ISLAMABAD - Insomnia can have a serious impact on a person’s health and well-being. Now, a study of females aged 50 and over has found that some parts of the diet most likely contribute to this sleep disorder. The findings of a new study suggest that refined carbohydrates contribute to insomnia among older females.

Insomnia affects many people all over the world. According to the National Sleep Foundation, up to 40 per cent of people in the United States experience some insomnia symptoms each year.

Researchers have taken due note of this, as numerous studies have suggested that insomnia is not just a mild annoyance: It may actually be linked with many other negative health outcomes.

According to the Centres for Disease Control and Prevention (CDC), short sleep duration and sleep disruptions are associated with Trusted Source cardiovascular problems, diabetes, and depression, to name a few.

For this reason, specialists have been looking for ways of preventing or treating insomnia and other sleep disorders — starting by looking for all the possible causes.

Existing research has already called attention to the fact that diet may influence a person’s sleep quality. Now, a study from Columbia University Vagelos College of Physicians and Surgeons in New York City, NY, suggests that a diet high in refined carbohydrates — particularly added sugars — is linked to a higher risk of insomnia. This, at least, appears to be the case among females aged 50 and over.

The research team reports these findings in a study paper that now appears in The American Journal of Clinical Nutrition.

“Insomnia is often treated with cognitive behavioural therapy or medications, but these can be expensive or carry side effects,” explains senior study author James Gangwisch, Ph.D.

But, he adds, “[b]y identifying other factors that lead to insomnia, we may find straightforward and low cost interventions with fewer potential side effects.”

The researchers worked with the data of 53,069 female participants aged 50-79, all of whom had enrolled in the Women’s Health Initiative Observational Study between September 1994 and December 1998.

To understand whether or not there really is a link between dietary choices and the risk of insomnia, the investigators looked for any associations between different diets and sleep disruptions.

Gangwisch and colleagues found a link between a higher risk of insomnia and a diet rich in refined carbohydrates. This includes foods with added sugars, soda, white rice, and white bread.

The researchers caution that it was unclear from their analysis whether the consumption of refined carbohydrates led to insomnia, or that people who experienced insomnia were more likely to consume refined carbs, especially sugary foods.

However, they do note that there is a possible underlying mechanism that might explain added sugars causing sleep disruptions.

“When blood sugar is raised quickly, your body reacts by releasing insulin, and the resulting drop in blood sugar can lead to the release of hormones such as adrenaline and cortisol, which can interfere with sleep,” Gangwisch explains.

The study authors also explain why not all foods that contain sugar will lead to the same effect. Fruits and vegetables — which naturally contain sugar — are unlikely to raise blood sugar levels nearly as quickly as foods containing added sugars.

This is because these natural foods are also high in fibre, which means that the body absorbs the sugar more slowly, preventing a spike in blood sugar levels.

Indeed, the female participants who had diets rich in vegetables and whole fruits — but not fruit juices — did not have an increased risk of insomnia.

“Whole fruits contain sugar, but the fibre in them slow the rate of absorption to help prevent spikes in blood sugar,” says Gangwisch.

“This suggests that the dietary culprit triggering the women’s insomnia was the highly processed foods that contain larger amounts of refined sugars that aren’t found naturally in food.”

The researchers only worked with females aged 50 and over, but they believe that the findings could also apply to males and people of other ages. Going forward, they argue that this idea is worth exploring in more detailed studies.

“Based on our findings, we would need randomized clinical trials to determine if a dietary intervention, focused on increasing the consumption of whole foods and complex carbohydrates, could be used to prevent and treat insomnia,” concludes Gangwisch.

Another new research in mice reveals the mechanisms through which two experimental drugs that may treat Alzheimer’s disease have broader, anti-aging properties and can reverse age-related cognitive decline.

Family history, genes, and some lifestyle choices all influence a person’s risk of Alzheimer’s disease, but age is the greatest risk factor that researchers are aware of.

Most people who receive a diagnosis of Alzheimer’s are at least 65 years old. In fact, after that age, the risk of developing the condition doubles every 5 years.

However, scientists do not yet fully understand, on a molecular level, how aging is involved in driving Alzheimer’s.

Previous research has shown that faulty glucose metabolism in the brain occurs before the onset of Alzheimer’s symptoms. Cerebral glucose metabolism declines with age anyway, but in Alzheimer’s, the decline is much more severe.

Furthermore, other studies have shown that dysfunctional mitochondria in the brain’s cells are a hallmark of both normal aging and Alzheimer’s.

Armed with this knowledge, researchers from the Salk Institute for Biological Studies and the Scripps Research Institute — both in La Jolla, CA — set out to test several drugs under conditions that “mimic numerous aspects of old age-associated neurodegeneration and brain pathology, including energy failure and mitochondrial dysfunction.”

Antonio Currais, a Salk staff scientist, is the first and corresponding author of the new paper, which now appears in the journal eLife.

Currais and team tested two experimental drugs — called CMS121 and J147 — that studies had already shown to be “very neuroprotective” in mouse models of Alzheimer’s, possibly even capable of reversing cognitive impairment.

Previous research first-authored by Currais suggested that the compounds boost memory and “prevent some aspects of aging” in mice engineered to age rapidly, especially when administered early in life.

Both compounds are derivatives of plants that have medicinal properties. CMS121 derives from the flavonol fisetin, and J147 is a derivative of a molecule present in the curry spice curcumin.

So, although previous tests had shown these two compounds to have neuroprotective benefits, the mechanisms behind these effects were less clear.

“[W]e hypothesized that [the compounds] may mitigate some aspects of aging brain metabolism and pathology via a common pathway,” write Currais and colleagues in their new paper.

The mechanisms that reverse aging

To test their hypothesis, the researchers fed rapidly aging mice the two compounds and used a multi-omics approach to identify the mechanisms at play.

They fed the rodents the two compounds when they were 9 months old, which is roughly the human equivalent of late middle-age.

Around 4 months into the treatment, the scientists tested the rodents’ memory and behaviour and examined the genetic and molecular changes in their brains.

The experiments revealed that the mice that received the treatment had a much better memory than those that did not. Importantly, in the treated mice, the genes associated with functional, energy-creating mitochondria continued to be expressed throughout the aging process as a result of the two drugs.

On a more detailed level, the experiments showed that the way in which these drugs worked was by raising levels of a chemical called acetyl-coenzyme A.

This improved mitochondrial function, cell metabolism, and energy production, thereby protecting brain cells from the molecular changes that characterize aging.

Co-corresponding study author Pamela Maher, a senior staff scientist at Salk, comments on the findings, saying: “There [were] already some data from human studies that the function of mitochondria is negatively impacted in aging and that it’s worse in the context of Alzheimer’s [...]. This helps solidify that link.”

“The bottom line was that these two compounds prevent molecular changes that are associated with aging.”

Currais also shares some of the team’s plans for future research, saying, “We are now using a variety of animal models to investigate how this neuroprotective pathway regulates specific molecular aspects of mitochondrial biology, and their effects on aging and Alzheimer’s.”