From the monthly archives: January 2012
English: Governor Mitt Romney of MA

Boston Business Journal by Mary Moore, Reporter

Date: Tuesday, January 24, 2012, 2:36pm EST – Last Modified: Tuesday, January 24, 2012, 4:15 pm EST

Former Massachusetts Gov. Mitt Romney‘s charitable foundation contributed $210,000 – a third of its donations – to organizations in Greater Boston in 2010, according to tax returns released Thursday by Romney’s presidential campaign.

The Tyler Charitable Foundation donated a total of $647,500 in 2010 to a wide range of nonprofit organizations nationwide, from the Church of Latter Day Saints to a cystic fibrosis organization in Cambridge. The largest gift the Romneys made locally was a $75,000 donation to the Boston-based Center for the Treatment of Pediatric MS.

An Internet search for the pediatric nonprofit did not turn up an organization by that specific name, but the Tyler Foundation doc**ent lists the organization’s address at 1 Autumn St. in Boston.

Romney’s wife Ann was diagnosed with multiple sclerosis in the late 1990s.

The organization MS Cure, of Boston, received $10,000 from the Romneys’ foundation, while Cambridge-based Joey Fund for Cystic Fibrosis received $20,000.

The Dana Farber Cancer Institute    received $10,000 from the Romney foundation and $20,000 went to the Dana Farber Pan Mass Challenge.

Friends of the Belmont Council – a nonprofit co-located with the Belmont Council on Aging – received $20,000 from the foundation. The Belmont Hill School, which the Romneys’ children attended, received $5,000.

Other Boston-area organizations that received funding from the Romneys include:

Non-Profits, Philanthropy, Higher Education

Ryan launches New Campaign & Petition’s Platform

Ryan Mclaughlin has launched a new health campaign “Let Kids Shine” and a petition calling for parents to Tell Prime Minister To Take Action, stop delaying and implement changes needed to current Policy  of Vitamin D aiming improve the health of children and pregnant mothers.

Ryan has created his new petition for Vitamin D and we ask that you join and support him or indeed start a campaign of your own!

The New feature plus the recent launch of the Social Pledge platform will put network on course to be a serious social action platform for change..

So what you waiting for ? Lets Go ! Get campaigning and make a difference !

We have also started a live poll on the system and we ask that all members vote and participate. To make it easy for members to use and locate we have installed a widget on the home page so its super easy for members to locate.

Please Give it a Spin and leave us feedback.


What is Citizens Voice about?

Citizens Voice application was created to enable social network users with a unique opportunity to come together for meaningful social causes. All of us are passionate about one or more positive changes. It could be about stopping corruption, fighting terrorism, feeding the hungry, restoring human rights, saving the environment, education for all, etc. What better place than Ning where you and your friends can come together to start and promote your cause.

How to use Citizens Voice?

Citizens Voice provides several options. You can Create Campaigns, Petitions, Polls, and Discussion Forums. Application also provides a powerful invite feature for you to gather support from friends and like minded people on Shineonms, Ning, Orkut and other networks. While we are providing some guidelines below on how to use them, it is up to you on unleashing the power of each of these features to start and support your cause.

One of the key things to keep in mind is the difference between a Campaign and a Petition. Campaigns are high level social causes that you can take up based on location and/or category. Petitions are meant to gather official support for the action to be taken with regards to your campaign. Once you have enough people supporting your campaign, you can create a petition for an action to be taken.

Once you gather sufficient and/or signatures on your petition, we will offer you Free further support and help take it to the next steps for further action.

Contact : Alan McLaughlin 07580 461976

Social Network : shineonms.com

Tags: citizens voice, Campaigns

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Computer-obsessed children who spend too long indoors and over-anxious parents who slap on excessive sunscreen are contributing to a sharp rise in cases of the bone disease rickets, doctors are warning.

Vitamin D deficiency, which causes the condition, could be rectified by adding supplements to milk and other food, a research team at Newcastle University suggests.

