No increased risk of lung disease with methotrexate .


VITALS

Key clinical point: Methotrexate is not associated with an increased risk of pulmonary disease.

Major finding: There was no increased risk of total adverse respiratory events – infectious or noninfectious – or pulmonary deaths in patients taking methotrexate, compared with controls.

Data source: Meta-analysis of seven double-blind, randomized, controlled studies, involving a total of 1,640 participants.

Disclosures: The investigators had no specific source of funding for the study and had no conflicts of interest to declare.

Methotrexate is not associated with an increased risk of pulmonary disease in patients taking it for the treatment of psoriatic arthritis, psoriasis, or inflammatory bowel disease, a meta-analysis has found.

The analysis of results from seven double-blind, randomized, controlled studies, involving a total of 1,640 participants, showed no increased risk of total adverse respiratory events – infectious or noninfectious – or pulmonary deaths in patients taking methotrexate, compared with controls, according to Dr. Richard Conway of the department of rheumatology at Galway (Ireland) University Hospitals and his coauthors.

Dr. Richard Conway
Dr. Richard Conway

Methotrexate has previously been implicated as a cause of lung toxicity, and the prevalence of methotrexate-related interstitial lung disease has been reported as high as 11.6% in rheumatoid arthritis, but studies of methotrexate-induced lung disease are confounded by the higher risk of pulmonary infections among patients with rheumatoid arthritis, the authors said (BMJ 2015 [doi:10.1136/bmj.h1269]).

“These findings, coupled with those of a previous study in rheumatoid arthritis, suggest that methotrexate-related lung disease is rare, if it exists at all,” the investigators wrote.

The investigators had no specific source of funding for the study and had no conflicts of interest to declare.

World’s first malaria vaccine could be available by October


The world’s first viable malaria vaccine could be available by as early as October, after final trial results showed it can potentially prevent millions of cases of the deadly disease every year.

The vaccine candidate (RTS,S/AS01) is the first to reach phase 3 clinical testing and is partially effective against clinical disease in young African children up to 4 years after vaccination, according to final trial data published in The Lancet journal.

The results suggest that the vaccine could prevent a substantial number of cases of clinical malaria, especially in areas of high transmission.

The findings show that vaccine efficacy against clinical and severe malaria was better in children than in young infants, but waned over time in both groups.

However, protection was prolonged by a booster dose, increasing the average number of cases prevented in both children and young infants.
“Over 3 years of follow-up, an average 558 cases were averted for every 1,000 infants vaccinated, and 983 cases in those also given a booster dose,” said Greenwood.

The results suggest that the vaccine could prevent a substantial number of cases of clinical malaria, especially in areas of high transmission.

“Given that there were an estimated 198 million malaria cases in 2013, this level of efficacy potentially translates into millions of cases of malaria in children being prevented,” Greenwood added.

In 2014, initial phase 3 results at 18 months showed vaccine efficacy of about 46 per cent against clinical malaria in children and around 27 per cent among young infants.

“The European Medicines Agency (EMA) will assess the quality, safety, and efficacy of the vaccine based on these final data. If the EMA gives a favourable opinion, WHO could recommend the use of RTS,S/AS01 as early as October this year. If licensed, RTS,S/AS01 would be the first licensed human vacc ..

Optogenetics: Harvesting the Power of Light for Neuronal Control


       

With accolades like “method of the year” and “breakthrough of the decade,” it’s easy to assume that optogenetics—a scientific technique for turning neurons on and off using light—is, indeed, a game-changing technology. The technique has already shown promise for treating blindness,1 quieting seizures,2 and homing in on the genetic causes of brain disorders like Parkinson’s disease.3 It has also played a large role in enabling the NIH’s BRAIN Initiative, which aims to map the activity of every cell in the human brain. But, has it lived up to its hype? And what does the future hold for using optogenetics beyond simply studying how the brain works—can it also be useful in treating diseases as diverse as autism, PTSD, and depression?

