Gov’t admits rotavirus vaccine causes intussusception, adds it to injury compensation program.

Because the Obama administration quietly announced their plans for 3,400-plus new regulations[1] last week just after Ferguson erupted and just in time for the Thanksgiving holiday, a lot of what’s actually going on in that rather long list was already lost and forgotten pretty much the moment it was released.

One regulation worth mentioning has to do with rotavirus vaccines and a condition called intussusception.

Intussusception is a serious condition where part of the intestine slides into an adjacent part of the intestines, and it is the most common abdominal emergency to hit kids under the age of two. Usually the intestines become blocked. This results in the veins becoming compressed, the intestines swelling, and ultimately, obstruction. Reduced blood flow can actually kill the affected intestine, causing it to become gangrenous. Intussusception can cause internal bleeding, and it can even cause the intestine to rupture. Symptoms include cramps and abdominal pain which for infants seems like a colicky reaction, vomiting, and lack of appetite. Failure to catch this condition early or misdiagnosis can lead to death.


Babies under a year old are most susceptible to intussusception.

One of 3,415 new rules (which surely should’ve been in place when rotavirus vaccines first began being administered) officially adds intussusception[2] to the Vaccine Injury Table for rotavirus vaccines under the National Vaccine Injury Compensation Program.

The rule states:

The National Vaccine Injury Compensation Program allows a family of a child, a person, or their estate to receive monetary compensation if they experience a vaccine-related injury or death after receiving a covered vaccine. Currently, no adverse event is listed on the Vaccine Injury Table for rotavirus vaccines. However, recent data point to a small risk of intussusception, and the rule amends the Vaccine Injury Table to provide for this adverse event.
The rotavirus vaccine is administered at two, four, and six months of age in combination with other vaccines.

According to the VAERS Database at the time of writing this article, of the nearly 11,000 adverse events reported in children under three after receiving a rotavirus vaccine, there are 532 incidents listed where a child under the age of 3 received a rotavirus vaccine and later presented with intussusception. (Note: there were actually 542 cases, but age was unknown in 10 of them.)

The United States currently has the most aggressive vaccination schedule in the whole world. The U.S. Centers for Disease Control and Prevention (CDC) recommends we shoot up our infants up with 26 shots by age one, and then ten more shots before age five.

Considering what ends up reported in the VAERS Database is only a teeny tiny window into the true number of side effects suffered by patients who are administered vaccines (as most people aren’t even aware the Vaccine Adverse Event Reporting System even exists to report side effects to in the first place), coupled with the fact that the government has basically been forced to list intussusception as a side effect, this is yet another vaccine risk parents need to be aware of.

The World Health Organization officially recommended rotavirus vaccines be included in all national immunization programs in 2009. Only two rotavirus vaccines are approved for infants in the U.S.: Merck’s RotaTeq and GlaxoSmithKline’s Rotarix.

This particular vaccine has always stood out as especially controversial considering both its revolving door, conflict-of-interest origins and the fact that the FDA admitted in 2010 these vaccines were contaminated with DNA from two pig viruses.

First, about those pig viruses (via the National Vaccine Information Center[3]:

On May 7, 2010[4], the FDA announced that RotaTeq vaccine was contaminated with DNA from two porcine circoviruses: PCV1 and PCV2. To date the vaccine manufacturer, Merck, has not given any information regarding if, or when, PCV1 and PCV2 will be removed from this vaccine. Although PCV1 has not been associated with clinical disease in pigs, PCV2 is a lethal pig virus that causes immune suppression and a serious wasting disease in baby pigs that damages lungs, kidneys, the reproductive system, brain and ultimately causes death. The FDA recommended temporary suspension of the use of Rotarix vaccine on March 22nd after DNA from PCV1 was identified in Rotarix, but did not call for suspension of the use of RotaTeq vaccine after PCV2 was found in RotaTeq. On June 1st,[5] NVIC called on Merck to voluntarily withdraw RotaTeq from the market until PCV2, especially, is removed from the vaccine.
Now on to the origin story…

In the U.S., the CDC’s Advisory Committee on Immunization Practices (ACIP) is the body of supposed medical professionals and health experts that officially votes to recommend what vaccines will become part of the mandated childhood vaccine market. Dr. Paul Offit, who has sat on a Merck-funded $1.5 million dollar research chair (the Maurice R. Hilleman Chair in Vaccinology in fact) at The Children’s Hospital of Philadelphia since it was created in 2005, just so happened to be a voting member of ACIP from 1998 to 2003. He then went on to take a $350,000 grant from Merck to help develop the Big Pharma company’s RotaTeq pentavalent rotavirus vaccine which was approved by the FDA 2006.

When the Children’s Hospital of Philadelphia sold its worldwide royalty interest in the vaccine, Dr. Offit refused to admit how much his take was. The income distributed to Offit has been estimated as high as $46 million.[6]

So, essentially the guy who sat on a the board that helped create a captured market for the rotavirus vaccine then went on to create said vaccine.

