Month: October 2013

Gluten-free foods that make you gain weight

If you think you’re doing yourself a favor by eating gluten-free foods — even though you don’t have to — you’re not alone. Sixty-five percent of people who eat GF foods say they think they’re healthier, and 27 percent think it’ll help them lose weight, finds a new survey. But here’s the thing: GF foods aren’t automatically better for you — and plenty of them can make you gain lbs. Just check out these fattening GF products — and the much better alternatives (assuming you don’t actually have celiac disease — the substitutes aren’t gluten-free).

Granola

Don’t Eat This: Bakery on Main Rainforest Banana Nut Granola (1/2 cup)
Calories: 375
Fat: 11 g (1 g saturated)
Sodium: 23 mg
Sugar: 9 g

This contains the same number of calories as more than 65 Cheez-It crackers — before you even add any milk or yogurt to it.

Eat This: Special K Low-Fat Touch of Honey Granola (1/2 cup)
Calories: 190
Fat: 3 g (0.5 g saturated)
Sodium: 115 mg
Sugar: 9 g

This option has nearly half the calories of the gluten-free granola — and less than a third of the fat!

Bread

Don’t Eat This: Aleia’s Gluten-Free Farmhouse White Bread (2 slices)
Calories: 240
Fat: 7 g (0 g saturated)
Sodium: 190 mg
Sugar: 6 g

You’d have to eat 60 Jelly Belly jelly beans to consume the same number of calories that are in these slices!

Eat This: Arnold Whole Grain White Sandwich Thin Rolls (1 roll)
Calories: 100
Fat: 1 g (0 g saturated)
Sodium: 170 mg
Sugar: 2 g

Slash the fat, calories, and sugar by switching to sandwich thins instead.

Pizza

Don’t Eat This: Uno Chicago Grill Gluten-Free Pepperoni Pizza (half a pizza)
Calories: 500
Fat: 21 g (8.5 g saturated)
Sodium: 1,040 mg
Sugar: 6 g

You’d have to eat more than 60 tortilla chips to take in that much sodium!

Eat This: Domino’s Crunchy Thin Crust Pepperoni Pizza (2 small slices)
Calories: 240
Fat: 13 g (5.5 g saturated)
Sodium: 525 mg
Sugar: 2 g

While the fat is a little on the high side here, too, the Domino’s pizza is still the clear winner.

Chocolate Chip Cookies

Don’t Eat This: Amy’s Gluten-Free Chocolate Chip Shortbread Cookies (1 cookie)
Calories: 90
Fat: 6 g (2.5 g saturated)
Sodium: 25 mg
Sugar: 4 g

Eat two of these, and you’ll have consumed the same amount of fat as in a McDonald’s cheeseburger — and that’s assuming you can stop yourself at two cookies.

Eat This: WhoKnew Original Cookie (1 cookie)
Calories: 53
Fat: 2 g (1 g saturated)
Sodium: 18 mg
Sugar: 3 g

Talk about smart cookies: These pack 1 gram of fiber and 10 percent of your daily calcium requirement per cookie.

Source: Fox News

 

Docs tell parents to limit kids’ texts, tweets and computer use

Doctors 2 parents: Limit kids’ tweeting, texting & keep smartphones, laptops out of bedrooms.

The recommendations are bound to prompt eye-rolling and LOLs from many teens but an influential pediatricians group says parents need to know that unrestricted media use can have serious consequences.

It’s been linked with violence, cyberbullying, school woes, obesity, lack of sleep and a host of other problems. It’s not a major cause of these troubles, but “many parents are clueless” about the profound impact media exposure can have on their children, said Dr. Victor Strasburger, lead author of the new American Academy of Pediatrics policy

“This is the 21st century and they need to get with it,” said Strasburger, a University of New Mexico adolescent medicine specialist.

The policy is aimed at all kids, including those who use smart phones, computers and other Internet-connected devices. It expands the academy’s longstanding recommendations on banning televisions from children’s and teens’ bedrooms and limiting entertainment screen time to no more than two hours daily.

Under the new policy, those two hours include using the Internet for entertainment, including Facebook, Twitter, TV and movies; online homework is an exception.

