The 20 Min Morning Ritual For Weight Loss Success

The 20 Min Morning Ritual For Weight Loss Success

The 20 Min Morning Ritual For Weight Loss Success

It is a mistake to think that losing or gaining weight comes down to just calories. Many studies demonstrate the multitude of factors beyond what we eat that affect our weight. So the best way to assure a proper weight is to create balance on many different levels. And since the morning sets the tone for the entire day, a healthy morning routine will increase your odds of weight loss success.

And before your write off what I’m saying as “hippie talk”, understand one thing. How much fat we store as well as how hungry we feel is determined by the hormones leptin and insulin. In order for anyone to successfully lose weight, these two hormones must be working correctly. These hormones communicate with every other hormone in our bodies, so in order for these hormones to be working correctly, we must have something close to total body balance. Too much stress hormones, or too many inflammatory markers, and your weight loss hormones will be headed for a tailspin.

So, without further delay, here is my:


20 Minute Morning Routine For Weight Loss

1. Write in a gratitude journal

Before you even get out of bed, take a couple of minutes down what you are thankful for. Why a gratitude journal? Because as difficult as life can get, you still probably have good things in your life. Focusing on the positive at the start of the day will raise the “feel good” hormones and will relieve stress hormones.Stress is bad for the waist line for a couple of reasons. First, studies have shown that those who are stressed find fattening foods more rewarding, leading to overeating. Second, the cortisol spike that accompanies stress can actually make your body less receptive to insulin, the fat storing hormone. When sensitivity to insulin goes down, fat storage goes up and it becomes easy to pack on the pounds. Plus, taking a couple of minutes to focus on the good sets you up for a happier day. And a slim waist line doesn’t mean anything if you aren’t happy on the inside.

2. Stretch

This might mean touching your toes, stretching your arms, or anything else that improves flexibility. Stretching can help you have an improved range of motion and can relieve muscle tension. Muscle tension can create a similar stress response as emotional stress. This is especially true when muscle tension is also associated with physical pain. When you feel better physically, you are happier emotionally and that has a positive hormonal effect on the body. Additionally, stretching can get your blood flowing, giving you more energy. When the body is energized, you are less likely to crave fattening foods like sugar and refined carbohydrates which can provide the body with a quick burst of energy. Finally, feeling better physically will make you much more likely to exercise later in the day. Aches and pains can easily be an excuse to skip a trip to the gym. If you are looking for a quick stretching routine to start your morning, you can try this one.

3. Drink a Glass of Water

You are naturally dehydrated when you wake, even if you don’t feel signs of thirst. Dehydration will eventually lead to inflammation. The inflammatory markers associated with inflammation can interact with the hormones insulin and leptin, throwing them off balance. If that doesn’t provide enough motivation to stay hydrated, consider this 2003 study published in The Journal of Clinical Endocrinology and Metabolism. This study found that drinking 500ml of water had a thermogenic effect that increased metabolism by 30%. Once you feel signals of thirst, you are already in a severe state of dehydration. Start off the day with a glass of water before you are thirsty! For extra credit, add a squeeze of lemon. Lemon water first thing in the morning will help ready your digestive system for the day. And when your digestive system is more effective, your food is processed more effectively which will support a healthy weight.

4. Detoxify by body brushing

If you have never heard of body brushing before, you can get a detailed explanation right here. Most of us are exposed to a high level of toxicity in our daily lives. High levels of toxicity cause system-wide inflammation which, as already mentioned, has a disastrous effect on the hormones that are needed to control weight. While true detoxification is a detailed process, small habits can help allay the toll of living in a world of high toxicity. Body brushing is a simple process of brushing the skin to awaken the lymphatic system and get it moving. When the lymphatic system is working correctly, it effectively removes toxins from the body. When you lower the inflammation associated with toxicity, the body will be much more sensitive to insulin which means your body will be programmed to store less fat. Body brushing should only take a couple of minutes. Another positive side of body brushing is that it can be very energizing, which is just what you need first thing in the morning.

5. Eat Something

I’ve talked at length in the past about what constitutes a good breakfast. While having a good breakfast is extremely important, what is more important is just to eat something. So if you really don’t have time for breakfast. grab a piece of fruit or a few whole grain crackers or anything that will wake up your metabolism. Studies show that those who wait until later in the day to eat have higher levels of the hormone ghrelin during the day. Ghrelin is the hormone responsible for informing your brain that you’re hungry. Eating in the first half hour of the day will not only give your metabolism an early wake-up, meaning you will potentially burn more calories in the early part of the day. It will also better ensure that you will have more controlled hunger signals, which can improve your eating habits for the rest of the day.