The basics

Optogenetics uses light to control neurons that have been made artificially sensitive to illumination. In the lab, scientists employ viruses to introduce genes for light-sensitive proteins into neurons. First discovered in microbes, these naturally occurring proteins, called opsins, react to light. Some proteins react to light by turning neurons on, or prompting them to fire, while others turn off neuronal activity. In this way, optogenetics targets specific, modified neurons in order to discover their function and how they’re connected within larger neuronal networks.

In 2005, Dr. Karl Deisseroth, a bioengineering professor at Stanford University and a member of the Howard Hughes Medical Institute, and his then-graduate students Dr. Edward Boyden (now at MIT) and Dr. Feng Zhang (now also at MIT), published the first paper demonstrating the use of microbial opsin genes to control neuronal activity.4 In 2010, Nature Methods named optogenetics “Method of the Year,”5 and Science called it one of several “Breakthroughs of the Decade.”6

Current approaches

Optogenetics has indeed, come a long way since 2005. Its most valuable feature as a cutting-edge neuroscience tool is that it offers an unmatched level of precision in its ability to affect a specific neuron at a specific time.

Opsin proteins come from bacterial or algal genomes, where they fulfill their roles as light-activated membrane ion channels. Opsin genes are introduced into specific neurons via transfection where a virus transfers both the gene and its promoter into the host cell’s genome. “Thousands of labs around the world are now using these optogenetic techniques, and thousands of papers have been published with these methods,” Deisseroth says.

There are many tools in use, including engineered opsins that can be targeted to single neurons, groups of neurons, and connections between regions of the brain. Modified opsins include those engineered to recognize different colors of light (red, blue, or yellow); those that are activated quickly or slowly; and those that simply turn neurons on or off, resulting in a binary circuit that has many futuristic applications such as altering memories. Opsin-targeting strategies, Deisseroth says, are also using specialized viruses that only insert the opsin gene into cells of interest. “A key moment was when we were able to solve the structure of the microbial channel opsin, which allowed us to engineer it at will.”7,8,9

Recently, Ed Boyden’s group at MIT developed a “fast” opsin called Chronos,10 as well as two more opsins that are sensitive to red light, Chrimson and Jaws,11 which both silence neurons. It’s nice, Boyden notes, “because it goes deep in tissue,” reaching regions that were previously untouchable by standard fiberoptic tools consisting of lasers that send light to very small implanted optical fibers.12 “One of the obstacles to applying optogenetics is how to deliver light deep in the tissue or body,” Dr. Hiromu Yawo, a neuroscientist doing cutting-edge opsin engineering at Tokyo University, says. Fiber optic light sources are mainly used today; however, Deisseroth indicates that two-photon “spots” of light have been successfully used in living animals.

Challenges

When dreaming about the future of optogenetics, it’s important to consider that it is still early days. “We don’t have good maps of the brain, so using optogenetics is difficult for many scientific questions,” Boyden says. “We don’t often know where to stimulate.”

Activating deep brain tissue is also problematic. “As the visible light is absorbed by the tissue, the light sources have to be embedded in it for the optogenetic manipulation of deep tissue,” Yawo says. Infrared can go deep, but to date there is no opsin sensitive to this type of light. Additionally, viral vectors are difficult to apply to humans; neuronal selectivity depends on targeted promoters reaching their place in the genome. According to Yawo, these promoters are “mostly unidentified” in humans. “Even if identified, [the gene] is often too large to deliver efficiently or it is too weak to produce enough number of molecules to generate [a] response.”

There’s also cost. Says Deisseroth, “the main disadvantages include the light power requirements associated with targeting large numbers of individually specified cells. That requires fairly advanced and costly lasers.” However, standard optogenetics control is “actually relatively easy and cheap to do now, and we run training classes at Stanford to help people out in getting started,” he says.