The policy statement cites a 2010 report that found U.S. children aged 8 to 18 spend an average of more than seven hours daily using some kind of entertainment media. Many kids now watch TV online and many send text messages from their bedrooms after “lights out,” including sexually explicit images by cellphone or Internet, yet few parents set rules about media use, the policy says.

“I guarantee you that if you have a 14-year-old boy and he has an Internet connection in his bedroom, he is looking at pornography,” Strasburger said.

The policy notes that three-quarters of kids aged 12 to 17 own cellphones; nearly all teens send text messages, and many younger kids have phones giving them online access.

“Young people now spend more time with media than they do in school – it is the leading activity for children and teenagers other than sleeping” the policy says.

Mark Risinger, 16, of Glenview, Ill., is allowed to use his smartphone and laptop in his room, and says he spends about four hours daily on the Internet doing homework, using Facebook and YouTube and watching movies.

He said a two-hour Internet time limit “would be catastrophic” and that kids won’t follow the advice, “they’ll just find a way to get around it.”

Strasburger said he realizes many kids will scoff at advice from pediatricians – or any adults.

“After all, they’re the experts! We’re media-Neanderthals to them,” he said. But he said he hopes it will lead to more limits from parents and schools, and more government research on the effects of media.

The policy was published online Monday in the journal Pediatrics. It comes two weeks after police arrested two Florida girls accused of bullying a classmate who committed suicide. Police say one of the girls recently boasted online about the bullying and the local sheriff questioned why the suspects’ parents hadn’t restricted their Internet use.

Mark’s mom, Amy Risinger, said she agrees with restricting kids’ time on social media but that deciding on other media limits should be up to parents.

“I think some children have a greater maturity level and you don’t need to be quite as strict with them,” said Risinger, who runs a communications consulting firm.

Her 12-year-old has sneaked a laptop into bed a few times and ended up groggy in the morning, “so that’s why the rules are now in place, that that device needs to be in mom and dad’s room before he goes to bed.”

Sara Gorr, a San Francisco sales director and mother of girls, ages 13 and 15, said she welcomes the academy’s recommendations.

Her girls weren’t allowed to watch the family’s lone TV until a few years ago. The younger one has a tablet, and the older one has a computer and smartphone, and they’re told not to use them after 9 p.m.

“There needs to be more awareness,” Gorr said. “Kids are getting way too much computer time. It’s bad for their socialization, it’s over stimulating, and it’s numbing them.

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Your smart phone is destroying your memory

Your Android and iOS phones are killing cognitive thinking and declarative memory, say experts

Dr Hozefa A Bhinderwala, psychiatrist at Saifee and Prince Aly Khan Hospital, received a call from his brother last week. “He said, ‘You are the doctor, but I performed a surgery today’.”

The specialist’s brother was referring to having managed to get his nine-year-old son to let go off his smart phone, which he was worried had grown into “an extended limb”. “As soon as my brother would get back home, his son would grab the phone and stay glued to it right until bedtime, playing games and fiddling with apps,” says the psychiatrist.

This is not a lone case. Dr Sangeeta Ravat, Head of the Department of Neurology at Seth G S Medical College and KEM Hospital, says the co-relation between mild Attention Deficit Hyperactivity Disorder (significant difficulties of inattention and impulsiveness or a combination of the two) among young adults and the excessive use of gadgets has been the subject of debate at recent medical conferences.

And if the Indian smart phone user study is accurate, we have reason to worry. The survey conducted by AC Nielsen across 46 cities in September and October 2012 revealed that the number of smart phones had touched 40 million, and almost half of the users were under 25. The dramatic growth was driven by a desire ‘to stay connected and have instant access to social networking sites’, it said.

Although the gadgets are designed to make life easier, and the user, work-smart, experts warn that their unrelenting pings and blitzkrieg of updates can throw the brain into overdrive, affecting its cells and blunting the mind over time. Here’s all that’s at stake:

Declarative memory reduced

Culprit: Reminder features Declarative memory refers to data that can be consciously recalled, such as important phone numbers, date and time of important meetings, and critical dates like your birthdays that we store in our brain. “While earlier, we’d easily remember at least 10 important phone numbers by rote, today we can’t recall any other than our own. Our mind is not challenged. Everything is fed in the phonebook, and under categories — family, work, miscellaneous. Sometimes, there are so many, we can’t recall the face to the name and number,” says Dr Ravat.

