A latest study debunked the association between vitamin D levels in newborns and the risk of developing multiple sclerosis in adulthood.
This study was conducted by researchers at the Karolinska Institutet. Over the recent years, it was widely accepted that low levels of vitamin D in newborn babies increase the risk of multiple sclerosis (MS) in adulthood. This is based on the studies that highlighted infants born in spring have a high risk of developing the disease as compared to those born during autumn. It was believed that low levels of sun exposure during pregnancy doubles the risk of MS in children born after winter.
This is the first time that this hypothesis has been tested; till date it was assessed through indirect observations.
Multiple sclerosis (MS) is one of the most disabling neurological diseases that affect 250,000-350,000 people in the U.S. It is diagnosed in people aged between 20 and 40 years. It is estimated that nearly 2.5 million people worldwide have MS. It is not an inherited disorder, but researchers assume that there is a genetic predisposition to the development of the disease.
"There are several reasons why the link between vitamin D at birth and later risk of MS has not been directly assessed previously," explains Peter Ueda.
The levels of vitamin D at birth of MS sufferers were measured and compared with a control group. It included 459 participants with MS and 663 healthy control subjects. These participants were part of the EIMS project led by the Institute. Each participant with MS gave blood sample and was made to answer a questionnaire.
Using PKU register that contains blood samples from newborn Swedish babies from 1975 onwards, the researchers determined the levels of vitamin D from time of birth of MS patients and their controls. They developed a new technique to measure vitamin D levels in dried blood samples.
"We could not see any association between levels of vitamin D at birth and risk of MS in adulthood," said Peter Ueda. "However a weaker link cannot be ruled out, nor can the link be ruled out for people with certain genes. However, our results do not support the hypothesis of such a possibility for reducing MS risk."
The results have been published in the journal Annals of Neurology.
Source: Science World Report Copywrite Science World Report 2014 (12/08/14)
Factors Associated With Recovery From Acute Optic Neuritis in Patients With Multiple Sclerosis
Malik MT, Healy BC, Benson LA, et al
Using their multiple sclerosis (MS) database, the investigators aimed to identify clinical and demographic factors linked to severity and to prediction of recovery from acute optic neuritis (AON). Malik and colleagues enrolled 253 adults and 38 children whose first symptom of MS was AON. The investigators defined a mild AON attack as visual acuity (VA) ≤ 20/40, a moderate attack as VA 20/50-20/190, and a severe attack as ≥ 20/200. At 1 year after the AON attack, complete recovery was defined as VA ≤ 20/20, fair recovery as VA 20/40, and poor recovery as VA ≥20/50.
Proportional odds logistic regression allowed the investigators to identify demographic and clinical characteristics associated with attack severity and recovery among the entire sample. To determine the association of vitamin D level with AON severity and recovery, they analyzed a subgroup of patients for whom blood samples were available within 6 months of an AON attack.
AON recovery was worse in men (adjusted odds ratio [OR], 2.28; P = .03) and in patients with severe AON attacks (adjusted OR 5.24; P < 0.001). Although children and adults had similar AON severity, recovery was significantly better in children in the unadjusted analysis (P = .041) and in the analysis adjusted for sex (P = .029).
Vitamin D level was significantly associated with AON attack severity, after adjustment for season (OR for 10-IU increase in vitamin D level, 0.47; 95% confidence interval, 0.32-0.68; P < .001). However, vitamin D level was not associated with recovery from the AON attack in univariate analysis (P = .98) or after adjustment for AON attack severity (P = .10).
Study limitations include the observational design, relatively small sample size, and inability to prove causality. In addition, vitamin D levels were available for only a subgroup of patients. Nonetheless, the findings suggest that vitamin D levels may affect AON severity, whereas younger age, attack severity, and male sex may affect AON recovery. Further clarification of the underlying pathophysiology may uncover potential therapeutic targets and strategies to limit progression of disability in MS.
Primary Source: Neurology. 2014;82:2173-2179
Source: Medscape Multispeciality Copyright © 1994-2014 by WebMD LLC (22/07/14)
Ueda P, Rafatnia F, Bäärnhielm M, Fröbom R, Korzunowicz G, Lönnerbro R, Hedström AK, Eyles D, Olsson T, Alfredsson L.
Objective: Low vitamin D status at birth may be associated with risk of adult onset multiple sclerosis, but this link has not been studied directly. We assessed the relation between neonatal vitamin D concentrations, measured in stored blood samples, and risk of multiple sclerosis.
Methods: This was a population-based case-control study in Sweden including 459 incident cases of multiple sclerosis and 663 controls, randomly drawn from a national population registry and frequency matched on sex, age and residential area.
Results: There was no association between neonatal 25-hydroxyvitamin D quintile and risk of multiple sclerosis (crude odds ratio 1.0, 95% confidence interval 0.68 to 1.44, for the highest quintile compared to the lowest). Adjusting for a number of potential confounding factors in early life (month of birth, latitude of birth, breastfeeding) and in adult life (25-hydroxyvitamin D, sun exposure, vitamin D intake from dairy products, fat fish consumption, smoking, body mass index at 20 years of age) as well as ancestry, multiple sclerosis heredity, and socioeconomic group, did not considerably affect the result.
Interpretation: At a broad population level, 25-hydroxyvitamin D at birth was not associated with risk of multiple sclerosis.