So there you have it! This 20-minute routine which will help your body be balanced, will help give a positive start to your day and will help ready your body for weight loss. Of course, this routine doesn’t give you permission to overindulge later in the day. True weight loss comes from a consistent practice of health supporting habits. But this routine is a great foundation for your day. It will help you get the most out of all the other healthy choices you make later. And in weight loss, every little bit helps, doesn’t it?

This World Diabetes Day, watch out for these early signs of diabetes

Young adults and children are also prone to diabetes. Read to know how one could detect the early symptoms and keep this disease at bay.

46% people in the world suffer from this lifestyle disease and remain undiagnosed. Picture courtesy

So you too thought children are not amongst the ones who are affected by diabetes? You’re wrong, because most children are affected by Type 1 diabetes throughout the world. India, has the second highest number of people with diabetes, out of which more than half of them are undiagnosed. We spoke to Dr Sujeet Jha, Director, Institute of Endocrinology, Diabetes and Metabolism, Max Health Care and he gave us an insight into the world of diabetes–The Silent Killer.

Dr Jha said “As Indians, we are more prone to weight gain and when combined with our inherent genetics, it further increases our chances of developing the condition. As a result, we need to be extra careful with our carbohydrate and fat intake.  It is very important to detect diabetes at an early stage as this allows us to intervene sooner and prevent further onset of complications. Diabetes is rightly thought to be a silent killer, capable of affecting any organ in the body from our head to toe.  If you have diabetes mellitus, chances are it will stay with you for the rest of your life.”


What is Diabetes?
The condition exists in two different forms; namely Type 1 and Type 2. Type 1 occurs when the immune system destroys cells in the pancreas called beta cells which are the ones that make insulin. It’s a rare type and was previously known as juvenile diabetes since it targets only young adults and children. However, the age is not restricted and only about 5% of people with diabetes get diagnosed by Type 1. Type 2 diabetes mellitus results from a combination of factors (like an individual’s genetics or their lifestyle choices) and occurs when a person’s own insulin can no longer control the body’s blood sugar levels.

Dr Jha added, “What is even more shocking is close to 46% people in the world suffer from this lifestyle disease and remain undiagnosed.”

If you experience one or more of the following signs, you might be suffering from diabetes.

” Increased frequency of urination
” Increased thirst
” Increased hunger
” Blurring of vision
” Sudden, unexplained weight loss
” Increase in the occurrence of infections such as boils on the skin

Certain risk factors that can make you more susceptible to developing diabetes are:
” Physical inactivity
” First-degree relative with diabetes
” High body mass index (BMI)
” Hypertension
” Women with polycystic ovarian syndrome (PCOS)
” Other clinical conditions associated with insulin resistance like severe obesity, acanthosis nigricans–a velvety, hyper-pigmentation of the skin.

Even though there is no cure for diabetes but by following these simple things daily, you could make a big difference.
” Eating healthy meals: Sticking to a diabetic meal plan will help, as apart from direct sugar intake, you need to keep a check on the natural sugar that comes along with fruits and vegetables.
” Exercising regularly: Regular walks or mild jogging will help you keep in shape and normalize the blood glucose levels.

If you still have any further health concerns, you must visit the nearest physician the earliest.

How to cope with traumatic news – an illustrated guide.

How to cope with traumatic news, an illustrated guide


It’s hard not to be upset by rolling media coverage of an unfolding tragedy.

People exposed to more than six hours of daily coverage of a disaster are more likely to feel vulnerable, despairing, alienated and irritable.

They are also more likely to suffer from feelings of a loss of identity or a sense of failure, as well as sleeplessness.

They can also experience intrusive thoughts and images of the event. And small, daily events can have a bigger impact than usual.

Apart from limiting exposure to media, there are things people can do to look after themselves: make sure they get enough sleep; exercise regularly; eat well; avoid using drugs and alcohol to cope; spend time with loved ones; do things they enjoy; get back into their usual routine.

Children are especially sensitive to media coverage of disasters.

They might worry the same sort of thing will happen to them and their family, and fail to understand it’s a one-off, discrete event.

Parents shouldn’t necessarily try to shield their children. Keeping secrets is not possible in this day and age, and trying to hide events can make things more terrifying.

Instead parents should try to limit the amount of media the child is exposed to, while explaining what has happened and answering their questions.

