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Folat und Folsäure sind zwei verschiedene Formen der selben Vitamingruppe, des Vitamin B₉. Folat ist die natürlich vorkommende Form des Vitamins. Folsäure ist die synthetische Form, bzw. auch die chemisch einfachste Form, die vom Körper besser aufgenommen wird.

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https://www.dge.de/wissenschaft/referenzwerte/vitamin-d/?L=0

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Vitamin D (Calciferole)

Zuletzt überarbeitet: 2012

Vitamin D nimmt unter den Vitaminen eine Sonderstellung ein, da es sowohl über die Ernährung zugeführt als auch vom Menschen selbst durch UVB-Lichtexposition (Sonnenbestrahlung) gebildet wird. Die Zufuhr über die Ernährung mit den üblichen Lebensmitteln reicht nicht aus, um den Schätzwert für eine angemessene Zufuhr bei fehlender endogener Synthese zu erreichen, der die gewünschte Versorgung (25-Hydroxyvitamin-D-Serumkonzentration) in Höhe von mindestens 50 nmol/l sicherstellt. Die Differenz muss über die endogene Synthese und/oder über die Einnahme eines Vitamin-D-Präparats gedeckt werden. Bei häufiger Sonnenbestrahlung kann die gewünschte Versorgung ohne die Einnahme eines Vitamin-D-Präparats erreicht werden.
Schätzwerte für eine angemessene Vitamin-D-Zufuhr bei fehlender endogener Synthese

Alter

Vitamin D bei fehlender endogener Synthese µga/Tag

a1 µg = 40 Internationale Einheiten (IE); 1 IE = 0,025 µg

bDer Schätzwert wird durch Gabe einer Vitamin-D-Tablette zur Rachitisprophylaxe ab der 1. Lebenswoche bis zum Ende des 1. Lebensjahres bei gestillten und nicht gestillten Säuglingen erreicht. Die Gabe erfolgt unabhängig von der endogenen Vitamin-D-Synthese und der Vitamin-D-Zufuhr durch Frauenmilch bzw. Säuglingsmilchnahrungen. Die Prophylaxe sollte im 2. Lebensjahr in den Wintermonaten weiter durchgeführt werden (Deutsche Gesellschaft für Kinder- und Jugendmedizin).

c Die Vitamin-D-Zufuhr über die Ernährung mit den üblichen Lebensmitteln (1 bis 2 µg pro Tag bei Kindern, 2 bis 4 µg pro Tag bei Jugendlichen und Erwachsenen) reicht nicht aus, um die gewünschte Versorgung (25(OH)D-Serumkonzentration von mindestens 50 nmol/l) bei fehlender endogener Synthese sicherzustellen. Hierfür werden 20 µg/Tag benötigt. D. h., die Versorgung muss zusätzlich zur Zufuhr über die Ernährung über die endogene Synthese und/oder über die Einnahme eines Vitamin-D-Präparats sichergestellt werden. Bei häufiger Sonnenbestrahlung kann die gewünschte Vitamin-D-Versorgung ohne die Einnahme eines Vitamin-D-Präparats erreicht werden.

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Zuletzt überarbeitet: 2012 Vitamin D nimmt unter den Vitaminen eine Sonderstellung ein, da es sowohl über die Ernährung zugeführt als auch vom Menschen selbst durch UVB-Lichtexposition (Sonnenbestrahlung) gebildet wird. Die Zufuhr über die Ernährung mit den üblichen Lebensmitteln reicht nicht aus, um den Schätzwert für eine angemessene Zufuhr bei fehlender endogener Synthese zu erreichen, der die gewünschte Versorgung (25-Hydroxyvitamin-D-Serumkonzentration) in Höhe von mindestens 50 nmol/l sicherstellt.

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< 30 nmol/l : Vitamin D Mangel
> 50 nmol/l: ausreichend um Knochengesundheit sicherzustellen

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Ausgewählte Fragen und Antworten zu Vitamin D

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Gemeinsame FAQ des BfR, der DGE und des MRI vom 22. Oktober 2012 Vitamin D fördert die Aufnahme von Calcium aus dem Magen-Darm-Trakt sowie die Härtung des Knochens. Es hat Einfluss auf die Muskelkraft, reguliert den Calcium- und Phosphatstoffwechsel und ist auch an weiteren Stoffwechselvorgängen im Körper beteiligt.

