Clinicians can sift facts from fiction on diseases such as acne by checking Twitter, a letter by Boston-based Center for Connected Health researchers suggests.
Modern medicine – American Academy of Dermatology
Tag Archives: research
Research advances yield new treatments for skin disease
Brothers to brave Atlantic Ocean in row for skin cancer research
Two Lymington brothers are preparing to row the Atlantic Ocean in memory of their late father Peter Massey, who sufferer with basal cell carcinoma skin cancer and sadly passed away in 2015 aged 63.
Jude Massey, 17, and Dr Greg Bailey, 26, have launched a campaign to raise £100,000 for the British Skin Foundation – a charity that funds skin cancer research – whilst also raising awareness of the dangers of skin cancer.
The 3,000 mile trip is due to take place in January 2018 and will commence in the Canaries and end in Barbados. “It’s a gruelling trip’” explained Jude, “We’ll be rowing for two hours on and two hours off non-stop both day and night.”
Conditions on the boat will be basic, relying on solar panels to power a water maker for both vital drinking water and fresh water to rehydrate freeze-dried meals. They’ll also have GPS communication, along with radar alerts to avoid collisions with nearby vessels.
Once they have departed they will be at the mercy of the elements with the potential for hurricanes, capsizes, electrical failure, passage of large vessels, large marine life, sea sickness, injury and equipment breakages. Should conditions become unsafe to row, the brothers must deploy their para-anchor, a submersible parachute shaped piece of equipment which will keep the boat pointing into the waves and reduce the likelihood of a capsize as they sit and wait in the watertight cabin.
The challenge will be a good test of both physical and psychological strength. To add some perspective, only 317 crews have successfully crossed the Atlantic, with 153 unsuccessful crews and six crews who died attempting the challenge. Some 536 individuals have been into space and over 5,500 have climbed Mount Everest. The brothers have put their lives on hold to complete the challenge, directing all of their efforts into training and fundraising. The duo, who have never rowed before are aiming to take between four and eight weeks to complete the journey. If they succeed, Jude – a sailing instructor – is likely to become a record holder as the first vegan to complete this journey, shining the spotlight on endurance events for vegans.
Peter, Jude father and Greg’s stepfather, spent 16 years undergoing painful treatment for skin cancer. “There are no words to describe how awful this disease is both for the sufferer and their family” said NHS doctor Greg. “The more awareness we can raise, the better for everyone.”
The brothers will be packing plenty of sunscreen for their trip as they’ll need to be covering themselves from head to toe every day.
The boys are launching their sponsorship awareness campaign and are seeking support from different companies and organisations. They can be contacted through their website, email (contact@oceanbrothers.co.uk) or telephone (07590 926796). Please follow their Facebook & Twitter pages to keep up to date with their training and latest news.
How to Prevent Eczema – New Research on Eczema Prevention
By Mike Arsenault (bio below) Ten years ago my daughter Emily was born with eczema. Being an acupuncturist, I knew that using steroids on her tiny, infant body could be a very slippery slope, so I used my herbal training to make a simple herbal balm for her. It worked so well that I used […]
It’s an Itchy Little World
Comment on Following the low FODMAP diet long term…What is a modified low FODMAP diet? by Research on the reintroduction phase of the low FODMAP diet
There is a new term starting to emerge in relation to the low FODMAP diet and this is the modified low FODMAP diet.
Put simply this is the long term diet the majority of people follow after completing the reintroduction phase of the low FODMAP diet.
People with IBS who have been fortunate enough to see a dietitian will understand that there are actually 3 phases to a low FODMAP diet. Those who could not get access to a dietitian or have chosen to try the low FODMAP diet themselves may probably not have realised the low FODMAP diet has 3 phases. Certainly if you obtain most of your information from the internet the reintroduction phase and the long term maintenance phase are rarely mentioned. I have to admit the research into FODMAPs and IBS is pretty slim on these important phases too! The figure shows these 3 phases and is explained below.
So what are the 3 phases of the low FODMAP diet?
1. The first phase is the low FODMAP restriction (or elimination) diet. This is what most people know as the low FODMAP diet but this phase of the diet should only be followed for 2-6 weeks.
