Hypothesis explored in the current issue of the Journal of Alzheimer's Disease

Amsterdam, The Netherlands, May 26, 2009 � There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed.

Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases.

Several studies have correlated tooth loss with development of cognitive impairment and Alzheimer's disease or vascular dementia. There are two primary ways that people lose teeth: dental caries and periodontal disease. Both conditions are linked to low vitamin D levels, with induction of human cathelicidin by 1,25-dihydroxyvitamin D being the mechanism.

There is also laboratory evidence for the role of vitamin D in neuroprotection and reducing inflammation, and ample biological evidence to suggest an important role for vitamin D in brain development and function.

Given these supportive lines of evidence, Dr. Grant suggests that studies of incidence of dementia with respect to prediagnostic serum 25(OH)D or vitamin D supplementation are warranted. In addition, since the elderly are generally vitamin D deficient and since vitamin D has so many health benefits, those over the age of 60 years should consider having their serum 25(OH)D tested, looking for a level of at least 30 ng/mL but preferably over 40 ng/mL, and supplementing with 1000-2000 IU/day of vitamin D3 or increased time in the sun spring, summer, and fall if below those values.

Writing in the article, Dr. Grant states, "There are established criteria for causality in a biological system. The important criteria include strength of association, consistency of findings, determination of the dose-response relation, an understanding of the mechanisms, and experimental verification. To date, the evidence includes observational studies supporting a beneficial role of vitamin D in reducing the risk of diseases linked to dementia such as vascular and metabolic diseases, as well as an understanding of the role of vitamin D in reducing the risk of several mechanisms that lead to dementia."

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The article is "Does Vitamin D Reduce the Risk of Dementia?" by William B. Grant, Ph.D. It is published in the Journal of Alzheimer's Disease 17:1 (May 2009).

Since almost everyone over the age of 30 has substandard levels of vitamin D its seems pretty easy to be tempted to try to correlate it to almost every degenerative disease out there. Its getting to be the catchall cause of everything and hence perhaps we should watch out for givning it too much credit in some areas?

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Indeed I think that a lot of inflammatory conditions will progress more slowly if we have a full complement of natural anti inflammatory agents on board. However I think there is more to this than just the general consequences of being Vitamin D deficient.

VitaminDand neurocognitive dysfunction: Preventing “D”ecline? also draws the connection and explains how Vitamin D exhibits functional attributes that may prove neuroprotective through antioxidative mechanisms, neuronal calcium regulation, immunomodulation, enhanced nerve conduction and detoxification mechanisms. Compelling evidence supports a beneficial role for the active form of vitamin D in the developing brain as well as in adult brain function. The vitamin D receptor and biosynthetic and degradative pathways for the hydroxylation of vitamin D have been found in the rodent brain; more recently these findings have been confirmed in humans. The vitamin D receptor and catalytic enzymes are colocalized in the areas of the brain involved in complex planning, processing, and the formation of new memories. These findings potentially implicate vitamin D in neurocognitive function.

Similarly Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction? makes the point that there is ample biological evidence to suggest an important role for vitamin D in brain development and function and concludes recommendations for vitamin D supplementation of at-risk groups, including nursing infants, the elderly, and African-Americans appear warranted to ensure adequacy. These and other papers these reports lay the groundwork for the hypothesis that vitamin D can reduce the
risk of dementia.

If you look at Table 2 in Grant's paper you see the
Mechanisms whereby vitamin D metabolites protect the brain

Vasculoprotection
Advanced glycation end products 1,25(OH)2D blunts the impact on endothelial cells.
Neuronal protection Ca2+ regulation, stimulation of neurotrophin release, interaction with reactive oxygen and nitrogen species, and neuroimmunomodulatory effects of calcitriol
Facilitates detoxification through inhibiting synthesis of inducible nitric oxide synthase and increased glutathione levels.
Enhances neurotrophin synthesis.
Enhances antioxidant pathways.
Upregulates neurotrophin factors.
Neuron growth factor (NGF) Induces production of NGF
Neuronal calcium regulation Protects against excess calcium entry into the brain.
Reduces inflammatory factors
Downregulates proinflammatory cytokines such as serum tumor necrosis factor α, IL-1, and IL-6.
Reduces biomarkers of inflammation such as C-reactive protein.
Attenuates neuroinflammatory age-related changes.
Thrombosis Reduces risk of thrombosis.
Transition metal ion concentrations By increasing calcium absorption, may decrease transition metal (copper, iron, zinc) ion levels.