It is also important to speak to the child about their feelings and do something with them, like playing a game or heading outside. Providing comfort and affection will help the child to feel safe. Parents can also remind their child there are plenty of good things that happen that don’t make the news.

100 Years of the General Theory of Relativity.


It was 100 years ago this month that Einstein delivered four lectures to the Prussian Academy of Sciences in Berlin, which culminated in his discovery of the general theory of relativity. (If that theory rings a bell but you’re not entirely sure what it means.)

Einstein’s determined pursuit of mathematical equations that describe how the force of gravity works remains one of the most influential scientific discoveries of all time.

If you’re planning a party — a general relativity rave, maybe — November 25th is the day it all came together. That’s a Wednesday. But a Thanksgiving toast at dinner the next day works well, too.

To celebrate, physicist Brian Greene looks back on the intellectual and emotional journey Einstein took to arrive at the general theory of relativity in an article in Smithsonian Magazine. In March, Greene joined neurologist Frederick Lepore and filmmaker Thomas Levenson during the 92Y’s 7 Days of Genius Festival for a conversation about what made Einstein such a talented scientist. The conversation is moderated by Cynthia McFadden of NBC News.

If you still have room for more Einstein, the 2015 World Science Festival brought together Gabriela González, Samir Mathur, Andrew Strominger, Cumrun Vafa, Steven Weinberg and Brian Greene to discuss Reality Since Einstein.

Is it a rocket? Is it a plane?

A potentially game-changing rocket engine has attracted significant new investment to allow it to enter development.

A potentially game-changing rocket engine has attracted significant new investment to allow it to enter development.

The Synergetic Air-Breathing Rocket Engine (Sabre) combines elements of a jet and rocket engine. It is designed to enable a “spaceplane” to take off from a conventional runway and “fly” into orbit.

Once its mission is over it would return to land like any other aeroplane. Thus it is reusable, and should make launches cheaper than a conventional rocket.

Sabre is the brainchild of British engineer Alan Bond, who founded Reaction Engines in 1989 to develop his ideas.

The viability of the engine has been validated by the European Space Agency (ESA) during a review undertaken at the request of the UK government. This has resulted in the government’s awarding £50m to aid preparations for the design, manufacture and testing of demonstration engines. The ESA is currently drawing up a contract worth $10m.

Now a private investment has also been announced. Global aerospace companyBAE Systems will invest £20m in return for 20% of Reaction Engine’s share capital, and will enter into a working partnership with them. This will allow the firm to move towards the manufacture of ground-based test engines, a key milestone.

Sabre must first work as a jet engine and accelerate spaceplanes to more than five times the speed of sound. By changing the way it works, it then becomes a rocket engine, accelerating to more than 25 times the speed of sound, fast enough to put the spaceplane into orbit.

The Synergetic Air-Breathing Rocket Engine (Sabre) combines elements of a jet and rocket engine. It is designed to enable a “spaceplane” to take off from a conventional runway and “fly” into orbit.

Once its mission is over it would return to land like any other aeroplane. Thus it is reusable, and should make launches cheaper than a conventional rocket.

Sabre is the brainchild of British engineer Alan Bond, who founded Reaction Engines in 1989 to develop his ideas.

The viability of the engine has been validated by the European Space Agency(ESA) during a review undertaken at the request of the UK government. This has resulted in the government’s awarding £50m to aid preparations for the design, manufacture and testing of demonstration engines. The ESA is currently drawing up a contract worth $10m.

Now a private investment has also been announced. Global aerospace companyBAE Systems will invest £20m in return for 20% of Reaction Engine’s share capital, and will enter into a working partnership with them. This will allow the firm to move towards the manufacture of ground-based test engines, a key milestone.

Sabre must first work as a jet engine and accelerate spaceplanes to more than five times the speed of sound. By changing the way it works, it then becomes a rocket engine, accelerating to more than 25 times the speed of sound, fast enough to put the spaceplane into orbit.

Fingolimod May Protect Neurons from Degeneration

Effect appears independent of main mechanism of action in MS
  • Can the multiple sclerosis drug fingolimod (Gilenya) protect neurons from degenerating? An early cell study suggests it can, particularly in the presence of human immunodeficiency virus.

In a basic science laboratory study of HIV-exposed neurons, fingolimod upregulated the expression of a number of genes, including NESTIN, a structural protein found in progenitor cells; MAP2, a protein involved in microtubule processes; SOX2, a transcription factor found in immature cells; and S1Pr1, S1Pr3 and S1Pr5, three forms of the sphingosine-1-phosphate receptor that fingolimod binds to; as well as native immune response genes such as IFI6, which is thought to play a role in the regulation of apoptosis, lead investigator Micheline McCarthy, MD, of the University of Miami Miller School of Medicine and the Miami VA HealthCare System, told MedPage Today. The work was presented here at the American Neurological Association‘s annual meeting.

