Zonnen: de aanmaak van Vitamine D
Regelmatig 10 tot 30 minuten zonnen is heel gezond.

Te lang onbeschermd in de zon is weer ongezond.


Biologisch Medisch Centrum  Utrecht Epe        Arts Paul van Meerendonk
Vitamine D
Deze site is opgericht door een zeer tevreden
cliënt van het Biologisch Medisch Centrum

Biologisch Medisch Centrum
Behandeling CVS/ME
ATP energie
Dr Teitelbaum
Dr Meirleir
Dr Cheney
Arts Paul van Meerendonk

ADP-ATP efficiency
Cvs en fibromyalgie
CVS ME aantoonbaar
CVS legitiem
Research direction

Virus en DNA
Vitamine B12
Vitamine D
Zware metalen
Meetresultaten 1

Meetresultaten 2
Meetresultaten 3
Meetresultaten 4

Video Vitamine D   


Vitamine D veel belangrijker dan gedacht ook voor CVS ME

Vitamine D blijkt veel belangrijker voor de gezondheid dan gedacht. Het is bij heel veel processen in het lichaam betrokken en tekort vitamine D in het bloed komt veel voor bij CVS ME.

Twintig tot dertig minuten in de zon maakt 10.000 iu ofwel 250
µg vitamine D aan.
Behalve als je een zeer donkere huid hebt dan is daarvoor een uur noodzakelijk.

Twee tot drie maal per week 15 - 20 minuten met blote armen of benen als de zon hoog staat is optimaal voor de aanmaak van Vitamine D en tegelijkertijd ook noodzakelijk. Deste hoger de zon staat deste meer UVB er in het zonlicht zit en deste meer aanmaak vit D, voor 10.00  uur en na 15.00 uur is er geen aanmaak. In april tot en met september geeft zonlicht een zeer goede hoeveelheid vitamine D. In de winter (in Nederland van Oktober tot en met Maart) wordt geen vitamine D gemaakt door zonlicht omdat er dan geen UVB in het zonlicht zit. Dan neemt men om een goede gezondheid te behouden minimaal 1000 iu (25 µg) D2 of D3 per dag.  Optimaler 5000 iu 125 µg per 3 dagen of 2000 tot 4000 iu 50 - 100 µg per dag. Dit zijn indicaties van op dit moment door vitamine D onderzoekers aanbevolen hoeveelheden. Veel hoger dan de ADH. Volgens het NIH in de US is 2000 iu per dag zeker veilig.

Vitamine D activeerd je immuunsysteem het activeert peptides die virussen en bacteria doden. video
Het zorgt ervoor dat je tot 90% minder gevoelig bent voor virussen en bacteria
Het is ook heel belangrijk voor de tanden. En beter dan fluor.

Vitamin D3 is goed en Vitamine D2 is bijna net zo goed. De combinatie is ook net zo goed maar ook niet beter dan D3 of D2. Vitamine D is een hormoon.
Met zonlicht worden verschillende soorten vitamine D (D1 t/m D5) en andere fotoproducten gemaakt waarvan de werking nog onderzocht moet worden en is dus wel anders dan vitamine D inname.

Zonnebank is ook goed voor de aanmaak van vitamine D liefst wel een zonnebank met meer uvB dan de gemiddelde.

Per 100 iu (2.5 µg) Vitamine D inname per dag stijgt bloedhoeveelheid met 1 µg/L
30 µg/L is het echte minimum. Van 30 tot 50 µg/L is te laag. Vanaf 50 µg/L is goed. 60 tot 80 µg/L is optimaal.
Bij een bloedwaarde tussen de 30 en 50 µg/L is een supplement nodig.
Bij waarden beneden de 30 µg/L is een supplement noodzakelijk.


UVB 280-315nm UVA 315-400nm Vitamine D aanmaak 270-315nm. Boven 300nm steile afval.

Kan men met voldoende vitamine D, opgedaan in de zomer, de winter doorkomen?
Nee het lichaam kan een beperkte hoeveelheid opslaan en dit raakt op na twee weken als er niets binnenkomt zoals in de wintermaanden.

Vitamine D tekort heeft een verband met:
Autoimmuun-ziekten, multiple sclerose, osteoporose, fybromyalgia, hart en vaat ziekten, darm~, borst~ en prostaatkanker, diabetes type I, rachitis, osteomalacie, myopathie, depressie, chronische pijn, migraine, schizofrenie, hoge bloeddruk, reumatoďde artritis, verhoogd cholesterol niveau.

