutamate receptor subtypes in the hippocampus actually reduced levels of anxiety.

The authors of the latest study wanted to examine the role of glutamate in anxiety in more detail. To get a clearer picture, they ran a series of experiments on marmosets.

Glutamate and anxiety in primates

First, the team tested each marmoset’s anxiety levels when introduced to an unfamiliar human (one of their handlers wearing a mask). As expected, the animals with the greatest levels of anxiety — or high-trait anxiety — had significantly lower levels of glutamate in their hippocampus.

High-trait anxiety correlated with glutamate levels in the right anterior hippocampus.

Next, they artificially increased the level of glutamate in the highly anxious marmosets. They found that once glutamate levels reached normal levels, the animals responded less anxiously in psychological tests.

This second arm of the experimentation gave the researchers evidence of a causal relationship: Anxious primates naturally had lower levels of glutamate activity, and when glutamate was increased in the anxious primates’ hippocampi, anxiety was reduced.

To gain more information about the role of brain areas 25 and 32, the team carried out further experiments.

Blocking activity in these regions, they found that the anti-anxiety effects of increasing glutamate were abolished when area 25 was out of action. Blocking area 32, however, did not make a difference.

The study authors suggest that the hippocampal-area 25 pathway could be an interesting target for future pharmaceutical interventions. Overall, the authors outline their conclusions:

These findings provide casual evidence in primates that hippocampal glutamatergic hypofunction regulates endogenous high-trait anxiety, and the hippocampal-area 25 circuit is a potential therapeutic target.”

Though scientists are still unpicking glutamate’s role in anxiety, studies such as this bring us closer to having a full understanding.