As Dr. Mercola[7] put it, Offit effectively used his position on ACIP to “vote himself rich.” When the good doctor then goes on to write books with scaremongering titles like Deadly Choices: How the Anti-Vaccine Movement Threatens Us All[8] and advises parents on what vaccines to give their infants, just note that Offit has perhaps one of the most vested interests anyone could have – in both his bosses’ happiness and in his own wallet – in doing so.

Keep in mind, Dr. Offit is the same guy who once infamously said that according to his studies and in theory, “healthy infants could safely get up to 10,000 vaccines at once,”[9] because children have such great immune systems with such an enormous capacity to respond to “challenges” (not that the human body was designed to respond to all these vaccinations in the first place, which is why manufacturers have to create such a disgusting cocktail of ingredients including heavy metals, formaldehyde, fetal cells, animal tissues and emulsifiers like polysorbate which have been shown in studies to increase permeability[10] in the gut and blood brain barrier).

So when it comes to Dr. Offit and promoting vaccines (and the rotavirus vaccine in particular), the phrase “conflict of interest” doesn’t even remotely begin to cover it.

As usual, evidence continues to emerge that vaccine “science” is based more on corporate greed than health…[11]

And as evidence continues to emerge that ties linking the astronomical rise in autism in the U.S. to vaccines may have been covered up at the CDC,[12] the propaganda[13] is having less and less of an effect on parents as more are making informed choices about whether or not their children should even take so many shots.

Most people don’t even know that the government set up a no-fault compensation program through a special vaccine tribunal where parents and others harmed by vaccines have to submit their claims. Did you know the federal government has awarded more than $2 billion in damages to children and adults who have been injured by vaccinations?

If you think about this entire situation from a common sense standpoint, it’s absolutely absurd we even live in a nation where the parents of children who are harmed by vaccines aren’t even allowed to directly sue the vaccine manufacturer for creating a dangerous, sometimes life-altering, sometimes life-threatening, sometimes deadly product to begin with, let alone that those parents have to wait until the government admits that a specific vaccine can cause a specific side effect (like rotavirus vaccines officially causing intussusception in official government-funded studies) before that parent can even make a claim for damages because of it.

For more information on the corruption surrounding vaccines, watch Truthstream Media’s two-hour
expose “About all those vaccines…”
















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The ketogenic diet: high fat, high hopes .

Cure for epilepsy? Radical weight-loss programme? This increasingly popular regimen could have many benefits

The ketogenic diet encourages foods that are high in fat. Photograph: Alamy

In 1921, an endocrinologist named Dr Henry Rawle Geyelin arrived at the annual meeting of the American Medical Association to deliver a talk on therapeutic fasting in the treatment of epileptic seizures. Ninety years later, Geyelin would probably be surprised to find that the same diet is being heralded as the latest magic weight-loss programme.

The ketogenic diet has been called the “new Atkins” and is being taken up by an increasing number of people. But Professor Thomas Seyfried from Boston College, who has conducted research on the regimen, urges caution. “This diet is not to be taken lightly and there are healthcare professionals who work specifically in administering it,” he says. “Done incorrectly, you can alter your blood lipid parameters, which is not healthy. But when done the correct way, the blood parameters for the heart look beautiful.”

That the diet exists at all is down to the persistence of Geyelin, who was also one of the first doctors in New York to use insulin as a treatment for diabetes. But his ideas were not new. The ancient Greeks had discovered that one of the best ways to manage epileptic seizures was to stop eating, a finding that particularly fascinated Hippocrates. Unfortunately, it clearly was not a long-term solution. Both Hippocrates and Geyelin discovered that once fasting was over, the seizures invariably returned.

Epileptic seizures are brought on by abnormal electrical activity in the brain. The causes can vary, from a defective gene to a head injury, but one common mechanism of the condition is chronic inflammation throughout the whole body. Geyelin wondered what precisely happens during fasting that might be acting to counter this.

He found changes in two particular molecules in the blood: falling blood glucose and raised levels of fat metabolites, called ketones. So how to achieve this without starving the patient? Over the following decade the ketogenic diet was developed: a strict programme enforcing a 4:1 ratio of fats to proteins and carbohydrates.

Nuts, cream, butter and foods high in fat are encouraged while bread, pasta, sugar and grains are all forbidden. This results in ketones replacing glucose as an alternative fuel – and this transition from glucose to fat metabolism reduces the systemic inflammation that can underlie epilepsy and many other diseases. In addition, it induces a process of healthy weight loss. This differs from losses that occur as a result of insufficient nutrition.

Early studies showed enormus success in the treatment of epilepsy – but then in 1938, phenytoin, an anticonvulsant drug, was discovered. It became the epilepsy medication of choice and the ketogenic diet was dismissed and largely forgotten.

In 1994, Hollywood film director Jim Abrahams came across a recent paper on the diet by a doctor at Johns Hopkins hospital in Baltimore. Abrahams’ two-year-old son Charlie was in a critical condition, experiencing up to a hundred epileptic seizures a day and not responding to either drugs or brain surgery.

“We were desperate, so I did some research to find out the options,” Abrahams says. “We found out about the ketogenic diet, and about a herbalist in Texas. I asked Charlie’s doctor what we should try. He said, ‘Flip a coin. I don’t believe either is going to work.’”

