How to Heal all Diseases with Source Energy .


 “Sickness Is Not Because Cells Turned Bad. Sickness Is Because Cells Are Not Being Allowed Full Energy Response.

Everything is vibrational. The cells of your body are vibrational. You are an electronic being. Your wellness is about the transfer of Energy, (not different from electricity) from Universal Source to you on a cellular basis. You have many Energy points within your body. Sickness is not because cells have turned bad. Sickness is because cells are not being allowed the fullness of the Energy response. It’s sort of like an electrical short.

Mending a physical body is the simplest thing in the Universe, because the cells are eager to transmit and receive. Universal Energy, or God Force, is eager to transmit and receive. And if the consciousness involved, which is the personality that you know as you, is in an open and receiving way, then those responses can be restored in the moment — in this moment!

People tend to think that illnesses are progressive: Something goes wrong, and then the sickness just becomes more and more and more. That is not what is happening. What is happening is: the sickness calls attention to something that causes more contradiction or more resistance in the frequency. It is just in the moment.

You could be diagnosed with every deadly disease known to man — but you could be lying in your bed in a state of utter allowance, and allow the Energy of Source to flow through to the cells of your body — and you would have an instant healing! It is not about the body ne

Source: http://www.greatgenius.com/

Like Father, Like Son.


A 10-year-old boy spends his summer vacation helping his chemist dad solve the structure of complicated materials.

Chemist Sven Hovmöller of Stockholm University had been trying for nearly a decade to determine the structures of materials known as quasicrystals and their nearly identical approximants. Thought to be physically impossible until some 30 years ago, quasicrystals are aperiodic structures—meaning they don’t display the rigidly repeating patterns characteristic of crystals like sodium chloride, for example. Since their discovery in the lab, physicists had been working tirelessly to better understand the structure of quasicrystals. But because the existence of such materials was doubted for so long, computer programs currently used to interpret imaging data aren’t equipped to analyze the aperiodic structures.

Hovmöller has worked on and off in the field of quasicrystals for more than 25 years, focusing primarily on the aluminum-cobalt-nickel (Al-Co-Ni) system. Like other quasicrystal researchers, he studied not the elusive materials themselves but their approximants, which differ in atom placement by only 1 or 2 percent and have more tractable patterns of atomic arrangement. Hovmöller’s interest in quasicrystals was piqued when he saw a conference poster displaying an electron diffraction pattern of one of the Al-Co-Ni approximants. The image was “so beautiful, so clear, [that] it should be possible to solve it,” recalls Hovmöller, who immediately invited Markus Döblinger, the student who made the poster, to do a postdoc in his lab.

But after months of further electron microscopy studies, the duo couldn’t seem to solve the structure. “Not only him and me, but other people also involved, tried so hard, but we didn’t get anywhere,” Hovmöller recalls. “It was extremely annoying.”

The image was so beautiful, so clear, that it should be possible to solve it.
—Sven Hovmöller, Stockholm University

Döblinger eventually moved on to the University of Munich, but Hovmöller couldn’t let the idea go. “Every year, once or twice, I [tried] to solve these things, and I just couldn’t.” Then, last summer, he had a seemingly off-the-wall idea. He’d enlist the aid of his 10-year-old son, Linus. “I thought, He’s a smart guy; maybe he could help me,” Hovmöller says.

The father-and-son team sat at the kitchen table for 2 days, poring over the dozens of electron microscopy images Döblinger had generated, as well as some electron diffraction data, which provides more precise information on the materials’ atomic positions. Hovmöller would explain to Linus what he was thinking about how the images all fit together, and when Linus didn’t understand something, he’d interrupt his father to ask. This made Hovmöller realize that he was rushing to conclusions. When he slowed down to clear up Linus’s confusion, he’d get new ideas. “In 2 days, we solved four new structures.”

They published their findings in a special issue of Philosophical Transactions of the Royal Society A honoring the 85th birthday of Alan Mackay, who had predicted the existence of quasicrystals before they were identified in 1982. Linus was listed as a coauthor on the paper (370:2949-59, 2012).

“A kid [who] is clever and good at spatial things might well come up with a solution to a problem like that,” says surface physicist Renee Diehl of Penn State University. “I think there’s probably a lot of potential in 10-year-old kids that we’re not tapping.”

