Discussie over vitamine D

Denk aan vitamine D, vitamine B12, selenium, coeliakie, bijnier, vitiligo, gewrichten, vasculitis en borstimplantaten
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Re: Discussie over vitamine D

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High-Dose Vitamin D: Helpful or Harmful?
Karen E. Hansen

If the optimal serum 25(OH)D level for skeletal health is ≥30 ng/mL, then vitamin D insufficiency is widespread, affecting approximately 75% of adults based on a recent survey of over 20,000 Americans. However, after a comprehensive analysis of existing research studies, the Institute of Medicine recently concluded that nearly all individuals are vitamin D replete when their 25(OH)D levels are ≥20 ng/mL.

Furthermore, two recent publications challenge the belief that 25(OH)D levels >30 ng/mL are optimal for bone health. In a randomized, placebo-controlled trial, high-dose once yearly vitamin D therapy increased fractures and falls. The second study reported that high-dose vitamin D did not reduce levels of parathyroid hormone or bone resorption among adults with 25(OH)D levels <32 ng/mL at baseline. It is time to question whether serum 25(OH)D levels ≥30 ng/mL are necessary for all individuals.
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Re: Discussie over vitamine D

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BB1100XX schreef: 05 dec 2017, 20:40 Dat ben ik eindelijk aan het overwinnen!
time for a change!
Wat goed!
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Association Between Calcium or Vitamin D Supplementation and Fracture Incidence in Community-Dwelling Older Adults
A Systematic Review and Meta-analysis | Jia-Guo Zhao, Xian-Tie Zeng, Jia Wang, Lin Liu

Importance The increased social and economic burdens for osteoporosis-related fractures worldwide make the prevention of such injuries a major public health goal. Previous studies have reached mixed conclusions regarding the association between calcium, vitamin D, or combined calcium and vitamin D supplements and fracture incidence in older adults.

Objective To investigate whether calcium, vitamin D, or combined calcium and vitamin D supplements are associated with a lower fracture incidence in community-dwelling older adults.

Data Sources The PubMed, Cochrane library, and EMBASE databases were systematically searched from the inception dates to December 24, 2016, using the keywords calcium, vitamin D, and fracture to identify systematic reviews or meta-analyses. The primary randomized clinical trials included in systematic reviews or meta-analyses were identified, and an additional search for recently published randomized trials was performed from July 16, 2012, to July 16, 2017.

Study Selection Randomized clinical trials comparing calcium, vitamin D, or combined calcium and vitamin D supplements with a placebo or no treatment for fracture incidence in community-dwelling adults older than 50 years.

Data Extraction and Synthesis Two independent reviewers performed the data extraction and assessed study quality. A meta-analysis was performed to calculate risk ratios (RRs), absolute risk differences (ARDs), and 95% CIs using random-effects models.

Main Outcomes and Measures Hip fracture was defined as the primary outcome. Secondary outcomes were nonvertebral fracture, vertebral fracture, and total fracture.

Results A total of 33 randomized trials involving 51 145 participants fulfilled the inclusion criteria. There was no significant association of calcium or vitamin D with risk of hip fracture compared with placebo or no treatment (calcium: RR, 1.53 [95% CI, 0.97 to 2.42]; ARD, 0.01 [95% CI, 0.00 to 0.01]; vitamin D: RR, 1.21 [95% CI, 0.99 to 1.47]; ARD, 0.00 [95% CI, −0.00 to 0.01]. There was no significant association of combined calcium and vitamin D with hip fracture compared with placebo or no treatment (RR, 1.09 [95% CI, 0.85 to 1.39]; ARD, 0.00 [95% CI, −0.00 to 0.00]). No significant associations were found between calcium, vitamin D, or combined calcium and vitamin D supplements and the incidence of nonvertebral, vertebral, or total fractures. Subgroup analyses showed that these results were generally consistent regardless of the calcium or vitamin D dose, sex, fracture history, dietary calcium intake, and baseline serum 25-hydroxyvitamin D concentration.

Conclusions and Relevance In this meta-analysis of randomized clinical trials, the use of supplements that included calcium, vitamin D, or both compared with placebo or no treatment was not associated with a lower risk of fractures among community-dwelling older adults. These findings do not support the routine use of these supplements in community-dwelling older people.
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Re: Discussie over vitamine D

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hallo Eekhoorn,

Kun jij iets vertellen over de huidige stand van zaken rond vitamine D?
Wat is bijvoorbeeld een veilige dosis?
En hoe zit het met de halfwaardetijd?

Ik las van iemand dat zij 5000 IE per dag slikte.
Is dat niet heel veel?
laura

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Re: Discussie over vitamine D

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Patient education: Vitamin D deficiency (Beyond the Basics)

Author: Marc K Drezner, MD
Section Editor: Clifford J Rosen, MD
Deputy Editor: Jean E Mulder, MD

Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2019. | This topic last updated: Feb 08, 2019.

