Pets May Help Kids With Autism Develop Social Skills

HealthDay – 2 hrs 57 mins ago WEDNESDAY, Aug. 1 (HealthDay News) -- Introducing a pet into the home of a child with autism may help that child develop improved social behaviors, new research finds.

The study, from French researchers, is the first strong scientific evidence that animals may help foster social skills in individuals with autism, but it also reinforces what clinicians have been hearing anecdotally for years.

"We hear from parents a lot that having a pet or interacting with an animal really helps their child's social behavior, but there hasn't been a study so far that has looked at that scientifically," said Alycia Halladay, director of environmental research at Autism Speaks. "This offers some intriguing evidence to confirm what parents have been saying."

Halladay was not involved with the study, which was published online Aug. 1 in the journal PLoS ONE.

Problems with communication are one of the hallmarks of autism and strategies to combat this are central to autism therapy.

According to Halladay, some people with autism use service dogs but usually to address a particular handicap, such as problems with motor coordination or hearing loss, although not yet for social skills.

Previous studies have verified that having a pet in the house actually improves family bonding and can improve the social skills of a non-autistic child as he or she learns to share with the pet and care for it.

To see if pets might have the same effect in children with autism, the study authors compared the children's social interactions (as reported by the parents of the children with autism) in three different settings: households that had never had a pet; homes that had had a pet since the child's birth; and households that had acquired a pet after the child turned 5.

In total, 260 individuals with autism were involved and the researchers were most interested in social interactions when the child was 4 or 5 years of age, because this is when the social impairments are often at a peak.

Out of 36 measures, participants who had acquired a pet after they were born scored higher in the two categories of "offering to share" and "offering comfort" after having the pet for a few years.

There was no relationship between each individual's IQ and the impact of the pet, leading the authors to conclude that "the benefits that the animals may have on individuals with autism don't seem related to how serious the autism was," said study author Marine Grandgeorge, clinical research associate at the Autism Resource Center of Academic Hospital in Brest, France.

Pets may promote pro-social behavior by acting as "distracters," Grandgeorge suggested.

"When a human is in a stressful situation, a pet seems to distract him/her from the

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Health Tip: Help Baby Develop Healthy Sleep Habits

HealthDay – 1 hr 4 mins ago (HealthDay News) -- It's never too early to teach infants sleep habits that will help prepare them for a lifetime of healthy sleep.

The National Sleep Foundation offers these guidelines:

Look for baby's natural sleep patterns and when he or she starts to get sleepy.Place baby in the crib sleepy, but not asleep.Create a consistent daytime and nighttime sleep schedule, and a soothing bedtime routine.Make sure the environment is dark, cool, and otherwise conducive to sleep.Teach baby to fall asleep on his or her own and to self-soothe to sleep.

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Feces fossils show connection between Native-Americans, diabetes: Did fat-hoarding genes develop from the nature of ancient feasts?

ScienceDaily (July 24, 2012) — Why do Native Americans experience high rates of diabetes? A common theory is that they possess fat-hoarding "thrifty genes" left over from their ancestors -- genes that were required for survival during ancient cycles of feast and famine, but that now contribute to the disease in a modern world of more fatty and sugary diets.

See Also:Health & MedicineNutritionDiet and Weight LossCholesterolFossils & RuinsAncient CivilizationsArchaeologyFossilsReferenceDiabetic dietSouth Beach dietGlycemic indexMediterranean diet

A newly published analysis of fossilized feces from the American Southwest, however, suggests this "thrifty gene" may not have developed because of how often ancient Natives ate. Instead, researchers said, the connection may have come from precisely what they ate.

The research, which appears in the latest edition of the journal Current Anthropology, suggests that the prehistoric hunter-gatherer civilizations of the Southwest lived on a diet very high in fiber, very low in fat and dominated by foods extremely low on the glycemic index, a measure of effects food has on blood sugar levels. This diet, researchers said, could have been sufficient to give rise to the fat-storing "thrifty genes."

