How Americas Diet Culture Hinders Those With Eating Disorders

The inevitable January advertising of New Year, New You has arrived, and with it, the societal pressure to drop weight.

For some, this can be motivating, even goodafter all, Americas obesity rate is at a record high, according to research from the Centers for Disease Control and Prevention. But for many, the pressure to lose weight can be quite triggering, especially for those predisposed to developing eating disorders.

Longstanding research has shown that eating disorders can be hereditary, meaning some people are simply more likely to develop them than others. But new research from the Eating Recovery Center shows there might be a more specific genetic link than previously thought.

The risk of developing an eating disorder is largely inherited, meaning that people with a family history of eating disorders are more likely to have one, but the identity of which genetic variation increases that risk is unknown, Michael Lutter, who works as an attending psychiatrist for the Eating Recovery Center, told The Daily Beast.

Lutter researches the genetic and neurobiologic basis of eating disorders; his goal is to find a very specific genomic mutation that could cause eating disorders. While the genomic mutation hes looking for most likely affects a very small amount of people, it could be a game changer for treating eating disorders.

Lutter compared his search for this gene to that of breast cancers BRCA1 and 2 mutations.

Individuals with those mutations have a much higher risk of breast cancer, but only three percent of breast cancers are caused by these mutations, according to the CDC.

Similarly, we are trying to find something similar in the eating disorder population. If we can find the rare mutation, then it gives a better understanding of the underlying neurobiology of eating disorders, he said.

Lutters latest research sequenced the genes of 93 unrelated people with eating disorders, some who restrict their food and some who binge eat. Its pretty uncommon for an eating disorder patient to struggle exclusively with anorexia, bulimia or binge eating disorder, as people will cross over disordered eating behaviors in their lifetime, Lutter said, so the two groups of patients that were tested was a fair sample for this study.

He found specific links in two different genetic variations. For restrictive eaters, the variant is called neurotensin, which works in the brain to regulate appetite and tells your body it needs more food. For binge eaters, its called glucagon-like peptide 1, a hormone released by the gastrointestinal system after meals to tell you when youre full.

These results dont surprise Lutterhe says the fact that people with eating disorders would have genetic mutations for genes involved in appetite and fullness makes sensebut they had never been seen before. Still, the findings are in their preliminary stages; they cant be applied in a clinical setting yet.

Right now theres no way to use genetics to guide treatment but it does offer a better understanding of the pathophysiology of the illness that we can do these studies and measure levels of these hormones, Lutter said. He thinks that were close to developing treatment for eating disorders based on genetics in the next 10 or 20 years.

Lutter said that whats exciting is that there are drugs on the market that could target the hormones in the genetic variations his research found. For example, some diabetes medications might be able to restrict ones urge to binge eat. There are good drug targets so there are a lot of new potential leads for researchers to develop new treatments, he noted.

Until then, however, the New Years resolution madness can be quite challenging.

Lauren Muhlheim, Psy.D., a clinical psychologist for Eating Disorder Therapy LA, says that while this genetic research is important, its also relevant to know that there is no one single cause of someones eating disorder.

They are very complicated illnesses that dont stem from a single cause but from a complex interaction of biological, psychological and environmental factors. And I dont think you can ever tease it apart, she said.

Those environmental factors? The huge focus around losing weight or becoming a better version of yourself for the New Year.

Even though research shows that 80 percent of New Years resolutions (the top two being exercising more and eating healthier) fail, its easy to buy in to the idea that you need to lose weight, specifically at a time when were bombarded with messages that target body insecurities.

I cant remember who said it, but someone once said that the diet industry is brilliant because its the one product that repeatedly fails and makes you believe that its your fault, Muhlheim said. People are very susceptible to the newest fad diet, so I think its a very challenging time of year to people who are susceptible to eating disorders, especially with social media. Were getting more bombarded than we have in the past.

How do you know if youre susceptible to eating disorders? As its a very complex disease, its impossible to pinpoint this, but Tom Hildebrandt, Chief of the Division of Eating & Weight Disorders at Mount Sinai Health System, told The Daily Beast that some things to take note of are whether or not youre in an environment where restriction and dieting is valued in a critical way, are extremely stressed or are going through a big transition in your lifewhether thats high school to college, college to adulthood, becoming a parent, or even going through menopause.

The thing about this time of year is really not to get caught up in the swarm of information that comes from peers, social media and advertisers trying to sell you fixes to it, Hildebrandt said. Try to insulate yourself against that stuff.