INTRODUCTION

Vitamin D plays an important role in many places throughout the body, including the development and calcification of the bones.

Adequate exposure to sunlight and the use of dairy products with vitamin D have significantly reduced the incidence of vitamin D deficiency. However, vitamin D deficiency is still a common problem in many populations, particularly older adults.

This topic reviews the major causes of vitamin D deficiency, including how it is diagnosed and treated, and safe ways to prevent vitamin D deficiency.

WHAT IS VITAMIN D?

Vitamin D is an oil-soluble vitamin that has several important functions in the body:

●It helps to absorb dietary calcium and phosphorus from the intestines.

●It suppresses the release of parathyroid hormone, a hormone that causes bone resorption.

Through these actions, vitamin D keeps the calcium and phosphate levels in the blood normal, thereby promoting bone health. Vitamin D may have other benefits, such as improving muscle and immune function, but these areas require more research.

Natural sources of vitamin D — Vitamin D is made in the skin under the influence of sunlight. The amount of sunlight needed to synthesize adequate amounts of vitamin D varies, depending upon the person's age, skin color, sun exposure, and underlying medical problems. The production of vitamin D from the skin decreases with age. In addition, people who have darker skin need more sun exposure to produce adequate amounts of vitamin D, especially during the winter months.

Another important source of vitamin D is foods, where it may occur naturally (in fatty fish, cod liver oil, and [to a lesser extent] eggs). In the United States, commercially fortified cow's milk is the largest source of dietary vitamin D, containing approximately 100 international units (2.5 micrograms) of vitamin D per 8 ounces. Vitamin D intake, in international units, can be estimated by multiplying the number of cups of milk consumed per day by 100 (two cups milk = 200 international units vitamin D). In other parts of the world, cereals and bread products are often fortified with vitamin D.

Although vitamin D is found in cod liver oil, some fish oils also contain high doses of vitamin A. Excessive vitamin A intake can be associated with side effects, including liver damage and fractures.

CAUSES OF VITAMIN D DEFICIENCY

The main reasons for low levels of vitamin D are:

●Lack of vitamin D in the diet, often in conjunction with inadequate sun exposure

●Inability to absorb vitamin D from the intestines

●Inability to process vitamin D due to kidney or liver disease

Inadequate intake — Infants, children, and older adults are at risk for low vitamin D levels because of inadequate vitamin D intake. Human breast milk contains low levels of vitamin D, and most infant formulas do not contain adequate vitamin D. Older adults often do not consume enough vitamin D rich foods, and even when they do, absorption may be limited.

Inadequate sun exposure — Parents of infants and children are often advised to keep their child out of the sun, which reduces vitamin D synthesis from the skin. Exposure to the sun is not recommended as a source of vitamin D for infants and children, due to the potential long-term risks of skin cancer. (See "Patient education: Sunburn (Beyond the Basics)".)

Adults who have limited sun exposure are also at increased risk of vitamin D deficiency, especially if their skin is dark. In addition, reduced amounts of vitamin D are made in the skin and stored in the body as we age. This is especially true in the winter months in some northern areas, such as Boston, Massachusetts and Edmonton, Alberta, where the skin virtually ceases to produce vitamin D between October and April. In the summer months, the use of sunscreen limits vitamin D synthesis.

Diseases or surgery that affect fat absorption — Certain diseases affect the body's ability to absorb adequate amounts of vitamin D through the intestinal tract. Examples of these include celiac disease, Crohn's disease, and cystic fibrosis.

Surgery that removes or bypasses portions of the stomach or intestines can also lead to low vitamin D levels. An example of this type of surgery is gastric bypass. (See "Patient education: Weight loss surgery and procedures (Beyond the Basics)".)

Kidney and liver disease — The liver and kidney have important enzymes that change vitamin D from sun-exposed skin or food to the biologically active form of vitamin D. People with chronic kidney and liver disease are at increased risk of low active vitamin D levels because they have decreased levels of these enzymes.

Less common causes of vitamin D deficiency include familial or acquired diseases that impair the enzymes in the liver or kidney that create the biologically active form of the vitamin. This results in inadequate amounts of active vitamin D.

POTENTIAL COMPLICATIONS OF VITAMIN D DEFICIENCY

The most serious complications of vitamin D deficiency are low blood calcium (hypocalcemia), low blood phosphate (hypophosphatemia), rickets (softening of the bones during childhood), and osteomalacia (softening of the bones in adults). However, these complications have become less common over time because many foods and drinks have added vitamin D.

"Subclinical" vitamin D deficiency or vitamin D insufficiency is common and is defined as a lower than normal vitamin D level that has no visible signs or symptoms. However, vitamin D insufficiency is often associated with reduced gastrointestinal calcium absorption, decreased bone density (osteopenia or osteoporosis), and, in some cases, a mild decrease of the blood calcium level, elevated parathyroid hormone (which accelerates bone resorption), an increased risk of falls, and possibly fractures, all of which can seriously affect a person's quality of life.