Each of these is supported by references and if you are interested I'll provide links to the supporting research. But I think you've got to agree it appears that vitamin D metabolites, especially 1,25(OH)2D3, can counter many of the mechanisms linked to risk of dementia.

It would be interesting to know how people who have a history of living with a low level of sun light, such as Eskimo's, compensate for the lack of D produced from sun exposure.
Or maybe they do not compensate? What are their serum levels?

It would be more convincing to me if they can find normal levels in people that are healthy rather than low levels in sick people. There is a minority debate that low D is the result of some diseases and not the cause. It would be nice to have solid evidence that this is not the case.

Dan

They consumed lots of fish oil or seal blubber. Even the cariboo they hunted grazed on lichen in the winter so that meat would have been a source of D3.

don't know what they were, we know now they are eating non traditional diets they get rickets so it's now below 20ng.


but surely it is common sense that some conditions will also deplete 25(OH)D status. You can easily get into a viscous spiral of low levels of D3 causing obesity and as fat is stored rather than burned it locks up calcidiol in adipose tissue so less is available and the tendency to obesity continues ever faster. The way to break the spiral of decline is to take sufficient D3 for long enough to not only replete plasma 25(OH)D but also to build stores of D3. It takes around 3months to replete circulating 25(OH)D but a lot longer to rebuild all our cells with the omega 3/vitamin D3 makeup our DNA evolved with.

There are other ways 25(OH)D status can be lowered. High fibre diets can reduce 25(OH)D half life. There is some work on Fructose making it harder for vitamin D metabolism.

I'm not sure why anyone isn't aware that the human species evolved living outdoors naked nor that if you take off your clothes and spend the next six months living naked your 25(OH)D will naturally assuming you live in a sunny latitude, attain and maintain a 25(OH)D around 40~80ng.
Vitamin D status after prolong sun exposure

The best evidence to convince yourself is to actually get your own status above 55ng. and keep it above 55ng for a couple of years at least, that way half your cells at least will have been rebuilt in an adequate D3 environment.
Over that time note the prescriptions you do not need to renew.
Record the amount of pain medication you require.
Record every instance (if there are any) of colds/flu/upper respiratory tract infections.
Consider if your use of anti histamines could be lower?
See if you get any Urinary tract infections or ear infections (I will predict none)
If you have used anti depressants regularly in the past is this necessary now?
Also note if you now tan more easily and can stay in the sun longer without burning?

Considering you may get all the above benefits for a mere $15.70 for 250 days supply I really don't see why anyone is reluctant to Get the natural level that enables muscles to perform optimally and keeps brains sharp.

In my case I also changed to a low carbohydrate diet which reduced my intake of omega 6 oils, I had already increased my omega 3 levels and I'd improved my magnesium intake. So it's not fair to give all the credit to the Vitamin D3 but if you want me to add in the links to the research supporting the above then I'll edit them in if you think it would be helpful.

I already supplement D-3 in the Winter and Magnesium year round. But whenever there is a bandwagon going on, I start listening to the minority point of view as a counter balance.

I realize that anyone outside most of the time is going to have optimal D levels. But both myself and my wife have diseases. Mine is Crohn's and I supplement with D-3 because I am 95% sure that a weakened immune system is responsible for the symptoms of the disease. In another words, the weakened immune system came first. If D-3 weakens my immune response is not an issue due to my use of Low Dose Naltrexone which compensates. I do not know why I have a weakened immune system, I just know it is weak. It is not a problem as I have it under complete control.

My wife's Lyme disease is under some control but it is tough to eliminate. It may not even be possible. That is not the issue, but whether she should supplement with D-3 is a question. D-3 also acts as a steroid, which if it means it weakens the immune response similar to other steroids, would be a disaster in her particular case. This would be Trevor Marshalls line of thinking. I do not know if he is correct or not, but I know he is not a stupid man, and he has reasons for his conclusions. His conclusions can be wrong or incomplete, but no one has gave me a reason why they are wrong, only that they think they are wrong.