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Inhaltsverzeichnis

Die top 10 Lebensmittel mit Vitamin D

Eine genaue Übersicht über die top 10 Lebensmittel gibt die folgende Auflistung:

Gehalt an Vitamin D (Mikrogramm pro 100 Gramm):

1. Hering aus dem Atlantik: 25,00

2. Lachs: 16,00

3. Eigelb (Huhn): 5,60

4. Makrele: 4,00

5. Hühnerei, gesamt: 2,90

6. Pfifferlinge: 2,10

7. Champignons: 1,90

8. Rinderleber: 1,70

9. Käse (Gouda, 45% F. i. Tr.): 1,30

10. Butter: 1,20

Was ist Vitamin D?

Im Unterschied zu anderen Vitaminen kann der menschliche Körper Vitamin D selbst bilden, und zwar in der Haut. Dort werden die bereits vorhandenen Vorstufen mithilfe von Sonnenlicht - oder genauer von UV-B-Strahlung - in Vitamin D umgewandelt. Bei ausreichend Sonnenbestrahlung kann der Mensch dadurch 80 bis 90 % seines Bedarfs decken. Den Rest (also etwa 10 bis 20 %) nimmt er über die Nahrung auf.

Wie hoch ist mein Vitamin-D-Tagesbedarf?

Um den Vitamin-D-Status eines Menschen festzustellen, messen Mediziner den Gehalt an 25-Hydroxyvitamin-D (Speicherform) im Blut. Dieser sollte mindestens 50 Nanomol pro Liter (nmol/l) Blut betragen - ein Wert, der als optimal für die Gesundheit der Knochen gilt. Liegt er bei 30 nmol/l oder darunter, sprechen Mediziner von einem Mangel.

von Dagmar von Cramm

"Vitamin D ist für die Calcium-Aufnahme aus dem Darm sehr wichtig. Fehlt es, kommt es zu einem Absinken der Calcium-Konzentration im Blut. Das wiederum führt dazu, dass vermehrt Calcium aus dem Knochen ausgebaut wird, um diesen Mangel im Blut auszugleichen. So bleibt der Calcium-Spiegel konstant - aber die Knochendichte sinkt. Vitamin D wird in erster Linie im Körper selbst über die Haut durch Sonneneinstrahlung hergestellt und in geringen Mengen über bestimmte Lebensmittel wie Hering, Lachs, Hühnereigelb, Makrele, Pfifferlinge, Champignons und Rinderleber aufgenommen. Für den Erhalt starker Knochen sollte der Vitamin-D-Status vor allem im Winter vom Arzt überprüft und bei einem Mangel durch Supplementation ausgeglichen werden."

Dagmar von Cramm,

Ökotrophologin und Food-Journalistin

Welche Folgen hat ein Vitamin-D-Mangel?

Ein Mangel kann verschiedene Ursachen haben. Er entsteht, wenn die Haut zu wenig Sonnenlicht abbekommt oder wenn im Winterhalbjahr die Sonnenstrahlung zu schwach ist, damit der Körper ausreichend Vitamin D produzieren kann.
Das Sonnenvitamin spielt für verschiedene Vorgänge im Körper eine wichtige Rolle:

Es kontrolliert den Kalzium- und Phosphatstoffwechsel und unterstützt die Aufnahme von Kalzium aus dem Darm. Diesen Mineralstoff kann der Körper anschließend in die Zähne und Knochen einbauen. Das macht sie stabil und fest.

Es wirkt sich positiv auf die Muskelkraft aus.

Es unterstützt das Immunsystem und ist an weiteren Stoffwechselvorgängen beteiligt.

Eine langfristig schlechte Versorgung kann schwere Folgen haben:

Vitamin-D-Mangel bei Babys:
Bei Säuglingen und Kindern führt ein Mangel an dem Sonnenvitamin zum Beispiel dazu, dass nicht ausreichend Mineralstoffe in die Knochen eingelagert werden: Sie bleiben weich und können sich dadurch dauerhaft verformen. Mediziner bezeichnen dieses Krankheitsbild als „Rachitis".

Vitamin-D-Mangel bei Erwachsenen:
Auch bei Erwachsenen kann eine Störung des Knochenstoffwechsels auftreten und die Knochen weich werden lassen (Osteomalazie). Das ist oft mit großen Schmerzen und Muskelschwäche verbunden. Bei älteren Menschen steigt durch einen Vitamin-D-Mangel zudem das Risiko, an Osteoporose (Knochenschwund) zu erkranken.