Thus, identifying and treating vitamin D insufficiency or deficiency is important to maintain bone strength. Treatment may even improve the health of other body systems, such as the immune, muscular, and cardiovascular systems, although more research is needed in these areas.

DIAGNOSIS OF VITAMIN D DEFICIENCY

A low vitamin D level can be diagnosed with a blood test called 25-hydroxyvitamin D or 25(OH)D (OH = hydroxy, D = vitamin D). Although there is no formal definition of vitamin D deficiency, some groups use the following values in adults:

●A normal level of vitamin D is defined as a 25(OH)D concentration greater than 30 ng/mL (75 nmol/L)

●Vitamin D insufficiency is defined as a 25(OH)D concentration of 20 to 30 ng/mL (50 to 75 nmol/L)

●Vitamin D deficiency is defined as a 25(OH)D level less than 20 ng/mL (50 nmol/L)

Although there are differences of opinion regarding the 25(OH)D levels that define vitamin D insufficiency and deficiency, most experts agree that levels lower than 20 ng/mL (50 nmol/L) are suboptimal for skeletal health.

Who needs testing for vitamin D? — Testing for vitamin D deficiency or insufficiency is not recommended for everyone but may be advised for people who are home bound or in a long-term care facility (eg, nursing home); if the person has a medical condition that increases the risk of vitamin D deficiency or insufficiency; and for anyone with osteoporosis or a past history of a low-trauma fracture (eg, fracture after fall from standing), low blood calcium (hypocalcemia), or phosphate (hypophosphatemia). (See "Patient education: Bone density testing (Beyond the Basics)" and "Patient education: Osteoporosis prevention and treatment (Beyond the Basics)".)

TREATMENT OF VITAMIN D DEFICIENCY

Vitamin D supplements — There are many types of vitamin D preparations available for the treatment of vitamin D deficiency or insufficiency. The two commonly available forms of vitamin D supplements are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). We suggest vitamin D3 when possible, rather than vitamin D2, because vitamin D3 is the naturally occurring form of the vitamin and it may raise vitamin D levels more effectively.

Dosing — The recommended dose of vitamin D depends upon the nature and severity of the vitamin D deficiency.

In people who do not have problems absorbing vitamin D:

●In people whose 25-hydroxyvitamin D (25[OH]D) is <10 ng/mL (25 nmol/L), treatment usually includes 50,000 international units (1250 micrograms) of vitamin D2 or D3 by mouth once or more per week for six to eight weeks, and then 800 to 1000 international units (20 to 25 micrograms), or more, of vitamin D3 daily thereafter.

●In people whose 25(OH)D is 10 to 20 ng/mL (25 to 50 nmol/L), treatment usually includes 800 to 1000 international units (20 to 25 micrograms) of vitamin D3 by mouth daily, usually for a three-month period. However, many individuals will need higher doses. The "ideal" dose of vitamin D is determined by testing the individual's 25(OH)D level and increasing the vitamin D dose if the level is not within normal limits. Once a normal level is achieved, continued therapy with 800 international units (20 micrograms) of vitamin D per day is usually recommended.

●In people whose 25(OH)D is 20 to 30 ng/mL (50 to 75 nmol/L), treatment with 600 to 800 international units (15 to 20 micrograms) of vitamin D3 by mouth daily may be sufficient to maintain levels in the target range.

●In infants and children whose 25(OH)D is <20 ng/mL (50 nmol/L), treatment usually includes 1000 to 2000 international units (25 to 50 micrograms) of vitamin D2 by mouth per day (depending on the child's age) for two to three months. Children with rickets (softening of the bones, which can be seen on an X-ray) may need higher doses of vitamin D and should have medical follow-up to ensure that the rickets resolves.

In people who have diseases or conditions that prevent them from absorbing vitamin D normally (eg, kidney or liver disease), the recommended dose of vitamin D will be determined on an individual basis.

In people whose vitamin D level is normal (>30 ng/mL [≥75 nmol/L]), a dose of 800 international units (20 micrograms) of vitamin D per day is usually recommended. (See 'Prevention of vitamin D deficiency' below.)

Do I need other vitamins or minerals? — During treatment for vitamin D deficiency, it is important to consume at least 1000 mg of calcium per day for premenopausal women and men and 1200 mg per day for postmenopausal women.

Calcium can be found in food sources (table 1) or dietary supplements (table 2). (See "Patient education: Calcium and vitamin D for bone health (Beyond the Basics)".)

Monitoring — A blood test is recommended to monitor blood levels of 25(OH)D three months after beginning treatment. The dose of vitamin D may need to be adjusted based on these results and subsequent blood levels of 25(OH)D obtained to assure that normal levels result from the adjusted dose.