This, of course, is easier said than done. Muhlheim suggested curating a healthy, body-positive feed on your social media channels and consuming culture that steers away from harmful messaging. Muhlheim recommended following the hashtag #haes, or healthy at every size, and #intuitiveeatinga quick search yields registered dietitians like Claudia T. Felty and Alissa Rumsey, whose feeds are all about having a healthy relationship foodor downloading podcasts like Love, Food.

That said, eating disorders are dangerous. If you or someone you know is struggling, its important to get an evaluation by a physician or a therapist, Muhlheim said, referring those who may be binging or purging, is preoccupied by obsessive thoughts about food, is having trouble functioning normally, or is skipping social events to contact the National Eating Disorders Association Helpline or the Eating Recovery Center.

Read more: https://www.thedailybeast.com/how-americas-diet-culture-hinders-those-with-eating-disorders

Excitement as trial shows Huntington’s drug could slow progress of disease

Hailed as enormously significant, results in groundbreaking trial are first time a drug has been shown to suppress effects of Huntingtons genetic mutation

A landmark trial for Huntingtons disease has announced positive results, suggesting that an experimental drug could become the first to slow the progression of the devastating genetic illness.

The results have been hailed as enormously significant because it is the first time any drug has been shown to suppress the effects of the Huntingtons mutation that causes irreversible damage to the brain. Current treatments only help with symptoms, rather than slowing the diseases progression.

Q&A

What is Huntington’s disease?

Huntingtons disease is a congenital degenerative condition caused by a single defective gene. Most patients are diagnosed in middle age, with symptoms including mood swings, irritability and depression. As the disease progresses, more serious symptoms can include involuntary jerky movements, cognitive difficulties and issues with speech and swallowing.

Currently there is no cure for Huntington’s, although drugs exist which help manage some of the symptoms. It is thought that about 12 people in 100,000 are affected by Huntington’s, and if a parent carries the faulty gene there is a 50% chance they will pass it on to their offspring.

Prof Sarah Tabrizi, director of University College Londons Huntingtons Disease Centre who led the phase 1 trial, said the results were beyond what Id ever hoped … The results of this trial are of ground-breaking importance for Huntingtons disease patients and families, she said.

The results have also caused ripples of excitement across the scientific world because the drug, which is a synthetic strand of DNA, could potentially be adapted to target other incurable brain disorders such as Alzheimers and Parkinsons. The Swiss pharmaceutical giant Roche has paid a $45m licence fee to take the drug forward to clinical use.

Huntingtons is an incurable degenerative disease caused by a single gene defect that is passed down through families.

The first symptoms, which typically appear in middle age, include mood swings, anger and depression. Later patients develop uncontrolled jerky movements, dementia and ultimately paralysis. Some people die within a decade of diagnosis.

Most of our patients know whats in their future, said Ed Wild, a UCL scientist and consultant neurologist at the National Hospital for Neurology and Neurosurgery in London, who administered the drug in the trial.

The mutant Huntingtons gene contains instructions for cells to make a toxic protein, called huntingtin. This code is copied by a messenger molecule and dispatched to the cells protein-making machinery. The drug, called Ionis-HTTRx, works by intercepting the messenger molecule and destroying it before the harmful protein can be made, effectively silencing the effects of the mutant gene.

How the drug works to slow the progress of Huntington’s disease

To deliver the drug to the brain, it has to be injected into the fluid around the spine using a four-inch needle.

Prof John Hardy, a neuroscientist at UCL who was not involved in the trial, said: If Id have been asked five years ago if this could work, I would have absolutely said no. The fact that it does work is really remarkable.

The trial involved 46 men and women with early stage Huntingtons disease in the UK, Germany and Canada. The patients were given four spinal injections one month apart and the drug dose was increased at each session; roughly a quarter of participants had a placebo injection.

After being given the drug, the concentration of harmful protein in the spinal cord fluid dropped significantly and in proportion with the strength of the dose. This kind of closely matched relationship normally indicates a drug is having a powerful effect.

For the first time a drug has lowered the level of the toxic disease-causing protein in the nervous system, and the drug was safe and well-tolerated, said Tabrizi. This is probably the most significant moment in the history of Huntingtons since the gene [was isolated].

The trial was too small, and not long enough, to show whether patients clinical symptoms improved, but Roche is now expected to launch a major trial aimed at testing this.

If the future trial is successful, Tabrizi believes the drug could ultimately be used in people with the Huntingtons gene before they become ill, possibly stopping symptoms ever occurring. They may just need a pulse every three to four months, she said. One day we want to prevent the disease.

The drug, developed by the California biotech firm Ionis Pharmaceuticals, is a synthetic single strand of DNA customised to latch onto the huntingtin messenger molecule.