Unsere Empfehlung

Vitamin D von Donivital

Du hast einen Vitamin-D-Mangel? Die Kapseln von Donivital versorgen dich nicht nur mit dem Sonnenvitamin, sondern liefern auch gleichzeitig Calcium und Vitamin K2, was für die Aufnahme von Vitamin D im Körper unerlässlich ist. Für eine rundum Versorgung sind die Kapseln zusätzlich mit 8 weiteren Vitaminen und Mineralstoffe angereichert. Das Praktische: Die Kapseln müssen nur alle 5 Tage eingenommen werden!

Möglicherweise hat die Versorgung mit Vitamin D auch einen Einfluss auf verschiedene andere Krankheiten wie Bluthochdruck, Diabetes mellitus Typ 2, Herz-Kreislauf-Beschwerden oder Krebs. Dafür gibt es aber lediglich Hinweise, ein wissenschaftlicher Nachweis fehlt bislang.

Vitamin-D-Bedarf über die Ernährung decken

In welcher Form kommt Vitamin D in Lebensmitteln vor?

In der Gruppe der Calciferole sind zwei 2 besonders wichtig für den Körper:

Vitamin D2 (Ergocalciferol) kommt ausschließlich in pflanzlicher Nahrung vor. Der Körper kann dieses Molekül in Cholecalciferol umwandeln.

Vitamin D3 (Cholecalciferol) vor allem in Lebensmitteln enthalten, die aus tierischen Quellen stammen. In der Niere wandelt der Körper Cholecalciferol in das biologisch aktive Calcitriol um.

So viel Vitamin D ist in Nahrungsmitteln enthalten

Zu den Nahrungsmitteln, die besonders viel Vitamin D enthalten, gehören vor allem

fetter Fisch (wie z.B. Hering, Makrele, Aal, Lachs etc.),

Innereien wie Leber,

Eigelb und

bestimmte Speisepilze.

Vitamin D: Lebensmittel richtig lagern und zubereiten

Im Gegensatz zu vielen anderen Vitaminen ist Vitamin D relativ stabil. Das bedeutet, dass es nicht empfindlich auf äußere Einflüsse wie Licht, Sauerstoff oder Temperatur reagiert und sich zersetzt. Lebensmittel mit Vitamin D kann man daher ganz normal lagern, ohne einen großen Verlust befürchten zu müssen. Auch Kochen schadet ihm nicht, da es Temperaturen bis zu 180° C ohne Probleme übersteht.

Vitamin-D-Präparate: Wann sind sie sinnvoll?

Für gesunde, aktive Erwachsene ist der Nutzen von Vitamin-D-Präparaten sehr gering. In bestimmten Fällen können sie aber durchaus sinnvoll sein. Es gibt mehrere Risikofaktoren, die eine Unterversorgung begünstigen:

Lebensalter: Je älter ein Mensch ist, desto mehr verliert die Haut die Fähigkeit, Vitamin D zu bilden. Säuglinge dagegen sollten im ersten Lebensjahr keiner direkten Sonnenstrahlung ausgesetzt werden, sodass auch hier ein Mangel entstehen kann.

Pflegebedürftigkeit: Bettlägerige oder anderweitig in ihrer Mobilität eingeschränkte Personen können sich nur sehr selten im Freien aufhalten.

Religiöse oder kulturelle Gründe: Wenn ein Großteil der Haut im Freien bedeckt ist, kann das zur Produktion von Vitamin D nötige Sonnenlicht nicht auf die Haut gelangen.

Hautfarbe: Dunkle Haut hat einen höheren Gehalt an Melanin und bildet daher weniger Vitamin D als helle Haut.

Chronische Krankheiten: Bestimmte Erkrankungen (z. B. des Dünndarms, der Leber, der Nieren) können die Vitamin-D-Produktion stören.

Medikamente: Auch Medikamente (z. B. gegen Epilepsie) können die Vitamin-D-Bildung hemmen.

Wichtig: Die Einnahme von Vitamin-D-Präparaten sollte man unbedingt mit seinem Arzt absprechen. Er kann feststellen, ob tatsächlich ein Mangel vorliegt und ob eine entsprechende Therapie nötig ist.