And in fact, Linus isn’t as unlikely a character as one might expect in the field of quasicrystals. “There have been a lot of highly creative and unusual people associated with the field,” says Carnegie Mellon University theoretical physicist Mike Widom. Amateur mathematician Robert Ammann, for example, made several significant contributions to quasicrystal theory before the crystals were even proven to exist. Others have pointed to the links between quasicrystals and art, such as aperiodic tilings and mosaics found in Persia. There’s even a company, called Zometool, that manufactures toys used to model quasicrystalline shapes, Widom notes. “The field is quite rich … [in] unusual personalities,” he says. “This boy is in the tradition of the field attracting some nontraditional scientists.”

But all the structures of the Al-Co-Ni quasicrystal and its approximants aren’t exactly solved. “What Sven Hovmöller did is quite nice,” says Walter Steurer of the Laboratory of Crystallography at ETH Zurich, but his methods are qualitative. Thus, Hovmöller and Linus merely mapped out some of the repeating motifs in four of the approximant structures, but “did not publish any atomic coordinates.” The precise locations of some of the crystals’ atoms have yet to be pinpointed.

“A lot of the interesting controversy in the field of quasicrystals has to do with fairly fine details,” which are critically important to understanding the materials’ true structures, Widom says. “You can know where 90 percent of the atoms are, but still not really know the structure because a minority of the atoms are doing interesting and crucial things. . . . What [Hovmöller and Linus] give us is a good starting point for future structure refinement.”

But if someone eventually solves the true structure of the Al-Co-Ni quasicrystal or its approximants, it won’t be Linus. “He’s refused” to work on the remaining structures, Hovmöller says with a laugh. “He’s still a little bit tired” from the last bout of structure solving.

http://www.sciencedaily.com

 

 

Potential New Class of Drugs Blocks Nerve Cell Death.


Diseases that progressively destroy nerve cells in the brain or spinal cord, such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), are devastating conditions with no cures.

Now, a team that includes a University of Iowa researcher has identified a new class of small molecules, called the P7C3 series, which block cell death in animal models of these forms of neurodegenerative disease. The P7C3 series could be a starting point for developing drugs that might help treat patients with these diseases. These findings are reported in two new studies published the week of Oct. 1 in PNAS Early Edition.

“We believe that our strategy for identifying and testing these molecules in animal models of disease gives us a rational way to develop a new class of neuroprotective drugs, for which there is a great, unmet need,” says Andrew Pieper, M.D., Ph.D., associate professor of psychiatry at the UI Carver College of Medicine, and senior author of the two studies.

About six years ago, Pieper, then at the University of Texas Southwestern Medical Center, and his colleagues screened thousands of compounds in living mice in search of small, drug-like molecules that could boost production of neurons in a region of the brain called the hippocampus. They found one compound that appeared to be particularly successful and called it P7C3.

“We were interested in the hippocampus because new neurons are born there every day. But, this neurogenesis is dampened by certain diseases and also by normal aging,” Pieper explains. “We were looking for small drug-like molecules that might enhance production of new neurons and help maintain proper functioning in the hippocampus.”

However, when the researchers looked more closely at P7C3, they found that it worked by protecting the newborn neurons from cell death. That finding prompted them to ask whether P7C3 might also protect existing, mature neurons in other regions of the nervous system from dying as well, as occurs in neurodegenerative disease.

Using mouse and worm models of PD and a mouse model of ALS, the research team has now shown that P7C3 and a related, more active compound, P7C3A20, do in fact potently protect the neurons that normally are destroyed by these diseases. Their studies also showed that protection of the neurons correlates with improvement of some disease symptoms, including maintaining normal movement in PD worms, and coordination and strength in ALS mice.

Of mice and worms

In the ALS mouse model, a highly active variant of the original P7C3 molecule, known as P7C3A20, which the investigators synthesized, largely prevented death of the nerve cells within the spinal cord that are normally destroyed by this disease. The P7C3 molecule also worked, but was not as effective at protecting neurons in this model.

As cell survival increased in the ALS model, coordination and strength of the mice improved as well. Mice that were given P7C3A20 were able to stay on a rotating rod much longer than untreated animals or animals that received the less active compounds. Animals receiving P7C3A20 also performed better in analysis of their walking gait, which typically worsens in these animals as the disease progresses.