Source: Ann Neurol. 2014 Jul 1. doi: 10.1002/ana.24210. & Pubmed PMID: 24985080 (21/07/14)
A new study published in Neurology has found that in patients with multiple sclerosis, vitamin D status may relate to acute optic neuritis severity but not to recovery.
Acute optic neuritis (AON) is an inflammatory condition that occurs in the nerve fibers that communicate information between the eye and the brain. It is characterised by color blindness, vision loss, and pain in the eye.
AON is common in people with multiple sclerosis, a disease in which the immune system mistakenly attacks the covering of the body’s nerves. AON is often the first symptom that is present in those with multiple sclerosis, where the immune system attacks the optic nerves.
Vitamin D’s role in multiple sclerosis is well-established. Research suggests that maintaining healthy vitamin D levels helps slow progression of multiple sclerosis and help manage some aspects of the condition.
To further explore the diverse roles that vitamin D plays in multiple sclerosis, researchers recently conducted a study to determine if vitamin D status was related to AON.
For this study, the researchers were interested in evaluating factors that may relate to severity and recovery of AON, such as age, gender and vitamin D status. For vitamin D, they looked at 101 patients who had their vitamin D levels tested within six months of an AON attack.
The researchers found that 52.5% of the patients had a moderate attack and 35.6% had a severe attack. They also found that 90.1% of this group had a full recovery from the attack.
According to their results, vitamin D status was significantly related to the severity of attack. Male gender, more severe attacks, and older age were related to worse recovery from AON, while vitamin D status was not related to recovery.
“No previous study has specifically investigated the importance of vitamin D in severity of AON, and our results support the hypothesis that low vitamin D levels are related to worse multiple sclerosis disease course,” the researchers stated.
The researchers call for future studies using larger samples to further evaluate the role that vitamin D may play in AON attack severity.
Malik, M. et al. Factors associated with recovery from acute optic neuritis in patients with multiple sclerosis. Neurology, 2014.
Source: Vitamin D Council (13/06/14)
Everyone seems to agree that vitamin D is important throughout life. This is certainly as true in the first year of life as it is later on. For it is during the first year that, in addition to its role in calcium metabolism, this critical nutrient reduces both the risk of current infections and the late-life development of such autoimmune diseases as multiple sclerosis and type 1 diabetes.
Both the Institute of Medicine (IOM) and the American Academy of Pediatrics (AAP) agree that vitamin D intake during the first year of life should be 400 IU/d. My own estimation of the requirement (for different ages and body sizes) is 65-75 IU/kg body weight per day. For average body weights in infants during the first year of life that rule of thumb computes to somewhere between 300 and 500 IU/d for infants. So, while there is still contention with respect to the optimal intake for adults, there really is no disagreement about how much is needed for infants, either among various authoritative sources or arising from different approaches to the evidence. With respect to infants, 400 IU/d seems to be just about right.
The question is, how is the infant to get that vitamin D? Human milk, in most nursing mothers, contains very little vitamin D. Infant formulas, from various manufacturers, all contain some added vitamin D in amounts calculated to be sufficient to meet an infant's needs. But extensive studies during the first year of life reveal that less than one-fifth of all infants ever get as much as the recommended 400 IU/d from any source, and fewer than one out of 10 breast-fed infants meet the requirement. As a result, the AAP urges that all infants, regardless of whether they are breast or formula fed, receive their 400 IU/d as pediatric drops. Unfortunately, this recommendation, while appropriate, is not often followed. Most babies are just not getting the vitamin D they need. The late-life consequences of this shortfall could be enormous.
It must seem strange that on the one hand we stress that human milk is the best source of nourishment for our babies, and on the other seem to ignore the fact that human milk doesn't contain the vitamin D those babies need. The explanation, very simply, is that the disconnect is artificial. Nursing mothers have so little vitamin D in their own bodies that there is little or none left over to put into their milk. But it has not always been this way. We know that the vitamin D blood concentrations that are regularly found today in Africans living ancestral lifestyles are high enough to support putting into breast milk all the vitamin D an infant needs. But the bulk of the world's population today is not living on the high equatorial plains of East Africa nor exposing much of its skin for most of the day.
Fortunately, we don't have to return to East Africa. It turns out that, if we give nursing mothers enough vitamin D to bring their blood levels up to the likely ancestral levels, then they automatically put all of the vitamin D their baby needs into their own milk, thereby ensuring that the infant gets total nutrition without the need to resort to vitamin D drops.
How much vitamin D does the mother need so as to ensure an adequate amount in her milk? As with everything else related to vitamin D, there is a lot of individual variation, but it appears that the daily intake must be in the range of 5,000-6,000 IUs. As no surprise, that's just about the amount needed to reproduce the vitamin D blood levels in persons living ancestral lifestyles today. And while 5,000-6,000 IU may initially seem high, it is important to remember how much the sun produces for us. A single 15 minute whole body exposure to sun at mid-day in summer produces well over 10,000 IU.
There is one important proviso for nursing mothers concerning the needed intake. Those who live in North America and have to rely on supplements should be certain that they take their supplements every day. While for other purposes it is possible to take vitamin D intermittently (e.g., once a week), that doesn't work for putting vitamin D into human milk. The residence time of vitamin D in the blood is so short that, if the mother stops taking her vitamin D supplement for a day or two, vitamin D in her milk will be low (or absent altogether) on the days she skips.