There are several hundred cases of the preventable condition among children in the UK every year, according to a clinical review paper in the British Medical Journal by Professor Simon Pearce and Dr Tim Cheetham.

“More than 50% of the adult population [in the UK] have insufficient levels of vitamin D and 16% have severe deficiency during winter and spring,” they say. “The highest rates are in Scotland, Northern Ireland and northern England. People with pigmented skin are at high risk as are the elderly, obese individuals and those with malabsorption.”

Most vitamin D is synthesised in the body by absorption of sunlight. Some comes from foods such as fish oil. People with darker skins need more sunlight to top up their vitamin D levels.

One of the main reasons for the reappearance of rickets – once considered a disease of the industrial poor in 19th-century cities – is the changing ethnic makeup of the population, Pearce explained.

The most commonly affected are people of Asian or African descent who live in northern cities. He has examined cases among young Somali speakers who live in east Newcastle. But changing lifestyles are also contributing to lowering vitamin D levels in the general population.

“Some people are taking the safe sun message too far,” Pearce said. “It’s good to have 20 to 30 minutes of exposure to the sun two to three times a week, after which you can put on a hat or sunscreen.

“Vitamin D levels in parts of the population are precarious. The average worker nowadays is in a call centre, not out in the field. People tend to stay at home rather than going outside to kick a ball around. They stay at home on computer games.”

Pearce has written to the Department of Health proposing that vitamin D is added to milk. It is already added as a supplement to artificial baby milk. He has also asked the Royal College of Paediatrics to record cases of rickets but said figures were not being collected.

“A more robust approach to statutory food supplementation with vitamin D (for example in milk) is needed in the UK,” the paper concludes.

Meanwhile, figures obtained by the Tories show the number of patients leaving hospital with malnutrition has hit record levels in the last year. Those affected are primarily elderly people. The NHS figures show that last year 175,000 people were malnourished on entry to hospital but nearly 185,500 were in a similar condition on discharge, meaning more than 10,000 patients were more malnourished after medical treatment.

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Multiple sclerosis could be prevented through daily vitamin D supplements” reports The Times, stating that scientists have found the first causal link between the “sunshine vitamin” and a gene that increases the risk of the incurable neurological condition, known as MS.

The news comes from research into how vitamin D interacts with the genes that make certain people more likely to develop MS. The researchers claim their study strongly implies that vitamin D deficiency increases the risk of developing MS among susceptible individuals. This study was not attempting to find a cure or treatment for MS.

The Times reports that spending more time in the sun (which makes the body produce vitamin D) might protect against the condition. However, exposure to high levels of sunlight can damage the skin and cause cancer. The newspaper also suggests the use of vitamin supplements by pregnant women might reduce their children’s risk of the condition. Current advice for pregnant women is that they can choose to take up to 10 micrograms of vitamin D a day and to contact their GP for specific advice.

Although preliminary, this important study does point the way to future research into the actions of vitamin D and particularly the complex interactions between sunlight, vitamin D and genes.

Where did the story come from?

“There are remarkable implications for this work but of course it’s only part of the story, and there’s much still to be done…”

Simon Gillespie, of the MS Society

This study was conducted by Prof. George Ebers, Dr Julian Knight and colleagues from Oxford University, John Radcliffe Hospital and various institutions in Canada. The study was funded by the Multiple Sclerosis Society of Canada, the Scientific Research Foundation and the Multiple Sclerosis Society of the United Kingdom. It was published online in the peer reviewed journal PLoS genetics.

What kind of scientific study was this?

This genetic and laboratory study looked at whether there might be a relationship between vitamin D and genetic susceptibility for MS. The authors explain that MS is an inflammatory disease of the nervous system.

One particular area in the genome (genetic make up) on chromosome 6, called the Major Histocompatibility Complex (MHC), is reported to have the greatest genetic influence on a person’s risk of MS. Within this MHC one particular section called the HLA-DRB1 locus is known to influence MS risk. Having one particular variation of this locus, called the HLA-DRB1*15 haplotype, increases the risk of MS three fold.