Underdeveloped human intelligence

Culprit: Absence of external stimuli Shraddha Shah, clinical psychologist with the Department of Neurology at KEM, is most concerned about the smartphone’s impact on children. She discusses Piaget’s Theory of Cognitive Development — a comprehensive theory about the nature and development of human intelligence, which deals with the nature of knowledge itself and how humans gradually acquire, construct and use it. Shah explains, “This mental process of awareness, perception, reasoning and judgement can only be built if the child experiences something physical, like playing with clay, blocks or a bat and ball. It isn’t possible if s/he is staring into a screen and conquering angry birds.” Physical activities, she adds, help build a child’s motor skills (a learned sequence of movements that combine to produce a smooth, efficient action in order to master a task) that can range from cutting a paper with a scissor to running and jumping. Phones can’t play a role here.

Human mind not meant to multi-task

Culprit: Multi-tasking features Dr Ravat is critical of the Internet which none of us can do without. Our increasing dependency on search engines like Google is making us poor thinkers, she argues. “Our minds are getting lazy because gadgets ensure we don’t use them enough,” she says.

In another interesting argument by neuro experts, the very advantage of smartphones becomes a cause for worry. Smartphones encourage you to carry out multiple tasks at once. Clifford Nass, professor of communication at Stanford University, reckons, “It is not physiologically healthy for you because (humans) are not built to do a multitude of tasks at one time. Your phone makes you feel like you have to respond, which then increases your stress and harms your cognitive thinking.”

Dr Bhinderwala agrees. Multitasking, he says, lessens our ability to focus on what is relevant, and rewires the brain to make us shallow thinkers. Varied communication features (SMS, video, Whatsapp, BBM, Facebook, Twitter) available on our finger tips, makes us less responsive to the immediate environment.

Dr Sandy Chapman, chief director for the Center for Brain Health in Dallas, who has studied the effects of technology on the brain, was quoted in nbcdwf. com, saying: “It’s really keeping us at this distracted level, so everything that we’re thinking about tends to be quicker, less synthesized, and that’s what’s making us dumber.”

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China to monitor link between smog and health

China’s Health Ministry will set up a national network within five years to provide a way of monitoring the long-term impact of chronic air pollution on human health, state media said on Monday.

The network will gather data on PM2.5, or particulate matter with a diameter of 2.5 micrometers, in different locations around the country, the report said, citing a ministry statement.

“The document noted that the absence of a long-term, systematic monitoring system has prevented the country from uncovering the link between air pollution and human health,” the report said.

The network will first cover cities where smog is most prevalent, it added.

“The evaluation will be based on the integrated and long-term analysis of PM2.5 data, weather information and cases of local residents’ diseases and deaths,” Xinhua said.

An international study published in July showed that air pollution is shortening the lives of people in northern China by about 5.5 years compared to the south, a legacy of a policy that provided free coal for heating in the north.

Air quality is of increasing concern to China’s stability-obsessed leaders, anxious to douse potential unrest as a more affluent, urban population turns against a growth-at-all-costs economic model that has besmirched much of the country’s air, water and soil.

The government has announced many plans to fight pollution over the years, but has made little apparent progress, especially in the north and northeast.

Last week, the PM2.5 index reached a reading of 1,000 in some parts of Harbin, the gritty capital of northeastern Heilongjiang province and home to some 11 million people, virtually shutting it down.

A level above 300 is considered hazardous, while the World Health Organization recommends a daily level of no more than 20.

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12 Worst Endocrine Disruptors Revealed

An environmental health advocacy organization has released a list of what it says are the 12 worst hormone-disrupting chemicals.

These chemicals, known as endocrine disruptors, interfere with the actions of hormones in the human body in some way — for instance, by imitating natural hormones, or increasing or decreasing hormone production, according to Environmental Working Group (EWG), the organization that put together the list.

The list includes some chemicals that have been scrutinized for their potential ability to interfere with hormones and affect reproduction, such as bisphenol A (BPA) and phthalates, although studies on these chemicals are not definitive.

Other chemicals on the list — such as arsenic, mercury and lead — may surprise consumers, as people may not be aware that these chemicals disrupt hormones, according to EWG.