There is a glaring disconnect here between these well-attested physiological facts and the official IOM recommendation for nursing mothers, i.e., only 400 IU/d - the same intake for her as IOM recommends for her baby (whose body weight is less than 10% of her own). The IOM, if it were to be explicit about its current recommendations, would be telling nursing mothers something like this:
"The evidence we analyzed indicates that your own body needs only 400 IU of vitamin D each day. Unfortunately, that won't allow you to put any vitamin D into your breast milk. Sorry about that . . . So, if you want to ensure that your baby is adequately nourished, you are going to have to resort to giving your infant vitamin D drops."
That would be a hard message to sell, and clearly, it makes little sense on its face. As I have already noted, women living ancestral lifestyles (whether or not they are nursing an infant) have far higher blood levels of vitamin D than contemporary urban Americans. Milk production (and its optimal composition) are simply two of the many functions that vitamin D supports in a healthy adult. This breast-feeding example is not a special case; it is just one of the many pieces of evidence that point to the fact that current vitamin D recommendations for adults are too low - way too low.
Vitamin D supplements - and in this case vitamin D drops - are literal lifesavers for infants today. But what about two or three generations back - before nutritional supplements come into existence, but long after migration out of Africa? Ninety years ago vitamin D had not yet been discovered, and there certainly were no vitamin D supplements that could have been used. How did we get by through those thousands of years? There are two answers. Most of us, living in temperate latitudes, got a lot more sun exposure than we do today, and of course there were no sunscreens, so there was no blocking of the solar radiation that produces vitamin D in our skin. Those of us living in far northern latitudes survived mostly by depending upon diets that were very high in seafood, which is naturally a rich source of vitamin D. And those of us who got vitamin D by neither route were at increased risk of a whole host of vitamin D-related disorders, most obvious and most easily recognized being rickets.
The bony deformities of rickets were common a century ago in Europe, North America, and East Asia, and were largely eradicated in growing children by use of cod liver oil and, in the US, by the introduction of vitamin D fortification of milk in the 1930s. Fortunately, growing children can repair some of the bone deformities of rickets if they are given vitamin D soon enough. But, repairing rickets, while a good and necessary thing to do, is not sufficient. It is too late, by the time we recognize the deformities of rickets, to ensure maximal protection against the autoimmune diseases (for example), for which susceptibility is mainly determined in the first year of life.
To sum up, we now better recognize the importance of vitamin D in the earliest stages of life. Furthermore, there is, as noted earlier, quite good agreement on how much an infant needs. Where we lack consensus is how to make certain that all of our babies get the amount they need. Why not rely on giving nursing infants vitamin D drops, as the AAP recommends? Two reasons: 1) It's been tried and has failed; and, 2) When it does work in individual infants, it provides no benefit for the mother. By contrast, ensuring an adequate vitamin D input to the mother during pregnancy and lactation is almost certainly the best way to meet the needs of both individuals.
An "adequate" intake for nursing mothers, as noted earlier, is not the 400 IU/d the IOM recommends, but is instead in the range of 5,000-6,000 IU/d, taken daily. If they get that much, they will meet not only their own needs, but their infant's as well. And they will have the satisfaction of knowing that they are supplying all their baby's needs, the natural way.
Source: News-Medical.Net Copyright 2000-2014 AZoM.com Limited (09/06/14)
An award-winning writer and scientist believes a deficiency of Vitamin D in pregnant women is behind the increase in conditions such as MS, diabetes, schizophrenia and asthma.
Scientists often liken the process of discovery to doing a jigsaw. At first, few pieces fit and the picture is a mystery. Then suddenly two or three pieces lock together and an image starts to take shape.
This is what is happening in the study of apparently unrelated, chronic diseases such as multiple sclerosis, schizophrenia, diabetes and asthma. These conditions are increasingly common both in the UK and elsewhere; their causes have puzzled doctors and scientists for decades.
Now pieces of the jigsaw are starting to fit together – and they focus on vitamin D which is produced naturally in the skin when exposed to sunlight.
A deficiency in this crucial vitamin, thanks to our increasingly indoor lifestyles, is already blamed for the reappearance of rickets, the painful and deforming bone disease in children, in the UK. But gradually, evidence is emerging that links low vitamin D levels to a rise in a whole host of “modern” diseases, some of which were virtually unheard of in the pre-industrial era.
As a scientist and writer, I first realised the significance of vitamin D for prevention of ill-health some 12 years ago, at a time when it was only recognised as important for bone growth. I have researched and written extensively on the topic, including a report on the health benefits of sunlight - this at a time when official advice was to avoid the sun at all costs, especially when the sun is at its highest.
The report, published in 2004, gained support from the late Sir Richard Doll, the eminent epidemiologist who co-discovered the link between smoking and lung cancer. He had completed a clinical trial which found that people who took vitamin D supplements may live longer - and had he lived had wanted to do another. It has taken eight years to get that clinical trial started with Professor Julian Peto of the London School of Hygiene and Tropical Medicine. Called VIDAL, the trial is looking at benefits of supplementation and for any increase in life expectancy in over 65s.
Highlighting the benefits of vitamin D has led to at least some degree of change in official attitudes. We are now advised to spend some time in the sun at midday, while vitamin D supplements are advised for breastfed (but not bottlefed) babies from the first month of life.
My belief is that we could go much further – that vitamin D, given freely to all women in pregnancy, could be used to curb or prevent some major diseases including multiple sclerosis, diabetes, schizophrenia, asthma and several cancers; and that it might also be used to treat established disease, at least in early stages.