But after a month on the diet, Charlie was both drug- and seizure-free and has only the faintest memories of his traumatic start to life. “It was like a miracle,” Abrahams says. “But back in the 1990s, there were several myths used to talk people out of the diet. It was suggested that it stunts growth or may have long-term side-effects. Another popular argument is that it’s too difficult. The diet isn’t easy – but what’s more difficult, controlling what your kid eats or watching them have lots of seizures?”

Anticonvulsant drugs work in 70% of epileptics but if one drug fails, there is only a 10-15% chance that another will work. In addition, the side effects of long-term usage range from problems in bone density and hair growth to cognitive impairment. In a bid to bring the dietary option to the attention of similar families, Abrahams made the 1997 film First Do No Harm, starring Meryl Streep, based loosely on the experiences of his family.

It caused a new explosion of interest. Understanding exactly how the combination of low blood glucose and high ketones prevents seizures has become the subject of intense research. The diet is also viewed by some as a potential way of slowing down the growth of tumours and significantly delaying the onset of Alzheimer’s disease.

“It enhances the metabolic efficiency of all your normal cells,” Seyfried says. “With cancer cells, they can only produce the energy they need to grow via fermentation, which requires glucose. If you’re limiting glucose, you’re taking away their fuel. We know of many people who have had their tumours stop growing or become very indolent as a result of this diet, making these cells vulnerable to other kinds of non-toxic drugs and treatment.”

Aside from the risks from insufficient monitoring, the main difficulty the ketogenic diet poses has always been one of self-control. Therefore, the ultimate aim is a drug that can replicate its effects while allowing a normal diet. However, this remains a long way off.

But Abrahams believes that the problem is not so much human willpower as finance. “Ultimately hospitals are businesses, especially in the US,” he says. “The diet requires a trained dietitian, it is work-intensive, involves lots of hours and there is no pot of gold at the end of that, apart from the benefit to the family.”

Have A Certain Skull Shape, And Other Science Behind Carrying A Tune

The science behind why we’re all not pop stars. 

Besides gorgeous blonde locks and a bootylicious backside, what is it exactly that sets Beyoncé apart from the rest of us mere mortals? Is it natural talent, a lifetime of dedication, or top-notch vocal training? Well, to be fair, it’s most likely a combination of all three. Singing is a beautiful yet complicated art form, and although we all possess the ability to sing at some level, the ability to sing well is based on a number of physical, mental, and environmental factors.

Can We All Sing?

“The voice can be trained in just about everyone,” Justin Stoney, founder of New York Vocal Coaching in New York City, explained to Medical Daily, giving hope to all those who unfortunately have not yet mastered the ability to carry a tune. “The evidence that we have says that if you really apply good technique, just about anyone can sing well.” This is, of course, unless they have some sort of severe vocal limitation. According to Stoney, training your voice is similar to going to the gym and training any other muscle. “Not everyone is going to be a top athlete,” Stoney said, but with the right coach and lots of practice, you can surely see results.

As for why not everyone’s singing voice is as beautiful as a pop star’s? A 2012 study from the University of Montreal on what prevented those who were not musically trained from singing well found that 20 percent of people didn’t have good control of their vocal muscles, 35 percent had trouble matching the pitch of their voice to the desired musical note, and five percent completely lacked the ability to hear differences in pitch or difference between two sounds. The root of these “musical deficiencies” differs from person to person.

Why Can’t We All Sing Well?


A singer is a musician no different from a guitarist or pianist — only their instrument of choice is their body. Differences in a person’s physical make up can account for differences in their singing abilities. “Everyone is sort of built differently,” Stoney explained. “For some people, you can go, ‘Wow they must really work out,’ and it turns out they never go to the gym. People have vocal athleticism in the same way.” For example, the researchers of the Canadian study observed that the physiological shape of some individuals’ vocal tracts resulted in a more pleasing natural voice sound than others.

There’s also a genetic factor to singing. “Different races and cultures actually have different sound too,” Stoney said. This has to do with the shape and size of the vocal folds and the larynx. The shape of a person’s skull is also responsible for the shape and size of the pharynx and the nasal cavities, a person’s natural resonators.

“If you took 10 different guitars with the same exact string, they will all sound a little different because of the size and shape. The skulls are basically the resonator of the instrument.” There has been much research on the connection of the voice and physical appearance, with scientists concluding that the sound of a person’s voice is influenced not only by race and gender, but also by gender within a race, io9 reported.

Not only does the physical appearance you inherited from your parents play a role in your musical potential, but based on a study published in the Journal of Medical Genetics, so does your DNA. The concept of nature rather than nurture was found to be associated with as much as half of the musical talent of the musicians who partook in the study.


Although our physical and genetic makeup is accountable for slight variations in our musical potential, we all have the ability to sing. Sometimes it’s a mental boundary rather than physical limitation that’s keeping us from achieving our musical goals. “When one is quite hesitant about their singing … they may be doubting themselves and thinking too hard about it,” Stoney said.