Applications

While it has been mainly used as a way to study how individual neurons fire alone or in concert with other neurons or circuits of neurons, a slew of recent papers have helped elucidate pathways of many different diseases. For instance, research has demonstrated the use of optogenetics on D1 and D2 cells (types of dopamine receptors) in the striatum13 and subthalamic nucleus14 in mice, as a way to explore their role in Parkinson’s disease. Other work has involved finding what cells can be manipulated to alter fear memories, applicable to treating PTSD and other illnesses that revolve around conditioned fear responses;15 elucidating neural networks involved in autism;16 and testing the causal link between dopamine expression and positive reinforcement in mental health disorders like addiction17 and depression.18 Clinically, optogenetics could theoretically be used to treat diseases as diverse as Parkinson’s disease, PTSD, autism, schizophrenia, addiction, and depression, to name a few.

The future of optogenetics seems wide open. GenSight Biologics19, a company founded by leaders in the fields of ophthalmology and optogenetics, is aiming to use the technique to treat blindness caused by diseases resulting from cell loss in the retina, including glaucoma and retinal pigmentosa. Using optogenetics on other cell types has already gained some traction in research labs, with cardiac cells and stem cells being some of the prime non-neuronal targets. It’s also been adapted to study biochemical, instead of electrical, events, “opening the door to control of specific events in any cell in biology,” Deisseroth says. According to Yawo, events as diverse as “ionic microenvironment, signal transduction, enzymatic activity, and gene regulation are now under the targets of optogenetics.”

Optogenetics is being used in conjunction with other technologies too, to speed up the translation from lab to clinic. In a recent Science paper,20 scientists at the University of Geneva used a combination of deep brain stimulation—a proven tool to treat Parkinson’s disease—and a drug to block specific dopamine receptors to produce an “optogenetic-like” effect in lab mice. Ultimately, the mice’s cocaine use was reduced, underscoring the possibility of achieving the same effect in humans without having to solve the technological hurdles that applying optogenetics poses.

“The future is continued widespread use as a research tool,” Deisseroth says, to advance our still-small understanding of how individual neurons function in larger circuits. Indeed, when it comes to the brain, the whole is much greater than the sum of its parts, and optogenetics might be the best bet for probing not only deep, but far and wide.

Editor’s Note: Listen to Ed Boyden discuss his research in The Scientist’s on-demand webinar: New Models and Tools for Studying Synaptic Development and Function.

References
  1. 1. Picaud S et al. (2013) Retinitis pigmentosa: eye sight restoration by optogenetic therapy. [Article in French] Biol Aujourdhui 207(2):109-121.
  2. 2. Kullmann DM et al. (2012) Optogenetic and potassium channel gene therapy in a rodent model of focal neocortical epilepsy. Sci Transl Med 4(161):161ra152.
  3. 3. Vazey EM, Aston-Jones G (2013) New tricks for old dogmas: optogenetic and designer receptor insights for Parkinson’s disease. Brain Res 1511:153-163.
  4. 4. Deisseroth K et al. (2005) Millisecond-timescale, genetically targeted optical control of neural activity. Nat Neurosci 8(9):1263-1268.
  5. 5. Editorial (2011) Method of the Year 2010. Nat Methods 8(1).
  6. 6. News Staff (2010) Insights of the decade. Stepping away from the trees for a look at the forest. Introduction. Science 330(6011):1612-1613.
  7. 7. Staff (2012) Channelrhodopsin’s crystal structure. Nat Methods 9(224).
  8. 8. Deisseroth K et al. (2014) Structure-guided transformation of channelrhodopsin into a light-activated chloride channel. Science 344(6182):420-424.
  9. 9. Hegemann P et al. (2014) Conversion of Channelrhodopsin into a Light-Gated Chloride Channel. Science 344(6182):409-412.
  10. 10. Boyden ES et al. (2014) Independent optical excitation of distinct neural populations. Nat Methods 11(3):338-346.
  11. 11. Boyden ES et al. (2014) Noninvasive optical inhibition with a red-shifted microbial rhodopsin. Nat Neurosci (8):1123-1129.
  12. 12. Deisseroth K et al. (2007) An optical neural interface: in vivo control of rodent motor cortex with integrated fiberoptic and optogenetic technology. J Neural Eng 4(3):S143-156.
  13. 13. Kreitzer AC et al. (2010) Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry. Nature 466:622–626
  14. 14. Deisseroth K et al. (2009) Optical deconstruction of parkinsonian neural circuitry. Science 324(5925):354-359.
  15. 15. Deisseroth K et al. (2011) Dynamics of Retrieval Strategies for Remote Memories. Cell 147(3):678-689.
  16. 16. Deisseroth K et al. (2014) Natural neural projection dynamics underlying social behavior. Cell 157(7):1535-1551.
  17. 17. Deisseroth K et al. (2011) Recombinase-driver rat lines: tools, techniques, and optogenetic application to dopamine-mediated reinforcement. Neuron 72(5):721-733.
  18. 18. Deisseroth K et al. (2013) Dopamine neurons modulate neural encoding and expression of depression-related behaviour. Nature 493(7433):537-541.
  19. 19. GenSight http://www.gensight-biologics.com
  20. 20. Creed M, Pascoli VJ, Lüscher C (2015) Refining deep brain stimulation to emulate optogenetic treatment of synaptic pathology. Science 347(6222):659-664.