50% van de wereld bevolking heeft vitamine D tekort.
Kleding houdt UVB tegen.
Zonnebrand creme houdt UVB tegen en voorkomt de aanmaak van vitamine D.
Een donkere huidskleur of een aanleg voor een donker huidskleur houdt UVB gedeeltelijk tegen en zorgt voor een sneller ontstaan van vitamine D tekort.

De menselijke huid maakt onder invloed van zonlicht ook fumaarzuur aan. Fumaarzuur ofwel fumarate is een stof die ook noodzakelijk is in de mitochondrien voor atp productie.

Vitamin D and backpain

The report, "Vitamin D A Neglected 'Analgesic' for Chronic Musculoskeletal Pain," which was peer-reviewed by a panel of 8 experts, includes the following important points:

-- Vitamin D is essential for calcium absorption and bone health. Inadequate vitamin D intake can result in a softening of bone surfaces, or osteomalacia, that causes pain. The lower back seems to be particularly vulnerable to this effect.

-- In one study of 360 patients with back pain, all of them were found to have inadequate levels of vitamin D. After taking vitamin D supplements for 3 months, symptoms were improved in 95% of the patients. All of them with the most severe vitamin D deficiencies experienced back-pain relief.

-- The currently recommended adequate intake of vitamin D up to 600 IU per day is outdated and too low. According to the research, most children and adults need at least 1000 IU per day, and persons with chronic back pain would benefit from 2000 IU or more per day of supplemental vitamin D3 (also called cholecalciferol).

-- Vitamin D supplements have a highly favorable safety profile. They interact with very few drugs or other agents, and are usually not harmful unless extremely high doses such as 50,000 IU or more are taken daily for an extended period of time.

Vitamin D deficiency

In some people, the problem might not be enough magnesium, but instead might be not enough vitamin D, which has an effect on magnesium absorption.  Up until recently, doctors only associated a vitamin D deficiency with weak bones, and they believed that a vitamin D deficiency in young people was rare in countries like the US.  However, both of these beliefs have been proven false.  Not only does it occur in young people, but sometimes a vitamin D deficiency can manifest itself mainly as pain.  Initial symptoms in adults can often appear as vague musculoskeletal pains, muscle weakness, and fatigue, symptoms commonly found in fibromyalgia.   Also, studies on the muscles of vitamin D deficient patients, show a reduction of ATP levels, similar to that of fibromyalgia patients.

In some cases, the deficiency leads to myopathy, with quite severe muscle weakness, especially affecting the legs and ability to walk.  On the other hand, sometimes the symptoms are less severe, in which case it could be easily overlooked in fibromyalgia patients.  In fact, several small studies have shown that at least 40% of patients with fibromyalgia have a vitamin D deficiency.vitamin D subnutrition is common in patients with FM


And while some blood tests can possibly indicate a vitamin D deficiency, often a deficiency can exist without any other biochemical changes.   Thus, the only definite way to tell if you have this problem, is by testing vitamin D levels.  Unfortunately, very few doctors do this.  So It's quite possible that some people who have fibromyalgia, might also have a vitamin D deficiency.  Or perhaps they never had fibromyalgia to begin with.  In the following study from Canada, only 12% of patients referred to rheumatologists with the diagnosis of fibromyalgia, actually had fibromyalgia:


Vitamin D deficiency is often misdiagnosed as ME/CFS or fibromyalgia as the major symptoms include muscle pain and weakness, according to Michael F. Holick, MD, PhD, of the Boston University School of Medicine. Other researchers (Shinchuk & Holick) agree saying that all patients presenting with symptoms suggestive of ME/CFS should be tested for vitamin D deficiency.

Some studies have suggested that over 25% of ME/CFS patients have low vitamin D levels.

Studies have shown that vitamin D supplements can significantly reduce pain with one showing that vitamin D deficient people require twice as many painkilling drugs.

People getting no sunlight should supplement with at least 1,000 IU of vitamin D, which is 5 times the usually recommended amount [Glerup].