Side effects — Side effects of vitamin D are uncommon unless the 25(OH)D level becomes very elevated (>100 ng/mL or 250 mmol/L) and the person is taking high dose calcium supplements. However, it is important to follow dosing instructions closely and to avoid taking multiple products that contain vitamin D (eg, multivitamin and vitamin D).

If 25(OH)D levels do become very elevated, complications such as high blood calcium levels or kidney stones can develop.

PREVENTION OF VITAMIN D DEFICIENCY

As mentioned previously, the amount of vitamin D you need per day to maintain a normal level of 25-hydroxyvitamin D (25[OH]D) depends upon your skin color, sun exposure, diet, and underlying medical conditions.

In general, adults are advised to take a supplement containing 800 international units (20 micrograms) of vitamin D per day to maintain a normal vitamin D level. Older people who are confined indoors may have vitamin D deficiency even at this intake level. (See 'Vitamin D supplements' above.)

All infants and children are advised to take a vitamin D supplement containing 400 international units (10 micrograms) of vitamin D, starting within days of birth. For infants and children, vitamin D is included in most nonprescription infant multivitamin drops. In some countries, it is possible to buy infant drops that contain only vitamin D. (See "Patient education: Breastfeeding guide (Beyond the Basics)" and "Patient education: Starting solid foods during infancy (Beyond the Basics)".)

Exposure to the sun or tanning beds is not recommended as a source of vitamin D, because of the risk of skin cancer.

WHERE TO GET MORE INFORMATION

Your health care provider is the best source of information for questions and concerns related to your medical problem.

This article will be updated as needed on our website (www.uptodate.com/patients). Related topics for patients, as well as selected articles written for health care professionals, are also available. Some of the most relevant are listed below.

Patient level information — UpToDate offers two types of patient education materials.

The Basics — The Basics patient education pieces answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.

Patient education: Vitamin D deficiency (The Basics)
Patient education: Osteoporosis (The Basics)
Patient education: Calcium and vitamin D for bone health (The Basics)
Patient education: Vitamin supplements (The Basics)
Patient education: Vitamin D for babies and children (The Basics)
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Re: Discussie over vitamine D

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Martijn Katan op Facebook: https://www.facebook.com/martijnkatan/p ... 5980282159

Te weinig vitamine D is slecht voor je botten. Kan een tekort aan vitamine D ook hoge bloeddruk veroorzaken, of overgewicht, hart- en vaatziekten, griep, depressie, multiple sclerose, diabetes of astma?

Dat wordt wel gedacht.

Daarom laten sommige dokters bij veel patiënten vitamine D in het bloed bepalen. Maar die effecten van vitamine D zijn schijn. Het effect op hartinfarcten en beroertes bijvoorbeeld is getest in 21 experimenten bij 83.291 mensen. Daarvan kregen er 41.669 vitamine D en 41.622 een neppil. Effect: nul, niks, nihil.

Voor overgewicht, griep etc. werd ook nooit iets gevonden: https://www.mkatan.nl/nrc-columns/523-v ... l-het-idee.

Dokters moeten stoppen met vitamine D meten, het kost een vermogen en het zegt niets.

BRONNEN:
Barbarawi M et al. Vitamin D Supplementation and Cardiovascular Disease Risks in More Than 83 000 Individuals in 21 Randomized Clinical Trials: A Meta-analysis. JAMA Cardiol. 2019. www.ncbi.nlm.nih.gov/pubmed/31215980
Quyyumi AA, Al Mheid I. The Demise of Vitamin D for Cardiovascular Prevention. JAMA Cardiol. 2019.
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Eekhoorn
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Lid geworden op: 13 okt 2013, 12:09

Re: Discussie over vitamine D

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hallo Eekhoorn,

Kun jij iets vertellen over de huidige stand van zaken rond vitamine D?

laura
Er zijn meer aanwijzingen dat associaties tussen allerlei gezondheidsproblemen enerzijds en vitamine D-gebrek anderzijds, géén causaal verband hebben. Zie bijvoorbeeld https://jamanetwork.com/journals/jama/f ... d=76716975:
It now seems safe to conclude that many prior epidemiological associations between vitamin D deficiency and adverse health outcomes were driven by unmeasured residual confounding or reverse causality.
Wat is bijvoorbeeld een veilige dosis?
Wat betreft de maximaal veilige dosis heeft de EFSA in 2012 een 'scientific opinion' uitgegeven. Voor volwassenen en kinderen vanaf 11 jaar wordt een maximum van 4000 IE/dag geadviseerd. Daarbij is overwogen dat bij onderzoek geen nadelige gevolgen zijn gezien bij doses tot 10.000 IE/dag. Dat daarbij toch voor 4000 IE/dag is gekozen, kun je zien als het in acht nemen van een 'veiligheidsmarge'. Zie https://www.efsa.europa.eu/en/efsajournal/pub/2813