– See more at: http://www.neuroscientistnews.com/neuroinsights/optogenetics-harvesting-power-light-neuronal-control#sthash.s9TXGYPg.dpuf

Quantum Equation Suggests The Big Bang Never Occurred – The Universe Has No Beginning


bigbang
When it comes to the science regarding the true nature of our reality, you won’t find a shortage of theories, or a shortage of criticisms of each theory. We are like a race with amnesia, trying to discover and search for an answer that most probably exists, but has yet to be discovered. How did the universe begin?

According to new research, there might not have been a big bang. Instead, the universe might have existed forever. The theory was derived from the mathematics of general relativity, and compliment Einstein’s theory of general relativity.

“The Big Bang singularity is the most serious problem of general relativity because the laws of physics appear to break down there.”  – Ahmed Farag Ali, Benha University, Co-Author of the study.

The big bang theory postulates that everything in existence resulted from a single event that launched the creation of the entire universe and that everything in existence today was once part of a single infinitely dense point, also known as the “singularity.”

Here is a good picture representing what the big bang theory is referring to.

bang

So the big bang, again, postulates that the universe started out as an infinitely small point in space called a singularity, then exploded and created space where there was no space before, and that it is continually expanding. One big question regarding that expansion is; how did it happen? As you can see in the picture, “who is that guy?!”

According to Nassim Haramein, the Director of Research for the Resonance Project

“For every action there is an equal opposite reaction.” is one of the most foundational and proven concepts in all of physics. Therefore, if the universe is expanding then “the guy” (or whatever “he” is), who is blowing up that balloon, has to have some huge lungs that are contracting to be able to blow it up. This a concept that Nassim Haramein began exploring when creating an alternative unified field theory to explain the universe.” 

This is one out of many criticisms regarding the big bang theory. There are many considerations to be pondered. Can something come from nothing? What about quantum mechanics and the possibility that there is no moment of time at which the universe did not exist?

Again, so many considerations to be pondered.

According to Phys.org:

“The scientists propose that this fluid might be composed of gravitons—hypothetical massless particles that mediate the force of gravity. If they exist, gravitons are thought to play a key role in a theory of quantum gravity.In a related paper, Das and another collaborator, Rajat Bhaduri of McMaster University, Canada, have lent further credence to this model. They show that gravitons can form a Bose-Einstein condensate (named after Einstein and another Indian physicist, Satyendranath Bose) at temperatures that were present in the universe at all epochs.” (source)

The theory also suggests (obviously) that there are no singularities or dark matter, and that the universe is filled with a “quantum fluid.” These scientists are suggesting that this quantum fluid is filled with gravitons.

According to Phys.org:

“In a related paper, Das and another collaborator, Rajat Bhaduri of McMaster University, Canada, have lent further credence to this model. They show that gravitons can form a Bose-Einstein condensate (named after Einstein and another Indian physicist, Satyendranath Bose) at temperatures that were present in the universe at all epochs.”

