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Comments will follow news articles, This one from Medical News Today on Calcium, vitamin D and brain lesions.

Brain Lesions In Seniors Associated With Higher Calcium And Vitamin D Intakes

Main Category: Neurology / Neuroscience
Also Included In: Alzheimer's / Dementia;  Depression;  Stroke / Neuroprotection
Article Date: 07 May 2007 - 13:00 PDT

"Elderly men and women who consumed higher levels of calcium and vitamin D are significantly more likely to have greater volumes of brain lesions, regions of damage that can increase risk of cognitive impairment, dementia, depression and stroke.

Duke University scientist Dr. Martha Payne reported this finding at Experimental Biology 2007, in Washington, DC. Her presentation is part of the scientific program of the American Society for Nutrition.

Dr. Payne and her co-investigators from Duke and the University of North Carolina examined magnetic resonance imaging (MRI) scans from 232 men and women (79 men, 153 women) between the ages of 60 and 86 (average age 71). All the subjects had at least some brain lesions of varying sizes, including the extremely miniscule ones often seen in even healthy older persons, but those who reported consuming more calcium and vitamin D were markedly more likely to have higher total volume of brain lesions as measured across numerous MRI scans.

Age, hypertension, and other medical conditions - all factors related to the presence of brain lesions - were taken into account during statistical analysis (were controlled for) and were found not to account for the strong relationship between total lesion volume and high intake of calcium and vitamin D. Since the calcium/vitamin D research was part of a longitudinal study of late-life depression, almost half the subjects had been diagnosed with depression. However, the presence or absence of depression also did not appear to influence of relationship between calcium, vitamin D, and brain lesions.

In earlier studies, Dr. Payne's team had found that individuals who consumed more high-fat dairy products had more brain lesions than those who did not follow such a diet but that fat intake in general was not a significant factor. If not the fat, the researchers asked, what was it about a high fat dairy diet that accounts for the positive correlation with brain lesions? This new study points the finger to a prominent component of dairy - namely calcium - and the Vitamin D that is found in many dairy products and vitamin D-fortified foods.

In addition to its well-known function in bone health, calcium is important to the functioning of nerve and muscle cells. But when too much calcium is taken up into blood vessel walls, the calcium becomes incorporated into bone-like deposits that can lead to loss of elasticity and narrowing of the blood vessels. Vitamin D helps regulate calcium retention and activity, which may further enhance this arterial calcification. If blood vessels in the brain are affected, damage could lead to brain lesions.

"At this point," says Dr. Payne, "we do not know if high calcium and vitamin D intake are involved with the causation of brain lesions, but the study provides support to the growing number of researchers who are concerned about the effects of too much calcium, particularly among older adults, given the current emphasis on promoting high intakes of calcium and vitamin D."

Dr. Payne and her colleagues are continuing to investigate the effect and significance of high calcium and vitamin D intakes on brain lesions, including possible causality, in older patients with and without late-life depression. This research was funded by grants from the National Institute of Mental Health. MRI brain scans of a person with lesions are available to reporters, courtesy of Duke University's Neuropsychiatric Imaging Research Laboratory."

ANALYSIS: This information causes one to re-think the mentality of taking extra calcium for bone building. What is happening is that calcium is being deposited into the walls of arteries that exhibit lesions. The scenario is that the build up of calcium in the lesions reduces the blood flow from the lost of vessel elasticity and narrowing of vessels leading to increased blood pressure and cardiovascular disease. 

Vitamin D would be a participant since it facilitates the absorption of calcium, plus it also is now known that vitamin D participates in the calcification process right in the artery wall cells. Low magnesium intake accelerates this calcification action and people measuring high calcium intake, especially from dairy, just might really be low in magnesium which is responsible instead of the calcium. This process is identical to and involves the same cells as found in mineralizing bone building.

Calcium does not belong in artery walls at such high levels. Yes, while it is true that calcium deposits in arteries can be found at all levels of calcium intake, the taking of extra calcium habitually could speed up the process. The body has built in mechanisms to prevent too much calcium from binding to artery walls. Vitamin K controls this mechanism by building and activating proteins such as Matrix GLA. Thus it just might be a deficiency of vitamin K that allows the calcification process to progress after a lesion is formed in the artery wall. The calcium buildup process might actually be an attempt by the body to protect a weak spot on the artery wall. The addition of cholesterol to the calcium buildup may also be part of the process under normal levels and conditions. But normal is a far stretch for the American health scene. ref  

This concept has been studied and verified by research, low vitamin K equals greater calcium artery deposits. ref   Line from this ref-  "the involvement of vitamin K–dependent proteins in diverse biological mechanisms besides coagulation may have significant clinical impact with respect to influences on the progression and thrombogenicity of atherosclerotic plaque."  

Another factor with the consumption of extra calcium far above the amount that is lost every day is that these high levels might cause the body to turn off activating hormone Vitamin D. If the only function of vitamin D was just to aid calcium absoprtion, then this action would not cause major problems. But, vitamin D has many other roles to play and it is in some of these areas that body health would be jeopardized. One is the immune system's anti-microbial action from LL-37, a vitamin D produced protein. Another is the protection of breast, prostate, colon tissues against cell mutations.

Thus, low ( or high ) vitamin K and or vitamin D could be a major factor in cardiovascular, breast, prostate, and bone health. Too much calcium might hinder vitamin D acitivation and participate in greater calcification of arteries if proper levels of vitamins D and K are not maintained, as well as magnesium and phosphorus.