Adele, best known for her international hit “Someone Like You,” has been quite open with the mental blocks that interfered with her ability to sing. “I get shitty scared. One show in Amsterdam, I was so nervous I escaped out the fire exit. I’ve thrown up a couple of times. Once in Brussels, I projectile-vomited on someone. I just gotta bear it. But I don’t like touring. I have anxiety attacks a lot,” the songstress told Rolling Stone.

Stoney also explained that although voice teachers provide a great deal of technical guidance for their students, one of their biggest responsibilities is also providing the singer with positive encouragement.


Some individuals are able to develop beautiful natural singing voices because of the environment they were raised in. “There are cultures and households where singing is celebrated and encouraged, and environments where they are not. If you say [to a child] ‘You can’t stay on pitch’ or ‘You’re not a singer,’ they take on that identity and the musculature and the brain begins to not work right,” Stoney said.

Being exposed to a musical environment is also a big contributor to an individual’s singing limitations. For example, those who started studying piano or violin at a young age and then picked up singing later in life may experience better results faster based on their background in musical training. Just like the best athletes in the world, the best singers are most likely to have completely dedicated their lives to honing their craft. According to Stoney, vocal training has a lot to do with it as well.

“It’s all coming from scientific truth. That’s why it works so well. Musical training, it’s really all science.”

Hybrid chemical / genetic therapy restores light sensitivity to retina in blind mice, dogs

A new genetic therapy helped blind mice and dogs regain some sensitivity to light – enough for the mice to distinguish flashing from non-flashing lights – setting the stage for future clinical trials in humans.

The therapy employs a virus to insert a gene for a common ion channel into normally blind of the retina that survive after the light-responsive rod and cone photoreceptor cells die as a result of diseases such as . Photoswitches – chemicals that change shape when hit with light -are then attached to the ion channels to make them open in response to light, activating the retinal cells and restoring light sensitivity.

Afflicting people of all ages, retinitis pigmentosa causes a gradual loss of vision, akin to losing pixels in a digital camera. Sight is lost from the periphery to the center, usually leaving people with the inability to navigate their surroundings. Some 100,000 Americans suffer from this group of inherited retinal diseases.

In a paper appearing online this week in the early edition of the journal Proceedings of the National Academy of Sciences, University of California, Berkeley, scientists who invented the photoswitch therapy and veterinary colleagues at the School of Veterinary Medicine of the University of Pennsylvania (UPenn) report that congenitally blind mice regained the ability to navigate a water maze as well as normal mice.

The treatment worked equally well to restore light responses to congenitally blind mice and dogs, indicating that it will be feasible to restore some light sensitivity in blind humans.

“The dog has a retina very similar to ours, much more so than mice, so when you want to bring a visual therapy to the clinic, you want to first show that it works in a large animal model of the disease,” said lead researcher Ehud Isacoff, professor of molecular and at UC Berkeley. “We’ve now showed that we can deliver the photoswitch and restore light response to the blind retina in the dog as well as in the mouse, and that the treatment has the same sensitivity and speed of response. We can reanimate the dog retina.”

Advantages over other gene therapies

The therapy has several advantages over other sight restoration therapies now under investigation, says vision scientist John Flannery, UC Berkeley professor of vision science and of molecular and cell biology. It uses a virus already approved by the Food & Drug Administration for other genetic therapies in the eye; it delivers an ion channel gene similar to one normally found in humans, unlike others that employ genes from other species; and it can easily be reversed or adjusted by supplying new chemical photoswitches. Dogs with the retinal degeneration provide a key test of the new therapy.

“Our ability to test vision is very, very limited in mice because, even in the healthy state, they are not very visual animals, their behaviors are largely driven by their other senses,” he says. “Dogs have a very sophisticated visual system, and are being used already for testing ophthalmic gene therapy.”

The dogs, which were rescued from breeders, were chosen because they have inherited a genetic disease caused by the same gene defect as some patients with human retinitis pigmentosa. Several of them at the PennVet colony were treated and are currently undergoing tests to determine what degree of light sensitivity they now have.

“Seeing that some of the UC Berkeley results with this pharmaco-optogenetic strategy that worked so nicely in mice could be reproduced by our group at PennVet in dogs with late stage retinal degeneration was really exciting,” said William Beltran, an associate professor of ophthalmology at the UPenn School of Veterinary Medicine. “Use of such a clinically-relevant large animal model allows us to begin tackling the next challenges on the road to translating this novel therapeutic strategy to human patients.”

Hybrid chemical-genetic therapy

Genetic diseases like retinitis pigmentosa destroy the photosensitive cells of the eye, the photoreceptors, but often leave intact the other cells in the retina: the bipolar cells that the photoreceptors normally talk to, and the ganglion cells that are the retina’s output to the brain. Isacoff, Flannery and UC Berkeley colleagues have developed several optogenetic techniques for restoring light-sensitivity to surviving retinal cells other than the photoreceptors. These involve using the adeno-associated virus – a common and harmless vector or carrier for gene therapy – to successfully carry a modified gene into these cells. The virus inserts the therapeutic gene into the cell’s DNA and uses its instructions to produce a receptor protein – a modified version of a common glutamate receptor ion channel- that they display on their surface.