As you can see, when quantum mechanics is thrown into the equation things appear to be far different. Again, this new theory is suggesting that the universe could have always existed, that it never was what we perceive to be as “the  beginning.” Perhaps it was just an event that did occur that we perceive as the beginning, perhaps the event occurred not from nothing, but something. Again, who is that guy blowing on the balloon in the picture? There is something there that has yet to be discovered.

“As far as we can see, since different points in the universe never actually converged in the past, it did not have a beginning. It lasted forever. It will also not have an end, in other words, there is no singularity. The universe could have lasted forever. It could have gone through cycles of being small and big. or it could have been created much earlier.” –  Saurya Das at the University of Lethbridge in Alberta, Canada, Co-Author of the study.

What We Know Is Often Just Theory

To conclude, it’s clear that we do not yet have a solid explanation regarding what happened during the Big Bang, or if it even happened at all. This new theory is combining general relativity with quantum mechanics, and at the end of the day these are all just theories.

Not to mention the fact that theories regarding multiple dimensions, multiple universes and more have to be considered. When looking for the starting point of creation, our own universe might not even be the place to start. It might be hard given the fact that we cannot yet perceive other factors that have played a part in the make up of what we call reality. What is even harder is the fact that quantum physics is showing that the true nature and make up of the universe is not a physical material thing!

We just don’t know yet, and there are still new findings in modern day physics that delve into non-materialistic science that many mainstream materialistic scientists have yet to grasp and acknowledge.

I’ll leave you with a quote that might give you something to think about:

“A fundamental conclusion of the new physics also acknowledges that the observer creates the reality. As observers, we are personally involved with the creation of our own reality. Physicists are being forced to admit that the universe is a “mental” construction. Pioneering physicist Sir James Jeans wrote: “The stream of knowledge is heading toward a non-mechanical reality; the universe begins to look more like a great thought than like a great machine. Mind no longer appears to be an accidental intruder into the realm of matter, we ought rather hail it as the creator and governor of the realm of matter.” (R. C. Henry, “The Mental Universe”; Nature 436:29, 2005)

“Despite the unrivaled empirical success of quantum theory, the very suggestion that it may be literally true as a description of nature is still greeted with cynicism, incomprehension and even anger. (T. Folger, “Quantum Shmantum”; Discover 22:37-43, 2001)

Sources:

http://arxiv.org/abs/1404.3093v3

http://phys.org/news/2015-02-big-quantum-equation-universe.html

Brugada Syndrome .


Brugada Syndrome is a genetic disorder characterised by right bundle branch block pattern with ST segment elevation and T wave inversion in right precordial leads. Life threatening ventricular arrhythmias are the hallmark of Brugada Syndrome. The disorder was described by Brugada brothers (Pedro, Joseph and Ramon) in 1992. Later on the genetic defect was localised to the sodium channel gene SCN5A. Patients with Brugada Syndrome may sometimes present with electrical storm. Medical treatment is generally unsatisfactory for Brugada syndrome. Drugs like quinidine and cilostozol have been useful in reducing the number of episodes of ventricular tachyarrhythmia. Those with previous cardiac arrest, especially with a family history of sudden cardiac death need to be protected by an implantable cardioverter defibrillator (ICD). ICDs can detect and treat ventricular tachycardia either by overdrive pacing suppression or cardioversion.

brugada

Image courtesy: Francis J, Sajeev CG, Venugopal K. Brugada Syndrome: The Enigma. Calicut Medical Journal 2003;1(1):e3

Sometimes the classical Brugada pattern in the ECG may not be obvious and has to be brought out by flecainide challenge.

Why People Love Their Dogs So Much, According to Science


Photo: Getty Images

You don’t have to tell dog lovers the feeling is both mutual (and very real), but a new study published in the journal Science reveals the fascinating reason why we feel so close to our furry companions: When humans and dogs look into each other’s eyes, both get a boost of the feel-good hormone oxytocin, which is the same hormone behind the special bond between new parents and their babies.

To reach their results, researchers had 30 dog-and-human pairs come into a lab to look in each other’s eyes and give urine samples. Oxytocin concentrations were then measured in the human and animal samples. In the end, the dogs had a 130% rise in oxytocin levels, and owners showed a 300% increase, regardless of gender.