In PD, dopamine-producing neurons necessary for normal movement are gradually destroyed. In patients, loss of these brain cells leads to tremors, stiffness, and difficulty walking. The study again showed that P7C3 protects these neurons from cell death and the more active analogue, P7C3A20, provided even greater protection.

The two compounds also potently blocked cell death of dopaminergic neurons in a C. elegans worm model of PD. Moreover, reduced cell death in this model was associated with improved movement in the worms.

Healthy C. elegans worms have a very characteristic swimming motion. This movement is disrupted in the PD worm. Hector De Jesus-Cortes, a graduate student of neuroscience at UT Southwestern Medical Center and lead author of the Parkinson’s study, videotaped and analyzed the PD worms’ mobility with and without treatment. Normal swimming was almost completely preserved with P7C3A20, and was also fairly well preserved with P7C3.

Tweaking the molecule

The research team compared the activity of several new P7C3-related compounds that they synthesized, in both the hippocampal neurogenesis screen and the mouse model of PD.

“Every variation of our P7C3 molecule that works in the neurogenesis assay also works in the PD model,” Pieper says. “As we continue to refine the molecule, our hope is that the results from the neurogenesis assay will accurately predict the neuroprotective potency of the compound, and thus aid in more rapidly optimizing a new neuroprotective agent.”

The team plans to continue tweaking the structure of the P7C3 molecule to improve its neuroprotective ability while eliminating potential side effects.

“Our hope is that this work will form the basis for designing a neuroprotective drug that could eventually help patients,” Pieper says.

http://www.sciencedaily.com

 

 

 

Homolog of Mammalian Neocortex Found in Bird Brain.


A seemingly unique part of the human and mammalian brain is the neocortex, a layered structure on the outer surface of the organ where most higher-order processing is thought to occur. But new research at the University of Chicago has found the cells similar to those of the mammalian neocortex in the brains of birds, sitting in a vastly different anatomical structure.

he work, published in Proceedings of the National Academy of Sciences, confirms a 50-year-old hypothesis about the identity of a mysterious structure in the bird brain that has provoked decades of scientific debate. The research also sheds new light on the evolution of the brain and opens up new animal models for studying the neocortex.

“If you want to study motor neurons or dopamine cells, which are biomedically important, you can study them in mammals, in chick embryos, in zebrafish. But for these neurons of the cerebral cortex, we could only do that in mammals before,” said Clifton Ragsdale, PhD, associate professor of neurobiology at University of Chicago Biological Sciences and senior author of the study. “Now, we can take advantage of these other experimental systems to ask how they are specified, can they regenerate, and other questions.”

Both the mammalian neocortex and a structure in the bird brain called the dorsal ventricular ridge (DVR) originate from an embryonic region called the telencephalon. But the two regions mature into very different shapes, with the neocortex made up of six distinct cortical layers while the DVR contains large clusters of neurons called nuclei.

Because of this divergent anatomy, many scientists proposed that the bird DVR does not correspond to the mammalian cortex, but is analogous to another mammalian brain structure called the amygdala.

“All mammals have a neocortex, and it’s virtually identical across all of them,” said Jennifer Dugas-Ford, PhD, postdoctoral researcher at the University of Chicago and first author on the paper. “But when you go to the next closest group, the birds and reptiles, they don’t have anything that looks remotely similar to neocortex.”

But in the 1960s, neuroscientist Harvey Karten studied the neural inputs and outputs of the DVR, finding that they were remarkably similar to the pathways traveling to and from the neocortex in mammals. As a result, he proposed that the DVR performs a similar function to the neocortex despite its dramatically different anatomy.

Dugas-Ford, Ragsdale and co-author Joanna Rowell decided to test Karten’s hypothesis by using recently discovered sets of molecular markers that can identify specific layers of mammalian cortex: the layer 4 “input” neurons or layer 5 “output” neurons. The researchers then looked for whether these marker genes were expressed in the DVR nuclei.

In two different bird species — chicken and zebra finch — the level 4 and 5 markers were expressed by distinct nuclei of the DVR, supporting Karten’s hypothesis that the structure contains cells homologous to those of mammalian neocortex.

“Here was a completely different line of evidence,” Ragsdale said. “There were molecular markers that picked out specific layers of cortex; whereas the original Karten theory was based just on connections, and some people dismissed that. But in two very distant birds, all of the gene expression fits together very nicely with the connections.”

