all things vitamin D

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bromley
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Professor Ebers Vit D

Post by bromley » 10 years ago

I think I posted this in Summer 2007, but given today's research the talk by Professor Ebers may be of interest.

Ian

<shortened url>

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JoR
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Post by JoR » 10 years ago

Apologies for jumping in but this has been the first article that has compelled me to post instead of just lurking; does anyone know what Vitamin D supplement I should buy my 3 year olds? I have MS and I live in the UK (dim and dark North!) and feel this is something I cannot afford to ignore. I am unsure at what level I should be giving children so young and where I would be able to get it but any advice would be greatly appreciated.

Sorry if this is not an appropriate question to ask and please disregard if this is so however I ask out of concern for my children.

Many thanks

Jo :?

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jimmylegs
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Post by jimmylegs » 10 years ago

JoR you should be able to get a nice tasty baby liquid. do not neglect to balance any d3 supplementation plan with calcium and magnesium and zinc, all at appropriate levels for tiny bodies. you cannot give it all at the same time either because the minerals need some alone time with your body, it can't all be d3 interactions you know!
i think you'd be safe to say that if adults take 4000IU per day and weigh an average of 70kg, then scale back the dosage of d3 and the minerals relative to the kg weight of your child.
if you can't get an off-the-shelf liquid that fits the bill, you may be able to get the chemist to dilute a stronger liquid for you.
just be careful - that kind of thing you may need to keep in the refridgerator so it's not so easy to keep up high or locked.
if they are old enough to take pills it's really easy to get 1000 or 2000IU pills that are small and simple to take.
monitor the little ones' bloodwork to ensure it gets where you want it to be, but does not go too high. in one study where vitamin d3 status in adults was measured, the group with the lowest incidence of ms had serum levels 100 nmol/L and higher. if levels go too high you can expect side effects like hypercalcaemia and such so probably best to keep the max level under 150 until there is more research completed on optimal d3 status.

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cheerleader
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Post by cheerleader » 10 years ago

Hey Robbie...
Glad you're posting videos, since typing is getting harder for you. It's always good to see you. You bring up a really important question-
Why would folks who get plenty of sunshine get MS? I asked the same question about my husband, who grew up in the California sun, and was very outdoorsy. He even has basal cells (pre-skin cancer) to prove it!
I guess what the study is showing is that in people who have this genetic variant, a lack of vitamin D in their mother's wombs or childhood can turn on the MS process which will show up later in life.
This is just a good reminder for pregnant Moms to get enough vitamin D, and for Moms with MS in the family to make sure their kids get it, too. It's more about an ounce of prevention....
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com

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lyndacarol
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Welcome, JoR

Post by lyndacarol » 10 years ago

JoR--Before you begin administering D3 to your 3-year-olds, it would seem wise to find an endocrinologist to order tests to learn their D3 levels. (JimmyLegs can teach you all about Vitamin D and which exact test to request.)

And welcome to the site! You'll find a friendly, helpful community here.

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NHE
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More vitamin D news

Post by NHE » 10 years ago

I'm not sure if this has already been posted, but here's another recent article on vitamin D...


Lack of sunshine found to trigger MS

Research finds people with gene variant who lack vitamin D, produced from sun exposure, can develop condition

Women who are not exposed to sufficient sunshine in pregnancy may be at risk of giving birth to a child who will get multiple sclerosis in adulthood, research reveals today.

Oxford University researchers have identified a link between a shortage of the "sunshine vitamin" – vitamin D – and a specific gene which appears to be involved in the onset of the devastating and incurable disease.

Women are already urged to take folic acid in pregnancy to reduce the chances of a child being born with spina bifida. The research findings suggest that vitamin D could before long be advised for pregnant women as well – especially those who do not get much exposure to sunlight. The researchers think it is possible that vitamin D could play a part in other diseases whcih affect the immune system too.

"Our study implies that taking vitamin D supplements during pregnancy and the early years may reduce the risk of a child developing MS later in life," said lead author Dr Sreeram Ramagopalan. "Vitamin D is a safe and relatively cheap supplement with substantial potential health benefits. There is accumulating evidence that it can reduce the risk of developing cancer and offer protection from other autoimmune diseases."

Their work, published today in the journal PLoS Genetics, breaks new ground by revealing the interaction between a gene and an environmental factor – in this case, exposure to sunlight.