Voor kinderen van 1 tot en met 10 jaar geldt volgens dit stuk een geadviseerd maximum van 2000 IE/dag.
Voor kinderen tot 1 jaar is een apart advies gepubliceerd: https://www.efsa.europa.eu/en/efsajournal/pub/5365.
Ik las van iemand dat zij 5000 IE per dag slikte.
Is dat niet heel veel?
Dat is behoorlijk veel, maar waarschijnlijk niet zoveel dat het gevaar oplevert. Het is iets meer dan de 4000 IE/dag die de EFSA maximaal adviseert, maar zit nog ruim onder de 10.000 IE/dag. Het is waarschijnlijk wel zinloos zoveel te nemen.
En hoe zit het met de halfwaardetijd?
Die hangt af van de vitamine D 25OH-bloedspiegel: hoe hoger die is, hoe korter de halfwaardetijd. Dat komt doordat het enzym dat vitamine D afbreekt, actiever wordt naarmate de 25OH-spiegel hoger is. Voor 'normale' spiegels - zeg tussen de 50 en 80 nmol/L - is de halfwaardetijd van 25OH een week of vier.
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Re: Discussie over vitamine D

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The Role of Vitamin D in Thyroid Diseases
Dohee Kim

Abstract

The main role of vitamin D is regulating bone metabolism and calcium and phosphorus homeostasis. Over the past few decades, the importance of vitamin D in non-skeletal actions has been studied, including the role of vitamin D in autoimmune diseases, metabolic syndromes, cardiovascular disease, cancers, and all-cause mortality. Recent evidence has demonstrated an association between low vitamin D status and autoimmune thyroid diseases such as Hashimoto’s thyroiditis and Graves’ disease, and impaired vitamin D signaling has been reported in thyroid cancers. This review will focus on recent data on the possible role of vitamin D in thyroid diseases, including autoimmune thyroid diseases and thyroid cancers.

Limitations in the Study of Vitamin D

Although many studies have suggested an association of low vitamin D status with AITD and thyroid cancer, epidemiological studies simply show correlative relationships which cannot be used to determine cause and effect [3,72]. Low vitamin D status may be not the cause but rather a consequence of the disease [41,84]. The low vitamin D levels of patients with thyroid diseases can be explained by low vitamin D intake, malabsorption, lack of sun exposure, or reduced outdoor activity [21,29,72,84,85].

In addition, it is likely that good vitamin D status represents a general marker of good health. A young individual with a normal body weight and a healthy lifestyle, including good dietary and exercise habits, is more likely to not only have higher 25(OH)D levels, but also a lower risk of cancer or chronic illness. Therefore, it is difficult to separate the effects of these characteristics from those that may be attributed to 25(OH)D levels [55,76,86].

Similarly, low vitamin D status may be the result of chronic illness, which prevents outdoor activities and sun exposure. Vitamin D is rarely ingested in isolation; therefore, additional nutrients that are co-ingested with vitamin D may have independent or synergistic effects [86]. Additionally, because serum vitamin D levels were measured only once in almost all observational studies, the values obtained might not be representative [70,72,86].

The controversial and varying results of studies are partly due to inter-assay and inter-laboratory variability in the measurements of 25(OH)D, seasonal variations in blood sampling of 25(OH)D, and the different cut-off levels used to define vitamin D deficiency or insufficiency. In addition, the conflicting results could be explained by limitations in study design, such as cross-sectional studies with a small number of subjects, and therefore, the potential for selection bias, as well as the heterogeneity of the study population and the diverse methods used for the diagnosis of AITD, HT, GD, or thyroid cancer [11,29,41,72].

Conclusions

The pleiotropic roles of vitamin D have been recognized through preclinical and observational studies which have suggested a beneficial role of vitamin D in the management of thyroid disease. However, only an ambiguous causal relationship and few interventional studies have been reported to date, so the preventive and therapeutic potential of vitamin D or its analog in thyroid diseases remains debated.

Ongoing and future long-term, randomized controlled trials are required to determine whether individuals with low 25(OH)D levels are at increased risk of developing AITD and thyroid cancer, and to provide insight into the efficacy and safety of vitamin D as a therapeutic tool for these thyroid diseases.
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Re: Discussie over vitamine D

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Vitamine D tegen Covid-19? De wetenschap is er nog niet uit
Sander Voormolen | nrc.nl

Coronavirus: Mensen met een lage vitamine D-spiegel worden ernstiger ziek van het coronavirus. Maar is er wel een oorzakelijk verband?