Dugas-Ford called the evidence “really incredible.”

“All of our markers were exactly where they thought they would be in the DVR when you’re comparing them to the neocortex,” she said.

A similar experiment was conducted in a species of turtle, and revealed yet another anatomical possibility for these neocortex-like cells. Instead of a six-layer neocortex or a cluster of nuclei, the turtle brain had layer 4- and 5-like cells distributed along a single layer of the species’ dorsal cortex.

“I think that’s the interesting part, that you can have all these different morphologies built with the same cell types, just in different conformations,” Rowell said. “It’s a neocortex or a big clump of nuclei, and then in reptiles they have an unusual dorsal cortex unlike either of those.”

Future experiments will test the developmental steps that shape these neurons into various structures, and the relative pros and cons of these anatomical differences. The complex language and tool-use of some bird species suggests that the nuclear organization of this pathway is also capable of supporting advanced functions — and even may offer advantages over the mammalian brain.

“If you wanted to have a special nuclear processing center in Broca’s area to carry out language processing, you can’t do that in a mammal,” Ragsdale said. “But in a bird they have these special nuclei that are involved in vocalization. It’s as if you have additional flexibility: You can have shorter circuits, longer circuits, you can have specialized processing centers.”

Beyond the structural differences, the discovery of homologous neocortex cell types will allow scientists to study cortical neurons in bird species such as the chicken, a common model used for examining embryonic development. Such research could help scientists more easily study the neurons lost in paralysis, deafness, blindness, and other neurological conditions.

Source: http://www.sciencedaily.com

 

 

Obesity Epidemic Not Due to High Fructose Corn Syrup?


A staggering two-thirds of Americans are overweight, and about one-quarter to one-third of adults fall into the obese category and it is projected to go to FIFTY percent by 2030.

Obesity is now so common that it leads to more doctor visits than smoking1 – and rates have been on the rise for decades now.

The fact that obesity is now an epidemic is not up for debate. What’s causing it, however, is.

One of the forerunning theories is that dramatic changes in our dietary patterns such as the extensive use of sugar, primarily in the form of high fructose corn syrup (HFCS), which is added to virtually all processed foods, is prompting metabolic dysfunction that is making people gain weight.

Now a new study has come out claiming it has “proof” that HFCS is not to blame… but wouldn’t you know it, the study’s authors were funded by, or have links to, the corn industry.

No Link Between High Fructose Corn Syrup and Obesity?

The new report, published in the International Journal of Obesity, says there is no evidence to suggest that the U.S. obesity epidemic can be blamed on HFCS consumption.2 The authors reviewed existing HFCS research and concluded that there are no short-term health differences (such as weight gain, appetite, insulin or glucose levels) between the use of HFCS and sugar (sucrose), noting that both are similar in composition and absorbed identically in the GI tract.

This is the most common argument used by the corn industry to support their agenda that HFCS is safe. Sucrose (table sugar) is 50 percent glucose and 50 percent fructose. High fructose corn syrup (HFCS) is anywhere from 42 to 55 percent fructose depending on which type is used.

While it’s true that they are similar in composition – their parts are metabolized very differently in your body. Because high-fructose corn syrup contains free-form monosaccharides of fructose and glucose, it cannot be considered biologically equivalent to sucrose, which has a glycosidic bond that links the fructose and glucose together, and which slows its break down in the body.

Even if this obvious metabolic difference were not present, it is important to point out that glucose is the form of energy your body is designed to run on. Every cell in your body uses glucose for energy, and it’s metabolized in every organ of your body; about 20 percent of glucose is metabolized in your liver. Fructose, on the other hand, can only be metabolized by your liver, because your liver is the only organ that has the transporter for it.

Fructose is the Real Culprit

Since all fructose gets shuttled to your liver, and, if you eat a typical Western-style diet, you consume high amounts of it, fructose ends up taxing and damaging your liver in the same way alcohol and other toxins do. And just like alcohol, fructose is metabolized directly into fat – not cellular energy, like glucose.

While in times of complete glycogen depletion (i.e. post work-out or true hunger), fructose can be used to replenish these stores, any excess will mostly be converted to fat. So, eating fructose in excess of the very small amount our body can handle is really like eating fat – it just gets stored in your fat cells, which leads to mitochondrial malfunction, obesity and obesity-related diseases.