2. The second phase of the diet is the reintroduction phase. This involves both re-challenging and reintroducing FODMAPs to test your tolerance levels to FODMAPs and understand your FODMAP threshold. This phase takes about 10 weeks to complete. In a way it continues indefinitely as your tolerance to FODMAPs can change over time and you continue to re-challenge and reintroduce FODMAPs. More on reintroducing FODMAPs here.
3. The final phase is termed a modified low FODMAP diet. Once you have completed the reintroduction phase and reintroduced FODMAPs back into your diet most people will still restrict some high FODMAP foods. This combination of eating high FODMAP and low FODMAP foods to personal tolerance results in a modified low FODMAP diet.
The final terminology for these 3 phases has yet to be agreed or published but will be similar to what is discussed above. There is limited research available on what people do once they have completed the 2-6 week low FODMAP diet. Earlier this year I presented an abstract while working at King’s College London at the Digestive Diseases Federation conference which looked at the long term effects of the low FODMAP diet in the UK and answered some very interesting questions.
1. Do people reintroduce FODMAPs after starting a low FODMAP diet?
YES!
In fact 97 out of 103 people completed the reintroduction phase.
2. What sort of diet do people follow in the long term after completing the low FODMAP restriction diet and the reintroduction phase?
Out of the 103 participants when followed up one year later:
78 of them continued to follow an adapted low FODMAP diet. Meaning they had reintroduced FODMAPs to their own tolerance levels.
19 followed a normal diet. Meaning they had reintroduced FODMAPs and no longer followed any FODMAP restrictions.
6 continued to follow a low FODMAP restriction diet in the long term (a year later).
Therefore the vast majority of people do reintroduce FODMAPs but continue to follow a modified low FODMAP diet as their normal diet.
3. After you have reintroduced FODMAPs do you still have relief of your IBS symptoms in the long term?
YES!
There are two statistical points here. First of all 61% of people found relief of their IBS after following a low FODMAP restriction diet. This is similar to other studies looking at the effectiveness of the restriction phase of the low FODMAP diet. Importantly in those 61% of people 70% of them continued to have relief of their symptoms a year later.
This shows that in the vast majority of people who find the low FODMAP restriction diet effective, even once they have reintroduced FODMAPs they still have relief of their IBS symptoms in the long term.
The abstract is available here.
The full programme from the event is available here.
It is great that these questions are starting to be answered as it helps the low FODMAP diet become a long term treatment option for IBS symptoms. It also means that the full information about the low FODMAP diet will become known to more people. Hopefully this will result in more support for those who are following only phase one of the low FODMAP diet and unnecessarily restricting their diet.
The study also looked at quality of life, the long term nutritional adequacy and acceptability of the diet with some really interesting findings which I will discuss in a later post.
Want more information on the low FODMAP diet and IBS? Click here for the latest changes and important updates.
We are currently travelling around the world and plan to bring you‘Around The World In 80 Low FODMAP Dishes’ – a collection of the best low FODMAP foods and recipes as we travel the globe. See more on our low FODMAP diet travel section.
Good news! The first ever book dedicated to reintroducing FODMAPs is now available to purchase on Amazon Kindle. The book is titled ‘Re-challenging and Reintroducing FODMAPs – A self-help guide to the entire reintroduction phase of the low FODMAP diet’. Click on the logo for more details.
More information on Reintroducing FODMAPs here.
Low FODMAP recipes here.
We are offering very reduced rates for Skype consultations while we are travelling the world. For more information and for contacting R&MDietetics you can enquire here or email info@rmdietetic.com
Many Parasitic Worms Offer Host Benefits: Research Has Potential To Treat Obesity, Psoriasis
AppId is over the quota AppId is over the quota Main Category: Obesity / Weight Loss / Fitness
Also Included In: Infectious Diseases / Bacteria / Viruses;??Eczema / Psoriasis
Article Date: 10 Jan 2013 – 0:00 PST Current ratings for:
Many Parasitic Worms Offer Host Benefits: Research Has Potential To Treat Obesity, Psoriasis 
On the list of undesirable medical conditions, a parasitic worm infection surely ranks fairly high. Although modern pharmaceuticals have made them less of a threat in some areas, these organisms are still a major cause of disease and disability throughout much of the developing world.