Your pets do a lot more than just make you feel happiness and love: They can also help lower your cholesterol, relieve stress, and boost your self-esteem.

If this has finally convinced you it’s time to get a dog, do your research. Learn about active or hypoallergenic breeds, and don’t forget about the many shelter pets in need of homes!

Already have a dog? Now that it’s spring, get ready to hit the trails, beach, or sidewalk with your four-legged friend. Staying in shape is good for the both of you

This Stroke of Genius Could Allow You to Write With Your Brain


The notion of a nefarious power somehow dictating what individuals say and do by tampering with their brains is, for the moment at least, still fictional. But there’s a less diabolical kind of mind control and it’s very real, as Mick Ebeling is happy to show you.

In his Venice, California, laboratory he is developing a device that will permit disabled people to write with their minds—no pencil strokes or keystrokes required. Called the Brainwriter, it combines new, low-cost headsets that monitor the brain’s electrical activity with eye-tracking technology and open-source software. By thinking about a single idea or word, a person can command a computer cursor to enter writing mode, the equivalent of putting pen to paper. Then, as the eyes move, the cursor traces their path on-screen.

“I like to see things that are not supposed to be done, be done,” says Ebeling, co-founder of the hopeful-sounding company Not Impossible. He’s not an engineer himself—he’s a film and TV producer—so he recruits technical experts to help him solve real-world problems. “Help one, help many” is one of his mantras. For instance, Ebeling and his team 3-D-printed prosthetic arms for amputees in South Sudan, starting with a teenage boy named Daniel.

 Brainwriter was inspired by an L.A. graffiti artist named Tony Quan (tag name Tempt One), who is afflicted by amyo­trophic lateral sclerosis and no longer has control over his muscles. At first, Ebeling and his crew fashioned a device out of plastic eyeglasses, a coat hanger and a hacked-open PlayStation 3 camera. “Steve Jobs would roll over in his grave if he saw our stuff,” Ebeling says. In this version, Quan blinked to enter writing mode and select his drawing tools. But as his condition worsened, he could no longer control the device with his blinks.

So the next step was to tap into brain waves, monitored via electroencephalogram. A focusing brain produces a particular EEG pattern, which the computer software recognizes and processes the same way it processes the click of a mouse. Still in the testing phase, Brainwriter will give patients with paralysis a new way to communicate, more efficient than the current method of spelling out words letter by letter. In later iterations, it might be adapted for people with no control over their eye movements. “Mick will unashamedly and unabashedly say that our solution is not the end word,” says David Putrino (left), a neuroscientist who works with Not Impossible. “Our solution is a lesson that it can be done.”

Ebeling predicts that someday soon similar technologies will not only help disabled people but will also enhance the way everyone communicates. Ordinary baseball caps studded with EEG sensors will be sold at the mall. You won’t necessarily compose a sonnet with them, but you’ll be able to perform simple actions, like making a dinner reservation. While other developers hack the brain to make a toy robot walk or control a video game, Ebeling strives for a technology more akin to the telephone. “Just being able to convey information,” he says, “is huge.”

 

Immunity Against Contagious Diseases


Rubella is a mild viral disease occurring usually in early childhood. It would be disregarded except for the fact that when the disease occurs in a pregnant woman, strong likelihood exists that the fetus will suffer serious adverse effects. This fact accounts for the extensive efforts to administer rubella vaccine to all children to ensure that they will not acquire and transmit the disease to nonimmune pregnant mothers.

Schiff et al,1 reported the extent of rubella susceptibility among high school students in a remote resort town in north central Wisconsin. Blood was collected from the students during school hours and later tested for rubella immunity at the Clinical Virology Laboratories in Cincinnati. With parental permission, 127 boys and 215 girls participated, only ten of whom had received rubella immunization. Although 37% of the students gave a history of previous rubella, there was no correlation between the history and susceptibility to the disease; 48% of students with such a history were found to be susceptible.

