Findings reveal brain mechanisms at work during sleep

One in five American adults show signs of chronic sleep deprivation, making the condition a widespread public health problem. Sleeplessness is related to health issues such as obesity, cardiovascular problems, and memory problems.

Today’s findings show that:

• Sleepiness disrupts the coordinated activity of an important network of brain regions; the impaired function of this network is also implicated in Alzheimer’s disease (Andrew Ward, abstract 909.05).
• Sleeplessness plays havoc with communication between the hippocampus, which is vital for memory, and the brain’s “default mode network;” the changes may weaken event recollection (Hengyi Rao, PhD, abstract 626.08).
• In a mouse model, fearful memories can be intentionally weakened during sleep, indicating new possibilities for treatment of post-traumatic stress disorder (Asya Rolls, abstract 807.06).
• Loss of less than half a night’s sleep can impair memory and alter the normal behavior of brain cells (Ted Abel, PhD, abstract 807.13).

Other recent findings discussed show:
• How sleep enables the remodeling of memories — including the weakening of irrelevant memories — and the coherent integration of old and new information (Gina Poe, PhD).
• The common logic behind seemingly contradictory theories of how sleep remodels synapses, aiding cognition and memory consolidation (Giulio Tononi, MD, PhD).

McGill researchers link genetic mutation to psychiatric disease and obesity

neurosciencestuff:

McGill researchers link genetic mutation to psychiatric disease and obesity

Deletion of brain-derived neurotrophic factor leads to major depression, anxiety, and obesity

McGill researchers have identified a small region in the genome that conclusively plays a role in the development of psychiatric disease and obesity. The key lies in the genomic deletion of brain-derived neurotrophic factor, or BDNF, a nervous system growth factor that plays a critical role in brain development.

To determine the role of BDNF in humans, Prof. Carl Ernst, from McGill’s Department of Psychiatry, Faculty of Medicine, screened over 35,000 people referred for genetic screening at clinics and over 30,000 control subjects in Canada, the U.S., and Europe. Overall, five individuals were identified with BDNF deletions, all of whom were obese, had a mild-moderate intellectual impairment, and had a mood disorder. Children had anxiety disorders, aggressive disorders, or attention deficit-hyperactivity disorder (ADHD), while post-pubescent subjects had anxiety and major depressive disorders. Subjects gradually gained weight as they aged, suggesting that obesity is a long-term process when BDNF is deleted.

“Scientists have been trying to find a region of the genome which plays a role in human psychopathology, searching for answers anywhere in our DNA that may give us a clue to the genetic causes of these types of disorders,” says Prof. Ernst, who is also a researcher at the Douglas Mental Health University Institute. “Our study conclusively links a single region of the genome to mood and anxiety.”

The findings, published in the Archives of General Psychiatry, reveal for the first time the link between BDNF deletion, cognition, and weight gain in humans. BDNF has been suspected to have many functions in the brain based on animal studies, but no study had shown what happens when BDNF is missing from the human genome. This research provides a step toward better understanding human behaviour and mood by clearly identifying genes that may be involved in mental disorders.

“Mood and anxiety can be seen like a house of cards. In this case, the walls of the house represent the myriad of biological interactions that maintain the structure,” says Ernst, “Studying these moving parts can be tricky, so teasing apart even a single event is important. Linking a deletion in BDNF conclusively to mood and anxiety really tells us that it is possible to dissect the biological pathways involved in determining how we feel and act.

We now have a molecular pathway we are confident is involved in psychopathology,” adds Ernst, “Because thousands of genes are involved in mood, anxiety, or obesity, it allows us to root our studies on a solid foundation. All of the participants in our study had mild-moderate intellectual disability, but most people with these cognitive problems do not have psychiatric problems – so what is it about deletion of BDNF that affects mood? My hope now is to test the hypothesis that boosting BDNF in people with anxiety or depression might improve brain health.”

Activity, not just calories, key to kids’ weight

shychemist:

It makes sense for early childhood interventions to focus specifically on caloric intake, while for those in later childhood or adolescence the focus should instead be on increasing physical activity, since overweight children tend to be less active,” says pediatrician Asheley Cockrell Skinner. (Credit: “child holding sandwich” via Shutterstock)

UNC-CHAPEL HILL (US) — Obesity may begin by eating more in early childhood, but by adolescence, overweight kids may actually take in fewer calories than their peers.

Children younger than 9 who are overweight or obese consume more calories per day than their healthy weight peers—but among overweight adolescents between the ages of 9 and 17, the pattern is reversed, according to a new study published online September 10 in the journal Pediatrics.

How to explain such a seemingly counterintuitive finding?

“Children who are overweight tend to remain overweight,” says lead author Asheley Cockrell Skinner, assistant professor of pediatrics at University of North Carolina at Chapel Hill.

So, for many children, obesity may begin by eating more in early childhood. Then as they get older, they continue to be obese without eating any more than their healthy weight peers,” she says. “One reason this makes sense is because we know overweight children are less active than healthy weight kids.