The researchers then inject a chemical photoswitch into the eye, “basically, a glutamate dangling on a light-sensitive string,” says Isacoff, “which anchors to the modified receptor and stuffs the glutamate into its docking site on the receptor when activated by light.” The newest version of the photoswitch is fast enough to turn the activity of retinal neurons on and off at a rate that approaches video rate of 30 frames per second.

In mice, they can successfully insert the gene into almost every one of the million or so retinal ganglion cells. This, the researchers say, should restore useful vision.

“So we have reasonable speed and a lot of pixels, now the question is: What can the treated animals see? So far we can say that the treated mice can distinguish between steady light and flashing light. Our next step is to figure out how good they are at telling images apart,” says Isacoff, who holds the Class of 1933 Chair.

Which cells get gift of sight?

One key question the researchers wanted to answer is whether it is best to insert photoswitches into ganglion cells or bipolar cells. Viruses can be made to target one or the other. Because activity flowing from upstream bipolar cells to the retina’s output ganglion cells undergoes a lot of processing in the retinal circuit, the researchers were hoping that this same processing would occur when bipolar cells were given a new function they never had before, .

The answer seems to be yes.

“When we put the photoswitched channels into bipolar cells and record the output of the ganglion cells, we see complicated patterns that look a lot like the activity you get in a normal retina, compared to the on-off activity you get when you put the same photoswitch into a ganglion cell,” Isacoff said.

“The dogs’ behavior should show us if there is a functional difference between driving the system from the versus the ,” Flannery says.

He notes that the therapy works only for about a week after a single “charging” with the photoswitch, because the protein and attached chemical get recycled by the cell. While the modified receptors are replaced continually, since the new gene remains forever in the DNA, the chemical photoswitch – maleimide-azobenzene-glutamate, or MAG – must be resupplied by injection into the eyeball. Right now this means injection every week or so, with the future development of a slow release formulation less often.

“This is not necessarily a disadvantage,” Isacoff said, “because the therapy can be stopped, and new photo-sensitive chemicals can be tried as they are improved.”

The researchers continue to study the effects of treatment in both mice and dogs, improve the photoswitch, and develop ways of attaching the photoswitch to other receptors, including some that could amplify the signal and allow perception of fainter light, as occurs normally in rods and cones.

NIH funding keeps giving

The experiments, analysis and much of the design of the study were performed by first co-authors Benjamin Gaub, a graduate student, and Michael Berry, a technician, along with post-doctoral fellows Michael Keinzler and Andreas Reiner and technician Amy Holt, all from UC Berkeley and Natalia Dolgova and Sergei Nikonov in the labs of Gustavo Aguirre and William Beltran of UPenn.

The work was funded by a nine-year grant from the National Institutes of Health for the Nanomedicine Development Center for the Optical Control of Biological Function (PN2EY018241), as well a NIH grants RO1EY06855 and P30EY001583, and by a grant from the Foundation Fighting Blindness, USA.

“The NIH funding got us all the way from designing the chemical photoswitch to an experimental therapy in the dog,” Flannery says, noting the essential role played by a UC Berkeley interdisciplinary team of chemists, molecular biologists and vision scientists.

“And along the way, we developed tools that could be applied to the basic science of how synapses work and how neural circuits work,” Isacoff adds. “These are spinoffs that themselves could have implications for the clinic.”

The Other Reason Canned Food Is Raising Your Blood Pressure .

Forget sodium—BPA might be the real canned food villain

If your food or drink comes out of a can, chances are it’s not the healthiest choice for your blood pressure (thanks to all that salt preserving your beans, for example.) But the latest research suggests there may be another reason to avoid canned goods. In a study published in Hypertension, researchers from South Korea found that drinking from cans, many of which have linings that contain the chemical bisphenol A (BPA), can raise blood pressure by 16 times compared to drinking from glass bottles.

Tinned sardines

But those studies have compared different populations of people at different times. The Korean scientists decided to study the same group of 60 older people who drank the same beverages from both cans and glass bottles. Because the same people were being studied, it was unlikely that other factors that can affect BPA concentrations were influencing the results.

Senior author Yun-Chul Hong from the department of preventive medicine and the environmental health center at Seoul National University and his colleague found that the containers the drinkers used made a big difference in their BPA levels. Each was given two servings of soy milk during each of three visits. The milk was served in either two cans, two glass bottles, or one can and one glass bottle. The volunteers’ urine BPA levels were lowest after drinking from the two glass bottles, and highest after consuming milk from the two cans.

This difference translated to a change in 5 mmHg in blood pressure. Hong notes that an increase of 20 mmHg doubles the risk of heart disease, so the rise from BPA exposure is concerning.

“Because hypertension is a well-known risk factor for heart disease, our study showing the link of BPA exposure to elevation in blood pressure strongly suggests that BPA exposure may increase the risk of heart disease,” Hong writes in an email discussing the results.