One crucial piece in the jigsaw has come from the study of birthdays. Links between birthdays and future life events have long been the territory of clairvoyants and mediums; and when evidence first emerged about a decade ago that people born at the end of winter were more likely to get multiple sclerosis and those born in autumn less so, many scientists found it hardly credible.
“It looked as if we were interested in star signs and futurology,” said George Ebers, emeritus professor in the Department of Department of Clinical Neurology at the Wellcome Trust Centre for Human Genetics, University of Oxford, whose career has never deviated from scientific correctness. “But now we know that MS is associated with end of winter births, when shortage of sunshine is demonstrable and vitamin D levels are lowest. This suggests, in line with other observations, that vitamin D protects against the disease.”
THE POWER OF THE SUMMER SUN
Summer sun is at its maximum in June and July but vitamin D, generated in the skin by sunlight, takes two or three months to get into the general circulation. So we reach our maximum level of vitamin D in about September. Babies born in October or November have the best chance of a relatively high level of vitamin D during their final months in the womb. And this, the birthday evidence suggests, can protect them from MS, while the risk is higher for babies born at the end of winter.
This seasonal pattern in the risk of MS has now been found in eight different countries including Australia, winning over previously sceptical scientists. Less well known is the link between end of winter birthdays and an increased risk of several other diseases. Studies of thousands of birthdays in Europe, Canada and Australia over some 30 years have found that people born at this time are also at greater risk of type 1 diabetes, coeliac disease (gluten intolerance), schizophrenia and autism.
For a long time experts did not know what to make of this data, since these diseases had no obvious links. But now more conditions are being added to this list by the Oxford team. Writing in the peer-reviewed journal, BMC Medicine, in July 2012, Professor Ebers, working with Dr Sreeram Ramagopalan, has shown that the risk of rheumatoid arthritis, a digestive disease called ulcerative colitis and a distressing condition called systemic lupus erythematosus follows the same pattern of seasonal births. These are all autoimmune diseases, which occur when the body is attacked by its own immune system. Diabetes type 1 is also an autoimmune disease and in the case of coeliac disease the immune reaction is to wheat in the bowel. To date, at least 18 autoimmune diseases have been linked to low vitamin D levels – more than enough to demonstrate a pattern.
''These immune-mediated diseases are one of the most common disease groups in modern economies today, affecting some 10% of the world population. Vitamin D deficiency is the most obvious risk factor” says Dr Ramagopalan. To test this theory Dr Ramagopalan has examined blood taken from the umbilical cords of 50 healthy babies born in November and 50 born in May when, after winter, levels of vitamin D are low. The May babies had a far higher frequency of newly generated white blood cells called T cells which are normally programmed to react against infection by an outside agent and to tolerate the body’s own tissues.
However certain types of T cells react against the body tissues and they may cause autoimmune disease later on if they persist. These unwanted T cells are normally removed from the body in the first year of life by a clever arrangement - they are deleted in the thymus gland, a process that requires vitamin D. So a low vitamin D level leaves the baby at risk. Dr Ramagopalan has explained his findings in detail in the open access, peer-reviewed PLOS Genetics, 2009, in which he writes: “The prevalence of diseases, such as multiple sclerosis, type 1 diabetes, inflammatory bowel disease, and rheumatoid arthritis correlate positively with latitude and reduced ultraviolet radiation exposure which is the primary determinant of vitamin D levels.”
The scientific jigsaw is now making more sense, but some pieces still do not seem to fit. Why should schizophrenia, a mental health condition, be linked to season of birth? In fact the birthday evidence on schizophrenia has provided a vital scientific clue to a disease which has puzzled doctors for over 100 years. Researchers now recognise that schizophrenia also has features of an autoimmune disease in which the body attacks its own tissues.
Schizophrenia and MS are both diseases of the nervous system. In MS myelin nerve sheaths deep in the nervous system are attacked by an immune reaction. If this can happen in MS, surely it is not so strange that schizophrenia may be explained similarly by an immune attack on crucial areas of the brain.
Dr John McGrath, international expert in schizophrenia based at the University of Queensland, Australia, says the evidence suggests that sun exposure in pregnancy and early life protects against schizophrenia and “raises the tantalising prospect that optimising vitamin D status during pregnancy may lead to the primary prevention of the disease”. “Being born in the country where there is more opportunity for sun exposure is associated with a lower risk of schizophrenia - while moving subsequently to an urban area where more time is spent indoors does not seem to increase the risk,” he points out.
Could lack of vitamin D in pregnancy also explain autism? The latest evidence suggests that a low vitamin D level in the mother’s body during pregnancy may induce her immune system to make antibodies which can damage the baby’s brain, as well as causing certain genes to malfunction. Last month, Rhonda Patrick and Bruce Ames from the Children’s Hospital Oakland Research Institute, in California, published research findings that these genes normally make the chemical serotonin.
Too little of this neurotransmitter is associated with abnormal social behaviour while too much in the digestive tract causes sensitivity to foods which may explain some autistic children’s difficult eating habits.
Patrick and Ames, both well-respected scientists in the field of autism, suggest: “Supplementation with vitamin D and tryptophan [which is made into serotonin in the brain] is a practical and affordable solution to help autism and possibly ameliorate some of the symptoms of the disorder.”