It has long been suspected that sunshine played a part in the condition's development. MS, the most common disabling neurological condition, affects 85,000 mainly young adults in the UK and 2.5 million worldwide and is markedly more common in cloudy northern climates. Scotland has a significantly higher concentration of MS cases than England.

A gene variant known as DRB1*1501 has been implicated in MS. While one in 1000 people in the general population develop the disease, it is one in 300 among those who have one copy of this gene variant and one in 100 of those who have two copies.

The Oxford study has found a direct relationship between vitamin D, produced in the body as a result of sun exposure, and this gene variant. In effect, proteins activated by vitamin D in the body switch the gene on. It appears, they say, that if people get too little sunshine, the gene may not function properly.

This interaction between gene and environment – so-called "epigenetics" – is being seen as increasingly important by scientists: that genetic make-up is not set in stone from conception, but is influenced for better or worse by the world around us.

"Epigenetics will have important implications, not only for MS, but for other common diseases," said Professor George Ebers, from the Wellcome Trust Centre for Human Genetics at Oxford, where the work was done. "For mothers, taking care of their health during their reproductive years may have beneficial effects on the health of their future children or even grandchildren."

· This article was amended on Friday 6 February 2009. George Ebers does not run the Wellcome Trust Centre for Human Genetics at Oxford. This has been corrected.

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furch
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Post by furch » 10 years ago

"Our findings are corroborated by previous observations that UV light has a preventive role in the development of MS, although the possibility of reversed causality cannot be completely ruled out. Am. J. Ind. Med. 2009 (c) 2009 Wiley-Liss, Inc."

<shortened url>

so vitamin d can actually cause MS? theres no question that its significant in ms - but obviously not in a "the more the better" kind of way.. if so the epidemic of autoimmune disease would be decreasing with the amount of supplementation in the food chain..

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jimmylegs
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Post by jimmylegs » 10 years ago

reversed causality means that rather than d3 deficiency causing ms, ms causes d3 deficiency. my neuro has thrown that at me regarding uric acid.
there've been some good n-sized studies where they looked at d status and ms risk and the quintile with d3 levels over 100 nmol/L had the lowest risk. the average person with osteoporosis probably has levels in the 70s or lower.

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Terry
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Post by Terry » 10 years ago

http://www.consumerhealth.org/articles/ ... 0214043340

Lengthy- sorry.
UV-B The ultraviolet wavelength that stimulates our bodies to produce vitamin D is UV-B.
The reason it is difficult to get adequate vitamin D from sunlight is that while UV-A is present throughout the day, the amount of UV-B present has to do with the angle of the sun's rays. Thus, at higher latitudes, UV-B is present only during midday hours and only has significant intensity in temperate or tropical latitudes. Only 5 percent of the UV-B light range goes through glass and it does not penetrate clouds, smog or fog.
Sun exposure at higher latitudes before 10 am or after 2 pm will cause burning from UV-A before it will supply adequate vitamin D from UV-B. This finding may surprise you, as it did the researchers. It means that sunning must occur between the hours we have been told to avoid. Only sunning between 10 am and 2 pm during summer months (or winter months in southern latitudes) for 20-120 minutes, depending on skin type and color, will form adequate vitamin D before burning occurs.(9)
It takes about 24 hours for UV-B-stimulated vitamin D to show up as maximum levels of vitamin D in the blood. Cholesterol-containing body oils are critical to this absorption process.(10) Because the body needs 30-60 minutes to absorb these vitamin-D-containing oils, it is best to delay showering or bathing for one hour after exposure. The skin oils in which vitamin D is produced can also be removed by chlorine in swimming pools.
If you have symptoms of vitamin D insufficiency or are unable to spend time in the sun, consider adding a supplement of 2,000 IU daily. Higher levels may be needed but should be recommended and monitored by your health care practitioner.
Adequate calcium and magnesium, as well as other minerals, are critical parts of vitamin D therapy. Without calcium and magnesium in sufficient quantities, vitamin D supplementation will withdraw calcium from the bone and will allow the uptake of toxic minerals. Do not supplement vitamin D and do not sunbathe unless you are sure you have sufficient calcium and magnesium to meet your daily needs. Weston Price suggested a minimum of 1,200-2,400 mg of calcium daily. Research suggests that 1,200-1,500 mg is adequate as a supplement for most adults, both men and women. (Magnesium intake should be half that of calcium.)
In my experience, high, infrequent dosing can lead to problems. In one recent study, blood levels rose from low to extremely high, (more than 300 nmol/l) 24 hours after a 50,000 IU oral dose,65 and then slowly returned to pretreatment suboptimal levels. Clearly this must disrupt normal feedback mechanisms in D and calcium regulation
Jimmy,
I have been taking D3- 5,000 iu.
I went from 2x a week (per doc instructions) to almost daily this last week. (and felt better) I have added no calcium. I take mag.
Please tell me again how much of these you take and how often.

