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Type 2 diabetes caused by buildup of toxic fat, study suggests

By Ana Sandoiu

Over 29 million Americans, or 9.3 percent of the United States population, live with diabetes, according to the Centers for Disease Control and Prevention (CDC). Type 2 diabetes accounts for 90-95 percent of all these cases.

In type 1 diabetes, patients do not produce enough of the hormone insulin. In type 2 diabetes, although the body produces insulin, it cannot use it properly.

Insulin is secreted by the pancreas when it detects sugar intake. Insulin enables cells to accept glucose, which is then processed by the cells and turned into energy.

In patients whose insulin is not administered effectively, glucose is not assimilated by the cells but instead builds up in the bloodstream. Diabetes occurs when levels of blood sugar are abnormally high.

Although being overweight or obese is a common risk factor for diabetes, researchers have pointed out that diabetes can still occur in people of a healthy weight.

Previous research has found that 12 percent of people diagnosed with diabetes between 1990-2011 were at normal weight. The same research indicates that once diagnosed, normal-weight participants were more likely to die from diabetes than their heavier counterparts.

Reasons for this were unknown, until now. New research may have shed light on not only why people of a healthy weight are still prone to type 2 diabetes, but also why some people are more susceptible to it than others.

It could be that a certain kind of fat is what makes people prone to type 2 diabetes, regardless of their weight.

Ceramides triggered insulin resistance, diabetes in mice

Senior author Scott Summers, Ph.D., chairman of the University of Utah Department of Nutrition and Integrative Physiology, believes it might be a toxic class of fat metabolites called ceramides that causes type 2 diabetes.

The new research from Summer and team shows that a buildup of ceramides prevents the fat tissue from working normally in mice.

When we overeat, some of the excess fat gets either stored or burned for energy. But for some people, excess fat just turns into ceramides.

“Ceramides impact the way the body handles nutrients. They impair the way the body responds to insulin, and also how it burns calories.”

Scott Summers, Ph.D.

When too many ceramides accumulate in the fat tissue, the body reaches a “tipping point,” as Summers puts it. Fat tissue stops working properly, and fat overspills into the blood vessels, heart, or goes on to damage the peripheral tissues.

Ceramides have previously been linked to diabetes by at least three different mechanisms: they cause the death of pancreatic beta cells, they increase insulin resistance, and they reduce insulin gene expression.

The new study further emphasizes the role of ceramides in creating insulin resistance.

Adding extra ceramides to fat cells in mice made them insulin-resistant and unable to burn calories. Conversely, mice that had fewer ceramides did not develop any insulin resistance.

Mice with excessive ceramides were also more likely to develop diabetes and fatty liver disease.

The results of the study were published in the latest issue of Cell Metabolism.

Implications for further research

This study suggests that some people are predisposed to turning excess fat into ceramides instead of calories.

“[The research] suggests some skinny people will get diabetes or fatty liver disease if something such as genetics triggers ceramide accumulation,” said lead author Bhagirath Chaurasia, assistant professor at the University of Utah.

Summers points out that some Asian countries have a higher diabetes rate than the U.S., even though the obesity rate is relatively low.

Diabetes has already been linked to certain races/ethnicities, with African-Americans, Hispanics, Native Americans, some Asians, and Native Hawaiians or other Pacific Islanders being at a particularly high risk for type 2 diabetes, according to the CDC.

2-days sleep loss may alter gut microbiota

By Honor Whiteman

For optimal health and well-being, the American Academy of Sleep Medicine recommend adults aged 18-60 years get at least 7 hours of sleep every night.

However, earlier this year, a report from the Centers for Disease Control and Prevention (CDC) revealed that more than a third of adults in the United States are not meeting these recommendations.

Lack of sleep has been linked to increased risk of numerous health problems, including high blood pressure, stroke, heart disease, obesity, and type 2 diabetes.

Previous research has also associated changes in gut microbiota – the community of microorganisms that reside in the digestive tract – with obesity and type 2 diabetes. Whether sleep loss plays a role in this relationship, however, has been unclear.

According to the researchers of the new study – including first author Christian Benedict of the Department of Neuroscience at Uppsala University in Sweden – some studies in mice and humans have suggested that gut bacteria have a circadian rhythm that might be disrupted by sleep loss.