Fingolimod is a sphingosine-1-phosphate receptor modulator that prevents MS relapses by sequestering lymphocytes in lymph nodes, it is believed, preventing them from circulating and contributing to an autoimmune reaction. But the current study suggests it may have an independent neuroprotective effect.

“If validated, the data indicate that fingolimod may have a protective role on human neuronal progenitors and maturing neurons by promoting neurogenesis and preventing apoptosis,” McCarthy said. The results were interesting, she added: “People don’t think of neurons as immunologically active cells but they do actually have some capacity to mount an immune response.”

During phase III clinical trials of fingolimod, the first oral disease-modifying drug approved by the FDA for the relapsing form of MS, there were indications that brain volume loss was slower in patients taking the drug, McCarthy said: “That’s raised the question of whether fingolimod has the ability to protect neurons.”

HIV, one of McCarthy’s areas of interests, “is well known for its devastating effects on the brain, and even though neurons are not known to be to be infected directly by HIV, exposure to HIV or HIV proteins causes neuronal toxicity and neuronal cell death,” she said. “Even in well-controlled infection in which antivirals suppress the virus replication in circulation, there is still a long-term impact of the chronic infection and inflammation that goes with it on cognition.”

For the study, McCarthy and colleagues adapted human neuronal progenitor cell line hNP1, derived from human embryonic stem cell line WA09, to test the neuroprotective capacity of fingolimod in neurons exposed to HIV.

HNP1 cells were differentiated in medium alone, or in medium with added supernatants from mock-infected or HIV-infected lymphocytes, with or without added fingolimod. Fingolimod’s effect on the cells initially was studied in concentrations of 10 μM, 1μM, 100 nM, and 10 nM. Higher concentrations of the drug proved to be toxic to the cells.

In other experiments, duplicate cultures of hNP1 cells were incubated with differentiation medium alone (untreated) or with differentiation medium containing 100 nM unphosphorylated fingolimod. On days 11, 12, 18, and 20, McCarthy and colleagues harvested cells and used reverse transcriptase polymerase chain reaction (RT-PCR) to look for expression of genes for neurogenesis, neuronal function, and immune response.

The team also studied the drug’s impact on cells incubated alone or with mock supernatants from uninfected peripheral blood mononuclear cell (PBMC) cultures stimulated with phytohaemagglutinin and interleukin-2, performing RT-PCR on the cells on days 12, 18, and 20. And they studied fingolimod’s effect on hNP1 cells incubated with differentiation medium containing 10 mg p24 equivalent per ml of HIV, or mock supernatants from uninfected, mitogen activated PBMC cultures, conducting RT-PCR on days 12, 18, and 20.

Gene expression in cells exposed to mock supernatants was not affected by fingolimod. “Thus, fingolimod may enhance the expression of certain neuronal genes in HIV-exposed human neurons, possibly protecting against negative viral effects on gene expression,” McCarthy and colleagues wrote in their abstract.

“The implication is that the drug could be used to protect neurons from the degenerative phase of (MS),” McCarthy said. “The other possibility is it might have some role in HIV infection in chronic, well-controlled HIV infection to prevent neurologic decline.” She and her colleagues are planning a larger microarray study of genes affected by HIV and fingolimod.

Hope for Chronic Fatigue Syndrome

The debate over this mysterious disease is suddenly shifting.

That might sound like good news—but I knew these researchers’ past work very well, and it had only added to the misery of CFS patients like me. Back in 2011, I watched the headlines spread around the world when the team, funded by the British government, published the first results in the Lancet—while I was desperately ill in bed, reading the news on my phone, too weak to sit up to use my computer.

 I—and a lot of other people with knowledge of CFS—couldn’t believe what we were reading. Psychotherapy had helped me keep my sanity while my body fell apart, but it had never made me less sick. And the hallmark symptom of the illness is that exertion can make patients much, much worse. I’d learned through hard experience that the only way I could exercise safely was to stop as soon as the thought “I’m a little tired” wafted through my brain. Walking five minutes yesterday was no guarantee I could safely walk six minutes today—and if I misjudged and overdid it, I’d be semi-paralyzed later.

But according to the theory underlying this psychiatric research, my problem was that I was out of shape, afraid of exercise, and obsessed about my symptoms. The path to wellness was to drop the idea that I had a physical disease and steadily increase my exercise, no matter how bad it made me feel.