But parasites are not all bad, according to new research by a team of scientists now at the University of Georgia, the Harvard School of Public Health, the Universite Francois Rabelais in Tours, France, and the Central South University, Changsha, Hunan, China.
A study published recently in Nature Medicine demonstrates that once inside a host, many parasitic worms secrete a sugar-based anti-inflammatory molecule that might actually help treat metabolic disorders associated with obesity.
The sugar molecule, or glycan, is released by parasites to help them evade the body’s immune system. By reducing inflammation, they are better able to hide in tissues, and humans experience fewer symptoms that might reveal their presence. http://www.eczemablog.net/
“Obesity is an inflammatory disease, so we hypothesized that this sugar might have some effect on complications related to it,” said Donald Harn, study co-author who worked on the research while at Harvard School of Public Health and is now Georgia Research Alliance Distinguished Investigator in the UGA College of Veterinary Medicine’s Department of Infectious Diseases.
The researchers tested their hypothesis on mice fed a high-fat diet. Those in the control group exhibited many of the symptoms associated with excessive weight gain, such as insulin resistance, high triglycerides and high cholesterol.
Mice that received treatment with the sugar still gained weight, but they did not suffer the same negative health effects as those in the control.
“All of the metabolic indicators associated with obesity were restored to normal by giving these mice this sugar conjugate,” said Harn, who is also a member of UGA’s Faculty of Infectious Diseases and the Center for Tropical and Emerging Global Diseases. “It won’t prevent obesity, but it will help alleviate some of the problems caused by it.”
The same sugars excreted by the parasites are also found in the developing human fetus and in human breast milk, which Harn suspects may establish proper metabolic functions in the newborn infant. Beyond infancy, however, sugar expression is only found on a few cells, and the only external source for the sugar is parasitic worms.
Because parasites co-evolved with mammals over millions of years, some scientists believe that the relationship between humans and worms is more symbiotic than parasitic, and that small worm infections might actually have some benefits.
“Prevalence of inflammation-based diseases is extremely low in countries where people are commonly infected with worms,” Harn said. “But the minute you start deworming people, it doesn’t take too long for these autoimmune diseases to pop up.”
This doesn’t mean that people should actively seek out parasitic infections as treatment, he said. But it is an indication that the compounds secreted by worms may serve as the basis for future therapies.
In addition to obesity-related disease, Harn and his colleagues have demonstrated that the sugar molecule released by parasites may alleviate a number of other serious inflammatory medical conditions.
It may work as a treatment for psoriasis, a disease that causes skin redness and irritation. The sugar also appears to serve as a powerful anti-rejection drug that may one day be used in patients who have received organ transplants. And it has been shown to halt or even reverse the symptoms of multiple sclerosis in mice.
More research is needed before this sugar molecule can be tested in humans, but Harn and his colleagues are hopeful that they can create effective treatments that provide all the benefits of parasitic worms without the worms themselves.
“We see great promise in this sugar, and we hope that future research and collaborations will eventually lead to marketable therapies for people suffering from disease,” he said.
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‘Many Parasitic Worms Offer Host Benefits: Research Has Potential To Treat Obesity, Psoriasis’
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Eczema Blog
Supreme Court gene patent decision means little for eczema research
Following last week’s decision by the US Supreme Court that human genes cannot be patented, I’d say nothing has changed for eczema patients.
What I mean is that it makes little difference to eczema therapies now or in the future whether companies can obtain US patents on human genes.
I see two major issues: moral and commercial. Morally, I feel it’s a great triumph that even the famously conservative justices of the Supreme Court—who we really expected to side with big bucks, as they seem reliably to do—unanimously affirmed that nobody can own naturally-occurring human DNA. No company can own a piece of my genetic heritage.
Commercially, the issue is intellectual property. I work in biotech, and every day I hear about how it’s crucial for companies to control their IP. No investor is going to back a company that can obviously be sued in the future or that is developing a product that could instantly be copied by a competitor without penalty.
The loser in the decision was Myriad Genetics, which owned the US patent on BRCA1 and BRCA2, two human genes in which mutations increase one’s chances of getting breast cancer. (From what I can tell, Myriad had patents on the normal genes as well as common cancer-linked mutations.) Myriad had exclusive rights to DNA tests that could determine whether patients had mutations. Now many other companies are developing similar tests, and the competition will drive down the price of the tests.