Vitamin D is a powerful immune system modulator with most immune cells having receptors for the active form of the vitamin. It is suggested that vitamin D may enhance innate immunity and inhibit the development of allergies and certain autoimmune conditions. These actions may be important for the immune dysfunction in ME/CFS.


Technically not a "vitamin," vitamin D is in a class by itself. Its metabolic product, calcitriol, is actually a secosteroid hormone that targets over 2000 genes (about 10% of the human genome) in the human body. Current research has implicated vitamin D deficiency as a major factor in the pathology of at least 17 varieties of cancer as well as heart disease, stroke, hypertension, autoimmune diseases, diabetes, depression, chronic pain, osteoarthritis, osteoporosis, muscle weakness, muscle wasting, birth defects, periodontal disease, and more.

Vitamin D's influence on key biological functions vital to one's health and well-being mandates that vitamin D no longer be ignored by the health care industry nor by individuals striving to achieve and maintain a greater state of health.

Sunshine and Your Health Vitamin D

If well adults and adolescents regularly avoid sunlight exposure, research indicates a necessity to supplement with at least 5,000 units (IU) of vitamin D daily. To obtain this amount from milk one would need to consume 50 glasses. With a multivitamin more than 10 tablets would be necessary. Neither is advisable.

The skin produces approximately 10,000 IU vitamin D in response 20–30 minutes summer sun exposure—50 times more than the US government's recommendation of 200 IU per day!

Sun exposure
The maximum amount of vitamin D that is cutaneously produced under UV light stimulation, creating serum 25(OH)D concentrations similar to those resulting from an oral dose of 250 µg

OBJECTIVE: To estimate the amount, type, and tissue distribution of vitamin D in the adult body under typical inputs. METHODS: Review and reanalysis of published measurements and analysis of tissue samples from growing pigs raised in confinement on diets providing about 2000 IU vitamin D/day. Cholecalciferol and 25-hydroxyvitamin D [25(OH)D] concentration measured by HPLC. RESULTS: Mean serum 25(OH)D in all studies combined was 45 nmol/L. At the level of vitamin D repletion represented by this concentration, total body vitamin D would be 14,665 IU for a 70 kg adult woman. 65% of this total was present as native cholecalciferol and 35% as 25(OH)D. Nearly three-quarters of the cholecalciferol was in fat, while 25(OH)D was more evenly distributed throughout the body (20% in muscle, 30% in serum, 35% in fat, and 15% in all other tissues). At the daily vitamin D consumption rates in these animals total body stores provided only a approximately 7-day reserve. CONCLUSIONS: At total intakes on the order of 2000 IU/day, an adult has very little vitamin D reserve, despite intakes 10x the current recommendations. Those recommended inputs need to be increased by at least an order of magnitude. Food tables that fail to take into account 25(OH)D content of various meat products lead to underestimation of dietary vitamin D intake.

In a trial conducted by Barger-Lux et al, vitamin D3 doses of 25, 250, and 1250 µg per day were administered to 38 healthy men for 8 wk.
New save DRA 250 µg per day?

Many vitamin D-containing dietary supplements for adults are formulated to provide 5–10 µg/d, when used according to the label instructions. Although rare and not widely available, a few supplements now contain as much as 1250 µg vitamin D/d.

Exposure of a person in a bathing suit to a minimal erythemal dose of sunlight, which is typically no more than 15-20 minutes on Cape Cod in June or July at noon time, is the equivalent to taking 20,000 IU of vitamin D orally. It is now well documented that in the absence of any sun exposure 1,000 IU of vitamin D3 a day is necessary to maintain healthy levels of 25-hydroxyvitamin D in the circulation.


Vitamin D deficiency results in chronic fatigue and multi-system

Vitamin D should be taken with high dose Calcium 1200 mg and in severe cases up to  2400 mg/day divided in 4 doses of 300 to 600 mg.

Author: Dr. med. Anna Dorothea Hoeck, MD, Mariawaldstr. 7, 50935 Cologne, Germany. E-Mail: ad.hoeck@tonline.
No potential conflicts of interest exist in this paper.