The unexpected success raises the tantalising possibility that a similar approach might work for other degenerative brain disorders. The drugs like Lego, said Wild. You can target [any protein].

For instance, a similar synthetic strand of DNA could be made to target the messenger that produces misshapen amyloid or tau proteins in Alzheimers.

Huntingtons alone is exciting enough, said Hardy, who first proposed that amyloid proteins play a central role in Alzheimers. I dont want to overstate this too much, but if it works for one, why cant it work for a lot of them? I am very, very excited.

Prof Giovanna Mallucci, associate director of UK Dementia Research Institute at the University of Cambridge, described the work as a tremendous step forward for individuals with Huntingtons disease and their families.

Clearly, there will be much interest into whether it can be applied to the treatment of other neurodegenerative diseases, like Alzheimers, she added. However, she said that in the case of most other disorders the genetic causes are complex and less well understood, making them potentially harder to target.

About 10,000 people in the UK have the condition and about 25,000 are at risk. Most people with Huntingtons inherited the gene from a parent, but about one in five patients have no known family history of the disease.

The full results of the trial are expected to be published in a scientific journal next year.

Read more: https://www.theguardian.com/science/2017/dec/11/excitement-as-huntingtons-drug-shown-to-slow-progress-of-devastating-disease

Jennifer Doudna: I have to be true to who I am as a scientist

Crispr inventor Jennifer Doudna talks about discovering the gene-editing tool, the split with her collaborator and the complex ethics of genetic manipulation

Jennifer Doudna, 53, is an American biochemist based at the University of California, Berkeley. Together with the French microbiologist Emmanuelle Charpentier, she led the discovery of the revolutionary gene-editing tool, Crispr. The technology has the potential to eradicate previously incurable diseases, but also poses ethical questions about the possible unintended consequences of overwriting the human genome.

Were you nerdy as a child? What got youhooked on science?
Yes, I was nerdy. My father was a professor of American literature in Hawaii and he loved books. One day I came home from school and he haddropped a copy of The Double Helixon the bed, by Jim Watson. Onerainy afternoon I read it and Iwasjust stunned. I was blown awaythat you could do experiments about what a molecule looks like. I was probably 12 or 13. I think that wasthebeginning ofstarting to think,Wow, that could be an amazingthing to work on.

Youve spent most of your career uncovering the structure of RNA and never set out to create a tool to copy andpaste human genes. How did you endup working on Crispr?
I think you can put scientists into two buckets. One is the type who dives very deeply into one topic for their whole career and they know it better than anybody else in the world. Then theresthe other bucket, where I wouldput myself, where its like youre at a buffet table and you see an interesting thing here and do it for a while, and that connects you to another interesting thing and you take a bit of that. Thats how I came to be working on Crispr it was a total side-project.

But when you first started your collaboration with Emmanuelle Charpentier, did you have a hunch youwere on to something special?
We met at a conference in San Juan, Puerto Rico, and took a walk around the old town together. She was so passionate, her excitement was very infectious. I still remember walking down this street with her and she said: Well Im really glad you want to work with us on the mysterious [Cas9 the enzyme that snips DNA at the chosen location in the editing process]. It was this kind of electrifying moment. Even then I just had this gut feeling that this was something really interesting.

How important is personal chemistry inscience collaborations?
Its essential. Working in a lab is analogous to being in a high-school play: youre rehearsing long hours, itscrowded, there are stressful things that come up. Its the same thing in science. Things never work as you think they will, experiments fail and so to have people around that really get along with each other is super important. Many collaborations dont work out, usually just because peoples interests arent aligned or people dont really like working together.

The real frenzy around your work started in 2012, when you showed that Crispr-Cas9 could be used to slice up DNA at any site [of the DNA molecule] you wanted. Did you realise this was abig deal gradually orimmediately?
It wasnt a gradual realisation, it was one of those OMG moments where you look at each other and say holy moly. This was something we hadnt thought about before, but now we could see how it worked, we could see it would be such a fantastic way to do gene editing.

After you demonstrated Crispr could edit bacterial DNA, two rival labs (Harvard and the Broad Institute) got there first in human cells. How come they beat you to it?
They were absolutely set up to do that kind of experiment. They had all the tools, the cells growing, everything was there. For us, they were hard experiments to do because its not thekind of science we do. What speaksto the ease of the system was that a lab like mine could even do it.

The Broad Institute won the latest round of an ongoing legal battle over patent rights they claim that it wasnt obvious that Crispr could be used to edit human cells too. Where do you stand?
People have asked me over and over again: Did you know it was going to work? But until you do an experiment you dont know thats science. Ive been lambasted for this in the media, but I have to be true to who I am as a scientist. We certainly had a hypothesisand it certainly seemed likea very good guess that it would.