Kan het slikken van extra vitamine D beschermen tegen corona? De wetenschap heeft daarop nog geen definitief antwoord. Veel Nederlanders lijken daarop niet te willen wachten: bij drogisterijen en apotheken is deze herfst opvallend meer vraag naar vitamine D-supplementen dan in andere jaren, meldde het Algemeen Dagblad vorige week. De krant citeerde daarbij een aantal wetenschappers die bevestigden dat het zinvol zou zijn preventief extra vitamine D te slikken. Daarmee begeven ze zich op glad ijs, want er ligt hier een kip-of-ei-probleem op de loer. Ja, mensen met een laag gehalte vitamine D in het bloed worden ernstiger ziek van het nieuwe coronavirus, maar wat is hier oorzaak en gevolg?

Grote kans op vertekening

Wat er ligt is niet meer dan een aantal „aanwijzingen” dat een tekort aan vitamine D een rol kan spelen bij de bevattelijkheid voor het coronavirus of de ernst van de ziekte. Dat is diverse keren in zogeheten observationele studies geconstateerd. Lastig is dat mensen die extra risico lopen op Covid-19 vaak óók een lage spiegel vitamine D hebben. Het gaat om ouderen, mensen met overgewicht, mensen met een onderliggende ziekte, of mensen die door hun slechtere economische omstandigheden meer risico lopen besmet te raken. Een lagere vitamine D status hangt sowieso samen met een minder goede gezondheid. Dat maakt de kans op vertekening groot.

Wetenschappelijke studies rond Covid-19 en vitamine D rapporteerden meer dan eens grote effecten, maar die moeten niet argeloos geïnterpreteerd worden als bewijs voor het nut van vitamine D-supplementen in deze pandemie. Zo laat een grote Israëlische studie onder ruim 7.800 mensen zien dat een vitamine D-tekort het risico op ziekenhuisopname vanwege Covid-19 verdubbelde. Dat gold althans voor de tien procent van de deelnemers die in de drie maanden dat de studie liep tenminste één keer positief testte op SARS-CoV-2. En dat verband was statistisch significant, meldden de auteurs. Maar dat gold ook voor het verband met leeftijd (boven de vijftig jaar), het behoren tot het mannelijk geslacht of het hebben van een lage sociaal-economische positie in de maatschappij.

Een recent gepubliceerd Spaans onderzoek uitgevoerd in maart in een ziekenhuis in Santander laat zien dat meer dan 80 procent van de Covid-19 patiënten een laag vitamine D- gehalte in het bloed had. Maar het gaat hierbij om metingen bij mensen die al met ernstige klachten in het ziekenhuis waren opgenomen, dus het is de vraag of de infectie zelf niet de daling in het vitamine D-gehalte heeft veroorzaakt. Een duidelijk verband tussen de concentratie vitamine D in het bloed en het risico dat een patiënt op de IC belandt of komt te overlijden, konden de Spanjaarden niet ontdekken.

In het artikel vermelden de onderzoekers ook nog een groep van 19 opgenomen coronapatiënten die voorafgaand aan hun ziekenhuisopname vitamine D-supplementen slikten. Dat leek hen echter geen extra bescherming te bieden, maar volgens de auteurs kan dat komen doordat deze groep relatief ook minder gezond was (en om die reden dus al supplementen kreeg).

Een groot Amerikaanse onderzoek onder bijna 200.000 mensen liet zien dat mensen die positief testen op corona gemiddeld een grotere kans hebben ook een tekort te hebben aan vitamine D. Maar een harde conclusie dat vitamine D beschermt tegen coronabesmetting durven ze niet te trekken: ze beschouwen hun onderzoek als opmaat naar gecontroleerde studies die de invloed van vitamine D op het besmettingsrisico onderzoeken.

Visolie

En dat onderzoek komt eraan. Uit de Amerikaanse databank van klinische studies clinicaltrials.gov blijkt dat er inmiddels al tientallen vergelijkende studies naar het verband tussen Covid-19 en vitamine D-status zijn gestart. En er staan er nog tientallen andere in de startblokken. Ze zullen van alles in kaart proberen te brengen, van het mogelijk effect op de bevattelijkheid voor het virus, tot het genezend effect op mensen die al ziek zijn en de invloed op de sterfte aan Covid-19.

In Noorwegen staat een grote studie met 80.000 beoogde deelnemers op stapel om komende winter het effect van een supplement met visolie (dat net als levertraan in voorbije jaren veel vitamine D bevat) te vergelijken met een maïsolie-capsule, als placebo.

Een snel antwoord op de vraag of extra vitamine D zin heeft tegen corona is echter niet te verwachten. Ook de interpretatie van effectiviteitsstudies is lastig, omdat de toediening van dit vitamine niet onder goed gecontroleerde omstandigheden kan plaatsvinden. Mensen nemen vitamine D immers ook op uit hun voeding én ze maken de stof in de huid zelf aan.

LICHAAM MAAKT ZELF VITAMINE D

Vitamine D is voor iedereen belangrijk om goed gezond te blijven. De vitamine is nodig voor een goede regulatie van de fosfaat- en calciumhuishouding in het lichaam en daarmee belangrijk voor sterke botten en tanden. Vitamine D kan ook de immuniteit versterken en mensen minder vatbaar maken voor luchtweginfecties, variërend van verkoudheid tot tuberculose.