There is also evidence to suggest that environmental factors act at a population level to influence the geographical distribution of MS. This is unusual, and even in populations of the same ethnicity the risk can vary by up to three times depending on geographic location. There is also a trend for a higher incidence of the disease in areas with less sunshine, such as Scotland and Northern European countries.

This has led to the suggestion that sunshine and particularly vitamin D, which is synthesised in the body in response to sunlight, may be connected to the environmental causes of MS. This study aimed to look at whether vitamin D might directly affect the function of specific genes within the MHC.

Once in the body vitamin D can switch certain genes on. To do this it needs to bind to a protein called the vitamin D receptor (VDR), which in turn binds to a particular sequence of the letters in the DNA called vitamin D response elements (VDREs).

To investigate this, the researchers used a computer program to look at genes within the MHC for VDREs in DNA from a person with the HLA-DRB1*15 haplotype on both of their copies of chromosome 6. They looked at the HLA-DRB1, -DQA1 and -DQB-1 genes, and at the DNA around them, as well as the IL2RA and IL7RA genes.

The computer program identified a piece of DNA that looked like a VDRE. The researchers then carried out a case-control study in 322 people to see if its sequence varied in people with MS (cases) and people without MS (controls). These people were all homozygous for (had two copies of) the HLA-DRB1*15 haplotype. The researchers also looked at the DNA from 168 people who did not carry this high-risk haplotype, but were homozygous for other haplotypes, which were not associated with increased risk of MS, or conferred only a modest increase in risk.

To further test whether vitamin D could bind to the VDRE-like sequence, the researchers carried out experiments where they mixed the VDR with a piece of DNA containing the VDRE-like sequence. This was to see if  there was evidence that the two were specifically binding to each other. Cells were then grown in the laboratory that were homozygous for the HLA-DRB1*15 haplotype. Half of the cells were treated with vitamin D for 24 hours, and the other half had no vitamin D. The researchers then used specific techniques to see if the VDRE was bound to the VDRs.

They then investigated if the VDRE could affect how genes are switched on in living cells. They took a piece of DNA containing the VDRE and attached it to a gene that produces a protein that can cause a light-producing reaction under certain conditions (called a reporter gene because of the ability to tell if it is switched on or off). This piece of DNA was then inserted into cells in the laboratory to see whether exposing the cells to vitamin D caused the reporter gene to be switched on. The researchers repeated this experiment using the variant forms of the VDRE found in the no- or moderate-MS-risk haplotypes.

Finally, the researchers investigated whether having the VDRE could affect the switching on of the HLA-DRB1 gene. They did this by comparing the level of HLA-DRB1 protein on the surface of cells that carried two copies of the HLA-DRB1*15 and cells that carried two copies of the less active VDRE variant haplotypes. They also looked at how treating these cells with vitamin D affected levels of HLA-DRB1.

What were the results of the study?

The researchers identified a possible site for vitamin D binding (a possible VDRE) in the region that controls the switching on of the HLA-DRB1 gene (called its promoter region). They found no variations in this possible VDRE sequence in people who had two copies of the high risk HLA-DRB1*15 haplotype, regardless of whether they had MS or not.

However, people who had two copies of the haplotypes that were not associated with MS, or conferred only a modest risk of MS, did have variations within the possible VDRE that might affect vitamin D binding. Tests in the laboratory showed that the VDR protein could bind to the potential VDRE when mixed together, and that the two would bind to each other in cells grown in the laboratory.

They also found that the VDRE could lead to switching on of reporter genes in the presence of vitamin D in cells in the laboratory, but that the variants of VDRE found in the lower risk MS haplotypes did not. Cells that had two copies of the HLA-DRB1*15 haplotype, and therefore the working VDRE, had higher levels of HLA-DRB1 protein than those that did not. Treating the cells that had two copies of the HLA-DRB1*15 haplotype with vitamin D increased the levels of this protein even more, but did not affect the other cells.