So both sugar and HFCS play a role in the obesity epidemic, but it’s important to understand that the claim you hear on TV, that “sugar is sugar” no matter what form it’s in, is a misstatement that can, quite literally, kill you – albeit slowly.

The more fructose a food contains, and the more total fructose you consume, the worse it is for your health.

It’s important to note that both sugar and HFCS are problematic, as they both contain similar amounts of fructose, the true culprit. But the reason why HFCS may, in fact, be even worse than table sugar, despite having similar fructose content, is both due to the aforementioned difference in metabolizing it (sucrose’s glycosidic bond) and due to its liquid form. When you consume fructose in liquid form, such as drinking a soda, it places an even more intense burden on your liver. The effect on your liver is not only sped up but also magnified.

Cost Is King

Even if one were to ignore the evidence reviewed above and accept the corn industry’s argument that there is no significant biochemical difference between the fructose in HFCS and regular table sugar, one can’t escape the quantity argument. There is simply no defense against it. In the mid ’70s, Japanese scientists discovered how to manufacture HFCS cheaply from corn. Because it is so cheap it is used in massive quantities.

Fructose in small quantities is relatively harmless. Our ancestors would typically consume some on a regular basis, typically in the form of fruits, but they would rarely consume it in quantities greater than 15 grams (one tablespoon) a day. Now the average intake is FIVE times that at 75 grams and some people consume more than 10 times that amount. At those levels fructose becomes a pernicious liver and metabolic toxin.

Another Case of Industry-Funded Propaganda?

But here is where it gets really interesting. There are actually clever forces at work behind the scenes that have carefully orchestrated this information to deceive you and the rest of the public. So why does this new study make it sound like HFCS has been nothing more than an unfortunate scapegoat in this whole scenario?

As I have explained in a previous video, it is usually helpful to examine who authored the study, and where their funding and true loyalties lie. And in this case, doing so proved to be very revealing. Research shows that industry funding of nutrition-related scientific articles may bias conclusions in favor of sponsors’ products, with potentially significant implications for public health.3

This is now becoming widely accepted, so much so that still more research found physicians are less likely to believe and act on research findings when they are industry-sponsored.4 If that’s the case, many may have a hard time believing the featured HFCS/obesity study. There are four authors to the featured study: lead author James M. Rippe and co-authors David M. Klurfeld, John Foreyt, and Theodore J. Angelopoulos. Each one has his own ties to industry, making for a very concerning conflict of interest:

  1. Rippe: Disclosed in the journal that he and his Rippe Lifestyle Institute had received research grants and consulting fees from a variety of companies and organizations including ConAgra, Kraft Foods, PepsiCo, Weight Watchers and the Corn Refiners Association. He also disclosed in other research completed in 2012 that he has received funding from the Corn Refiners Association.5

Rippe also is an advisor to the food and beverage industry. On his health website he lists ConAgra and PepsiCo as two of several “partners.” He also disclosed in a press release on this most recent study that he is an advisor to the food and beverage industry including the Corn Refiners Association, “which funded this research with an unrestricted educational grant.”

  1. Foreyt: Disclosed in the study that he is a member of the scientific advisory panel of the Corn Refiners Association.6
  2. Klurfeld: Is a scientific and policy advisor on the American Council on Science and Health (ACSH),7 which has published material criticizing the “demonizing of high fructose corn syrup.”8
  3. Angelopoulos: Is the author of at least one other study vindicating HFCS – which was funded by PepsiCo.9 Plus he got a $200,500 research grant from Rippe Health and Lifestyle Institute for “consulting services.”10

How Sensitive are You to Fructose?

Some people may be able to process fructose more efficiently than others, and the key to assess this susceptibility to fructose-induced damage lies in evaluating your uric acid levels. The higher your uric acid, the more sensitive you are to the effects of fructose. The safest range of uric acid appears to be between 3 and 5.5 milligrams per deciliter (mg/dl), and there appears to be a steady relationship between uric acid levels and blood pressure and cardiovascular risk, even down to the range of 3 to 4 mg/dl.

Dr. Richard Johnson suggests that the ideal uric acid level is probably around 4 mg/dl for men and 3.5 mg/dl for women. I would strongly encourage everyone to have their uric acid level checked to find out how sensitive you are to fructose.