Initially, all metabolic disorders cause nonspecific symptoms combined with fatigue
It was in 1993, when I detected, that not only such common metabolic disorders, like thyroid
diseases, iron and vitamin B12 deficiencies, cause nonspecific symptoms like chronic fatigue
and functional disorders, but as well vitamin D deficiency (1). Not only these symptoms could
be observed in vitamin D deficiency, but as well frequent infections, allergies and widespread
intolerances, pains, sleep disorder, mood and personality changes (1,2).
In these early days, I found out an optimal treatment dose of 5,000 – 10,000 IU (125-250
mcg) cholecalciferol by dose-response trials (2). Initially, I hesitated to combine such high
doses with calcium, because of potential hypercalcemia and hypercalciuria. But addition of a
base powder, containing multi-minerals, and calcium as well, seemed to optimize treatment
results (2).
The striking resemblance between the symptoms of vitamin D deficiency and chronic fatigue
syndrome (CFS/ME), as well as the low levels of the meanwhile accepted biomarker for
vitamin D deficiency, 25-hydroxyvitamin D 3, which is named as well 25-
hydroxycholecalciferol (25OHD3), induced me to treat CFS/ME patients with cholecalciferol
(vitamin D3). However, though patients with mere chronic fatigue recovered soon, most with
full-blown CFS/ME did not respond remarkably to treatment. In particular patients with
calcium serum levels near the lowest or highest normal range seemed to be the most vitamin
D resistant (2).
When I realized that combination with calcium is mandatory for treatment response, I
substituted with 500 to 1,000 mg elementary calcium per day, which might have been, in
retrospective view, a perhaps too low dose for assumed severe calcium deficiency following
chronic vitamin D deficiency (3-10).
Vitamin D deficiency is a hidden disorder of high frequency
Vitamin D deficiency is by no means rare (3,11-15). In particular, highly gifted and engaged
people working most of time indoors, but as well poor and socially deprived people are at
high risk, due to their common problem, the lack of sunlight.
Vitamin D insufficiency, showing 25OHD3 levels from 20-30 ng/ml (50-80 nmol/L) even in
summer time, is quite common, but already entailing the threat of chronic depletion of body
calcium stores, and chronic infections (11-14). Levels from 10-20 ng/ml (25-50 nmol/L) are
measured frequently in winter season. This aggravates calcium deficiency substantially.
Severe vitamin D deficiency with levels below 10 ng/ml (25 nmol/L) causes severe fatigue
and personality changes, depression-like symptoms, chronic sleep disorder, multiple
intolerances, obvious immune dysfunctions and in the long time, multi-system symptoms and
multi-system diseases (1,2).
Vitamin D deficiency leads inevitably to calcium and other mineral deficiencies
Long lasting or chronically repeated 25OHD3 levels beneath 30 ng/ml (80nmol/L) result in
compromised calcium absorption in the bowel, and inefficient fixation of calcium and
phosphate, as well as all other minerals, stored in bone (4-10). This means, chronic vitamin D
deficiency can not be separated from the clinical consequences of calcium and phosphate, and
overall mineral and base deficiency (11-15).
Due to lowered body stores of calcium, a special “calcium rescue-hormone”, synthesized in
little glands (parathyroidea) positioned very closely (“para”) to the thyroid, augments its
production and secretion. This hormone is called parathormone (PTH) (5,7,8,10).
PTH enhances calcium absorption in the bowel and tubular calcium “re-uptake” (reabsorption)
in the kidney (5,7). Thus PTH helps to compensate for net calcium deficiency.
However, PTH mobilizes as well bone calcium stores thus acting as a so-called “osteolytic”
hormone (5,7). That means, at the costs of bone calcium, PTH tries to normalize appropriate
serum levels of calcium which are mandatory for proper neural and general cellular function
If enough stores of 25OHD3 and calcium circulate in blood, PTH levels are undulating with
peaks and troughs. In case of low stores, in contrast, PTH will be constantly elevated. As PTH
enhances the conversion from the pro-hormone 25OHD3 to the more metabolically active
hormone 1,25-dihydroxycholecalciferol [1,25(OH)2D3] (5,7,8), the latter will also be
constantly elevated, as long as any 25OHD3 will be available. Due to the high conversion
rate, 25OHD3 stores become depleted more quickly. Moreover, depleted stores compromise
a constant rate of conversion. It is important to realize that a persistent elevation of PTH and
low stores of 25OHD3 are no healthy conditions, and disturb profoundly cell functions and
metabolism. Normally, 1,25(OH)2D3 is converted only when the cell needs it. Furthermore,