And still other chemicals might be less familiar to consumers, such as glycol ethers, which are solvents in paints and cleaning products that have been linked to lower sperm count, among other health problems, in painters, according to EWG.

The list also includes: dioxin, atrazine, phthalates, perchlorate, fire retardants, perfluorinated chemicals (PFCs) and organophosphate pesticides

Dr. Kenneth Spaeth, director of the Occupational and Environmental Medicine Center at North Shore University Hospital in Manhasset, N.Y., said the list was reasonable. “The larger value of a list like this is raising the discussion about endocrine-disrupting chemicals,” Spaeth said.

While it is generally accepted that there is no safe level of exposure to chemicals like lead, there is still a lot of work to be done in determining whether other chemicals, such as BPA and phthalates, pose a risk to human health at the concentrations present in the environment, Spaeth told LiveScience.

“Endocrine-disrupting chemicals are a work in progress in determining what levels are, indeed, hazardous,” Spaeth said. Still, “there’s enough evidence for many of these [chemicals] that it’s reasonable to have some concern about them,” he said.

Spaeth said he might not have included lead, organophosphate pesticides and perchlorate on the list, because use of these chemicals has declined considerably in recent years, significantly lowering people’s level of exposure to these chemicals.

The full list, which is intended for readers of all ages, includes ways for consumers to avoid exposure to these chemicals. However, EWG says that ultimately, the best solution is better regulation to prevent such chemicals from coming to the market.

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Cataract treatment without surgery may lie in activating protective protein

The ability of the lens in the human eye to change focus relies on a dense formation of proteins that can result in clumps that cloud the lens and lead to cataracts – except for special protective proteins that prevent this. Now a team in Munich, Germany has discovered an activation mechanism that can switch on one of these protective proteins to keep the lens clear.

The team, from the Technische Universitaet Muenchen (TUM), writes about their findings in a recent online issue of the Proceedings of the National Academy of Sciences (PNAS).

They suggest the discovery may lead to alternative treatments for cataracts that do not require surgery.

Lens cells perform a remarkable feat. They produce a dense mix of proteins that give the lens its refractive power – its ability to change focus so we can see distant and close objects – yet at the same time keep the lens clear.

To overcome the problem of cloudiness, the lens cells produce and eliminate proteins in a completely different way to other cells – they make them once in the embryonic stage and preserve them for life. Unlike the proteins in the rest of our body, those in our lenses are as old as we are.

But to make the proteins last a lifetime, the lens cells have to keep them in a dissolved state, or they clump together and produce the cloudiness that is characteristic of cataracts.

And herein lies the clue to the German team’s discovery – they have found one of the mechanisms the cell uses to keep the proteins in a dissolved state for so long.

Two crystallin proteins stop other proteins clumping together

Scientists already knew that two related “heat shock” proteins, αA-crystallin and αB-crystallin, were involved. Heat shock proteins are present in all human cells and help stop other proteins clumping when the cell experiences strong heat or stress.

But until this study, little was known about the structure and behavior of the two crystallins, despite intensive research, as study author Johannes Buchner, professor for biotechnology at TUM, explains:

Molecular switch triggers the protective protein

A few years ago, scientists at TUM solved the mystery of one of the crystallin proteins – they decoded the molecular structure of one of the most important forms of αB-crystallin. The protein is made of 24 subunits.

Under normal conditions, when a lens cell is not stressed, the protein exists in the form that the scientists decoded. But they realized this is just a resting form, and not the form that helps prevent other proteins clumping. So they reasoned there must a switching mechanism that triggers the formation of active forms of the protein.

In the study they describe how they found the trigger – when the cell is exposed to stress, such as heat, phosphate groups attach to the crystallin protein causing it to break up into its subunits. Protein subunits bind to other proteins and stop them clumping. This is the active form of the crystallin.

The main challenge the team faced was resolving the structure of the protein, as co-author Sevil Weinkauf, professor for electron microscopy at TUM, explains:

The team believes their discovery of how the crystalline behaves could lead to new treatments for cataracts that do not require surgery. It may be possible to develop a drug that activates the αB-crystallin mechanism to clear up clouded lenses.

There could also be other applications, because the protein also plays a role in other cells. For instance it is too active in cancer cells and can stop them committing suicide. In that example, a drug could be developed to deactivate the protein.

