Blood biomarker identified for episodic migraines

A biomarker in the blood has been identified that indicates episodic migraines.- JR

A team of researchers at the Johns Hopkins University School of Medicine in Baltimore claims to have identified a biomarker present in the blood for episodic migraine. According to the researchers, the study findings could potentially have significant implications in diagnosis and treatment of episodic migraine.

A person suffers from episodic migraine when he or she experiences less than 15 headaches in a month. The author of the study, published in the journal Neurology, B. Lee Peterlin, says that “while more research is required to confirm the initial findings, the possibility of discovering a new biomarker for migraine is exciting.”

During the study, the researchers analyzed the neurological exam, blood samples and body mass index of a group of 52 women with episodic migraine and 36 women with no history of migraine headaches. The first group of the women had an average of 5.6 headache days in a month.

In the blood samples, the researchers looked for a group of lipids called ceramides, which plays a role in homeostasis and also helps regulate brain inflammation. The researchers found that in women with episodic migraine, the level of ceramides decreased.

Women suffering from migraine had 6,000 nanograms per milliliter of ceramides in their blood as compared to the women with no headache, who had 10,500 nanograms per milliliter of ceramide. Therefore, the researchers associated the standard deviation increase in levels of ceramide with a 92 percent less risk of developing migraine.

In another small random study, the researchers studied the levels of ceramide in a group of 14 subjects. Based on the levels of the ceramide, the team was able to correctly identify whether the participant had episodic migraine or not.

"This study is a very important contribution to our understanding of the underpinnings of migraine and may have wide-ranging effects in diagnosing and treating migraine if the results are replicated in further studies," said Karl Ekbom of the Karolinska Institutet in Stockholm, Sweden.

Ekbom further said that some of the shortfalls of the study include non-inclusion of males and exclusion of chronic migraine.

Read more here

Children with autism have higher cortisol levels

According to a recent study, children with autism were found to have elevated cortisol levels.

Researchers at the Institute for Autism Research at Canisius College have found that functional level appears to play a critical role in the stress levels of children with autism spectrum disorder (ASD). Specifically, lower-functioning children with ASD (LFASD) exhibited significantly higher levels of cortisol, the primary stress hormone in humans, than both high-functioning children with ASD (HFASD) and typical children.

Prior research has suggested that individuals with ASD experience elevated stress and related problems such as anxiety, however, many of the studies relied on informant rating scales and behavioral observations which have significant limitations for children with ASD. Attempts to more directly measure stress in this population using physiological measures such as cortisol have yielded mixed results. According to Susan K. Putnam PhD, chair and professor of psychology, the study's lead author, some of the inconsistent results may have been due to the prior studies not taking into account the significant differences in functional levels of individuals with ASD. "The inclusion of functionally-different individuals with ASD in studies has led to a need for studies of more precisely-defined subgroups with ASD, including subgroups based on functional level," said Putnam. This was the first study to assess cortisol (stress) levels in groups that were clearly differentiated based on functional level, specifically cognitive level.

Given the limitations in existing studies, the research team attempted to examine stress levels in ASD by examining the pattern of salivary cortisol across the day (morning, midday, and evening) and potential differences between lower-functioning children with ASD (LFASD IQ below 70), high-functioning children with ASD (HFASD IQ 85 or higher), and typical children. "It was important to determine whether the ASD groups exhibited the typical diurnal pattern of high cortisol in the morning, followed by a decrease at midday, and a further decline in the evening to determine if this typical pattern was present, and then examine the effect of functional level on stress level," said IAR co-director, Marcus Thomeer PhD, one of the study authors. Saliva samples were collected three times per day over four days on weekends from 13 children with LFASD, 16 children with HFASD, and 14 typical children. Results indicated that all three groups showed the typical pattern in which cortisol levels were highest at waking, followed by midday, and were lowest at bedtime. These findings are consistent with several prior studies of individuals with ASD.

The most significant finding, however, was that cortisol levels differed between the groups across the day. "Children with LFASD had significantly higher cortisol, the stress indicator, across the day than both the HFASD and typical children and, interestingly, children with HFASD did not significantly differ from the typical children across the day," said Putnam.

These findings have significant implications as they suggest that differences in cortisol levels and stress may be linked to the functional level, specifically IQ, of children with ASD. According to Putnam, this is an area in need of further study as it is unknown whether the elevated cortisol in the children with LFASD (compared to HFASD) is indicative of more significant neurological impairment and/or greater sensitivity to environmental stressors (associated with ASD symptoms), or whether a bi-directional relationship exists. IAR co-director Christopher Lopata PsyD, one of the study authors, noted that "identifying stress-level differences between functionally-differentiated groups with ASD has critical implications for how we assess and treat stress and stress-related reactions and conditions in children with ASD."