That’s great if you want to get tested for breast cancer. But what does it mean for companies that are developing diagnostic tests for other conditions? These companies may abandon their efforts. Or the companies may never get started.
At least that is what one commercially-minded person whose views I respect tells me.
The Faster Cures blog, conversely, makes the point that patenting DNA could, and has, led to R&D on diseases being blocked by legal obstruction. Lilly, apparently, spent eight years fighting Harvard, MIT and others over the rights to one particular gene, NF-kB. Presumably lots of money got spent that might have gone to actual research instead of lawyers.
But for a gene patent to be useful, there must first of all be a strong link between genetics and disease. Eczema, despite being known to have a strong genetic component, has not been definitively linked to genes except in the case of filaggrin. There are a few mutations that seem to correspond to particularly severe eczema but they don’t occur in many people.
In any case, the sequence of filaggrin was made public in 2006 so the point is moot—once made public, an invention can’t be patented. (I searched the US Patent and Trademark Office database and didn’t see anything.)
Also a diagnostic test is only useful if it gives you information you can act on. There’s no point telling an adult that they have severe eczema, because they already know that. And if parents learn that their child is at risk—not guaranteed—of developing eczema, what can they do to prevent it?
Not much that I know of.
Diagnostics aside, how might a gene patent be useful?
Many drugs or biotherapies being developed affect how genes are regulated—how the process of turning their information into protein is amplified or damped. Perhaps owning a gene patent would let you control work that other people are doing to regulate that gene. We’ll never know now! What is certain, though, is that if you had a gene patent and lots of money, you could probably intimidate other companies by threatening them with expensive legal action.
I don’t think enough is known about eczema at this point that a gene patent would have been a factor. Look at the existing therapies and the few in the pipeline (such as Anacor’s). They are all either anti-inflammatories or calcineurin inhibitors. They don’t affect genes directly.
Researchers are starting to put together useful models of how itch signals get transmitted from the skin to the brain. For itch, we wouldn’t be interested in a diagnostic, but we would like to have a therapy. It’s conceivable that one or two genes may turn out to be key, and we might want drugs to regulate them. But gene patents would not be necessary for scientists or companies to do that work.
In short: last week’s Supreme Court decision, while morally important and laudable, will have little effect on the field of eczema research and therapy.
End Eczema
Three years in: what has the $42M Atopic Dermatitis Research Network produced?
In July it will be three years since the NIH awarded National Jewish Health in Denver, CO $ 31 million to create and administer the Atopic Dermatitis Research Network, a consortium of five academic sites across the US. A contractor, Rho Federal Systems of Chapel Hill, NC, won an $ 11 million contract to operate a center to coordinate statistics and clinical trials for the project.
That makes $ 42 million—spread over five years—which puts the project on the large end of NIH funding for individual biomedical efforts. The typical NIH research grant ranges from $ 100 thousand to $ 2 million, and anything bigger is fodder for university news releases. Which raises the question: what have US taxpayers gotten in return?
I ask this as a patient who is grateful that these scientists are working to understand a disease that affects me, my family, and millions in the US and worldwide.
The answer is not obvious, since the publications page on the ADRN website hasn’t been updated since July 2011.
According to the website:
The Atopic Dermatitis Research Network (ADRN) is a consortium of academic medical centers that will conduct clinical research studies in an attempt to learn more about skin infections associated with atopic dermatitis (AD). The studies will focus on antibiotic-resistant Staphylococcus aureus infections and widespread viral infections of the skin, both of which are more prevalent among AD patients. The ADRN will build on the work of the Atopic Dermatitis and Vaccinia Network (ADVN) which conducted clinical studies focused on making smallpox vaccinations safer for people with AD.
This research will lead to a greater understanding of the immune system in AD patients and may lead to novel therapeutic strategies to manage or prevent infectious complications associated with this disease.
The ADRN will conduct a number of clinical studies over the next five years and will be enrolling large numbers of people with AD.
A search on clinicaltrials.gov returns two entries for the ADRN: one (open) to create a database of patients for the study of genetic markers connected to susceptibility to infections, and one (completed) to look into how AD patients respond to a new flu vaccine.
