Each reflects the operation of psychological mechanisms that were designed through evolution to serve important adaptive functions, but that nevertheless can produce harmful consequences.

What do anxiety disorders, domestic violence, racial prejudice, and obesity all have in common?

wehave found instances of people using relatively heavy-weightJavascript frameworks like Exhibit [11] just for the compar-atively minuscule feature of sortable HTML tables

People with eating disorders are often found to have a history of insecure-ambivalent attachment styles. It is thought that sufferers believe they have earned the closeness of others only when they meet their expectations. They then transfer this to their appearance and thus to their eating behaviour

What was new was a realization for me that I didn’t have a very good language to defend the value of my life, the worthiness of my life

ideal percentage for adult men will be between 50 and 65% of the total body. For the real athletic body types it is even recommended to have 5% more body water than the average adult range.

Nigg said it might help me grasp what’s happening if we compare our rising attention problems to our rising obesity rates. Fifty years ago there was very little obesity, but today it is endemic in the western world. This is not because we suddenly became greedy or self-indulgent. He said: “Obesity is not a medical epidemic – it’s a social epidemic. We have bad food, for example, and so people are getting fat.” The way we live changed dramatically – our food supply changed, and we built cities that are hard to walk or cycle around, and those changes in our environment led to changes in our bodies. We gained mass, en masse. Something similar, he said, might be happening with the changes in our attention.

half of the calories you consume can be burned off simply by fidgeting

Alzheimer's disease (AD) is not normally diagnosed until later in life, although evidence suggests that the disease starts at a much earlier age. Risk factors for AD, such as diabetes, hypertension and obesity, are known to have their affects during mid-life, though events very early in life, including maternal over-nutrition, can predispose offspring to develop these conditions. This study tested whether over-nutrition during pregnancy and lactation affected the development of AD in offspring, using a transgenic AD mouse model. Female triple-transgenic AD dam mice (3xTgAD) were exposed to a high-fat (60% energy from fat) or control diet during pregnancy and lactation. After weaning (at 3 weeks of age), female offspring were placed on a control diet and monitored up until 12 months of age during which time behavioural tests were performed. A transient increase in body weight was observed in 4-week-old offspring 3xTgAD mice from dams fed a high-fat diet. However, by 5 weeks of age the body weight of 3xTgAD mice from the maternal high-fat fed group was no different when compared to control-fed mice. A maternal high-fat diet led to a significant impairment in memory in 2- and 12-month-old 3xTgAD offspring mice when compared to offspring from control fed dams. These effects of a maternal high-fat diet on memory were accompanied by a significant increase (50%) in the number of tau positive neurones in the hippocampus. These data demonstrate that a high-fat diet during pregnancy and lactation increases memory impairments in female 3xTgAD mice and suggest that early life events during development might influence the onset and progression of AD later in life.

Cilia in the brain may be busier than previously thought

Subject ID, age, race, sex, visit age, BMI, BODE index, distance walked, forced expiratory volume, GOLD stage, MRC dyspnoea score, prognostic index, SGRQ, subject group, and visit description of participants with or without lung disease and involved in the \"Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE)\" project.

This subject phenotype table includes gender, race, age, asthma status, anthropometric measurements (n=3 variables; height, weight, and bmi), and smoking status (n=6 variables; ever, current, and former smoking status, number of cigarettes/day, average cigarettes and packs/year).

Slower metabolisms were not the only reason the contestants regained weight, though. They constantly battled hunger, cravings and binges. The investigators found at least one reason: plummeting levels of leptin. The contestants started out with normal levels of leptin. By the season’s finale, they had almost no leptin at all, which would have made them ravenous all the time. As their weight returned, their leptin levels drifted up again, but only to about half of what they had been when the season began, the researchers found, thus helping to explain their urges to eat.Leptin is just one of a cluster of hormones that control hunger, and although Dr. Hall and his colleagues did not measure the rest of them, another group of researchers, in a different project, did. In a one-year study funded by Australia’s National Health and Medical Research Council, Dr. Joseph Proietto of the University of Melbourne and his colleagues recruited 50 overweight people who agreed to consume just 550 calories a day for eight or nine weeks. They lost an average of nearly 30 pounds, but over the next year, the pounds started coming back.