Findings from the study were recently published online first in the Journal of Developmental and Physical Disabilities.

Read more here

The link between not getting enough sleep and diabetes

Not getting enough sleep causes changes in the body which can mimic diabetes thus explaining the link between the two.

Lack of sleep can elevate levels of free fatty acids in the blood, accompanied by temporary pre-diabetic conditions in healthy young men, according to new research published online February 19, 2015, in Diabetologia, the journal of the European Association for the Study of Diabetes.

The study, the first to examine the impact of sleep loss on 24-hour fatty acid levels in the blood, adds to emerging evidence that insufficient sleep -- a highly prevalent condition in modern society -- may disrupt fat metabolism and reduce the ability of insulin to regulate blood sugars. It suggests that something as simple as getting enough sleep could help counteract the current epidemics of diabetes and obesity.

"At the population level, multiple studies have reported connections between restricted sleep, weight gain, and type 2 diabetes," said Esra Tasali, MD, assistant professor of medicine at the University of Chicago and senior author of the study. "Experimental laboratory studies, like ours, help us unravel the mechanisms that may be responsible."

The researchers found that after three nights of getting only four hours of sleep, blood levels of fatty acids, which usually peak and then recede overnight, remained elevated from about 4 a.m. to 9 a.m. As long as fatty acid levels remained high, the ability of insulin to regulate blood sugars was reduced.

The results provide new insights into the connections, first described by University of Chicago researchers 15 years ago, between sleep loss, insulin resistance and heightened risk of type 2 diabetes.

The researchers recruited 19 healthy male subjects between the ages of 18 and 30. These volunteers were monitored through two scenarios in randomized order. In one, they got a full night's rest -- 8.5 hours in bed (averaging 7.8 hours asleep) during four consecutive nights. In the other, they spent just 4.5 hours in bed (averaging 4.3 hours asleep) for four consecutive nights. The two studies were spaced at least four weeks apart.

Each subject's sleep was carefully monitored, diet was strictly controlled and blood samples were collected at 15 or 30 minute intervals for 24 hours, starting on the evening of the third night of each study. The researchers measured blood levels of free fatty acids and growth hormone, glucose and insulin, and the stress hormones noradrenaline and cortisol. After four nights in each sleep condition, an intravenous glucose-tolerance test was performed.

They found that sleep restriction resulted in a 15 to 30 percent increase in late night and early morning fatty acid levels. The nocturnal elevation of fatty acids (from about 4 a.m. to 6 a.m.) correlated with an increase in insulin resistance -- a hallmark of pre-diabetes -- that persisted for a nearly five hours.

Cutting back on sleep prolonged nighttime growth hormone secretion and led to an increase in noradrenaline in the blood, both of which contributed to the increase in fatty acid levels.

Although glucose levels were unchanged, the ability of available insulin to regulate blood glucose levels decreased by about 23 percent after a short sleep, "suggesting," the authors note, "an insulin-resistant state."

"It definitely looks like a packaged deal," said the study's lead author, Josiane Broussard, PhD, a former graduate student at the University of Chicago who is now a post-doctoral research scientist at Cedars-Sinai Medical Center's Diabetes and Obesity Research Institute in Los Angeles.

"Curtailed sleep produced marked changes in the secretion of growth hormone and levels of noradrenaline -- which can increase circulating fatty acids," Broussard said. "The result was a significant loss of the benefits of insulin. This crucial hormone was less able to do its job. Insulin action in these healthy young men resembled what we typically see in early stages of diabetes."

Plasma free or non-esterified fatty acids are an important energy source for most body tissues. The demand for fatty acids goes up during exercise, for example, where they are used by cardiac and skeletal muscle; this preserves glucose for use by the brain. But constantly elevated fatty-acid levels in the blood are usually seen only in obese individuals as well as those with type 2 diabetes or cardiovascular disease. A 2012 study by a related research team emphasized the connections between sleep loss and the disruption of human fat cell function in energy regulation.

"This study opens the door to several intriguing questions," according to a Commentary in the journal by sleep specialists Jonathan Jun, MD, and Vsevolod Polotsky, MD, PhD, of Johns Hopkins University School of Medicine. Could variations in individual responses to short sleep explain susceptibility to metabolic consequences? Could dysregulation of fatty acid metabolism represent a common pathway linking various sleep disorders to metabolic syndrome? And why don't clinicians routinely ask their patients about sleep?

The study provides evidence for "potential mechanisms by which sleep restriction may be associated with insulin resistance and increased type 2 diabetes risk," the authors conclude. It supports the growing sense that insufficient sleep may disrupt fat metabolism. And it suggests that an intervention as simple as getting enough sleep could counteract the current epidemics of diabetes and obesity.

Read more here