“However, to date, there are no studies that have investigated the impact of insufficient sleep on the composition of the human gut microbiota,” they add.

“Studies are therefore lacking that assess whether important adverse metabolic changes that may increase the risk of [type 2 diabetes] and obesity, such as impaired insulin sensitivity, are associated with changes in the gut microbiome and associated SCFAs [short chain fatty acids] that could result from recurrent sleep loss.”

Restricted sleep linked to obesity-associated changes in gut microbiota

To find out more about the link between sleep loss, gut microbiota, and metabolic changes, Benedict and team enrolled nine healthy, normal-weight males to their study.

The researchers analyzed fecal samples from the men after two sleep conditions: 1 day of normal sleep (around 8 hours) and 2 days of restricted sleep (around 4 hours each night).

Meal times and food intake can affect the composition of gut bacteria, so these were kept consistent across both sleep conditions.

While the team found no evidence that sleep loss alters the diversity of gut bacteria, their analysis did identify changes in microbiota – such as an increase in the ratio of Firmicutes to Bacteriodetes – that previous studies have associated with obesity.

Additionally, the researchers found that following sleep restriction, subjects showed a 20 percent reduction in sensitivity to insulin – the hormone that regulates blood glucose levels.

“This decreased insulin sensitivity was however unrelated to alterations in gut microbiota following sleep loss,” says Benedict. “This suggests that changes in microbiota may not, at least in the short-term, represent a central mechanism through which one or several nights of curtailed sleep reduce insulin sensitivity in humans.”

While these findings suggest sleep loss can trigger changes in gut bacteria, the researchers say further investigation is warranted to better understand whether these changes influence metabolic health.

Genes for dreaming, deep sleep identified in new study

By Honor Whiteman

In a study published in the journal Nature, investigators describe the discovery of a gene that regulates the amount of rapid eye movement (REM) sleep in mammals, as well as a gene that controls the amount of non-rapid eye movement (NREM) sleep.

According to the National Sleep Foundation, REM is a recurring sleep stage that makes up around 25 percent of a typical night’s sleep.

REM is described as a period of sleep involving intense brain activity that is comparable to waking-state brain activity. Vivid dreaming is most likely to occur during REM sleep.

NREM accounts for the remaining 75 percent of sleep, and it is characterized by a reduction in brain activity. NREM sleep consists of three stages: drowsiness, light sleep, and slow wave sleep – the deepest sleep stage, where no eye movement or muscle activity occurs.

Understanding the mechanisms behind sleep

Both REM and NREM are considered important for health and well-being, aiding tissue growth and repair and ensuring the brain and body are able to function effectively during the day.

However, the underlying mechanisms that regulate both of these sleep stages have been unclear. Now, for the first time, researchers have pinpointed two genes that they believe control REM and NREM sleep.

For their study, co-author Joseph S. Takahashi, of the O’Donnell Brain Institute at the University of Texas (UT) Southwestern Medical Center in Dallas, and colleagues introduced random mutations to the genes of more than 8,000 mice.

The team them used electroencephalogy (EEG) to monitor the brain waves of the rodents, with the aim of seeing whether any of the genetic mutations they introduced affected their sleep.

Two new genes linked to REM, NREM sleep

The researchers identified two genes – Salt-Inducible Kinase 3 Sik3 (Sik3) and Sodium Leak Channel Non-selective (Nalcn) – that appear to play a role in REM and NREM sleep.

Mice that had a mutation in the Sik3 gene – referred to as “Sleepy” mice – were found to have 50 percent more NREM sleep than mice without this mutation, the team reports.

“We noticed that Sleepy mutants showed an exaggerated response to sleep deprivation,” notes first author Hiromasa Funato, of the University of Tsukuba in Japan. “Examining the brains of sleep-deprived mice revealed changes in the phosphorylation of amino acids within the SIK3 protein. These changes were disturbed by the Sik3 mutation in Sleepy mice, which is why they have an increased sleep need.”

Additionally, they found that mice with a mutation in the Nalcn gene – named “Dreamless” mice – were found to have much less REM sleep than mice without a Nalcn gene mutation.

“The Dreamless mutation causes increased ion conductance through the channel and increased activity of REM-terminating neurons, which is compatible with REM sleep instability,” explains co-author Chika Miyoshi, also of the University of Tsukuba.