Many people who are overweight likely have uric acid levels well above 5.5. Some may even be closer to 10 or above. Measuring your uric acid levels is a very practical way to determine just how strict you need to be when it comes to your fructose consumption.

The major problem with fructose lies in the excessive amounts so many people consume. And fructose has actually been linked to over 70 health conditions in the biomedical literature, indicating that this is far bigger than just a “weight problem.”11

It’s no secret that we are eating more sugar than at any other time in history. In 1700, the average person ate four pounds of sugar a year. Today, about 25 percent of all Americans consume over 134 grams of fructose a day, according to Dr. Johnson’s research.

For most people, including if you’re overweight or obese, it would actually be wise to limit your fruit fructose to 15 grams or less, as you’re virtually guaranteed to get “hidden” fructose from just about any processed food you might eat, including condiments you might never have suspected would contain sugar.

Keep in mind that fruits also contain fructose, although an ameliorating factor is that whole fruits also contain vitamins and other antioxidants that reduce the hazardous effects of fructose. Again, one way to determine just how strict you need to be in regard to fruit consumption is to check your uric acid levels. If your levels are outside the healthy ranges listed above, then I strongly suggest you listen to your body’s biochemical feedback and reduce your fructose consumption, including that from fruit, until your uric acid levels normalize.

Bonus Weight Loss Tips You Might Not Have Heard of

For the majority of people, severely restricting non-vegetable carbohydrates such as sugars, fructose, and grains in your diet will be the key to weight loss. Refined Carbohydrates like breakfast cereals, bagels, waffles, pretzels, and most other processed foods quickly break down to sugar, increase your insulin levels, and cause insulin resistance, which is the number one underlying factor of nearly every chronic disease and condition known to man, including weight gain.

As you cut these dietary villains from your meals, you need to replace them with healthy substitutes like vegetables and healthy fats (including natural saturated fats!). You will probably need to radically increase the amount of high-nutrient, low-carbohydrate vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.

I’ve detailed a step-by-step guide to this type of healthy eating program in my comprehensive nutrition plan, and I urge you to consult this guide if you are trying to lose weight.

Next, you’ll want to add in proper exercise. The key to boosting weight loss and getting the most out of your exercise routine is to make sure to incorporate high-intensity, short-burst-type exercises, such as my Peak Fitness Program, two to three times per week. Several studies have confirmed that exercising in shorter bursts with rest periods in between burns more fat than exercising continuously for an entire session.

Now here’s the bonus: A growing body of research suggests that intermittent fasting may in fact be a key weight loss tool. It appears particularly powerful when combined with exercise – i.e. working out while in a fasted state. Intermittent fasting is not the same thing as starving yourself; it can be as simple as skipping breakfast. You can find more details on intermittent fasting here.

Sourc: Dr. Mercola

Spice Girl Mel B.’s Topless Breast Cancer Campaign Is Hotter Than Pink Ribbons.


My favorite Spice Girl hands down?Scary Spice,” aka Mel B. I admit, I got a bit of a girl crush on her well after the Spice Girls’ heyday, when her fitness DVD became my go-to workout. She just has so much personality, attitude, and has never seemed to shy away from being herself. Hence why she’s putting it all out there by going topless in a new breast cancer awareness campaign for the U.K. charity, CoppaFeel!, which aims to remind us all that, “Knowing your boobs could save your life.” Too true!

The topless pic appears in the latest issue of Cosmopolitan UK, and features Mel with her hubby Stephen Belafonte “giving her a hand” with the shot — a la Janet Jackson‘s 1993 Rolling Stone cover. And in the interview she reveals she “loves boobs” and “me and the other Spice Girls are always having a feel of each other’s — Geri came up behind me and grabbed mine the other day!” Ha, wow! But then goes on to explain the more serious reason she’s involved in the campaign.

Mel shares:

I found a lump when I was 17 and freaked out. It turned out it was nothing but it terrified me. Ever since, I’ve always been one for checking, then double checking.

But as she and CoppaFeel! note, there’s nothing wrong with being incredibly well-versed with how your breasts feel. It only makes it that much easier to know when there’s a change that strikes you as off. Mel’s such a fan of breast self-exam that she says:

I have three daughters and one stepdaughter so I’ll show them as they get older. My eldest, Phoenix, 13, does it already.