Funds from the German Research Foundation helped finance the study.

In 2012, researchers at the Missouri University of Science and Technology in the US, found that eye drops containing an antioxidant can prevent or heal cataracts and other degenerative eye disorders.

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Scientists regenerate fully functional tear and saliva glands

A research group at Tokyo University of Science has successfully regenerated fully functional bioengineered salivary and lacrimal (tear) glands. The results signify a substantial advance in the development of next generation organ replacement regenerative therapies. The results are published in the scientific journal Nature Communications.

Organ replacement regenerative therapy has been proposed as having the potential to enable the replacement of organs that have been damaged by disease, injury or aging. The research group led by Professor Takashi Tsuji (Professor in the Research Institute for Science and Technology, Tokyo University of Science, and Director of Organ Technologies Inc.) has provided a proof-of-concept for bioengineered organ replacement as the next step for regenerative therapy.

For the salivary glands, Tsuji’s group reports the fully functional regeneration of a salivary gland that reproduces the morphogenesis induced by reciprocal epithelial and mesenchymal interactions through the orthotopic transplantation of a bioengineered salivary gland germ as a regenerative organ replacement therapy. The bioengineered germ developed into a mature gland through acinar formations with the myoepithelium and innervation. The bioengineered submandibular gland produced saliva in response to the administration of pilocarpine and gustatory stimulation by citrate, protected against oral bacterial infection and restored normal swallowing in a salivary gland defect mouse model. Thus, this study provides a proof-of-concept for bioengineered salivary gland regeneration as a potential treatment for xerostomia.

For the lacrimal (tear) glands, Tsuji’s group reports the successful orthotopic transplantation of a bioengineered lacrimal gland germ into an adult extra-orbital lacrimal gland defect model mouse, which mimics the corneal epithelial damage caused by lacrimal gland dysfunction. The bioengineered lacrimal gland germ and harderian gland germ both developed in vivo and achieved sufficient physiological functionality, including tear production in response to nervous stimulation and ocular surface protection. This study demonstrates the potential for bioengineered organ replacement to functionally restore the lacrimal gland.

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Blindness ‘could be prevented’ with new treatment

Researchers have revealed a new approach for treating human eye disease that has proved to be successful in preclinical studies. This is according to a study published in theJournal of Clinical Investigation.

The research team from The Scripps Research Institute (TSRI) in California, Mount Sinai Hospital in Canada and the University of California, San Diego (UCSD), say their findings could lead to new treatments to prevent blindness.

Many types of blindness, including diabetic retinopathy and macular degeneration, can be linked to the abnormal growth of blood vessels (neovascularization) in the retina at the back of the eye, the researchers explain. The retina is a thin layer of soft tissue consisting of blood vessels and light-sensing cells.

According to the Centers for Disease Control and Prevention (CDC), around 1.6 million Americans over the age of 50 suffer from macular degeneration, while 5.3 million people worldwide aged 18 or over have diabetic retinopathy, emphasizing the need for treatments for these diseases.

VEGF ’causes abnormal blood vessel growth’

In order to determine how the abnormal growth of blood vessels in the retina can be stopped, many studies over the last decade have focused on a molecule in the human body called vascular endothelial growth factor (VEGF).

The researchers explain that when the body senses too little oxygen, it triggers VEGF. Once the vessels in the eye sense high levels of VEGF, this causes them to produce more “shoots.”

Furthermore, VEGF and other molecules that prompt the growth of blood vessels, activate a gene called Ras that has to be triggered before new blood vessels can grow. Using this information, researchers believed that if VEGF can be stopped, this could potentially provide a cure for blindness.

However, research from the team at TSRI last year found that VEGF plays an important part in maintaining healthy vision. If VEGF were to be blocked, this could kill light-sensing cells in the eye, causing severe loss of vision.

This discovery meant researchers were now on the hunt for new ways to prevent abnormal blood vessel growth, and David Cheresh and colleagues at the Department of Pathology at UCSD found that microRNAs may be the answer.

MicroRNAs can ‘target’ blood vessel growth

Testing the theory on mice, the UCSD laboratory discovered that microRNAs – small pieces of RNA known to adjust gene activation and expression – could be used to target neovascularization in the VEGF pathway at a “downstream” point, preventing Ras activation.