New sleep-regulating drugs a possibility

All in all, the researchers believe their findings suggest Sik3 and Nalcn play significant roles in mammalian sleep, and the discovery of these genes may pave the way for new treatments for sleep disorders.

The National Sleep Foundation recommend that adults aged 18-64 get around 7-9 hours of sleep daily, while adults aged 65 and older should aim to get around 7-8 hours of sleep.

However, according to the Centers for Disease Control and Prevention (CDC), more than 25 percent of people in the United States often fail meet the sleep recommendations, and around 50-70 millionAmerican adults have some form of sleep disorder.

According to the researchers, it is possible that proteins produced by the Sik3 and Nalcn genes could be drug targets for sleep disorders.

“At least in theory, this study opens up future possibilities to create new sleep-regulating drugs, but doing so will occur in the distant future,” notes senior author Dr. Masashi Yanagisawa, professor of molecular genetics at UT Southwestern.

What is more, the researchers believe their study may fuel the discovery of other genes that play important roles in mammalian sleep.

Zinc for anti-infection, fighting bacteria and fungus

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Connie’s comments:  My mom has skin disorders and uses zinc oxide for most of it.

If stomach upset occurs, take zinc with a meal. Zinc also interacts negatively with several common minerals, namely calcium and iron. … Iron is best absorbed if taken on an empty stomach and should not be taken with compounds such as calcium, zinc, and vitamin E, which may interfere with proper absorption. Take your iron in the morning and your calcium+magnesium+zinc + Vit D in the evening since iron cancels calcium,magnesium and zinc absorpbtion.

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DNA variants can also predict probability of a woman remaining childless

For the first time, scientists have identified areas of DNA—specifically, 12—associated with reproductive habits, in this case the age when men and women have their first kid and how many kids they…

Source: DNA variants can also predict probability of a woman remaining childless

DNA variants can also predict probability of a woman remaining childless

For the first time, scientists have identified areas of DNA—specifically, 12—associated with reproductive habits, in this case the age when men and women have their first kid and how many kids they have. Reporting in the journal Nature Genetics, researchers at the University of Oxford analyzed more than half a million men and women in the Netherlands and Sweden and found what they are calling a “biological basis for reproductive behavior,” though they acknowledge social and environmental factors reign supreme. Still, “we now know where to find the DNA areas linked to reproductive behavior,” lead author Melinda Mills says in a statement. “For example, we found that women with DNA variants for postponing parenthood also have bits of DNA code associated with later onset of menstruation and later menopause.”

As such, the findings could one day have implications for fertility and help doctors advise women on how long they can wait based on these DNA variants. But when taken together, those variants “predict less than 1% of the timing … and of the number of children [men and women] have in the course of their lifetime.” The paper—co-authored by more than 250 sociologists, biologists, and geneticists—acknowledges that the figure seems “extremely small,” but it notes the variants can predict a woman’s likelihood of never having children. The findings are being modestly hailed by one of the researchers as a “small piece to understanding this very large jigsaw puzzle.” (This world-renowned chef has been accused of pregnancy discrimination.)


The genetic architecture of human reproductive behavior—age at first birth (AFB) and number of children ever born (NEB)—has a strong relationship with fitness, human development, infertility and risk of neuropsychiatric disorders. However, very few genetic loci have been identified, and the underlying mechanisms of AFB and NEB are poorly understood. We report a large genome-wide association study of both sexes including 251,151 individuals for AFB and 343,072 individuals for NEB. We identified 12 independent loci that are significantly associated with AFB and/or NEB in a SNP-based genome-wide association study and 4 additional loci associated in a gene-based effort. These loci harbor genes that are likely to have a role, either directly or by affecting non-local gene expression, in human reproduction and infertility, thereby increasing understanding of these complex traits.

Loneliness can be an Alzheimer’s sign

“People who are starting to accumulate amyloid may not be as well-functioning in terms of perceiving, understanding or responding to social stimuli or interactions,” says lead researcher Dr. Nancy Donovan. So while loneliness doesn’t necessarily lead to dementia, it can be a sign of it, suggesting a potential build-up of amyloid plaque in the part of the brain that plays a key role in memory, attention, and perception.