What interpretations did the researchers draw from these results?

The researchers say that their study provides further support for vitamin D as a strong environmental risk factor for MS. They say that their findings “imply direct interactions between HLA-DRB1, the main genetic susceptibility locus for MS, and vitamin D, a strong candidate for mediating the environmental effect”. They also say that as there is a high frequency of vitamin D insufficiency in the general population their data support the case for supplementation to reduce the number of people who have MS.

What does the NHS Knowledge Service make of this study?

This is important research and will be of major interest to people living with MS. However, this study concentrated on susceptibility to MS among populations, rather than looking for a cure or treatment to help those already living with the condition. “These are exciting advances, but unfortunately we have yet to find and solve the cause of MS… what I think we’ve done is add another piece to the jigsaw” said Dr Julian Knight, one of the authors.

Multiple genetic and environmental factors play a role in the development of MS, and this work advances scientific understanding of how these factors interact. This particular study focused on how vitamin D might interact with sections of the DNA of certain susceptible people.

Although The Times speculates that pregnant women might reduce their child’s risk of developing MS by taking vitamin D supplements, the authors state that the decision to use supplements “should still be between the patient and their physician”. Current NICE guidance states that pregnant or breastfeeding women may choose to take up to 10 micrograms of vitamin D a day and that women should speak to their GP for specific advice.
The newspaper also discusses the possibility of changing the recommended sun exposure limits. While sunlight does stimulate vitamin D production, the dangers of high levels of sun exposure are well documented, and sunbathing to increase vitamin D levels may be harmful. In addition, the study did not compare whether sunlight or supplements are a better source of vitamin D, but only looked at the chemical and biological interaction of vitamin D and genes in a laboratory.

This work will undoubtedly lead to further research into the risk factors behind MS, and potentially other serious conditions. Simon Gillespie, Chief Executive of the Multiple Sclerosis Society said that the research “is, of course, only part of the story, but what strikes me is opportunities and avenues for future research that it opens up.” At present trials are being conducted into whether vitamin D supplements can improve the symptoms of people living with MS.

The Multiple Sclerosis Society can give individuals further advice on this study through their website and helpline, on 0808 800 8000.

Links to the headlines
Vitamin D is ray of sunshine for multiple sclerosis patients. The Times, February 05 2009

Links to the science

Ramagopalan SV, Maugeri NJ, Handunnetthi L et al. Expression of the Multiple Sclerosis-Associated MHC Class II Allele HLA DRB1*1501 Is Regulated by Vitamin D PLoS genetics, 2009 [Advance online press release]

Related review by Cochrane:
Farinotti M, Simi S, Di Pietrantonj C, McDowell N, Brait L, Lupo D, Filippini G. Dietary interventions for multiple sclerosis. Cochrane Database of Systematic Reviews 2007, Issue 1

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Three novel multiple sclerosis genetic susceptibility loci have been identified, according to a meta-analysis published in the December issue of theAnnals of Neurology.

FRIDAY, Jan. 6 (HealthDay News)

Three novel multiple sclerosis (MS) genetic susceptibility loci have been identified, according to a meta-analysis published in the December issue of the Annals of Neurology.

Nikolaos A. Patsopoulos, M.D., Ph.D., from the Brigham and Women’s Hospital in Boston, and colleagues investigated MS susceptibility and explored the functional consequences of novel susceptibility loci. They performed a one-stage meta-analysis of seven genome-wide association studies involving 2,529,394 unique single nucleotide polymorphisms obtained from 5,545 patients with MS and 12,153 controls. Quantitative trait analysis in peripheral blood mononuclear cells (PBMCs) of 228 individuals with demyelinating disease were used to explore RNA expression data.

The researchers identified three novel susceptibility alleles: rs170934T on chromosome 3p24.1 (odds ratio [OR], 1.17), rs2150702G on chromosome 9p24.1 (OR, 1.16), and rs6718520A on chromosome 2p21 (OR, 1.17). There was no strong cis effect on RNA expression in PMBCs associated with these loci. Suggestive associations were seen in 10 additional loci.