“Additionally, this is in line with other research that obesity is not a simple matter of overweight people eating more—the body is complex in how it reacts to amount of food eaten and amount of activity.”

Click title to read more.

Latinos and blacks more likely to suffer health disparities due to wealth differences

univisionnews:

Latinos and black children have poorer physical and psychological health.

By ALBERT SABATÉ

A recent study found that health disparities among Latino, black and white children -– but when adjusted for socioeconomic factors, differences had more to do with class than race.

Read More

(Source: thisisfusion)

At a time when America is facing an obesity epidemic, crushing debt and a weak economy, billions of taxpayer dollars are subsidizing junk food ingredients.

In this report, we find that in 2011, over $1.28 billion in taxpayer subsidies went to junk food ingredients, bringing the total to a staggering $18.2 billion since 1995. To put that figure in perspective, $18.2 billion is enough to buy 2.9 billion Twinkies every year—21 for every single American taxpayer.

In contrast, only $637 million has gone to subsidies for apples since 1995. That’s enough to buy 77 million apples per year on average—just half of one apple per taxpayer.

OH NO LET’S HOPE NOBODY FINDS OUT SO THEY CAN KEEP BLAMING POOR PEOPLE, PEOPLE WHO LIVE IN FOOD DESERTS, PEOPLE WHO ARE NOT VEGAN BECAUSE OF IT, AND FAT PEOPLE IN GENERAL LOLOLOLOL

Ahem.

http://organicconnectmag.com/wp/junk-food-subsidies-twinkies-versus-apples/

Junk food is mainly produced by Masterfoods, Hershey’s, and Nestle, also known as the “big three”. They are multinational corporations that don’t really need subsidies period.

(via aboutmaleprivilege)

Obese Kids as Bright as Thinner Peers

neurosciencestuff:

ScienceDaily (July 12, 2012) — Obesity is not to blame for poor educational performance, according to early findings from research funded by the Economic and Social Research Council (ESRC). In a study that combines statistical methods with genetic information, researchers dispel the false idea that being overweight has damaging educational consequences.

Previous studies have shown that children who are heavier are less likely to do well at school. However, Dr Stephanie von Hinke Kessler Scholder from University of York argues it’s vital to understand what drives this association. “We sought to test whether obesity ‘directly’ hinders performance due to bullying or health problems, or whether kids who are obese do less well because of other factors that are associated with both obesity and lower exam results, such as coming from a disadvantaged family,” Dr Scholder explains.

Researchers examined data on almost 4,000 members of the Children of the 90s Birth Cohort Study. These data include the children’s DNA. It is well known that genes are randomly allocated within a population, irrespective of factors such as socio-economic position. The researchers combined the latest developments from genetic epidemiology with statistical methodologies in economic and econometric research. Using two carefully chosen ‘genetic markers’, the research team was able to identify children with a slightly higher genetic pre-disposition to obesity.

“Based on a simple correlation between children’s obesity as measured by their fat mass and their exam results, we found that heavier children did do slightly worse in school,” Dr Scholder points out. “But, when we used children’s genetic markers to account for potentially other factors, we found no evidence that obesity causally affects exam results. So, we conclude that obesity is not a major factor affecting children’s educational outcomes.”

These findings suggest that the previously found negative relationship between weight and educational performance is driven by factors that affect both weight and educational attainment. Future research should focus on other determinants of poor educational outcomes, such as social class or a family’s socio-economic circumstances, Dr Scholder points out.

The finding that obesity is not a cause of poorer educational performance is, the researchers suggest, a positive thing. “Clearly there are reasons why there are differences in educational outcomes, but our research shows that obesity is not one of them,” Dr Scholder argues.

Source: Science Daily

Environmental Factors Spread Obesity, Study Shows

neurosciencestuff:

ScienceDaily (June 14, 2012) — An international team of researchers’ study of the spatial patterns of the spread of obesity suggests America’s bulging waistlines may have more to do with collective behavior than genetics or individual choices. The team, led by City College of New York physicist Hernán Makse, found correlations between the epidemic’s geography and food marketing and distribution patterns.

Supermarket. Physicists found correlations between the obesity epidemic’s geography and food marketing and distribution patterns. (Credit: © flashpics / Fotolia)

“We found there is a relationship between the prevalence of obesity and the growth of the supermarket economy,” Professor Makse said. “While we can’t claim causality because we don’t know whether obesity is driven by market forces or vice versa, the obesity epidemic can’t be solved by focus on individual behavior.”

The teams findings, published online this week in Scientific Reports, come as a policymakers are starting to address the role of environmental factors in obesity. For example, in New York Mayor Michael Bloomberg wants to limit serving sizes of soda sweetened with sugar to 16 ounces as a way to combat obesity.

The World Health Organization considers obesity a global epidemic similar to cancer or diabetes. It is a non-communicable disease for which no prevention strategy has been able to contain the spread.