Terry

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DIM
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Post by DIM » 10 years ago

Jimmy I give to my wife 5000IU D3 3 times per week with 1200mg Calcium-600mg Magnesium daily.
I don't think the above quantities Cal-Mag aren't enough for the vitamin D3 intake as we take some minerals from our food and we eat 3-4 times per week fishes etc.

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jimmylegs
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Post by jimmylegs » 10 years ago

i agree dim, those daily cal and mag amounts sound good.
that's what i try for too terry, 1200mg Ca and 600mg Mg daily.

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Terry
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Post by Terry » 10 years ago

Thanks JL.

Frank
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Post by Frank » 10 years ago

As far as I remember, previous research had shown that people with MS do NOT have eleviated levels of autoreactive T-Cells compared to healthy controls.

How can that be consistent with the new findings regarding a flawed selection process in the thymus?

Wouldn't the quantities of autoreactive T-cells be a benchmark for that theory?

--Frank
Treatment: Gilenya since 01/2011, CCSVI both IJV ballooned 09/2010, Tysabri stopped after 24 Infusions and positive JCV antibody test, after LDN, ABX Wheldon Regime for 1 year.

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cheerleader
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Post by cheerleader » 10 years ago

Here's what the study says about t-cells, Frank. It's more about the specificity of autoantigen presentation in the "central deletion" process, as opposed to elevated levels of autoreactive t-cells.
A T cell repertoire with millions of specificities provides surveillance against a multitude of foreign pathogens [32]. An inherent danger in recognizing so many foreign proteins is the potential to respond to self-proteins. To circumvent this problem T cells are scrutinised for self-reactivity as they mature in the thymus with deletion of those posing the greatest threat (central deletion) [32]. One constraint on central deletion is the requirement for the relevant autoantigen to be present in the thymus. Whether or not these are expressed as proteins at levels sufficient to induce T cell deletion is not clear. Given the results of this study, variable expression of HLA-DRB1 could affect central deletion of autoreactive T cells. It is plausible that a lack of vitamin D in utero or early childhood can affect the expression of HLA-DRB1 in the thymus, and impacting on central deletion. For MS, in HLA-DRB1*15 bearing individuals, a lack of vitamin D during early life could allow auto reactive T cells to escape thymic deletion and thus increase autoimmune disease risk. Indeed it has been shown that antigen presentation in the thymus of VDR knock-out mice is impaired [33]
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com

Frank
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Post by Frank » 10 years ago

cheerleader wrote: Here's what the study says about t-cells, Frank. It's more about the specificity of autoantigen presentation in the "central deletion" process, as opposed to elevated levels of autoreactive t-cells.
You are right, the study discusses what kind of antigene representation in the thymus might be relevant for autoreactive T-cell (ARTC) deletion.
But anyway the study concludes that HLA-DRB1*1 bearing people with a lack of Vit D are at risk for ARTCs to escape the selection process, so ARTC should be elevated in these people, shouldnt they?
Given the results of this study, variable expression of HLA-DRB1 could affect central deletion of autoreactive T cells. It is plausible that a lack of vitamin D in utero or early childhood can affect the expression of HLA-DRB1 in the thymus, and impacting on central deletion. For MS, in HLA-DRB1*15 bearing individuals, a lack of vitamin D during early life could allow auto reactive T cells to escape thymic deletion
--Frank
Treatment: Gilenya since 01/2011, CCSVI both IJV ballooned 09/2010, Tysabri stopped after 24 Infusions and positive JCV antibody test, after LDN, ABX Wheldon Regime for 1 year.

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