“These results extend the list of loci associated with MS from earlier genome scans and confirm theoretical predictions that increasing sample sizes will lead to additional discoveries given the magnitude of effect seen for non-major histocompatibility complex MS susceptibility loci,” the authors write.

Several authors disclosed financial ties to the pharmaceutical industry.

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Newswise — BOSTON – January 6, 2012

Scientists at Joslin Diabetes Center, Harvard University, and the University of Cambridge have found that the age-related impairment of the body’s ability to replace protective myelin sheaths, which normally surround nerve fibers and allow them to send signals properly, may be reversible, offering new hope that therapeutic strategies aimed at restoring efficient regeneration can be effective in the central nervous system throughout life.

In a proof-of-principle study published in the journal Cell Stem Cell, the researchers report that defects in the regeneration of the myelin sheaths surrounding nerves, which are lost in diseases such as multiple sclerosis may be at least partially corrected following exposure of an old animal to the circulatory system of a young animal. Myelin is a fatty substance that protects nerves and aids in the quick transmission of signals between nerve cells.

Using a surgical technique, the researchers introduced an experimental demyelinating injury in the spinal cord of an old mouse, creating small areas of myelin loss, and then exposed those areas to cells found the blood of a young mouse. By doing so, they found that the influx of certain immune cells, called macrophages, from the young mouse helped resident stem cells restore effective remyelination in the old mouse’s spinal cord. This “rejuvenating” effect of young immune cells was mediated in part by the greater efficiency of the young cells in clearing away myelin debris created by the demyelinating injury. Prior studies have shown that this debris impedes the regeneration of myelin.

“Aging impairs regenerative potential in the central nervous system,” says author Amy J. Wagers, PhD, an associate professor of stem cell and regenerative biology at Harvard University and Joslin, who co-led the study with Professor Robin Franklin, director of the MS Society’s Cambridge Centre for Myelin Repair at the University of Cambridge. “This impairment can be reversed, however, suggesting that the eventual development of cell-based or drug-based interventions that mimic the rejuvenation signals found in our study could be used therapeutically.”

This could be particularly useful, she adds, in treating MS, which typically spans many decades of life, and thus is likely to be influenced by age-dependent reductions in the ability of myelin to regenerate. In MS, the body’s own immune system attacks the myelin sheath and prevents nerve fibers in the brain from sending signals properly, which can cause mild symptoms such as limb numbness or more serious ones like losing the ability to walk or speak. As people with MS age, remyelination decreases significantly, eventually causing permanent loss of nerve fibers.

“For MS sufferers,” says Franklin, “this means that, in theory, regenerative therapies will work throughout the duration of the disease. Specifically, it means that remyelination therapies do not need to be based on stem cell transplantation since the stem cells already present in the brain and spinal cord can be made to regenerate myelin, regardless of a person’s age.”

Other Joslin co-authors of the study were Tata Nageswara Rao and Jennifer L. Shadrach.

About Joslin Diabetes Center

Joslin Diabetes Center, located in Boston, Massachusetts, is the world’s preeminent diabetes research and clinical care organization. Joslin is dedicated to ensuring that people with diabetes live long, healthy lives and offers real hope and progress toward diabetes prevention and a cure. Joslin is an independent, nonprofit institution affiliated with Harvard Medical School.

For more information about Joslin, visit www.joslin.org.

Keep up with Joslin research and clinical news at Inside Joslin at www.joslin.org/news/inside_joslin.html,

Become a fan of Joslin on Facebook atwww.facebook.com/joslindiabetes

Follow Joslin on Twitter @JoslinDiabetes

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Lack of vitamin D is being linked to rickets, MS and asthma, so it’s time to confront the Victorian villain once again

Editorial: ”Down with this Dickensian disease

LAST month, Rohan Wray and Chana Al-Alas walked free from the Old Bailey court in London after being cleared of killing their 4-month-old son Jayden in 2009. The injuries to his skull, knee, elbow, shoulder, hip, ankle and wrist – and haemorrhages in his skull and eyes – had seemed to suggest that the pair was responsible for their baby’s death.