That is my personal reasons for questioning whether increasing D-3 is always indicated regardless of the persons condition. Or is the low D-3 in some diseased people the bodies way of protecting itself, as Marshall is proposing? Which came first, the Chicken or the Egg?

Dan

Hopefully at levels equivalent to those that our early ancestors would have enjoyed.

By all means consider what is being said but don't leave your own common sense behind.
But only if they take their clothes off and check their 25(OH)D to check that they are getting what they think they are getting. Some of us live under clouds of upper atmospheric haze that absorbs the uvb before it reaches the ground. Unless you check your Vitamin D levels you cannot be sure

but with Crohn's can you be certain your digestive system is up to absorbing it. I'm not a great fan of Mercola but his new
Sublingual spray may solve that problem.

But having optimum vitamin D3 status improves your immune function.
We've got a Marshall thread I'm not prepared to waste any more time refuting his theory. I really cannot understand why you can't trust evolution. Get yourselves 25(OH)D tested. Get your levels above 50ng ASP. Then keep them there for at least a year then see how much better you are.

I had my B-12 and D levels checked. 42 was the number. That was without supplementing, other than whatever small amount the multivitamin had in it. It also was Winter when I had it checked. I will have it checked annually because of my disease it is normal to check for at least B-12 and Iron. I threw in the D.

The only indication of malabsorbtion I have is protein. I am always on the low end of normal in spite of a high protein diet. I think it is not a malabsorbtion problem because nothing else is abnormal. I do not know why this is, but it has been this way for over 25 years.

I can pretty much be sure that my ancestors were not running around without clothes. They were near the arctic circle, so direct sun light was somewhat seasonal, and warm weather was only a short period of time. People live in vastly different climates, then and today.

Different cultures likely have different adaptations due to environment. Such as skin color.
I think that should be a consideration, especially if you are dark skinned living in a Northern latitude. This would certainly cause problems without supplementation. It is not a natural environment for this type of skin.

People have not supplemented throughout time, so it really is not an evolutionary question.
We also have no record of the levels of vitamin D in earlier people. It is being assumed at this point that it was higher. We do not know today what is optimal, it is being debated at this time.



Dan

I just sent a grandaughter, a college freshman, 3 bottles of Vit D3.
One of my Health Newsletters said that Vit D3 will keep the Swine
Flu at bay. I old her to take 2 daily for now; if her college in
Louisville has a Swine flu outbreak, then increase to 3 or 4 daily.
Luckily she lives at home and commutes, doesn't live in a dorm.
The D3 should help her to build up her immune system for colds
too.

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I still see people talking about doses of 1000 or 2000 IU. This is very low if you are depleted and will not raise levels to optimum. donaldmiller.com has a presentation on this and you need 5000 units to raise your levels up to optimum over several weeks.

vitamindcouncil.org newsletter reported recently of E german children receiving 600,000 units every few months. 1/3 did see elevated calcium but there were no bad effects. They did this up to 36 months old for 30+ years! So 10,000 won't hurt anyone and would probably be better for a few months. And I think one should supplement even if you get some sun in the summer. Males need 5000/day to maintain.

I am uncomfortable taking too high of levels of vitamin D daily. I prefer to stay under 4000 right now.

"Vitamin D is well known as a hormone involved in mineral metabolism and bone growth. Its most dramatic effect is to facilitate intestinal absorption of calcium, although it also stimulates absorption of phosphate and magnesium ions. In the absence of vitamin D, dietary calcium is not absorbed at all efficiently."
https://www.vivo.colostate.edu/hbooks.../vitamind.html

Otherwise, I am very pleased with it. I don't get out much. We just came out of a spell of 100+ degree days for 2 months. We are having a fall cooling trend of upper 90s. Too hot to get out and do any activity.

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It makes a difference where you live and how much skin you are able to expose to sunlight. The way to be certain about your current Vitamin D status is to check your 25(OH)D level. It's cheap enough and that way you can be sure your level is around the 55ng/mL mark associated with peak muscle performance, least incidence of chronic illness and at which human breast milk flows replete with D3. You may think this last is only relevant to pregnant or lactating females but IMO that is a NATURAL biomarker for Vitamin D sufficiency.

Those interested in understanding the latest science about vitamin d3 rather than merely repeating out of date myths may care to read Vitamin D and Cancer Mini-Symposium: The Risk of Additional Vitamin D Reinhold Vieth