Love it! And yeah, although this campaign is very sensual — and some are even calling it risque — it’s also brilliant. Because it’s so bold — and so not the same old pink ribbon campaign. And anything that can nab and keep our attention like this does, that encourages us to keep up with be more in tune with our bodies and be more comfortable “copping a feel” deserves a round of applause. Go, Mel B.!

How do you feel about Mel. B.’s topless pic? Do you do breast self-exams?

OCTOBER IS BREAST CANCER PREVENTION MONTH.

Source: cafemom.com

Implications of New Autism Diagnosis in DSM-5.


Most children with an existing diagnosis of pervasive developmental disorder (PDD) will still qualify for an autism diagnosis under the proposed fifth edition of the Diagnostic and Statistical Manual of Mental Disorders — contrary to earlier concerns that many children would be excluded and therefore lose access to social services — according to an American Journal of Psychiatry study.

Researchers analyzed parental behavior reports for three groups of children, comprising nearly 4500 with PDD diagnoses and 700 with non-PDD diagnoses under DSM-IV. The DSM-5 criteria correctly identified 91% of children with PDD. When using parental report or clinical observation, the sensitivity increased to roughly 99%.

The authors write: “These results … provide evidence that the proposed criteria would likely be able to correctly classify a phenotypically wide range of children” with autism.

DSM-5 is expected to take effect in May 2013, the New York Times reports.

Source: American Journal of Psychiatry

 

 

Patients with Rheumatoid Arthritis Face ‘Moderately’ Increased Thrombosis Risk .


Rheumatoid arthritis is associated with increased risk for venous thromboembolism, according to a JAMA study.

Using Swedish national registries, researchers identified roughly 38,000 patients with prevalent RA, 8000 patients with incident RA, and 210,000 age- and sex-matched individuals from the general population (comparison cohort).

During follow-up, patients with prevalent RA were twice as likely as the general population to have a first hospitalization for VTE (5.9 vs. 2.8 events per 1000 person-years). Similarly, incident RA was associated with a higher risk for VTE hospitalization (4.5 vs. 2.8 per 1000 person-years); this increased risk was observed within a year after RA diagnosis.

The researchers note that in inflammatory diseases like RA, upregulation of procoagulatory factors might increase the risk for thrombotic events. They conclude: “In general, patients with RA should be considered at a moderately elevated risk of VTE.”

Source:JAMA

Beta-Blockers Might Not Reduce CV Events in Patients with Stable Heart Disease .


Beta-blockers might not lower the risk for major cardiovascular events in patients with — or at risk for — stable coronary artery disease (CAD), according to a JAMA study.

Investigators compared outcomes with and without beta-blocker therapy in about 22,000 participants in the REACH (Reduction of Atherothrombosis for Continued Health) registry who had prior myocardial infarction, CAD without MI, or CAD risk factors only. Patients were followed for roughly 44 months.

In both cohorts with CAD, risk for the primary outcome — a composite of cardiovascular death, MI, or stroke — did not differ significantly between beta-blocker recipients and nonrecipients. In the risk-factor-only group, the primary outcome occurred more often among beta-blocker recipients (14% vs. 12% among nonrecipients).

The authors note that their findings support recent changes in secondary prevention guidelines, giving class I status only to the short-term use of beta-blockers after MI.

Source:JAMA

 

More Evidence for Increased Skin Cancer Risk with Indoor Tanning.


Exposure to ultraviolet radiation through indoor tanning devices is associated with increased risk for nonmelanoma skin cancer, according to a meta-analysis in BMJ.

The analysis included 12 studies (mostly case-control) comprising over 80,000 participants and 9300 cases of basal cell carcinoma or squamous cell carcinoma. Overall, individuals who’d ever used an indoor tanning device were about 25% more likely to have basal cell disease and nearly 70% more likely to have squamous cell disease, relative to unexposed participants. Risk for basal cell carcinoma was even higher among those with higher levels of exposure, as well as those exposed before age 25.

The authors calculate that in the U.S., more than 170,000 cases of nonmelanoma skin cancer each year can be attributed to indoor tanning.

Editorialists emphasize the role of healthcare providers in warning patients, especially young patients, about the risks of indoor tanning.

Source:BMJ