Onze huid kan vitamine D zelf aanmaken onder invloed van zonlicht en ook via de voeding krijgen we wat binnen. Mensen met een donkere huid en mensen die nauwelijks buiten komen kunnen een tekort aan vitamine D krijgen dat zij kunnen aanvullen met supplementen. Ook ouderen hebben doorgaans een iets hogere vitamine D-behoefte. Te veel vitamine D is weer niet goed: dat kan nierstenen veroorzaken.

De menselijke huid maakt een voorloperstof van vitamine D onder invloed van zonlicht. Een kwartiertje zonnebaden in de zomer in zwembroek levert iemand met een lichte huid al ruimschoots de dagelijks benodigde hoeveelheid previtamine D op die later door de lever en de nieren kan worden omgezet in de actieve vorm. Bij mensen met veel pigment gaat de productie in de huid tot wel zes keer langzamer. In de wintermaanden is het aandeel UV-B-straling in het zonlicht op onze breedtegraad te zwak om voldoende bij te dragen aan de aanmaak in de huid.

In de voeding zijn vooral vette vis (o.a. haring , zalm, makreel), vlees en eieren (dooiers) een bron van vitamine D. Ook paddenstoelen bevatten een vorm van vitamine D.
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laura
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Lid geworden op: 11 sep 2013, 22:42
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Re: Discussie over vitamine D

Bericht door laura »

Why USPSTF still finds insufficient evidence to support screening for Vitamin D deficiency

In 2014, the United States Preventive Services Task Force (USPSTF) concluded that among community-dwelling asymptomatic adults aged 18 years and older, there was insufficient evidence (ie, I statement) to assess the balance of benefits and harms of screening for vitamin D deficiency in asymptomatic adults.1 Over the past 7 years, many randomized clinical trials (RCTs) have evaluated vitamin D supplementation for improving primary or secondary outcomes of cardiovascular disease, cancer, diabetes, depression, bone health, and falls,2-8 necessitating a reevaluation of whether screening for vitamin D insufficiency might be worthwhile. The evidence is still not there to inform this decision.9,10

Screening is the routine evaluation of an asymptomatic population with the goal of detection of a disease, when the natural course of that disease can be altered by early intervention. The benefits of screening in a population need to outweigh any potential harms that might arise from false positive tests, inappropriate downstream testing, and overtreatment of so-called pseudodisease.11 Thus, the rationale for screening a broad population by measuring blood 25-hydroxyvitamin D (25[OH]D) levels would be to identify a deficiency state, with the expectation that eliminating the deficiency in individuals (through an intervention) will improve health.

In epidemiological studies, low blood levels of 25(OH)D have consistently been a factor strongly associated with many health outcomes, such as depression, fractures, frailty, falls, diabetes, hypertension, cardiovascular diseases, cancer, and others.7 However associations do not equal causation, and low 25(OH)D status might reflect a poorer health status in general owing to reverse causation or confounding by other health or behavioral factors.7 For example, individuals with obesity, reduced outdoor physical activity, and less healthy diets are more likely to have lower 25(OH)D levels. Importantly, high quality RCTs have not found that supplementation with vitamin D meaningfully mitigates these outcomes.2-7 Even the benefit of vitamin D on bone health and musculoskeletal outcomes has been challenged,5,12 and its efficacy may depend on whether concomitant calcium supplementation is given.13 While many of these RCTs did not specifically enroll individuals with a documented deficiency state, post hoc subgroup analyses failed to find outcome benefit for vitamin D supplementation among those with low 25(OH)D levels (ie, <20 ng/mL [to convert to nanomoles per liter, multiply by 2.496]), with less data available for the subgroup of those below 12 ng/ml.2,3,7

Might the commonly used vitamin D measure be the wrong measure? In the blood, 25(OH)D is the major circulating form and reflects both endogenous and exogenous sources. It has a half-life of 2 to 3 weeks and has long been considered to be the best marker of vitamin D status,14 although 25(OH)D is largely biologically inert. The activated form, 1,25-dihydroxyvitamin D (also known as calcitriol), confers the biological activity through the binding of the vitamin D nuclear receptor in the small intestine, kidneys, and other tissues. However, given its short half-life and tightly controlled regulation, calcitriol levels do not adequately reflect vitamin D stores. Furthermore, it has been challenging to measure 25(OH)D accurately, with substantial overestimation or underestimation of 25(OH)D levels with the most commonly used immnoassays.15 This has improved with implementation of the Vitamin D Standardization Program and, currently, liquid chromatography-mass spectrometry is the criterion standard, although it is unknown how broadly this is used across commercial laboratories. Additionally, 25(OH)D circulates predominately in the bound form, with only 10% to 15% being bioavailable; current clinical assays do not discern between bound and bioavailable states. Other novel vitamin D markers, such as free vitamin D, may more adequately reflect vitamin D status and thus more accurately identify those who would benefit from vitamin D supplementation; this has been an active area of investigation.3,7