Patients rapidly discovered serious scientific problems with the 2011 Lancet paper. Despite these errors, the study, known as the PACE trial, went on to inform recommendations from such influential bodies as the Centers for Disease Control and Prevention, the Mayo Clinic, and the British National Health Service. So the new follow-up study, I feared, seemed destined for a warm and uncritical reception from the medical establishment regardless of whether its findings were legitimate.

But just days before the new study was released, on Oct. 21, the San Francisco journalist David Tuller published a major investigation exposing deep methodological flaws in the entire PACE trial that put its validity in serious doubt.

And this time, the new study has been met with intense criticism from outside the world of patients and advocates. On Friday, six researchers, including prominent scientists such as virologist Vincent Racaniello of Columbia University and geneticist Ronald Davis of Stanford University, released an open letter to the Lancetdemanding an independent review of the PACE trial.

“The whole study is unbelievably amateur,” says Jonathan Edwards, a biomedical researcher at University College London who signed the letter. “The trial is useless.”

The PACE trial has exerted a strong influence on American physicians: If you ask your doctor about CFS, odds are good you’ll hear that cognitive behavioral therapy (the flavor of psychotherapy used in the trial) and exercise are the only proven treatments for CFS.

The American scientific research community, on the other hand, has rejected the psychiatric model that PACE epitomizes and is instead looking for physiological explanations for the disease. Research efforts have been hamstrung, though, by scarce funding: the National Institutes of Health spends $5 million to $6 million a year on a disease that affects a million Americans. (For comparison, about the same number of people with HIV/AIDS, which receives $3 billion in NIH funding.)

Just two days after the follow-up PACE study was released, the NIH made the stunning announcement that it is starting a program to study CFS (which is also referred to as myalgic encephalomyelitis or ME/CFS) at the NIH Clinical Center in Bethesda, Maryland. Francis Collins, the director of the NIH, has also promised increased funding for universities to research the illness. “It will be substantially greater than the current $5 [million] or $6 million a year,” he told NPR. “We are going to ramp this up.”

After so many years of scarce funding, bad science, and uncritical journalism, the events of the past few weeks have left me feeling something I’ve never felt before about this illness: hope. It almost frightens me to say it, but we may be on the verge of clearing up the massive misunderstandings about this disease—and even of starting to figure the damn thing out.

Questions about the 2011 Lancet paper emerged soon after the PACE team announced its first results at a press conference. One of the researchers said that, compared with other study subjects, “twice as many people on graded exercise therapy and cognitive behavior therapy got back to normal.” In a follow-up paper two years later, the researchers claimed that 22 percent of participants who received cognitive behavioral therapy or exercise on top of regular medical care “recovered” by the end of the trial.

But patients who analyzed the PACE trial and its follow-up studies discovered that these statements depended on a remarkably weak definition of “recovery”—one so weak that participants could enter the trial, get worse on two out of four criteria, and then be called “recovered.” These supposedly recovered patients could furthermore have poorer physical function than 92 percent of the British working-age population. And 13 percent of participants qualified as “recovered” on at least one of the criteria even before they received treatment.

Peter White, a psychiatrist at Queen Mary University of London and the lead PACE investigator, told me by email in late October that “some small overlap might be expected” between the criteria for entry into the trial and those for recovery, and he pointed out that there were two additional criteria. He didn’t, however, mention that those criteria were also weakened. When I inquired why such an overlap “might be expected,” he declined to answer further questions.

Starting in 2011, patients analyzing the study filed Freedom of Information Actrequests to learn what the trial’s results would have been under the original protocol. Those were denied along with many other requests about the trial, some on the grounds that the requests were “vexatious.” The investigators said they considered the requests to be harassment.

The patients found many other problems as well. The study participants hadn’t significantly improved on any of the team’s chosen objective measures: They weren’t able to get back to work or get off welfare, they didn’t get more fit, and their ability to walk barely improved. Though the PACE researchers had chosen these measures at the start of the experiment, once they’d analyzed their data, they dismissed them as irrelevant or not objective after all. In addition, the patients researching the study found statistical errors, actions that might have pumped up the subjective ratings, measurement problems that allowed participants to deteriorate without being detected, conflicts of interest, and more.

The patients wrote detailed letters to the Lancet and other journals describing PACE’s scientific shortcomings. In responding, the researchers either didn’t address the core problems, dismissed them as unimportant, or accused the critics of beingprejudiced against psychiatry.