Theres the patent dispute and you and Emmanuelle Charpentier also ended up pursuing rival projects to commercialise the technology. Are you all still friends?
If theres a sadness to me about all of this and a lot of its been wonderful and really exciting its that I wouldve loved to continue working with Emmanuelle, scientifically. For multiple reasons that wasnt desirable to her. Im not blaming her at all she had her reasons and I respect her a lot.

The media loves to drive wedges, but we are very cordial. I was just with her in Spain and she was telling me about the challenges [of building her new lab in Berlin]. I hope on her side, certainly on my side, we respect each others work and in the end were all init together.

In your book you describe a nightmare youhad involving Hitler wearing a pig mask, asking to learn more about your amazing technology. Do you still have anxiety dreams about where Crispr mightleave the human race?
I had the Hitler dream and Ive had a couple of other very scary dreams, almost like nightmares, which is quite unusual for an adult. Not so much lately, but in the first couple of years after I published my work, the field was moving so fast. I had this incredible feeling that the science was getting out way ahead of any considerations about ethics, societal implications and whether we should be worrying about random people in various parts of the world using this for nefarious purposes.

In 2015, you called for a moratorium on the clinical use of gene editing. Where do you stand on using Crispr to edit embryos these days?
It shouldnt be used clinically today, but in the future possibly. Thats a big change for me. At first, I just thought why would you ever do it? Then I started to hear from people with genetic diseases in their family this is now happening every day for me. Alot of them send me pictures of their children. There was one that Icant stop thinking about, just sent to me in the last 10 days or so. A mother who told me that her infant son was diagnosed with a neurodegenerative disease, caused by a sporadic rare mutation. She sent me a picture of thislittle boy. He was this adorable little baby, he was bald, in his little carrier and so cute. I have a son and myheart just broke.

What would you do as a mother? You see your child and hes beautiful, hes perfect and you know hes going to suffer from this horrible disease and theres nothing you can do about it. Its horrible. Getting exposed to that, getting to know some of these people, its not abstract any more, its very personal. And you think, if there were away to help these people, we should do it. It would be wrong not to.

What about the spectre of designerbabies?
A lot of it will come down to whether the technology is safe and effective, are there alternatives that would be equally effective that we should consider, and what are the broader societal implications of allowing gene editing? Are people going to start saying I want a child thats 6ft 5in and has blue eyes and so on? Do we really want to go there? Would you do things that are not medically necessary but are just nice-to-haves, for some people?Its a hard question. There area lot of grey areas.

Are you worried about cuts to science funding, including to the National Institutes of Health (NIH) budget?
I am very concerned. Science funding is not a political football but in fact a down payment on discovery, the seed money to fund a critical step toward ending Alzheimers or curing cancer.

Researchers currently working on projects aimed at improving numerous aspects of our agriculture, environment and health may be forced to abandon their work. The outcome is that people will not receive the medical treatments they need, our struggle to feed our exploding population will deepen, and our efforts to manage climate change will collapse.

Over the long term, the very role of fundamental science as a means to better our society may come into question. History and all evidence points to the fact that when we inspire and support our scientific community we advance our way of life and thrive.

Were you disturbed when Trump tweeted, If U.C. Berkeley does not allow free speech and practices violence on innocent people with a different point of view NO FEDERAL FUNDS? in response to a planned alt-right speaker being cancelled due to violent protests on campus?
Yes. It was a confusing tweet since the university was clearly committed to ensuring that the event would proceed safely and first amendment rights were supported. Few expected the awful actions of a few to be met with a willingness from the highest office to deprive more than 38,000 students access to an education.

Youve spoken at Davos, shared the $3m2015 Breakthrough prize, been listedamong the 100 most influential people in the world by Time magazine. Areyou still motivated about heading intothe lab these days?
Yesterday I was getting ready to go to a fancy dinner. I was in a cocktail gown and had my makeup on and my hair done, but I wanted to talk to a postdoc in my lab about an experiment he was doing, so I texted him saying can we Skype? It was 8am in California, I was over here [in the UK] in my full evening gown, talking abouttheexperiment.Thats how nerdy I am.

A Crack in Creation: The New Power to Control Evolution by Jennifer Doudna and Sam Sternberg is published by The Bodley Head (20). To order a copy for 17 go to bookshop.theguardian.com or call 0330 333 6846. Free UK p&p over 10, online orders only. Phone orders min p&p of 1.99

Read more: https://www.theguardian.com/science/2017/jul/02/jennifer-doudna-crispr-i-have-to-be-true-to-who-i-am-as-a-scientist-interview-crack-in-creation