Post-mortems revealed a different story. Jayden had rickets, a Dickensian disease caused by a shortage of vitamin D, making his bones abnormally weak and vulnerable to damage.

Further investigations showed that Jayden’s mother was also suffering from a lack of vitamin D. She had been unable to supply Jayden with enough of the vitamin, either before his birth or afterwards in her breast milk.

The case has highlighted a resurgence in rich countries of the potentially fatal diseases that result from a lack of vitamin D (see “Rickets is just the start”).Irene Scheimberg, the clinical pathologist at the Royal London Hospital who discovered Jayden’s rickets, says there is evidence to suggest vitamin D deficiency was to blame for the deaths of two other babies she had examined, and may have contributed to the deaths of the 27 infants she has autopsied in the last few years, including deaths attributed to asthma, viruses and sudden infant death syndrome.

In the UK, cases of childhood rickets have leapt from 147 in 1997 to 762 in 2010. The story may be similar in the US: a study published by the US Centers for Disease Control (CDC) in Atlanta, Georgia, found that only 5 to 13 per cent of breastfed infants and 20 to 37 per cent of formula-fed babies got enough vitamin D to meet the recommended daily dose of 400 international units (IUs) – or 10 micrograms (PediatricsDOI: 10.1542/peds.2009-2571). The American Academy of Pediatrics came up with this figure in 2009 and it was endorsed in 2010 by the US Institute of Medicine.

There is no national surveillance of rickets in the US. “However, hospitalised cases of rickets among infants, indicating severe vitamin D deficiency, do continue to be reported,” says Cria Perrine, lead author of the CDC study.

So why the deficiencies? The body makes its own vitamin D in skin, but only if the skin is exposed to sunlight – something which tends to be discouraged because it raises the risk of skin cancer. Rickets flourished during Britain’s industrial revolution, when smog blocked sunlight and children were forced to work all day in factories.

Up to a quarter of the body’s vitamin D needs are provided by our diet. It is abundant in oily fish and eggs, but modern diets may not include enough of these foods to provide sufficient vitamin D. Supplements can boost levels of the vitamin, but the few studies available in the US suggest physicians seldom recommend vitamin D supplements for infants, says Perrine.

Gillian Killiner of the British Dietetic Association says the importance of vitamin D has been overlooked in the past decade because of the disproportionate focus on folic acid supplements, which can help prevent spinal defects in infants if given to pregnant women.

There is even uncertainty over the appropriate dose of vitamin D to give to pregnant or breastfeeding women. A recent study of 350 women who were between 12 and 16 weeks into pregnancy explored whether daily doses of 400, 2000 or 4000 IUs of vitamin D should be given. The women were tracked through to delivery. The results suggest that the highest dose was required to sustain normal metabolism in the women, and no adverse effects were found (Journal of Bone and Mineral Research, DOI: 10.1002/jbmr.463).

London-based coroner Andrew Walker recently concluded that vitamin D deficiency had claimed another infant by causing heart-valve failure and impairing immunity to an infection. On 6 December, he wrote to the UK’s health minister urging him to ensure that supplemental vitamin D is offered to all woman who are pregnant or breastfeeding.

In response, the Department of Health has promised to review the evidence on vitamin D requirements, and repeated a pledge from 1991 to provide vitamin D to pregnant women.

Boosting awareness is important: disease from vitamin D deficiency is preventable.

Rickets is Just the Start

Low levels of vitamin D through pregnancy and early childhood might increase the risk of food allergies, asthma and even multiple sclerosis.

George Ebers at the University of Oxford, and colleagues, discovered that MS is more common in those born in the northern hemisphere in May – following winter – than those born in November. The incidence of MS also increases further from the equator. Both results hint that lack of exposure to UVB light and subsequent low levels of vitamin D could be linked to a higher risk of the disease.