Richard Horton, the editor of the Lancet, aggressively defended the trial. In a radio interview, he called the critics “a fairly small, but highly organized, very vocal and very damaging group of individuals who have, I would say, actually hijacked this agenda and distorted the debate so that it actually harms the overwhelming majority of patients.” He didn’t address the substance of the criticisms.

 In the United States, ME/CFS researchers largely dismissed the PACE trial findings. Their research on the role of exercise in the illness has instead focused on unraveling the physiology of patients’ abnormal response to it. Multiple teams found that when patients exercise to exhaustion two days in a row, their performance drops dramatically the second day, as shown by physiological indicators that can’t be faked. Other researchers documented changes in how genes function in patients after moderate exercise.
Jennifer Brea and her partner, Omar, visiting a nature preserve near their home, where she once had been able to walk for a mile but can’t anymore.

Courtesy of Canary in a Coal Mine

Still, each time the PACE team publishes a new follow-up study, a flurry of ill-informed news coverage follows, including after the release last month. The Telegraph front page blared “Chronic Fatigue Syndrome Sufferers ‘Can Overcome Symptoms of [Myalgic Encephalomyelitis] with Positive Thinking and Exercise’: Oxford University has found ME is not actually a chronic illness.”

When I read the study itself, I quickly found that this headline went far beyond even the researchers’ claims—but I also saw that the researchers’ claims went far beyond their own data.

According to the researchers, their work proved that the purported improvements from cognitive behavioral therapy and exercise stood up over time. But what the data actually showed was that after 2½ years, the benefits of CBT and exercise had entirely vanished. The patients who hadn’t been assigned to those therapies had by then improved as much as those who had, though all groups were still sick.

The PACE researchers acknowledged this but discounted the significance of the improvement of the patients who hadn’t received therapy or exercise. They pointed out that some of these patients had received CBT or exercise after the trial had ended, and they argued that this might explain the improvement. However, their data showed that the additional therapy didn’t help these patients at all.

The reception of this new study among researchers was very different from in the past, in part because Tuller, a public health and journalism lecturer at the University of California–Berkeley, published his long story on the site Virology Blog just days before this latest study came out. His work persuaded researchers outside the ME/CFS community to scrutinize the study for the first time—and they condemned it. For example, James Coyne, a psychologist at the University Medical Center Groningen in the Netherlands, who was previously uninvolved in ME/CFS research, wrote a blog post for the Public Library of Science calling the researchers’ interpretation of their new study “unsubstantiated spin in favor of the investigators’ preferred intervention.”

And now researchers and patients are demanding that the PACE team release its data (with any patient-identifying information made anonymous), either publicly or to a team of highly qualified independent investigators, for re-analysis.

The PACE researchers have refused to release the data in the past, arguing that “activists seeking to discredit the PACE trial and its researchers” would somehow decrypt the anonymous details in the data and publish the names of participants. And White told me that the changes to the original protocol “improved the science and interpretation. We see no reason why we should do a further analysis based on an inferior method.” Horton, editor of the Lancet, didn’t respond to my request for comment.

“The Lancet needs to stop circling the wagons and be open,” says Bruce Levin, a biostatistician at Columbia University who signed the open letter. “One of the tenets of good science is transparency.”

Davis, the Stanford geneticist, has a son with ME/CFS so severe that he can’t walk, talk, or eat. Davis goes even further: “The Lancet should step up to the plate and pull that paper,” he says. “It has lots of flaws, and I worry that it hurts patients.” Davis has now started his own effort to find a cure for the disease, called the End ME/CFS Project. He is collecting a vast amount of data on severe patients like his son, who have almost never been included in studies because they are too frail to go to a doctor or clinic.

Ron Davis and his son, Whitney Dafoe, who has severe ME/CFS, in September 2014. Davis helps his son by shaving his beard and head, since he cannot get out of bed to bathe.

Courtesy of the family of Whitney Dafoe

As encouraging as the public criticism of the PACE trial has been, only one thing is likely to excise the notion from the minds of doctors and the public that ME/CFS is a psychiatric condition: a truly effective treatment for the disease. My condition has improved remarkably after I pursued a treatment that has hardly been researched at all: taking extreme measures to avoid mold. But there hasn’t been the money to follow up on promising leads like that one and others.

That makes the NIH announcement of its research plans for the disease a huge step in undoing the damage PACE has caused. The NIH plans to analyze 40 patients whose illness began suddenly with an apparent infection, using big data methods. And if the NIH follows through on its promises for increased funding for research at universities, scientists like Davis will have new opportunities.