But the vitamin D jigsaw puzzle is not finished yet. Some 15 or more different cancers have been consistently associated with low vitamin D levels in a way that accords with established criteria, according to epidemiologist Dr William B Grant, from the non-profit organisation the Sunlight Nutrition and Health Research Center in California. In his paper published in 2009, the link is most clearly seen in breast and bowel cancer. Insufficient vitamin D leads to loss of control of several genes which regulate proliferation of cancer cells and inhibit the cell cycle.
In fact there are more than 900 genes that Vitamin D is now known to switch on and off - and in doing so alters our vulnerability to disease. The large number of genes involved explains how so many quite different diseases can be caused by insufficient sunshine. In this way sunshine exposure directly alters the action of genes which may actually be passed on in their altered state – a newly understood process known as epigenetics. So it is possible to see how some diseases may emerge for the first time in one generation and be passed on to the next.
There is understandable opposition to these theories from some in the medical establishment. In an editorial published last December,the journal The Lancet argued that failure of “gold standard” clinical trials of vitamin D to treat disease in adults disproves the possibility that insufficient vitamin D is a causal factor.
In my view, this ignores a wealth of experimental and observational evidence associating low vitamin D levels with higher risk of certain diseases. Also, vitamin D given in adulthood cannot necessarily be expected to cure a condition that has arisen through lack of vitamin D in early life. This is an error in scientific reasoning which I call the The Lancet’s “gold standard fallacy”.
INDOOR LIFESTYLES BLAMED
At the same time researchers are finding links between vitamin D and chronic disease, the world is facing an epidemic of these same conditions, caused by our indoor lifestyles. Even in the height of summer people in cities often have sub-optimal levels of vitamin D, and so babies born at any time of year may develop these diseases. It’s well recognised that multiple sclerosis has become increasingly common in the UK over the last century. Today, in cloudy Orkney, off the north of Scotland, one in 150 women suffer from MS, believed to be the highest prevalence in the world.
Less well known is that a generation ago the disease was much less common in southern than in northern Europe. But MS has increased rapidly in the Mediterranean over recent years, reflecting the increased movement of people away from rural subsistence farming to town and a life in urban apartments. In the Greek island of Crete MS has increased almost four fold over the last generation.
One striking example of the rise in MS is in Iran where, after the Islamic revolution in 1979, women were compelled by law to wear the veil outdoors together with clothing covering most of the body. Between 1989 and 2006, the incidence of MS in Iran increased more than eight fold, from an incidence of about one case in 100,000 to nearly one in 10,000 in the city of Isfahan.
“The Islamic revolution can potentially explain the observed increase in MS incidence in Iran in just over 30 years,” said Dr Ramagopalan. “Veiled women have lower vitamin D levels compared to unveiled women, giving an increased risk of low vitamin D in pregnancy which can account for the increase in MS.”
There have been similar increases in other autoimmune diseases, some rare or even unknown a century ago. Type 1 diabetes has seen an annual 4 per cent increase across Europe in a generation, with larger increases in the under-fives and the number of cases in this age group expected to double between 2005 and 2020. Crohn’s disease, a life threatening inflammation of the bowel, has since the 1930s become increasingly common in most developed countries.
Between 1965 and 1997 the incidence of schizophrenia doubled in London’s Camberwell. Much, but not all, of the increase is attributed to second generation dark-skinned immigrants who have a five times greater risk of the disease than their parents or people with white skin. Dark skin blocks absorption of weak northern sunlight, preventing vitamin D synthesis.
Autism was also rarity a generation ago. Between 1988 and 1995 the incidence in UK children increased some five fold, according to a nationwide survey by a 1000 GPs; arguably such a large rise cannot all be explained as improvements or changes in diagnosis of the condition, which is generally held to be difficult to miss. A similar increase occurred in the United States in the 1990s.
Over the last generation there has also been a global increase in asthma. Tests on frozen blood show that the epidemic is not caused by changes in diagnosis. Allergic reactions to mixed pollens, animal dander and house dust mites have increased by 4.5 per cent per decade in the UK during last quarter of the 20th epidemic has been followed closely by a rapid increase in food allergy. In extreme cases allergy can cause anaphylactic shock which has increased in England by 50 per cent between 2001 and 2005.
Professionals dealing with overflowing clinics are talking about a 'double tsunami’ – a giant wave of asthma followed by a second wave of food allergy, suggesting that they are two parts of a continuing epidemic. Two distinguished professors, Augusto Litonjua and Scot Weiss, from Harvard University School of Medicine calculate that some 300 million people worldwide now suffer from asthma and blame social changes: “...as populations grow more prosperous and more westernised”, they say, “more time is spent indoors and there is less exposure to sunlight, leading to vitamin D deficiency, subsequently resulting in more asthma and allergy.”
Why has the wave of food allergy followed the wave of asthma rather than occurring simultaneously: and why are second generation immigrants more at risk of diseases such as schizophrenia or Crohn’s than their first generation parents? The new science of epigenetics explains how the environment can influence genes which are then passed on in an altered state, in apparent contradiction of classical genetics.
Women who are severely vitamin D deficient may pass on de-activated genes, which make their children more vulnerable to disease. Multiple sclerosis, Type 1 diabetes, Crohn’s, schizophrenia, autism, asthma and food allergy have all been increasing in the same overlapping time frame and all have links to low vitamin D and low sunshine exposure. A further 11 autoimmune diseases have been linked to serious vitamin D deficiency in an Oxford study published in BMC Medicine in 2013. This makes at least 18 autoimmune diseases clearly linked to low vitamin D levels - more than enough to demonstrate a pattern.