persistent elevation of PTH augments constantly the relation of free to protein-bound calcium
in the cells (3-15). This as well is detrimental for cells, finally causing multisystem diseases
The multiple actions of vitamin D become more and more acknowledged in research
Besides the classical and well known actions on bone, gut and kidney, most tissues possess
nuclear vitamin D receptors (11,12,15-18,20). More than 200 genes are now known to be
influenced by vitamin D (11,12). Besides these actions on gene expression, it acts as well on
cell signalling by multiple mechanisms (8,15,19,20). Many common and frequent diseases,
like heart problems, diabetes, hypertension, Parkinson’s disease, multiple sclerosis, and colon,
prostate and breast cancer, as well as chronic inflammatory and autoimmune diseases, are
now discussed as co-induced by vitamin D deficiency (8,21-34). This points to the impact of
vitamin D deficiency and vitamin D resistance for the general population (8,21-34), and to the
importance to substitute vitamin D and calcium in many chronic health problems (21-34).
In particular, immune system takes profit from treatment (22-30). Vitamin D supports the
primary (innate) immune answer strongly (22-27), but regulates, modifies and mitigates the
secondary (cognate) immune answer (22,26-29), and inhibits the nuclear factor kappa-B (NFKB)
which is an important pro-inflammatory switch signal in cells (30), thus preventing
chronic inflammation and autoimmunity by multiple mechanisms (22-30). Meanwhile, recent
new research about immune regulatory cells elucidates more clearly the connection between
chronic fatigue and chronic inflammation (35). These insights fit very well to already existing
results of vitamin D research (22).
Chronic fatigue syndrome, a condition of vitamin D resistance?
As sufficient stores of vitamin D and calcium are mandatory for general health (8-15),
CFS/ME as a severe health problem, accompanied by immune dysfunctions and high grade
disability, should be focussed as well (11), though not yet broadly discussed in literature (3).
In case of chronic disease, lifetime-stabilization of seasonal fluctuations of vitamin D level
will enhance calcium absorption (11,12); calcium substitution will restore already existing
calcium body deficits (5,8,11,12), thus reducing high turnover of vitamin D (8,38,39) and
vitamin D resistance (8,38,39).
Vitamin D de- or insufficiency can be easily identified by serum 25OHD3 levels. However, it
is difficult to prove chronic calcium deficiency by serum measurements. The well known
osteolytic actions of parathormone and inflammatory cytokines result in misleading rise of
serum calcium levels obscuring the real whole body calcium deficits (4-6,14).
Furthermore, it must be kept in mind that both calcium deficits (36) and high oxidativenitrosative
stress (37) result in altered protein shapes (secondary structure) which highly
compromise enzymatic and other biologic functions. Both mechanisms may substantially
contribute to the observed vitamin D resistance of patients with CFS/ME.
In order to overcome this resistance, substitution doses should be high enough. 25OHD3
levels should be higher than 40 ng/ml (100 nmol/L) (13,38). As ergocalciferol is less potent,
but nevertheless raises 25OHD3 levels, cholecalciferol would be the preferred compound, if
locally available (9). At least 2,000 IE (50 mcg) cholecalciferol, but often higher doses up to
10,000 IE (250 mcg) per day, are necessary (38,39). The daily amount of calcium should be at
least 1200 mg, given 3-4 times a day, in divided single doses between 300 - 600 mg (5,8).
Calcium needs in severe diseases are reported to be as high as 2400 mg per day (5,8,10,39).
Last, but not least, it should be mentioned that cholecalciferol as chemical derivative of
cholesterol is an important antioxidant (40), and is able to restore redox balance (36). Both
actions are supposed to be of additional usefulness in CFS/ME.
Physicians should realize that chronic fatigue is not a primary mental disease. Vitamin D deor
insufficiency seems to be the most frequent cause. If untreated, calcium depletion and
vitamin D resistance, presumably further deficiencies, and for instance, chronic fatigue
syndrome will develop, later on followed by other more obvious diseases. Vitamin D
resistance of chronic fatigue syndrome should be treated with much higher doses of vitamin D
and calcium, than applied in osteoporosis prophylaxis.
Clinical high quality studies would be helpful to get an overview which doses of calcium and
vitamin D will be optimal and appropriate in CFS/ME, and reveal the rate of treatment
responses. Possibly, further micronutrient co-medications will be necessary in severe cases of