Just a year ago, both the public criticism of the PACE trial and the moves by the NIH were nearly unimaginable. But to me, these events feel like the fruits of change that’s been cultivated over years. When the PACE trial first came out in 2011, few journalists took serious interest in the disease, and much of the coverage was dreadful. Now, several journalists, in addition to Tuller,have been producing great work. In 2011, the cadre of dedicated researchers was tiny and isolated. Now, giants in their own fields have become fascinated by the illness. The patient community has long been divided and fractious, but now, platforms like #MEAction are supporting more united action, and patients are developing recommendations for research priorities, modeling their efforts on AIDS and breast cancer activists’ methods to earn respect and influence in the scientific community.

Coyne, the psychology researcher whose interest was sparked by the controversy over PACE, suggested on Twitter that PACE might be the ME/CFS Stonewall, and it does feel like I’m watching the emergence of a new movement.

Of course, there’s still a long way to go. Patients are still suffering, derided, and without treatment. But it no longer seems quixotic to anticipate the day when patients as sick as I was in 2011 won’t have their misery exacerbated by prejudice and bad science.

Could wearable ‘artificial kidney’ change dialysis?

A small, experimental wearable device has moved a step closer to helping patients who rely on kidney dialysis, according to a report.

Victor Gura fits a "wearable artificial kidney," which filters a patient's blood continuously.

For patients with kidney failure, the common treatment is to be hooked up to a dialysis machine at a hospital or clinic several times a week. In addition to the inconvenience, patients develop buildup of fluids and minerals between dialysis sessions, which can result in high blood pressure and breathing problems and require severe dietary restrictions.

“I was very frustrated — I still am — because for decades, we’ve been doing dialysis with big machines that prolong the life of the patient a little bit … and in addition, they have a lousy quality of life,” said Victor Gura, an associate clinical professor of medicine at the David Geffen School of Medicine at the University of California, Los Angeles.

Gura and his colleagues are developing the Wearable Artificial Kidney, or WAK, which would filter a patient’s blood continuously, instead of a few times a week. “This is to reduce a lot of the complications that make patients sick … (and) to give patients back their life,” such as allowing them to have jobs again, he said.

The researchers presented the results of a small trial of the device on Saturday at Kidney Week, the annual meeting of the American Society of Nephrology. The trial involved seven patients in Seattle with end-stage kidney disease who wore the device for 24 hours. During that time, the device removed water and salts from the blood at the same rate as healthy kidneys, and patients did not complain of discomfort or experience side effects, Gura said.

New rules give hope to people waiting for donated kidneys

The current research has not been published in a peer-reviewed journal and should be considered preliminary; however, Gura and his colleagues have previously published studies of patients wearing WAK devices for up to eight hours.

Participants in the current and previous trials were able to sleep with the devices, and should be able to take showers and carry out other normal activities, Gura said.

“We encouraged patients to eat bananas and mashed potatoes and drink orange juice, (and) they enjoyed ice cream and cheesecake, which they couldn’t before,” Gura said. Normally, these foods would be off-limits because they can lead to a dangerous buildup of potassium and phosphorus between dialysis sessions.

However, the device had one important pitfall: Two of the seven patients stopped wearing it before the 24 hours were up because it stopped working properly. Gura and his colleagues are working to correct technical problems before they start their next trial, which will probably involve a group of patients wearing the device for a week.

“Getting the machine to be reliable and consistent is going to be (Gura’s) greatest challenge. … I’ll be convinced when they can keep patients stable for seven or 14 days,” said Leslie Spry, medical director for the Dialysis Center of Lincoln in Lincoln, Nebraska, and spokeswoman for the National Kidney Foundation, a patient advocacy organization.

The WAK device weighs 10 pounds, though Gura and his colleagues are working to get it down to 5 pounds, and patients in the study wore them on their belts. The device connects to a large vein in the body via a catheter and, similar to a conventional dialysis machine, contains filters that separate water, salts and minerals out of the blood.

Users would have to remove the WAK from the catheter once a week to replace the filter and add chemicals once per day to purify the water that is filtered out. Other than those steps, the device would take care of itself, running on 9-volt batteries.

“Anytime you maintain a connection with a machine to your blood vessel system, infection is going to be your No. 1 enemy,” Spry said, adding that he will be interested to see whether patients in longer-lasting trials develop infections. However, it would be “very possible” to teach patients to maintain their devices properly, just as those with home dialysis machines do, he added.