PREVENTION IS CRUCIAL
Although The Lancet may insist otherwise, some clinical trials have shown that people with MS, asthma or Crohn’s may do better or have fewer relapses when they take vitamin D, if disease is not too advanced. For example, MS begins with optic neuritis, a temporary form of blindness, in 20 per cent of cases. Doctors at Isfahan University, Iran, have shown in a clinical trial that giving vitamin D (about 7,000 IUs per day) at this early stage can reduce risk of a relapse in blindness by 68 per cent and lower the incidence of lesions and “black holes” in the brain. They are hopeful that vitamin D may delay the usual conversion of optic neuritis to subsequent MS. Symptoms of Crohns’ disease can be reduced dramatically by 5,000 IUs per day of vitamin D according to a clinical trial at the Center for Molecular Immunology, University of Pennsylvania. Another study at Massachusetts General Hospital, described in the journal Inflammatory Bowel Disease, 2013, shows that risk of surgery is reduced in Crohns’ patients who took a vitamin D supplement that increased their blood level to normal.
While the Lancet remains trapped in its “gold standard” fallacy, doctors working with these autoimmune diseases, previously sceptical, are now privately hopeful that vitamin D will prove to be a useful addition to treatment. But increasing vitamin D later in life cannot always restore what has been lost when vitamin levels are low: for example, in the case of diabetes type 1, an enterovirus may attack the islet cells in the pancreas that make insulin, wiping them out. This is why prevention is so crucial: the link between high vitamin D levels in pregnancy and a reduction in diabetes risk was shown as long ago as 2001.
BRITAIN'S CLOUDY SKIES ARE BAD NEWS
THE UK has least sunshine of almost any advanced economy; our cloudy weather is arguably one of the unhealthiest climates in the world. And even when the sun shines we spend too much time indoors, detained by our computers and TVs. Fear of sunlight has been spread by misguided advice from cancer charities urging people to “seek the shade” rather than enjoy the sun safely and often. Extensive use of suncreams since the 1970s, has reduced exposure to UVB, the part of sunlight which generates vitamin D. The Chief Medical Officer, Dame Sally Davies, has said she is “profoundly ashamed” at the return of rickets in the UK. But the increase in rickets is small compared with the pandemic of immune system disease, the cost of which can be calculated in billions. MS costs the UK £3 billion a year, type 1 diabetes £9 billion, and schizophrenia £12 billion IN 1942, when Britain was besieged by German submarines, the government was eager to maintain the nation’s health by providing all children with cod liver oil, the best natural source of vitamin D. Since then successive governments have pursued a false economy and restricted free supplies of vitamin D supplements to a small percentage of pregnant and breastfeeding women and under-fives who are on state benefits.
I believe a great advance could be made by returning to heroic wartime thinking, providing all pregnant women and babies with free vitamin D supplements. I would argue that an intensive programme reaching 80-90 per cent of people, as modern vaccinations do, would greatly reduce and might even virtually eradicate MS, type 1 diabetes and several other autoimmune diseases.
Even lesser measures could at least halt or slow the pandemic. At little cost, the government could encourage voluntary fortification of foods such as milk and bread with vitamin D and give better advice on benefits of sunshine and how to enjoy the sun safely. Failure to act soon will be a cause for profound national shame.
Source: Daily Telegraph © Copyright of Telegraph Media Group Limited 2014 (10/03/13)
Vitamin D status appears to be associated with reduced disease activity in patients with multiple sclerosis (MS) and a slower rate of disease progression, according to a study by Alberto Ascherio, M.D., Dr.P.H., of the Harvard School of Public Health, Boston, and colleagues.
MS is a common cause of neurological disability and vitamin D status may be related to the disease process, according to the study background.
Researchers examined whether blood concentration of 25-hydroxyvitamin D (25[OH]D), a marker of vitamin D status, was associated with MS disease activity and progression in patients with a first episode suggestive of MS.
Blood 25[OH]D levels were measured as part of a randomized trial originally designed to study patients given interferon beta-1b treatment. A total of 465 patients (of the 468 enrolled) had at least one 25[OH]D measurement. Patients were followed for up to five years with magnetic resonance imaging.
Increases of 50-nmol/L in average blood 25[OH]D levels within the first 12 months appeared to be associated with a 57 percent lower risk of new active brain lesions, 57 percent lower risk of relapse, 25 percent lower yearly increase in T2 lesion volume and 0.41 percent lower yearly loss in brain volume from months 12 to 60.
"Among patients with MS mainly treated with interferon beta-1b, low 25[OH]D levels early in the disease course are a strong risk factor for long-term MS activity and progression," the study concludes.
Source: MNT © 2004-2014 All rights reserved (21/01/14)
Researchers have discovered a vitamin D-based treatment that can halt and even reverse the course of the disease in a mouse model of Multiple Sclerosis (MS).
The treatment involves giving mice that exhibit MS symptoms a single dose of calcitriol, the active hormone form of vitamin D, followed by ongoing vitamin D supplements through the diet.
Lead scientist biochemistry professor Colleen Hayes said that all of the animals just got better and better, and the longer we watched them, the more neurological function they regained.
While scientists don’t fully understand what triggers MS, some studies have linked low levels of vitamin D with a higher risk of developing the disease.
Hayes has been studying this “vitamin D hypothesis” for the past 25 years with the long-term goal of uncovering novel preventive measures and treatments.