When doctors evaluate patients for high blood pressure, asking them how many canned products they consume may be worthwhile, since the exposure to BPA from those containers could be pushing their blood pressure higher. “Clinicians and patients, particularly hypertension or heart disease patients, should be aware of the potential clinical problems for blood pressure elevation when consuming canned foods or using plastics containing BPA,” Hong says. And if you have a choice of getting your vegetables from the preserved aisle or the produce aisle, it might be better for your heart to kick the can.

Is Serotonin The Obesity Hormone? Better Brown-Fat Burning Linked To Hormone Blockage

Through a series of blocked signals in the body, peripheral serotonin may be responsible for preventing normal calorie burns. 

Whenever you feel really happy (like too happy) or even just healthy and content, your brain is releasing the neurotransmitter serotonin. But while this form of serotonin is the most popular, it only makes up five percent of the body’s total supply. The other 95 percent, a new study finds, is busy regulating how well your body burns calories through brown fat.

Stored around your collarbone are deposits of brown adipose tissue (fat) that help burn energy. Brown fat is scarcer in obese people, and for years researchers have wondered about the mechanism behind the reduction. Recently, a team from McMaster University has found the presence of so-called “peripheral serotonin” makes brown fat less active due to enzyme blockage.

“Too much of this serotonin acts like the parking brake on your brown fat,” said Gregory Steinberg, a professor of medicine and the paper’s co-author, in a statement. “You can step on the gas of the brown fat, but it doesn’t go anywhere.”

Brown fat was once believed to be a vestige of evolution — similar to the appendix — that helped keep warm other mammals that do not shiver. But several years of research have begun confirming brown fat’s advantages, principally a role in speeding up the body’s metabolism. As we age, however, the stores of beneficial brown fat, which burn the “bad” white fat that accumulates on our bellies and thighs, begin to diminish. And depending on our diets, they could stop working entirely.

As of late, these concerns have multiplied for researchers involved with obesity. In the U.S. alone, more than one-third of adults, or 79 million people, are obese. The annual cost for treating the conditions associated with obesity, including heart disease, stroke, type 2 diabetes, and some types of cancer, totals $147 billion in 2008 dollars, the latest year for which data are available. Individually, medical costs for the obese are $1,429 higher than for those of a normal weight.

Given these concerns, Steinberg and his colleagues wanted to understand how exactly brown fat’s energy burning comes to a halt. Previous work in their lab had shown the enzyme tryptophan hydroxylase, or Tph1, was overrepresented in lighter mice. Using Tph1 in their follow-up studies, they fed a second group of mice a high-fat diet that was designed to mimic a traditional Western diet. Those with the enzyme mutation produced less serotonin than the normal mice, in turn keeping them healthier.

“What we discovered is that if we remove this enzyme either genetically or if we inhibit its activity using a chemical, a drug, the mice have low levels of serotonin and they didn’t develop diabetes, obesity, or fatty liver disease,” Steinberg said.

This finding holds great promise for future weight loss drugs, the team argued. Most of the current options rely on suppressing people’s appetites to achieve a desired amount of weight loss. They also produce severe side effects, including heart complications and risks for depression. Inhibiting the enzyme that triggers energy storage tackles the problem from the other direction, helping to increase the amount of energy people burn normally.

“Moving forward, we think it’s a much safer method to work with increasing energy expenditure instead of decreasing the appetite, which involves more risks,” Steinberg said. He and his team are currently at work on a pharmacological approach that could stand in as a substitute for traditional weight loss pills.

Source: Crane J, Palanivel R, Mottillo E, et al. Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis. Nature Medicine. 2014.

‘Life on Earth is in peril. We have no future if we don’t go into space’

‘Life on Earth is in peril. We have no future if we don’t go into space’

Experts including Stephen Hawking look at the value of human and robotic spaceflight


Stephen Hawking
Stephen Hawking says robotic missions do not catch the public imagination in the same way as manned space missions. Photograph: Danita Delimont / Alamy/Alamy


Physicist and cosmologist

Robotic missions are much cheaper and may provide more scientific information, but they don’t catch the public imagination in the same way, and they don’t spread the human race into space, which I’m arguing should be our long-term strategy. If the human race is to continue for another million years, we will have to boldly go where no one has gone before. Life on Earth is at the ever-increasing risk of being wiped out by a disaster such as sudden global warming, nuclear war, a genetically engineered virus or other dangers … I think the human race has no future if it doesn’t go into space.


British astronaut

There is no future for us on Earth. If we survive as a human species, it’s inevitable – we are going to have to leave the planet. Now that’s an awful long time away, we hope, but at some point we have to make the leap, and we have to find other resources in the universe – and that starts now. To me it’s an insurance policy. It’s also all about exploration – it’s in our natural psyche to want to explore, to push the boundaries and take the next steps.

Tim Peake is set to fly on a mission to the International Space Station in November next year.


US space scientist

Only a tiny number of Earth’s six billion inhabitants are direct participants in human spaceflight. For the rest of us, the adventure is vicarious. At the end of the day, I ask myself whether the huge national commitment of technical talent to human spaceflight and the ever-present potential for the loss of precious human life are justifiable.

His work on the first US satellites revealed the existence of powerful radiation belts round the Earth, now known as the Van Allen radiation belts.