Home dialysis machines have alleviated some of the burden of treatment, allowing patients to receive dialysis up to seven days a week, Spry said. He has helped develop these machines and is a part-time employee of Nx Stage, which makes dialysis machines. However, these machines do not allow continuous dialysis, and patients use them for only up to eight hours a day (in the case of nocturnal machines), he added.

Although other wearable dialysis devices have been researched over the years, the WAK is the only one for which there are published clinical trials, Gura said.

If the researchers continue to receive funding to conduct clinical trials and further develop the technology, Gura estimates that WAK devices could be available for patients in two years.

The U.S. Food and Drug Administration announced last month that it would expedite the approval of the device once studies are able to demonstrate safety and efficacy.

Earth-like world could be ‘most important planet found outside solar system’ | Science | The Guardian

GJ 1132b is close enough for telescopes to observe any atmosphere it might have, which could help scientists spot signs of life on other planets in the future

In this artist’s conception GJ 1132b, a rocky planet very similar to Earth in size and mass, circles a red dwarf star.
In this artist’s conception GJ 1132b, a rocky planet very similar to Earth in size and mass, circles a red dwarf star.

A rocky Earth-sized planet that circles a small, nearby star could be the most important world ever found beyond the solar system, astronomers say.

The planet lies in the constellation of Vela in the southern sky and is close enough for telescopes to observe any atmosphere it has, a procedure that could help spot life on other planets in the future.

Named GJ 1132b, the alien world is about 16% larger than Earth, and at 39 light years distant, is three times closer than any other Earth-sized rocky planet yet found around another star. At that distance, it is hoped that telescopes will be able to make out the chemistry of its atmosphere, the speed of its winds and the colours of its sunsets.

Astronomers spotted the planet as it moved across the face of a red dwarf star only a fifth the size of the sun. Though much cooler and fainter than the sun, GJ 1132b orbits so close to its star that surface temperatures reach 260C.

The searing temperatures are too hot for the surface to retain liquid water, making it inhospitable to life, but not so hot as to burn off any atmosphere that formed on the planet.

“If this planet still has an atmosphere, then we might find other, cooler planets that also have atmospheres and orbit small stars. We can then imagine interrogating the atmospheres for molecules that come from life,” said Zachory Berta-Thompson at the MIT’s Kavli Institute for Astrophysics and Space Research.

This time-lapse video shows MEarth-South discovering the planet GJ 1132b. Credit: Jonathan Irwin

Researchers used the MEarth-South array, a group of eight 40cm robotic telescopes at the Cerro-Tololo Inter-American Observatory in Chile, to detect the planet. As it whipped around its star, completing an orbit every 1.6 days, it produced a faint 0.3% dip in the starlight picked up by the telescopes, according to a report in Nature.

The planet is tidally locked to its star, much as the moon is to Earth, and has one face in permanent daylight, the other in darkness. Given the world’s size and mass, researchers suspect it is rocky, like the inner planets of our solar system. It orbits 1.4m miles from its star, far closer than Mercury, which is never less than 36m miles from the sun.

Because the red dwarf is so small, and the planet is on such a close orbit, astronomers should find it fairly easy to detect and study any atmosphere the world has. The team has already requested time on the Hubble and Spitzer space telescopes to observe the planet in more detail.

Drake Deming, an astronomer at the University of Maryland, said GJ 1132b was “arguably the most important planet ever found outside the solar system”. Its proximity and orbit around a red dwarf will allow astronomers to study the planet with unprecedented fidelity. “It’s nearby, it’s Earth-like, and its star won’t interfere,” Drake said.

The planet will become a prime target for future missions too, including the James Webb Space Telescope, which is expected to launch in 2018, and the Giant Magellan Telescope, which is due to start operations in Chile in 2025.

The discovery came as scientists announced they had found the most distant object in the solar system, a frozen body that lies more than 100 times farther from the Sun than Earth does. The object lies beyond the edge of the Kuiper belt, home to the dwarf planet Pluto, and into the realm of space dominated by the so-called Oort cloud, a vast shell of icy objects where comets such as Hale-Bopp are thought to have formed.

Spotted from the Subaru telescope on Mauna Kea in Hawaii, the distant object is at least 500km across, but has not been tracked long enough to work out the full path of its orbit.

How to Look Younger: 10 Secrets Even Your Best Friend Doesn’t Know

Young, middle-aged, and older individuals studied thousands of photographs and were asked to guess the age of models with various facial expressions. Neutral expressions yielded the most accurate results, and fearful expressions made subjects look older; happy faces were rated as younger than they really were.