Ebers has called on the Scottish government to fortify essential foods with vitamin D. “Scotland has two new cases of MS a day and a lifetime cost per case of £1.2 million a year,” he says. “It also has the lowest vitamin D levels in the world.”

Lack of vitamin D has also been linked to food allergies. Carlos Camargo at Harvard University says that vitamin D deficiency in critical periods of development may increase intestine permeability, meaning the immune system is interacts with genes at over 2776 sites on the human genome, including those linked to asthma and diabetes. “It’s got to be an awful lot more important than people give it credit for,” says Ebers.

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Evidence for a direct link between Vitamin D deficiency and MS has just been bolstered, with a December publication of exciting new research.

2011 was a dramatic year in MS genetics research, with the results of the largest ever MS genetics experiment published in Nature. It not only identified 57 genes/gene regions affecting MS risk, but also identified specific aspects of the immune response as being pivotal. This study has provided the roadmap for the next few years of genetic research.

The next papers are now starting to appear. In the December edition of the prestigious journal, Annals of Neurology, a UK/Canadian collaboration headed by Prof George Ebers in Oxford and including Dr Julia Morahan (an Australian Research Fellow*), identified the gene from chromosome 12 as the most likely to contribute to MS risk and variants that appear to have a direct link. The gene, called CYP27B1, which activates vitamin D was first identified by the ANZgene collaboration of Australian MS researchers, then confirmed in the 2011 Naturepaper.

The UK/Canadian group has now shown that relatively rare variants of this gene, which can cause rickets (a common vitamin D deficiency disease), are nearly 5 times more common in people with MS than healthy controls. Remarkably, in the 35 families where an unaffected parent carried one of these variants of CYP27B1, all affected children inherited the variant, whereas unaffected children usually did not.

There are many other observations that link the Vitamin D deficiency with MS, such as:
• low blood vitamin D levels associated with increased risk of developing MS and increased risk of relapses;
• the latitude effect, where MS risk is highest where vitamin D activation is lowest;
• mouse models of MS showing how vitamin D protects against disease development; and
• another of the 57 genes known to affect MS risk that regulates vitamin D activation.

Vitamin D is known to regulate immune responses through turning genes on or off and many of the 57 genes associated with MS are responsive to vitamin D. This new research reflects the first potential direct genetic link.

The research adds support to proposals for clinical trials using vitamin D to treat MS, and studies to better understand how vitamin D exerts its protective effect, so that better interventions can be designed.

Contributed by A/Prof David Booth
The Hunt Family Foundation MS Senior Research Fellow, Westmead NSW

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UK POLITICIANS have been urged to bring in new legislation south of the Border to give doctors the right to be able to help the terminally ill die.

 The year-long Commission on Assisted Dying, chaired by Lord Falconer, has backed recommendations for reforms that would give adults with less than one year to live the right to ask their doctor for a lethal dose of medication that would end their life.

However, in a report published today, the body cautioned that stringent safeguards would have to be put in place to protect those who might not have the mental capacity to make such a choice, or were clinically depressed or under pressure from friends and relatives.

Scottish right-to-die campaigners, led by the independent MSP Margo MacDonald, backed the report’s recommendations, claiming it had once again put on the agenda attempts to change the legislation.

Ms MacDonald, who suffers from Parkinson’s disease, is weeks away from re-launching a Bill at Holyrood to give Scots the right to assisted suicide after her last attempt was rejected by fellow MSPs.

She said: “Public opinion can’t be ignored. Politicians will have to face it, and I think they will have to reflect a bit more what their constituents think rather than certain organised groupings of their constituents, whether they be faith groupings or otherwise.

“For me, it’s a human rights issue. People have the right to determine whether or not they want assistance to end their life earlier than nature would. I think that’s a right – it’s the sort of decision they make throughout their whole life and I don’t see why the last act of their life should be any different.