Obscenely expensive manned missions mean that practical, Earth-based science suffers, as does the genuinely valuable satellite research so essential to the way we live today. It is no wonder that the most articulate opposition to the Apollo missions came from Nobel scientists who objected to the way their budgets were bled in order to fund an ego trip to the Moon.

Gerard DeGroot, professor of modern history at St Andrews University, is author of Dark Side of the Moon: The Magnificent Madness of the American Lunar Quest.

Mild Stenosis Linked to Death in Diabetes

Even modest coronary plaque causing no symptoms has a long-term impact on mortality and heart disease in diabetes, an observational study showed.

Action Points

  • Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
  • In patients with diabetes, both nonobstructive and obstructive CAD by coronary computed tomographic angiography are associated with higher rates of all-cause mortality and MACE when followed for 5 years. The relative risk of nonobstructive disease is comparable to single vessel obstructive disease

The adjusted mortality risk was similarly elevated by twofold whether coronary CT angiography showed mild stenosis of less than 50% or obstructive stenosis of 50% or more (hazard ratios 2.0 and 2.1,P=0.003 and P<0.001, respectively), Philipp Blanke, MD, of the University of British Columbia and St. Paul’s Hospital in Vancouver, and colleagues found in the CONFIRM registry.

The mortality risk with nonobstructive coronary artery disease was similar to that of having single-vessel obstructive disease (P=0.42), the researchers reported at the Radiological Society of North America meeting here.

Overall major adverse cardiovascular events (death, myocardial infarction, unstable angina, or late coronary revascularization) showed about double the risk with obstructive disease as with the milder stenosis, but both were significant, with HRs of 10.4 and 4.9, respectively (both P<0.001).

“Coronary computed tomographic angiography in diabetics can be used for long-term prognostication with respect to mortality and major adverse cardiovascular events,” the group concluded.

However, screening of diabetes patients for asymptomatic coronary artery disease with coronary CT angiography to guide management wasn’t any better than simply aggressively targeting risk factors in the FACTOR 64 trial, reported in November at the American Heart Association meeting.

“A lot of patients end up having their first symptom as a heart attack or even death. We would like to be able to identify those patients and treat them before they die or have a heart attack,” said J. Brent Muhlestein, MD, of the FACTOR 64 trial. Muhlestein is from Intermountain Medical Center and the University of Utah in Salt Lake City.

While CT screening wasn’t the solution, “aggressive medical management of all patients significantly reduced the number of adverse events that happened in diabetic patients in both the patients who were in the control arm and also in the scanning arm,” he pointed out to MedPage Today. “We also found that 70% of the patients who did have asymptomatic diabetes also did have some degree of atherosclerosis in their coronary arteries which justifies secondary prevention risk management.”

The Coronary CT Angiography Evaluation For Clinical Outcomes: An International Multicenter (CONFIRM) Registry was designed to look for prognostic value of cardiac CT angiography in coronary artery disease-related events.

Among the more than 40,000 patients with CT angiography data from more than a dozen centers around the world, Blanke’s analysis included the 1,823 with diabetes and at least 5-years of follow-up but no prior clinically-apparent coronary artery disease.

10 dangerous substances in Coca-Cola®

10 dangerous substances in Coca-Cola®

Coca-Cola® is no doubt one of the most popular beverages in the world. Almost everyone loves it and must have drink it. In fact, i was an addict like you perhaps whereby your day is not complete without it until i became conscious and enlighten about my health and what our daily food and drinks can do to destroy our body system. It works like a slow poison.

Coca-Cola® has an unnatural drink has been mar with lots of accusations that it contain some dangerous health substance. We are aware of it high sugar content which makes it NOT a drink for people who are diabetics, want lose some weight and be eating healthy. You must stay out sugary foods and drinks, and one of such drinks is Coca-Cola®.

Apart from it high sugar content and caramel, studies have shown that it contain many other dangerous strikingly substances which are bad for our dear health. Some of these are artificial sweeteners which can cause weight gain, disruption of sleep patterns, sexual dysfunction, increases in cancer, MS, Lupus, diabetes, and a list of epidemic degenerative diseases. How ironic that a product originally intended for medicine can actually make you sick.

These are the 10 dangerous substances which studies have affirm to be in Coca-Cola® and even perhaps in the NEW Coca-Cola®Zero according to examiner because i guess there will be no changes.