"What we're saying is we don't really need to look to feast or famine as a basis for (the genes)," said Karl Reinhard, professor of forensic sciences at the University of Nebraska-Lincoln's School of Natural Resources and the study's lead author. "The feast-or-famine scenario long hypothesized to be the pressure for 'thrifty genes' isn't necessary, given the dietary evidence we've found."

Natives have some of the highest rates of Type 2 diabetes of any group and are more than twice as likely to develop the disease as are Caucasians. The notion the gene's origin goes back to feast-and-famine cycles among prehistoric hunter-gatherer ancestors has been discussed for nearly a half-century.

To fully understand the basis of the high rates, Reinhard said, "one has to look at the best dietary data one can find. That comes from coprolites (the official term for fossilized feces). By looking at coprolites, we're seeing exactly what people ate."

The coprolites are from Antelope Cave, a deep cavern in northern Arizona where, over several thousands of years, was home to various cultures. That includes the Ancestral Pueblan peoples, who are believed to have lived there seasonally for at least 450 years.

Reinhard and Keith Johnson, an archeologist at California State University, Chico, studied 20 coprolites found in the cave and combined it with analysis from other sites for hints of ancient Natives' diets. They found clues to a food regimen dominated by maize and high-fiber seed from sunflowers, wild grasses, pigweed and amaranth. Prickly pear, a desert succulent, was also found repeatedly in the samples.

By volume, about three-quarters of the Antelope Cave coprolites were made up of insoluble fiber. The foods also were low on the glycemic index; some research suggests that high-GI foods may increase risk of obesity and diabetes.

The analysts' findings led them to deduce that the nature of the feast, and not necessarily its frequency, was enough to lock the "thrifty" genes in place -- and leave modern Natives more susceptible to diabetes as their diets evolved to lower-fiber, higher-GI foods.

"These were not just famine foods," the authors wrote. "These were the foods eaten on a day-by-day basis during all seasons in both feast and famine. They continued to be eaten even after agriculture was developed. Antelope Cave coprolites show that this high-fiber diet was eaten during the warmer seasons of food abundance."

In addition to UNL's Reinhard and California State Chico's Johnson, the study was authored by Isabel Teixeira-Santos and Monica Viera of the Escola Nacional de Saude Publica in Rio de Janeiro, Brazil.

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Overfed fruit flies develop insulin resistance; Represent new tool to study human diabetes

ScienceDaily (June 5, 2012) — Researchers find that fruit flies overloading on carbs and protein not only gain weight but have shortened life spans -- and develop insulin resistance, a hallmark of Type 2 human diabetes.

See Also:Health & MedicineDiabetesDiet and Weight LossObesityPlants & AnimalsMolecular BiologyCell BiologyAnimalsReferenceDiabetes mellitus type 2Blood sugarSouth Beach dietDiabetic diet

With Type 2 human diabetes climbing at alarming rates in the United States, researchers are seeking treatments for the disease, which has been linked to obesity and poor diet.

Now biologists at Southern Methodist University, Dallas, report they have developed a new tool that will help researchers better understand this deadly disease.

By manipulating the diets of healthy adult fruit flies, the researchers developed flies that are insulin-resistant, a hallmark of Type 2 diabetes.

Until now, researchers largely have relied on rats, mice and other animals as model systems for exploring the metabolic and genetic changes that take place in diabetics.

The fruit fly Drosophila melanogaster has been widely deployed in labs to investigate a wide range of human diseases, from Alzheimer's to cancer. But the scientific literature hasn't documented use of the adult fruit fly for studying the metabolic disruptions that are the hallmark of Type 2 diabetes. The fruit fly's advantages include its low cost and a very short lifespan, both of which enable scientists to undertake rapid screenings in their search for new genetic and drug treatments.