You have one of six possible variations of the APOE gene, having inherited one variant—e2, e3, or e4—from each parent. Reporting in the journal Neuron, University of Hawaii researchers found that the brain development of children as young as preschool age with two copies of e4 or one of e4 and one of e2 seem most adversely affected—an intriguing find in light of previous research that has linked the e4 variant to Alzheimer’s. Researchers scanned the brains of 1,187 healthy people between the ages of 3 and 20 and found, for instance, that the size of the hippocampus tends to be smaller in those with the e2/e4 combination. They also found some kids with e4 didn’t perform as well on tests of memory, though they caught up with their peers by age 10, reports HealthDay News.

And while brain researcher Rebecca Knickmeyer, who didn’t participate in the study but wrote an accompanying editorial, says the variants aren’t necessarily predictive and people shouldn’t start testing their kids, the research suggests that Alzheimer’s may in fact be a developmental disorder, not strictly an aging one, reports the Los Angeles Times. That raises the possibility that adjustments to “diet or cognitive training” early on could change someone’s “trajectory,” per Knickmeyer. Three in four people have at least one copy of e3 which seems to offer a protective effect. About 14% of people have an e4 variant, which has been linked with an elevated risk of Alzheimer’s, but Knickmeyer points out that there are many Alzheimer’s patients without e4, and many with e4 who never develop Alzheimer’s. (Some research suggests that memories lost to Alzheimer’s are actually retrievable.)


For decades, scientists believed the memories lost by Alzheimer’s patients were gone for good, the Washington Postreports. But a new study out of MIT and published in Nature shows those memories may still be somewhere in the brain and, what’s more, could be recoverable. That’s because, contrary to earlier scientific thought, the problem in Alzheimer’s patients appears to be memory recovery, not memory storage. “Even if a memory seems to be gone, it is still there,” Nobel Prize-winning scientist Susumu Tonegawa tells the Post. “It’s a matter of how to retrieve it.” A Harvard neurology professor tells the Boston Herald the research conducted by Tonegawa’s team “shattered a 20-year paradigm of how we’re thinking about the disease.”

In the study, mice genetically altered to have Alzheimer’s-like symptoms didn’t seem to remember an earlier electric shock and fear further shocks. That changed when researchers stimulated brain cells associated with short-term memory in the mice. And while it opens the possibility of one day helping Alzheimer’s patients recover their lost memories, it’s not a process that is repeatable in humans and further research is needed. “We’re still many years away from knowing if it would be possible to restore lost memories in people,” one expert tells the Guardian. (Scientists believe they’ve found a link between Alzheimer’s and herpes.)

Frame your perspectives to fall in love or fall out of love

The researchers, Sandra Langeslag from the University of Missouri-St. Louis and Jan van Strien from Erasmus University Rotterdam, examined 40 participants in what was “the very first study” of its kind, according to Langeslag. Each participant came armed with 30 photos of their current or former partner — half of the participants were in a relationship, while half had recently been through a breakup — and were instructed to try to regulate their love feelings by using the technique of “reappraisal” — viewing a slideshow of the images and focusing each time on a positive aspect of their beloved for “up-regulation,” or a negative aspect for “down-regulation.”

The results? Well, participants did indeed feel more love after up-regulation, and less love after down-regulation. What’s more, brainwave measurements showed this wasn’t just an illusion: The Late Positive Potential brainwave, which “indicates how emotionally salient a stimulus is for you,” was diminished after down-regulation and somewhat enhanced after up-regulation, says Langeslag.

This is not a new concept — psychologists stretching all the way back to Freud have thought that our mind may be able to control certain emotions. So it’s a little surprising that more research like this hasn’t already happened. The field of emotion regulation research, says Gross, has tended to concentrate on strategies to regulate negative emotions, such as anger and anxiety, without much prior research on how to regulate positive emotions like love. Besides which, the members of Foreigner are not the only ones unsure of what love is. Many psychologists refer to love not so much as an emotion itself, but instead a motivational state to a variety of emotions such as happiness, or perhaps jealousy. Love is not obviously a “pure” or “basic” emotion, says Gross. “I think we can be pretty confident that there’s something moving around,” he says, “but we can’t yet be sure that it’s really love.”

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