Over the years, she and her researchers have revealed some of the molecular mechanisms involved in vitamin D’s protective actions, and also explained how vitamin D interactions with estrogen may influence MS disease risk and progression in women.
First, Hayes’ team compared the effectiveness of a single dose of calcitriol to that of a comparable dose of a glucocorticoid, a drug now administered to MS patients who experience a bad neurological episode.
Calcitriol came out ahead, inducing a nine-day remission in 92 percent of mice on average, versus a six-day remission in 58 percent for mice that received glucocorticoid.
Next, Hayes’ team tried a weekly dose of calcitriol. They found that a weekly dose reversed the disease and sustained remission indefinitely.
But calcitriol can carry some strong side effects it’s a “biological sledgehammer” that can raise blood calcium levels in people, Hayes says – so she tried a third regimen: a single dose of calcitriol, followed by ongoing vitamin D supplements in the diet.
Source: AM Authint Mail © AMPL 2014 (20/01/14)
Vitamin D could represent a natural therapeutic method against multiple sclerosis (MS), according to a new study. Researchers at John Hopkins University School of Medicine have discovered that the so-called sunshine vitamin can block nerve damage in a mouse model of the autoimmune disease. The findings may represent a significant step towards halting and ultimately reversing one of our most debilitating disorders.
For some time, researchers have been trying to figure out why the incidence of MS is significantly lower in regions close to the equator. Many now believe that the sustained sunlight of these areas may have a protective effect against the nerve-destroying disease. Published in the journal Proceedings of the National Academy of Sciences, the current study sought to determine whether vitamin D — a key nutrient derived from sunlight — is associated with this effect.
To investigate, the researchers designed a trial involving lab rodents afflicted with a mouse model of MS. They found that subjects who received a high dose of vitamin D did not exhibit the usual symptoms associated with the disorder. According to lead author Anne R. Gocke, this suggests that the “sunshine vitamin” may offer MS protection that parallels that of current drugs. "With this research, we learned vitamin D might be working not by altering the function of damaging immune cells but by preventing their journey into the brain," she said in a press release. "If we are right, and we can exploit Mother Nature's natural protective mechanism, an approach like this could be as effective as and safer than existing drugs that treat MS."
As subsequent biological analyses nonetheless confirmed a strong disease presence in the form of nerve-damaging T cells, the researchers theorize that vitamin D suppresses debilitating symptoms by keeping the disease out of the brain. "Vitamin D doesn't seem to cause global immunosuppression," Gocke explained. "What's interesting is that the T cells are primed, but they are being kept away from the places in the body where they can do the most damage."
According to the Mayo Clinic, MS is a so-called autoimmune disorder that turns the body’s own defenses against its most essential parts. Rogue T cells begin to erode myelin, the protective sheath that covers nerves. The degeneration, which disrupts communications between essential organs, eventually results in irreversible nerve damage.
Source: Medical Daily © Medical Daily 2013 (10/12/13)
Many people with MS start using some kind of mobility aid -- cane, walker, scooter or wheelchair -- by 45 or 50, and those with the most severe cases are typically bed-bound by 60. The medications that are currently available don't do much to slow the relentless march of the disease.
In search of a better option for MS patients, a team of University of Wisconsin-Madison biochemists has discovered a promising vitamin D-based treatment that can halt -- and even reverse -- the course of the disease in a mouse model of MS. The treatment involves giving mice that exhibit MS symptoms a single dose of calcitriol, the active hormone form of vitamin D, followed by ongoing vitamin D supplements through the diet. The protocol is described in a scientific article that was published online in August in the Journal of Neuroimmunology.
"All of the animals just got better and better, and the longer we watched them, the more neurological function they regained," says biochemistry professor Colleen Hayes, who led the study.
MS afflicts around 2.5 Million people worldwide, with 200 new cases diagnosed each week. Early on, this debilitating autoimmune disease, in which the immune system attacks the myelin coating that protects the brain's nerve cells, causes symptoms including weakness, loss of dexterity and balance, disturbances to vision, and difficulty thinking and remembering. As it progresses, people can lose the ability to walk, sit, see, eat, speak and think clearly.
Current FDA-approved treatments only work for some MS patients and, even among them, the benefits are modest. "And in the long term they don't halt the disease process that relentlessly eats away at the neurons," Hayes adds. "So there's an unmet need for better treatments."
While scientists don't fully understand what triggers MS, some studies have linked low levels of vitamin D with a higher risk of developing the disease. Hayes has been studying this "vitamin D hypothesis" for the past 25 years with the long-term goal of uncovering novel preventive measures and treatments. Over the years, she and her researchers have revealed some of the molecular mechanisms involved in vitamin D's protective actions, and also explained how vitamin D interactions with estrogen may influence MS disease risk and progression in women.
In the current study, which was funded by the National Multiple Sclerosis Society, Hayes' team compared various vitamin D-based treatments to standard MS drugs. In each case, vitamin D-based treatments won out. Mice that received them showed fewer physical symptoms and cellular signs of disease.
First, Hayes' team compared the effectiveness of a single dose of calcitriol to that of a comparable dose of a glucocorticoid, a drug now administered to MS patients who experience a bad neurological episode. Calcitriol came out ahead, inducing a nine-day remission in 92 percent of mice on average, versus a six-day remission in 58 percent for mice that received glucocorticoid.
"So, at least in the animal model, calcitriol is more effective than what's being used in the clinic right now," says Hayes.
Next, Hayes' team tried a weekly dose of calcitriol. They found that a weekly dose reversed the disease and sustained remission indefinitely.