The ADRN’s NIH contract number is HHSN272201000020C. A search in the NIH’s PubMed database returns 12 papers that acknowledge funding by that contract number. Three of those are review papers (which did not involve new research).
So that makes two clinical trials and nine research papers, three years into a five-year $ 42 million project.
Should US taxpayers expect more; be satisfied; or be impressed?
The answer is probably that we will have to wait to find out.
In each year, a typical top university research lab operates on about $ 2-3M a year and publishes somewhere around ten papers. That’s roughly $ 200k a paper.
Three of the five years in the ADRN contract are up; three-fifths of $ 42M is around $ 24M. We might therefore naively estimate that we should have seen upwards of 100 papers produced so far.
Most likely the reasons there are only 12 at the moment are that you don’t start publishing papers right at the outset of a project. The research must be done first and then written up; and the process of getting accepted to a journal takes months. And the ADRN appears largely to rely on clinical trials–which take time to set up.
So why do we only see two trials listed on clinicaltrials.gov?
I’ve never had anything to do with a clinical trial, but when I was a researcher, I conducted animal experiments, and there were formidable administrative hurdles to get over before I could start work. I imagine that trials with human subjects are heavily regulated by the government, and for good reason. So the apparently small output of the ADRN to date is, I’m guessing, because it takes a long time to plan trials, get approval, and conduct them, before you can begin analyzing data and reporting it.
Still, let’s keep in mind that the ADRN is an extension of the ADVN. It’s not like the ADRN began from scratch—the scientists had the momentum of existing expertise and administration and research aims.
Looking at the titles of the published papers, I can’t immediately judge which are the most important. So I emailed Donald Leung, the principal investigator for the ADRN (he’s a professor and head of the Division of Pediatric Allergy and Immunology at National Jewish Health), and asked him whether he could summarize the consortium’s findings so far and highlight key points. I hope to hear back from him soon and perhaps to interview him on the phone.
I’d like to know what ADRN scientists have found that surprises them. What have they learned that is truly new?
And what is going to be truly useful to patients in the end? Publishing papers should not be the be-all and end-all of scientific research. What about patents? I’d like to know whether anyone in the ADRN has thought about controlling intellectual property and commercialization. While it’s true that clinical studies may highlight the ideal dosing amount or schedule for existing therapies, and this does not involve creating a new commercial enterprise, most medical technology must pass through the marketplace before it can benefit the consumer/patient.
Someone has to do the dirty work of developing scientific discovery into therapy, and it’s not academic scientists.
More to come.
End Eczema
New NEA post: Atopic Dermatitis Research Network needs trial participants
This week you’ll find me blogging over at the National Eczema Association website. I interviewed Donald Leung of National Jewish Health about the Atopic Dermatitis Research Network. Three years in to a $ 42M program to investigate the links between genetics and our susceptibility to skin infections, the ADRN is registering patients with the NIH before proceeding with clinical trials.
They still need black and Hispanic patients to sign up–eczema, genetics, and skin pathogens are different for different ethnic groups. The better your demographic is represented in the trials, the more that scientists will learn that applies to you.
The ADRN has centers in Boston, Chicago, Denver, Los Angeles, Portland OR, and Rochester NY.
If you’re interested in participating, email Judy Lairsmith at National Jewish or call 1-888-413-5852.
End Eczema
Fishy research for eczema sufferers
Eating fish has long been associated with healthy skin but is fish good for eczema? Researchers from Sweden found that the early introduction of fish into a child’s diet reduces the risk of eczema and asthma.
How soon can you introduce fish into a child’s diet?
Norwegian researchers found that frequent fish consumption before age 1 is associated with a reduced risk of allergic disease for toddlers. In this study, the average age infants began eating fish was 9 months of age (another study suggested 8 months of age was ideal and it reduced the risk of allergy). The Norwegian researchers concluded that fish consumption in infancy was more important than maternal fish intake during pregnancy in preventing childhood eczema.
Eczema Diet readers: check out pages 78 to 80 for safe seafood and fish to avoid.
You can read more on the eczema fish studies here:
http://jech.bmj.com/content/64/2/124.short
http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2006.01115.x/full
http://www.ncbi.nlm.nih.gov/pubmed/20670305
FYI: Keep in mind that fish allergy is possible so avoid fish if your child is allergic to fish or seafood.