SIDEBAR: With all the hoopla over vitamin D regarding cancer protection and bone health, scientific protocols are being iqnored and higher dosages are being recommended and taken. The government has established the safe upper limit at 2000 IUs. Supplements have recently come out in 5000 IU's, even 10,000IU's. Nutritionists are failing to connect the logical dots. 

One particular statement being used to justify these higher dosages is that 20-30 minutes in the noon day sun would naturally produce 10,000 IUs in the skin. Let's look rationally at this statement, similar to how Sherlock would ask questions.  First, it is impossible for the body to naturally produce enough sunshine vitamin D to reach a toxic level in the body. There is a fail safe mechanism that turns off this sun created vitamin D production or conversion. No such mechanism is in place for supplements. 

Second, for every 100 IUs consumed, the inactive vitamin D pool increases by about 1 ng/ml. If 30 minutes in the sun created 10,000 IUs, this would increase the pool by 50-100 ng/ml similar to what consuming 10,000 IUs daily would do over about 3 months. A study of young healthy Hawaiian surfers revealed this did not happen, even averaging 3.5 sun hours per day. This fact by itself is enough to question the high dose theory. But there is more. ref

Third, most of the studies on Vitamin D to determine that 10,000 units is safe used Vitamin D2. While this plant based form is nearly identical in action to D3 at lower dosages, at higher doses D2, it is only about 35% as effective as D3. Thus, the 10,000 of D2 is probably closer to 3,000 units of D3. This fact is partly driven by the knowledge that D3 lasts longer in the body, but there are other considerations as well. D3 is preferred, but at lower dosages.

A researcher wanted to find out if there was a vitamin D pool level that was associated with lower mortality. He found that between 24-32 ng/ml exhibited the lowerst mortality rates. Both lower and higher had increasing overall mortality rates. This same level by the way was the peak average created from many hours in the sun per day in the Hawaiian study. 

There are nutritionists that would like to see 50+ levels. Yes, you might have to take 5000 IUs to get to this high level since 3 hours in the Hawaiian sun only acheived this level in about 10%, average was 30 ng/mL

One last fact, taking supplemental Vitamin D3 may increase the inactive vitamin D pool, but does not directly increase the highly active hormone form of vitamin D3, 1,25(OH)2 D3. This form is not governed by the level of the inactive vitamin D pool, but by parathyroid and thyroid hormones acting from the blood calcium level. There is an association where very low inactive pool levels start to limit the active hormone vitamin D production, but not at other levels. Increased vitamin D effects observed at higher levels may very well be from the inactive D pool itself and not from increased active D production. 

Now, what level for the inactive vitmin D do you think Sherlock deduced as healthiest and most benefical? Did he side with Nature or the Nutritionists?Unfortunately, many Americans are under even 15, but most are at 20 -25, so they only need a moderate dosage of at least 600-800 IUs to achieve a 5 to 10 increase over time. 400 IUs is just under what is needed and subjects at this consumption amount did not increase their pool level enough unless they included sun exposure time too.

Now Dr Watson, what are the ramifications over time of these higher vitamin D3 supplements?  A reduced brain capacity might present difficulties in finding this answer. 

If you are taking 5000 IUs of vitamin D3, limit daily use to only a couple of months, then take one every third day. Get your numbers tested to see where they are. The winter months are the appropriate time to maintain or increase D levels.

A study out of Germany found that women taking 500 IUs of D and 500 milligrams of calcium were able to slow down or prevent bone density reductions over the winter months.

The next referenced study gave 300,000 IUs of D3 once a month for 3 months to very deficient subjects, 10 ng/mL. They compared them to the healthy markers of the control group (30 ng/mL). As vitamin D pool levels went up, there was less lipid (fat) peroxidation. These results reveal that increasing a low vitamin D pool level supports a healthier cardiovascular system.

VITAMIN E on High Dosages and Mortality 

Biofactors. 2009 Nov-Dec;35(6):469-73.

No evidence supports vitamin E indiscriminate supplementation.


Department of Physiology and Pharmacology, Tel Aviv University, Sackler Medical School, Tel Aviv, Israel.


For many years, the prevailing concept was that LDL oxidation plays the central role in atherogenesis. As a consequence, supplementation of antioxidants, particularly vitamin E, became very popular. Unfortunately, major randomized clinical trials yielded disappointing results and recent meta-analyses concluded that indiscriminate, high dose vitamin E supplementation results in increased mortality. This conclusion raised (quite reasonable) criticism, much of which referred to the characteristics of meta-analysis. In our recent study, we used a Markov-model approach, which is free of most of the limitations of meta-analyses. Our major finding was that the average quality-adjusted life years (QALY) of vitamin E- supplemented individuals was 0.30 QALY (95%CI 0.21 to 0.39) less than that of untreated people. In our view, this supports the view that indiscriminate supplementation of high dose vitamin E can not be recommended to the general public.In the present communication we address several recent studies that demonstrated negative effects of vitamin E and raise possible mechanisms that may be responsible for the harmful effects of vitamin E supplementation. We also review recent studies conducted with specific groups of patients that gained from vitamin E supplementation, indicating that although, on the average, indiscriminate supplementation of high dose vitamin E is not beneficial, specific populations may gain from vitamin E. The challenge is to establish selection criteria that will predict who is likely to benefit from vitamin E supplementation. Such criteria may be based either on the assumption that antioxidants are likely to be beneficial for people under oxidative stress or on knowledge regarding the benefit of sick people with certain diseases. In short, we adopt the view that vitamin E is a "double-edge sword" that should not be consumed until criteria are defined to predict who is likely to benefit from high dose supplementation of vitamin E.

(c) 2009 International Union of Biochemistry and Molecular Biology, Inc.