But calcitriol can carry some strong side effects -- it's a "biological sledgehammer" that can raise blood calcium levels in people, Hayes says -- so she tried a third regimen: a single dose of calcitriol, followed by ongoing vitamin D supplements in the diet. This one-two punch "was a runaway success," she says. "One hundred percent of mice responded."
Hayes believes that the calcitriol may cause the autoimmune cells attacking the nerve cells' myelin coating to die, while the vitamin D prevents new autoimmune cells from taking their place.
While she is excited about the prospect of her research helping MS patients someday, Hayes is quick to point out that it's based on a mouse model of disease, not the real thing. Also, while rodents are genetically homogeneous, people are genetically diverse.
"So it's not certain we'll be able to translate (this discovery to humans)," says Hayes. "But I think the chances are good because we have such a broad foundation of data showing protective effects of vitamin D in humans."
The next step is human clinical trials, a step that must be taken by a medical doctor, a neurologist. If the treatment works in people, patients with early symptoms of MS may never need to receive an official diagnosis.
"It's my hope that one day doctors will be able to say, 'We're going to give you an oral calcitriol dose and ramp up the vitamin D in your diet, and then we're going to follow you closely over the next few months. You're just going to have this one neurological episode and that will be the end of it,'" says Hayes. "That's my dream."
Source: ScienceDaily Copyright 2013 by ScienceDaily, LLC (30/09/13)
In the time it took to cross a Melbourne suburban street, Simon McKeon went from seeing the world in full colour to one of fuzzy darkness. It was 1999 and the investment banker, philanthropist and former Australian of the Year had experienced an episode of multiple sclerosis, a disease that attacks the brain and spinal cord.
“I left the pavement on one side and by the time I got to the other side I could only literally see a vague shape of a tree,” he says.
“I hugged this tree because it happened without warning.”
McKeon was not far from his home, so shuffled along the path and doesn’t remember much from there. He was helped into hospital and did not recover his sight for about 10 days. He didn’t make the link between an episode a few months before when he suddenly experienced paralysis from the hip down. But his neurologist quickly tied the two events together to diagnose MS.
McKeon, who is executive chairman of Macquarie Bank, Melbourne, began working with MS Australia and in 2004 became the founding chairman of MS Research Australia.
MS occurs when white blood cells produced as part of a normal immune response erroneously attack myelin, which is like insulation that wraps around the nerves. The insulation allows electrical impulses to travel quickly to and from the brain, but when it is damaged, the messages are not relayed, which causes symptoms such as blindness and paralysis.
The disease afflicts about 23,000 Australians and this number is increasing at a rate of 5 per cent each year. Three out of four cases afflict women. There is no cure.
EQUATOR OFFERS CLUE
But a new trial being undertaken by MS Research Australia, the largest of its kind in the world, hopes to identify a link between the progression of MS and levels of Vitamin D in the body.
Researchers have long suspected such a link exists because of the varying incidence of MS depending on how far away from the equator a location is, said MSRA chief executive Matthew Miles.
Vitamin D is activated in the body by sunlight. How many degrees of latitude away from the equator a person lives generally gives a good indication of their levels of sun exposure and Vitamin D in the blood.
“The incidence of MS in Tasmania, Victoria or the ACT is much, much greater than the incidence in tropical far north Queensland or the Northern Territory,” Miles says. “That leads us to two things – either MS may be related to Vitamin D levels, or it might be related to UV radiation levels.”
The organisation hopes to recruit about 260 patients across 21 hospitals in Australia and New Zealand who have had their first clinically recognised episode of MS. Patients will be given one of three different doses of Vitamin D or a placebo.
The trial is double blind, which means neither the patient nor the doctor knows who gets which course of treatment. Participants’ exposure to sunlight will also be measured.
“What we’re hoping to find is that there is an ability of Vitamin D to prevent the onset or the incidence of people developing diagnosed MS,” Miles says.
CORPORATE WORLD BEHIND CAUSE
McKeon is excited about the prospects of the trial. “There really hasn’t been a large-scale [trial] done on this anywhere around the world, particularly on such a spread of population and with a placebo and different doses,” he says.
MSRA has tapped into corporate networks and received commitments to fund $3 million worth of research annually for the next 10 years. Within five years of its establishment, the annual amount spent on new medical research into MS increased five-fold to just over $2 million.
McKeon has since been replaced as chair by former Goldman Sachs banker and company director Paul Murnane, although he is patron.
MS is one of a number of causes that McKeon backs but, unlike his work on indigenous disadvantage and the environment, he says it was his only philanthropic interest with a direct personal link. He calls it his “selfish” work.
“I can remember saying at the time, ‘my gosh – have I sailed my last yachting race and kicked my last footy with my kids?’? [I thought] if I somehow am not sentenced to a life in a wheelchair or whatever else, I will never take a day for granted. I’ve had my own version of a near-death experience. I didn’t die, but I’ve had that taste of what vulnerability is all about.”
“Sometimes in the philanthropic space it’s okay to be a bit self-motivated, so long as it’s not the only motivation,” he said. “It does add to the passion. For me it’s not just a another disease.”
McKeon doesn’t talk much about his own condition. His reluctance stems from a relatively clean bill of health after the initial episodes that lasted for about 18 months more than a decade ago. He is one of the lucky ones.
Source: Financial Review © Copyright 2013 Fairfax Media Publications Pty Ltd (24/09/13)