This means that microRNAs are able to block the formation of abnormal blood vessel growth and still maintain the health of normal blood vessels in the eye.

Commenting on the findings, Prof. Martin Friedlander of the Department of Cell and Molecular Biology at TSRI, says:

Prof. Friedlander says it is hoped this approach will reach clinical trials. He notes that one pharmaceutical partner has already shown interest in teaming up with the research team once the therapy is advanced for human use.

However, he emphasizes that clinical trials could take many years, as the treatment needs to be proved safe and effective prior to routine availability.

“Are we ready to go to the clinic tomorrow? No,” adds Friedlander. “But is this class of therapeutics “drugable?” The answer is yes.”

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Obesity linked to “hunger gene”

New research points to a genetic reason behind why some people gain more weight than others regardless of what they eat.

Researchers from the University of Cambridge in the UK have found that the mutation of a particular gene (called KSR2) may cause slow down metabolism and increase feelings of hunger in people who are obese.

Researchers have known that the KSR2 gene plays a role in regulating energy balance and metabolism, as previous studies in mice have shown that the absence of the KSR2 gene may lead to obesity.

In the new study, researchers found that children with KSR2 mutations had increased appetite, slower metabolism and lower heart rate than children with normal KSR2 genes.

The findings don’t suggest that a healthy diet and exercise should be discarded as effective methods for preventing obesity; however, these findings do suggest that there are genetic factors that can contribute to obesity.

Further studies on the KSR2 gene may lead to the development of new treatment options for obesity and type 2 diabetes, researchers said.

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Forest Waste Used to Develop Cheaper, Greener Supercapacitors

Researchers report that wood-biochar supercapacitors can produce as much power as today’s activated-carbon supercapacitors at a fraction of the cost – and with environmentally friendly byproducts.

The report appears in the journal Electrochimica Acta.

“Supercapacitors are power devices very similar to our batteries,” said study leader Junhua Jiang, a senior research engineer at the Illinois Sustainable Technology Center at the University of Illinois. While batteries rely on chemical reactions to produce sustained electrical energy, supercapacitors collect charged ions on their electrodes (in this case, the biochar), and quickly release those ions during discharge. This allows them to supply energy in short, powerful bursts– during a camera flash, for example, or in response to peak demand on the energy grid, Jiang said.

“Supercapacitors are ideal for applications needing instant power and can even provide constant power– like batteries, but at lower cost,” he said. They are useful in transportation, electronics and solar- and wind-power energy storage and distribution.

Many of today’s supercapacitors use activated carbon – usually from a fossil-fuel source, Jiang said.

“Costly and complicated procedures are normally used to develop the microstructures of the carbon – to increase the number of pores and optimize the pore network,” he said. “This increases the surface area of the electrode and the pores’ ability to rapidly capture and release the ions.”

In wood-biochar supercapacitors, the wood’s natural pore structure serves as the electrode surface, eliminating the need for advanced techniques to fabricate an elaborate pore structure. Wood biochar is produced by heating wood in low oxygen.

The pore sizes and configurations in some woods are ideal for fast ion transport, Jiang said. The new study used red cedar, but several other woods such as maple and cherry also work well.

Expensive and corrosive chemicals are often used to prepare the activated carbon used in supercapacitors, giving the electrodes the physical and chemical properties they need to function well, Jiang said.

“The use of those chemicals will probably impose some environmental impacts,” he said. “This should be avoided or at least substantially reduced.”

Jiang and his team activated their biochar with mild nitric acid, which washed away the ash (calcium carbonate, potassium carbonate and other impurities) in the biochar. The byproduct of this process has a beneficial use, Jiang said: The resulting solution of nitrate compounds can be used as fertilizer.

These simple approaches dramatically cut the material and environmental costs of assembling supercapacitors.

“The material costs of producing wood-biochar supercapacitors are five to 10 times lower than those associated with activated carbon,” Jiang said. And when a biochar supercapacitor has reached the end of its useful life, the electrodes can be crushed and used as an organic soil amendment that increases fertility.

“The performance of our biochar materials is comparable to the performance of today’s advanced carbon materials, including carbon nanotubes and graphenes,” Jiang said. “We can achieve comparable performance with much less cost and probably much lower environmental costs.”

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