The insulin-resistant fruit fly was developed in the lab of SMU biologist Johannes H. Bauer, principal investigator for the study. It was accomplished by feeding fruit flies a diet high in nutrients, said Bauer, an assistant professor in SMU's Department of Biological Sciences. That process mimics one of the ways insulin resistance develops in humans -- overeating to the point of obesity.

The lab's insulin-resistant fruit flies now can serve as a highly relevant and efficient model for studying Type 2 diabetes.

"We learned that by manipulating the nutrients of fruit flies, we can make them insulin resistant," Bauer said. "With this insulin-resistant model we can now go in with pinpoint precision and study the molecular mechanisms of insulin resistance, as well as drug treatments for the condition, as well as how to treat obesity, how to block insulin resistance and how metabolic changes from a specific diet develop. The possibilities are endless."

The researchers reported their findings in the article "Development of diet-induced insulin resistance in adult Drosophila melanogaster," published in Biochimica et Biophysica Acta -- Molecular Basis of Disease.

Two overfeeding diets, carb and protein, both result in insulin resistance

Insulin, produced by the pancreas, is the hormone that tells our cells to absorb glucose, a necessary sugar molecule that provides our body, particularly the brain, with the energy to function, make repairs, move and grow.

In Type 2 diabetes, a person is insulin-resistant because his or her cells fail to respond to insulin's signal to absorb glucose. The disregulation of glucose upsets the body's delicate internal equilibrium, causing massive disruptions in normal cellular processes. These interruptions manifest in multiple disease symptoms, making Type 2 diabetes difficult to characterize, treat and cure.

To provide a good base model organism to study aspects of this complex disease, researchers in the Bauer lab wanted to determine whether flies develop diabetes-like metabolic changes when fed different diets. The researchers developed the insulin-resistant flies in two different ways: One group of fruit flies was overfed a carbohydrate-loaded diet; a second group of flies was overfed a protein-loaded diet. In both cases, the disruption had a profoundly detrimental effect on the flies' health and physiology.

SMU biologist Siti Nur Sarah Morris, lead author on the study, said the results the researchers observed were both expected and unexpected. The researchers expected the flies to gain weight, which they did. Carb-loaded flies gained excessive weight and got fat, just like humans who overeat sweets, french fries, pasta and ice cream. Protein-loaded flies also gained weight, but upon extreme overfeeding they lost weight, just like humans who follow the popular Atkins Diet, a weight loss program in which participants eat only meat, seafood and eggs.

The researchers expected the carb-loaded fruit flies to develop insulin resistance, which they did.

In a surprising result, however, the fruit flies that overate protein also developed insulin resistance, but at a quicker and more severe rate.

"Carb-loaded flies gain weight. Protein-loaded flies gain and then lose weight. So the two diets have exactly opposite effects on metabolism," Bauer said. "But too much of either one of them causes insulin resistance. That surprised us."

Overfed flies had shortened lifespans, differences in fertility

In other findings, carb-loaded flies experienced a profound decline in egg-laying, a measurement of fertility. In contrast, protein-loaded flies first experienced increased egg-laying, but the extreme diet led to decreased egg laying. Both diets led to shortened longevity, the scientists reported.

"The high-protein flies looked frail and unhealthy. They moved less, almost as if sedated," Morris said. "The fatter flies on the high-carb diet had massively decreased fertility; they flew less but still tried to move."

While both diets resulted in insulin resistance, differences were remarkable.

"The carb data imply a linear relationship between carb levels and health. The more carbs, the more weight, the more sugar storage and fat, the more insulin resistance and the less fertility," Bauer said. "But with protein, this relationship becomes parabolic, meaning all readouts go up, then come down again. The decreased storage we liken to a catabolic state that is primarily destructive for the body's optimum metabolic functioning, such as the ketosis typically seen in people eating Atkins-type diets."