Because obesity is related to increased calorie intake and physical inactivity, prevention has focused on changing individuals’ behaviors. However, prevalence of non-communicable diseases shows spatial clustering, and the spread of obesity has shown “high susceptibility to social pressure and global economic drivers.”

Professor Makse and his colleagues hypothesized that these earlier findings suggest collective behavior plays a more significant role in the spread of the epidemic than individual factors such as genetics and lifestyle choices. To study collective behavior’s role, they implemented a statistical clustering analysis based on the physics on the critical phenomena.

Using county-level microdata provided by the U.S. Centers for Disease Control Behavior Risk Factor Surveillance Systems for 2004 through 2008, they investigated spatial correlations for specific years. Over that time span, the pattern of the spreading of the epidemic, which has Greene County, Ala., as its epicenter, has shown that two clusters spanning distances of 1,000 kilometers have emerged; one along the Appalachian Mountains, the second in the lower Mississippi River valley.

The spatial map of obesity prevalence in the United States shows that neighboring areas tend to have similar percentages of their populations considered obese, i.e. have a body mass index greater than or equal to 30. Such areas are considered obesity clusters, and their spread can be seen in the maps from 2004 to 2008.

To assess the properties of these spatial arrangements, the researchers calculated an equal-time, two-point correlation function that measured the influence of a set of characteristics in one county on another county at a given distance. The characteristics studied were population density, prevalence of adult obesity and diabetes, cancer mortality rates and economic activity.

The researchers said the form of the correlations in obesity were reminiscent of those in physical systems at a critical point of second-order phase transition. Such systems are uncorrelated and characterized by short-range vanishing fluctuations when they are not at a critical stage.

However, at critical points long-range correlations appear, and these may signal the emergence of strong critical fluctuations in the spreading of obesity and diabetes. Consequently, they concluded the clustering patterns found in obesity were the result of “collective behavior, which may not merely be the consequence of fluctuations in individual habits.”

Professor Makse and his colleagues believe the correlations of fluctuations in the prevalence of obesity may be linked to demographic and economic variables. To test this hypothesis, they compared the spatial characteristics of industries associated with food production and sales, e.g. supermarkets, food and beverage stores, restaurants and bars, to other sectors of the economy.

Their analysis of spatial fluctuations in food economic activity gave rise to the same anomalous values as obesity and diabetes. Areas with above-average concentrations of food-related businesses had high-than-normal prevalence of obesity and diabetes.

In future studies, Professor Makse plans to apply physics concepts to measure the spread of cancer and diabetes. “The basic idea is that if a non-communicable disease is spreading like a virus, then environmental factors have to be at work,” he said. “If only genetics determined obesity, we wouldn’t have seen the correlations.”

Source: Science Daily

THIS!!!

Brain circuitry is different for women with anorexia and obesity

neurosciencestuff:

May 14, 2012

Why does one person become anorexic and another obese? A study recently published by a University of Colorado School of Medicine researcher shows that reward circuits in the brain are sensitized in anorexic women and desensitized in obese women. The findings also suggest that eating behavior is related to brain dopamine pathways involved in addictions.

Guido Frank, MD, assistant professor director of the Developmental Brain Research Program at the CU School of Medicine and his colleagues used functional magnetic resonance imaging (fMRI) to examine brain activity in 63 women who were either anorexic or obese. Scientists compared them to women considered “normal” weight. The participants were visually conditioned to associate certain shapes with either a sweet or a non-sweet solution and then received the taste solutions expectedly or unexpectedly. This task has been associated with brain dopamine function in the past.

The authors found that during these fMRI sessions, an unexpected sweet-tasting solution resulted in increased neural activation of reward systems in the anorexic patients and diminished activation in obese individuals. In rodents, food restriction and weight loss have been associated with greater dopamine-related reward responses in the brain.

“It is clear that in humans the brain’s reward system helps to regulate food intake” said Frank. “The specific role of these networks in eating disorders such as anorexia nervosa and, conversely, obesity, remains unclear.”

Scientists agree that more research is needed in this area. The study was published in Neuropsychopharmacology.

Provided by University of Colorado Denver

Source: medicalxpress.com

theatlantic:

Your Sugar Addiction is Killing You

Substances of abuse used to be the subject of much hand-wringing. It started with opium dens, moved to speakeasies, then to crack houses, then to “smoking permitted” anterooms. Since Nancy Reagan’s “Just Say No,” the war on drugs has taken a back seat, but not because it has been won. Rather, because a different war has cluttered the headlines — the war on obesity. And a substance even more insidious, I would argue, has supplanted cocaine and heroin. The object of our current affliction is sugar. Who could have imagined that something so innocent, so delicious, so irresistible — just one glucose molecule (not so sweet) plus one fructose molecule (very sweet) — could propel America toward economic deterioration and medical collapse?

Read more. [Image: Larina Natalia/Shutterstock]

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