  1. Aspartame (phenylalanine) Used in the majority of diet products, including Diet Coke®, Aspartame can be up to 200 times sweeter than regular (real sugar). The high levels of phenylalanine (detrimental to people with PKU disorder) and methanol in Aspartame destroys neurons and can lead to memory loss, brain tumors and cancer. Twelve ounces of Diet Coke® can contain about 200 mg of Aspartame. Aspartame is a half-billion dollar industry and is the main ingredient in Equal® and NutraSweet®
  1. Acesulfame-K (acesulfame potassium) or Ace-K an artificial sweetener used in Coca-Cola Zero®. Acesulfame-K is 150-200 times sweeter than sugar and is a potential cancer-causing agent. Similar to saccharin, Acesulfame-K enhances a beverages’ sweet taste while extending its shelf life. Acesulfame-K failed to meet FDA standards. Acesulfame-K is marketed under the brand, Sunett and is in Sweet One sweeteners.
  2. Neotame (dimethylbutyl) 7,000 to 13,000 times sweeter than sugar (one quarter teaspoon of neotame contains the equivalent of 22 pounds of sugar). Neotame is relatively new and is being marketed to replace high fructose corn syrup in many Coca-Cola products. Neotame can cause ADD/ADHD and other emotional and behavioral disorders. Currently not available in individually wrapped packages.
  1. Saccharin: Made from an organic petroleum molecule and can be 300 times sweeter than natural sugar. Saccharin is found in fountain Diet Coke® and should be avoided during pregnancy. Especially harmful to children, saccharin has been implicated as a carcinogen and can cause tumors in the bladder as well as cancer. Saccharin is used in Sweet and Low®
  1. Cyclamate or sodium cyclamate is found in Coke Zero and Coca-Cola Light. Banned by the FDA, cyclamate is especially harmful to the male reproductive system causing infertility and diminished testicles. Cyclamate is a carcinogen, which when combined with other harmful substances, can increase the onset of cancer. Look for this harmful sweetener in products when traveling overseas, especially in Latin America. Cyclamate is in Sugar Twin.
  1. Sucralose (E955) is 600 times sweeter than sugar and is found in Diet Coke. Preliminary research indicates that sucralose can cause organ damage and intestinal complications as it is removed from the blood stream by the kidneys. Sucralose has also been found to trigger migraines. Sucralose is the ingredient known as Splenda®.
  1. Maltodextrin: A bulking base for most, common artificial sweeteners. A type of carbohydrate, Maltodextrin is only slightly sweet or almost flavorless. Affects people with allergies to corn or wheat. It is found in Equal, Splenda and many others.
  1. Sucrose: Regular table sugar. In one can of Coke there can be over 40 grams of sugar, equivalent to eight to ten teaspoons. If you substitute water with cola beverages, you could gain 18 pounds in one year. Excessive sugar consumption can cause mood swings, nervous disorders, diabetes, heart disease and hypertension. Sugar feeds every cell including cancer cells. In Mexico, Coca-Cola is made with sugar.
  1. High Fructose Corn Syrup (HFCS 55): Quite possibly the single most common sweetener. High fructose corn syrup also extends the shelf life of products and is cheaper than sugar. Linked to obesity possibly due to the pervasiveness of its presence, digestion of high fructose corn syrup promotes the storage of fat in the human body. High fructose corn syrup is found Coca Cola Classic
  2. Alitame is 2000 time sweeter than sugar and not calorie free. It’s not approved in US.

What Chemicals are Really in Coca-Cola’s Coke Soda?

Perhaps you already know that the Coca-Cola Co. has committed atrocious ground-water polluting in other countries, along with creating water shortages. You probably know as well that the company is turning providing the mass population with toxic beverage choices. After reading this quick, informative article, you will understand exactly what you are putting into your body, and this just might make it easier to break the Coke-drinking habit.

soda chemicals 263x164 What Chemicals are Really in Coca Colas Coke Soda?

Here’s what’s really in Coca-Cola’s famous Coke soda:

  • Carbonated tap water – Whatever is in unfiltered municipal water is also in your Coke. The carbonation that is added increases gastric secretions and can make you flatulent. Here is what your tap water looks like, by the way.
  • E150D – This is a food coloring, which is made from processing sugar at certain temperatures. Ammonium sulfate is then added (also a constituent of Round Up Ready Chemicals used by Monsanto). This chemical has been known to increase asthma attacks.
  • E952 – This is a sugar substitute. It is 200 times sweeter than sugar and can cause your glycemic levels to sky-rocket. This can lead to diabetes, obesity and other diseases.
  • E950 – This is Acesulfame Potassium, and it aggravates the heart, vascular system, and nervous system. It is especially bad for children and pregnant women.
  • E951 – Aspartame – GMO product which can cause seriously negative impact on your body. Symptoms of aspartame poisoning include: unconsciousness, headaches, fatigue, dizziness, nausea, palpitation, weight gain, irritability, anxiety, memory loss, blurry vision, fainting, joint pains, depression, infertility, hearing loss and more. Aspartame can also provoke the following diseases: brain tumors, MS (Multiple Sclerosis), epilepsy, Graves’ disease, chronic fatigue, Alzheimer’s, diabetes, mental deficiency and tuberculosis. Later, this substance was initially illegal due to its dangers but was again made legal in a suspicious manner.
  • E338 – Orthophosphoric Acid – This causes skin and eye irritation, and can interfere with your body’s ability to absorb calcium, causing osteoporosis.
  • E330 – Citric Acid – This is preservative that is also used in the medical field for preserving blood. In small doses it is fine, but in large doses it can eat away at your stomach and esophageal lining.
  • Aromas – Unknown aromatic additives.
  • E211 – Sodium Benzoate – According to a study completed by Peter Piper at the Sheffield University in Britain, sodium benzoate can harm DNA.

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