Yet, what constitutes 25(OH)D sufficiency? The guidelines are generally in agreement that evidence is scant for better health, aside from skeletal health, in individuals with higher 25(OH)D levels; thus, recommendations for optimal 25(OH)D levels are benchmarked for optimizing bone health. Vitamin D deficiency results in decreased intestinal absorption of calcium and phosphate from dietary sources, leading to increased parathyroid hormone levels. Secondary hyperparathyroidism in turn results in calcium mobilization from the skeleton and phosphate wasting from the kidney, adversely impacting bone health. Vitamin D deficiency is also associated with muscle weakness, which may further contribute to an increased risk of fracture.

The Institute of Medicine16 has defined vitamin D deficiency as 25(OH)D less than 12 ng/mL, with levels greater than 20 ng/mL being considered adequate for bone and overall health; whereas the Endocrine Society14 has classified 25(OH)D less than 20 ng/mL as deficient and greater than 30 ng/mL as optimal. These cutoffs for vitamin D deficiency have been defined, in part, based on levels at which parathyroid hormone levels begin to normalize. A prominent issue with using 25(OH)D as a marker of bone health status is the paradoxical findings by race. Black adults living at northern latitudes have lower 25(OH)D levels than lighter-skinned individuals owing to reduced UV-B absorption, yet Black women generally have lower rates of fracture and higher bone mineral density than similarly aged White women.17 Thus, sufficiency may be hard to define at a population level.

Approximately half of adults would be considered vitamin D deficient or insufficient using current definitions, with higher rates in racial/ethnic minorities, including Black and Hispanic individuals,18 suggesting wide-spread vitamin D deficiency.15 There are unclear harms associated with assigning a diagnosis of vitamin D deficiency to asymptomatic people in regards to patient anxiety, costs of treatment for vitamin D repletion and monitoring of follow-up levels, and the pill burden of supplementation.11 Additionally there is the rare but real potential for vitamin D toxic effects with overtreatment, leading to the adverse clinical manifestations that stem from hypercalcemia and hypercalciuria. Even without overt hypercalcemia, some studies have suggested that daily vitamin D supplementation of greater than 4000 IU may even reduce bone health and increase fall risk.5,6 Combined vitamin D and calcium supplementation may increase the risk for kidney stones. Thus, vitamin D supplementation above the recommended daily allowances should not be considered as a benign intervention.

We note that the latest USPSTF statement about insufficient evidence relates to population-based screening.9,10 The recommendation does not preclude targeted measurement of 25(OH)D in the individual patient, where it is thought that the risk-to-benefit ratio may favor testing to guide intervention or risk stratification.9,10 This might include individuals with osteoporosis, chronic kidney disease, malabsorption syndromes, or medication use (ie, glucocorticoids) and pregnant and lactating women. This is concordant with recommendations from the Endocrine Society,14 which also concluded that there was insufficient evidence for broad screening of populations but that measurement could be considered selectively among individuals at high risk for deficiency.

Thus, in 2021, the USPSTF recommendation remains an I statement: the evidence is insufficient to assess the balance of benefits and harms of screening for vitamin D deficiency in asymptomatic adults.9,10 The biggest challenge remains that no studies have specifically evaluated the direct benefits or harms of screening for vitamin D deficiency. To move the needle, further data are needed to determine whether a broad populated-based screening approach is superior to a selective targeted measurement approach or to no measurement of 25(OH)D at all. Ideally, an RCT evaluating such a screening approach would generate the strongest evidence, yet would be challenging to conduct. A screening trial would need to carefully choose the clinical outcomes to target for evidence of benefit (bone health vs other). Additionally, the needed duration of a trial is uncertain, and there is likely to be substantial heterogeneity in benefits of screening among subgroups. Over the past 7 years, despite RCTs of vitamin D supplementation, everything has changed and yet nothing has changed regarding the approach to screening for vitamin D deficiency.

Article Information

Published: April 13, 2021. doi:10.1001/jamanetworkopen.2021.3627

Open Access: This is an open access article distributed under the terms of the CC-BY License. © 2021 Michos ED et al. JAMA Network Open.

Corresponding Author: Jodi B. Segal, MD, MPH, Division of General Internal Medicine, Johns Hopkins University School of Medicine, 624 N Broadway, Rm 644, Baltimore, MD 21287 (jsegal@jhmi.edu).

Conflict of Interest Disclosures: Dr Segal reported receiving grants from the National Institutes of Health, Patient-Centered Outcomes Research Institute, National Institute for Health Care Management, and Arnold Foundation and personal fees from Gilead, and ProventionBio. No other disclosures were reported.
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