Transgender Suicide Attempt Rates Are Staggering


Teenager Ash Haffner’s suicide last week is the latest example of an alarming statistic plaguing the trans and gender non-conforming community

Ash Haffner died in North Carolina last Thursday—another transgender teen lost to suicide. His mother says the 16-year-old had encountered bullying, which worsened when he began to transition publicly. “Ash had been so strong for years,” she said, using the female pronoun. “Ash started enduring the most bullying when she cut her hair short.”

Haffner’s death follows that of Leelah Alcorn, the 17-year-old transgender high schooler from Ohio, whose suicide attracted international attention last December and ignited a broader debate about early transition and conversion therapy. But perhaps most troubling about the deaths of these two young people is that they’re part of a broader trend in the U.S., which sees a disproportionate number of transgender and gender non-conforming teens and adults attempting suicide.

The most recent, comprehensive data on suicide attempts was gathered by The Williams Institute, in collaboration with the American Foundation for Suicide Prevention. Its report, Suicide Attempts Among Transgender and Gender Non-Conforming Adults, analyzed responses from 6,456 self-identified transgender and gender non-conforming adults (18+) who took part in the U.S. National Transgender Discrimination Survey. The results are staggering.

Beyond the overall number of suicide attempts, the rates are consistently high from respondents ages 18 to 65, when they begin to recede. Trans men are the most impacted, with 46 percent reporting an attempt in their lifetime. Trans women are close behind at 42 percent, and female-assigned cross-dressers report rates of 44 percent.

“Parents of transgender youth have to take the time to listen to their kids when they’re trying to assert their gender identity,” says Vincent Paolo Villano, Director of Communications at The National Center of Transgender Equality. “At the school level, teachers and administrators have to understand what policiesneed to be in place to make sure that transgender students are learning and thriving in school, and give them the space to be who they are.”

If you or someone you know is struggling with depression or suicidal thoughts, callThe Trevor Project on 866-488-7386.

Exercise ‘not key to obesity fight’


Physical activity has little role in tackling obesity – and instead public health messages should squarely focus on unhealthy eating, doctors say.

In an editorial in the British Journal of Sports Medicine, three international experts said it was time to “bust the myth” about exercise.

They said while activity was a key part of staving off diseases such as diabetes, heart disease and dementia, its impact on obesity was minimal.

Instead excess sugar and carbohydrates were key.

The experts, including London cardiologist Dr Aseem Malhotra, blamed the food industry for encouraging the belief that exercise could counteract the impact of unhealthy eating.

They even likened their tactics as “chillingly similar” to those of Big Tobacco on smoking and said celebrity endorsements of sugary drinks and the association of junk food and sport must end.

They said there was evidence that up to 40% of those within a normal weight range will still harbour harmful metabolic abnormalities typically associated with obesity.

But despite this public health messaging had “unhelpfully” focused on maintaining a healthy weight through calorie counting when it was the source of calories that mattered most – research has shown that diabetes increases 11-fold for every 150 additional sugar calories consumed compared to fat calories.

And they pointed to evidence from the Lancet global burden of disease programme which shows that unhealthy eating was linked to more ill health than physical activity, alcohol and smoking combined.

‘Unscientific’

Dr Malhotra said: “An obese person does not need to do one iota of exercise to lose weight, they just need to eat less. My biggest concern is that the messaging that is coming to the public suggests you can eat what you like as long as you exercise.

“That is unscientific and wrong. You cannot outrun a bad diet.”

But others said it was risky to play down the role of exercise. Prof Mark Baker, of the National Institute of Health and Care Excellence, which recommends “well-balanced diets combined with physical activity”, said it would be “idiotic” to rule out the importance of physical activity.

Ian Wright, director general at Food and Drink Federation, said: “The benefits of physical activity aren’t food industry hype or conspiracy, as suggested. A healthy lifestyle will include both a balanced diet and exercise.”

He said the industry was encouraging a balanced diet by voluntarily providing clear on-pack nutrition information and offering products with extra nutrients and less salt, sugar and fat.

“This article appears to undermine the origins of the evidence-based government public health advice, which must surely be confusing for consumers,” he said.