“No-one is bound to help them, whether a professional person or a lay person, but they should know that they can ask someone, and that person can accede to their request without being penalised and criminalised.”

The commission said MPs should consider developing a new legal framework for assisted dying, saying the “current legal status of assisted suicide is inadequate, incoherent and should not continue”.

The report found “there is a strong case for providing the choice of assisted dying for terminally ill people”.

“It is possible to devise a legal framework that would set out strictly defined circumstances in which terminally ill people might be assisted to die, supported by health and social care professionals, and which would employ robust upfront safeguards to prevent inappropriate requests that did not meet the eligibility criteria from going ahead.”

It added: “A person who provided assistance when the strictly defined circumstances were not present would be liable to be prosecuted for the crime of assisting suicide.”

It also called for more choice, saying clear and accessible information should be provided to those who want to die, linked to “the principles of improving open discussion and improving access to high quality end-of-life care”.

The right-to-die advocate, Dr Libby Wilson, said the report was a step in the right direction.

However, the former GP was critical of the 12-month stipulation, which she said would exclude many patients with degenerative conditions that destroyed their mental and physical faculties while having more than one year to live.

She said: “This is supposed to be about compassion. Why is your compassion limited by a timeframe?

“If you’ve got some horrible disease like motor neurone disease or the last stages of multiple sclerosis or Parkinson’s disease, you can go on living and suffering very severely for perhaps years, and yet compassion can’t extend to those people. I’m all for it in one sense – if indeed any notice is taken of it in the House of Lords – but from an ethical point of view I don’t understand it, especially with neurological diseases.

“There’s a terrible disease called Huntington’s disease which is genetic, where your brain just eventually disintegrates and you become paralysed, and you also become demented. And of course the people who inherit it have already seen their parents, aunts and uncles and so on die of it.”

Under Scots law an act of euthanasia by a third party, including physician-assisted suicide, is regarded as the deliberate killing of another, and would be dealt with under the criminal law relating to homicide.

A Scottish Government spokesman said: “While it is right that a patient who suffers from a life-limiting illness should receive the best palliative and end-of-life care available, deliberate taking of life remains illegal and there are no plans to change this.”

BMA Scotland said it was “firmly opposed to the legalisation of assisted dying”.

One member of the 11-person commission, the Reverend Canon Dr James Woodward, said he was unable to back its majority decision. He said the right time to consider changing the law was after a greater ethical, moral and social consensus had been generated on the issue.

Care not Killing, an anti-euthanasia group, said changes to the law could lead to around 13,000 deaths a year. Campaign director Dr Peter Saunders said the commission was paid for by those in favour of the right to die, with panel members “handpicked” by Lord Falconer, who they described as a “leading advocate” of changing the law, and the campaigners Dignity in Dying.

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CarersCarers will be disproportionately hit by government benefit cuts over the coming years, research published today shows.

Tax and benefit changes from 2010-15 will result in a real terms drop of 6% in net income for households where a person claims carer’s allowance, compared with a 4% fall for other households, found an analysis by the Institute for Fiscal Studies, commissioned by the Family and Parenting Institute.

The difference reflects the extent to which government benefit cuts are hitting disabled people cared for by loved-ones at home.

In particular, it arises from the government’s decision to replace disability living allowance with a new benefit, personal independence payment, with tighter eligibility criteria, and to limit eligibility for employment and support allowance to a year for claimants in households with savings or working spouses, except where the claimant is too ill or disabled to work at all.

The study also found that families with children were being disproportionately affected by the cuts. Average incomes for families with children are due to fall by 4.2% from 2010-15 in real terms, compared with 0.9% for all households, when all changes – not just those to taxes and benefits – are taken into account.

Larger families and those with younger children will be particularly badly hit, the research found.

“Many families will be left struggling to understand why they have been singled out in this way and how this sits alongside the Government’s ambition for the UK to become a family friendly nation,” said Family and Parenting Institute chief executive Katherine Rake.

Source: Communitycare © Reed Business Information Ltd (04/01/12)

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