Besides Morris and Bauer, other authors on the study were SMU students Claire Coogan, Khalil Chamseddin and Santharam Kolli. Other co-authors, from Pennington Biomedical Research Center, Baton Rouge, La., are Jeffrey N. Keller, director, Institute of Dementia Research & Prevention, and Sun Ok Fernandez-Kim. The research was funded by the National Institute on Aging.

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Kidney stone mystery solved: Why some people are more prone to develop kidney stones

ScienceDaily (Apr. 18, 2012) — Kidney stones strike an estimated 1 million Americans each year, and those who have experienced the excruciating pain say it is among the worst known to man (or woman).

See Also:Health & MedicineKidney DiseaseUrologyOsteoporosisWomen's HealthDiseases and ConditionsGenesReferenceKidney stoneUrologyExcretory systemInflammation of the kidney

Now, new research by scientists at Washington University School of Medicine in St. Louis provides evidence to explain why some people are more prone to develop the condition than others. Their discovery opens the door to finding effective drug treatments and a test that could assess a person's risk of kidney stones.

"Now, we finally have a more complete picture detailing why some people develop kidney stones and others do not," says senior author Jianghui Hou, PhD, assistant professor of medicine. "With this information, we can begin to think about better treatments and ways to determine a person's risk of the condition, which typically increases with age."

The research, in mice, is now available online in the EMBO Journal, published by the European Molecular Biology Organization.

Because kidneys function the same way in mice as in humans, the new findings can help scientists understand the root causes of kidney stones in patients. The mouse model used in the study can also serve as a platform for the preclinical testing of novel treatments for the condition, the researchers say.

Most kidney stones form when the urine becomes too concentrated, allowing minerals like calcium to crystallize and stick together. Diet plays a role in the condition -- not drinking enough water or eating too much salt (which binds to calcium) also increases the risk of stones.

But genes are partly to blame. A common genetic variation in a gene called claudin-14 recently has been linked to a substantial increase in risk -- roughly 65 percent -- of getting kidney stones. In the new study, the researchers have shown how alterations in the gene's activity influence the development of stones.

Typically, the claudin-14 gene is not active in the kidney. The new research shows that its expression is dampened by two snippets of RNA, a sister molecule of DNA, that essentially silence the gene.

When claudin-14 is idled, the kidney's filtering system works like it's supposed to. Essential minerals in the blood like calcium and magnesium pass through the kidneys and are reabsorbed back into the blood, where they are transported to cells to carry out basic functions of life.

But when people eat a diet high in calcium or salt and don't drink enough water, the small RNA molecules release their hold on claudin-14. An increase in the gene's activity prevents calcium from re-entering the blood, the study shows.

Hou and his team have found that claudin-14 blocks calcium from entering passageways called tight junctions in cells that line the kidney and separate blood from urine.

Without a way back to the bloodstream, excess calcium goes into the urine. Too much calcium in the urine can lead to stones in the kidneys or bladder. Intense pain develops when a large stone gets stuck in the bladder, ureter or urethra and blocks the flow of urine.

Hou's research supports the theory that people with a common variation in claudin-14 lose the ability to regulate the gene's activity, increasing the risk of kidney stones.

He is optimistic, however, that drugs could be developed to target the short stretches of RNA that are intimately linked to claudin-14. Drugs that mimic these so-called microRNAs could keep the activity of claudin-14 in check and reduce the likelihood that stones would form.

Also, it may one day be possible to develop a diagnostic test to measure levels of the claudin-14 protein excreted in urine. Elevated levels would indicate an increased risk of stones, and people could take steps to prevent stones by modifying their diet.

"Many genes likely play a role in the formation of kidney stones," Hou says. "But this study gives us a better idea of the way one of the major players work. Now that we understand the physiology of the condition, we can start to think about better treatments or even ways to prevent stones from developing in the first place."

The research was funded, in part, by the National Institutes of Health (NIH) and the American Heart Association.

Hou is working with Washington University's Office of Technology Management on an invention related to work described in the paper.

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