Wer auf Verdacht Vitamin-D-Pillen schluckt, riskiert nicht nur eine Überdosierung mit unangenehmen Nebenwirkungen wie Kopfschmerzen, Übelkeit oder sogar Nierensteinen. Diese Präparate können auch die Wirkung anderer Medikamente beeinflussen. Das kann zum Teil gefährliche Folgen wie zum Beispiel Herzrhythmusstörungen haben.

Häufige Fragen zu Vitamin-D-Lebensmitteln

Durch Sonneneinstrahlung kann der menschliche Körper Vitamin D selbst bilden. Nur ein geringer Anteil (etwa 10-20 %) wird über die Ernährung aufgenommen. Lebensmittel mit viel Vitamin D sind meist tierischen Ursprungs (wie fetter Fisch, Eigelb oder bestimmte Innereien). Zu den wenigen pflanzlichen Quellen zählen vor allem bestimmte Speisepilze.

Die deutsche Gesellschaft für Ernährung empfiehlt, maximal 20 Mikrogramm Vitamin D pro Tag zu sich zu nehmen. Das gilt allerdings nur, wenn die körpereigene Produktion nicht stattfindet. Grundsätzlich ist es für gesunde, aktive Menschen nicht sinnvoll, Nahrungsergänzungsmittel mit Vitamin D zu schlucken. Denn eine Unterversorgung tritt in der Regel nur in bestimmten Fällen (z. B. Krankheit) auf.

Welche Symptome entstehen bei Vitamin-D-Mangel?

Bei einem echten Mangel leiden vor allem die Knochen. Verformungen, Schmerzen oder Muskelschwäche sind die Folgen. Auch das Risiko, an Osteoporose (Knochenschwund) zu erkranken, ist erhöht.

Quellen:

Deutsche Gesellschaft für Ernährung e.V. (2018), D-A-CH-Referenzwerte für die Nährstoffzufuhr, 2. Auflage, 4. aktualisierte Ausgabe, Bonn.

Deutsche Gesellschaft für Ernährung e.V. (2012), Ausgewählte Fragen und Antworten zu Vitamin D, https://www.dge.de/wissenschaft/weitere-publikationen/faqs/vitamin-d/, aufgerufen am 24.04.2020.

Robert Koch-Institut (2019), Antworten des Robert Koch-Instituts auf häufig gestellte Fragen zu Vitamin D, https://www.rki.de/SharedDocs/FAQ/Vitamin_D/Vitamin_D_FAQ-Liste.html,

. (2015), Die große GU Nährwert Kalorien Tabelle, Gräfe und Unzer Verlag, 2. Auflage , München.

Psychrembel Online (2018), Wiesenauer, Markus: Vitamin D, https://www.pschyrembel.de/Vitamin%20D/H00DT, aufgerufen am 28.04.2020.

Bundesinstitut für Risikobewertung (2014), Ausgewählte Fragen und Antworten zu Vitamin D, https://www.bfr.bund.de/de/ausgewaehlte_fragen_und_antworten_zu_vitamin_d-131898.html, aufgerufen am 28.04.2020.

Bundesinstitut für Risikobewertung (2017), Vitamin D - aus Sicht der Risikobewertung, https://mobil.bfr.bund.de/cm/343/vitamin-d-aus-sicht-der-risikobewertung.pdf, aufgerufen am 28.04.2020.

Bundesamt für Verbraucherschutz und Lebensmittelsicherheit (2017), Stellungnahme zur Bewertung von Vitamin- D-haltigen Produkten, https://www.bvl.bund.de/SharedDocs/Downloads/01_Lebensmittel/expertenkommission/Zweite_Stellungnahme_VitaminD_Revision1.1.html, aufgerufen am 28.04.2020.

Berufsverband Deutscher Internisten e.V. (2018), Vitamin-D-Mangel - ein Hype?, https://www.internisten-im-netz.de/aktuelle-meldungen/aktuell/vitamin-d-mangel-ein-hype.html,

Inhaltsverzeichnis

Die top 10 Lebensmittel mit Vitamin D

Eine genaue Übersicht über die top 10 Lebensmittel gibt die folgende Auflistung:

Gehalt an Vitamin D (Mikrogramm pro 100 Gramm):

1. Hering aus dem Atlantik: 25,00

2. Lachs: 16,00

3. Eigelb (Huhn): 5,60

4. Makrele: 4,00

5. Hühnerei, gesamt: 2,90

6. Pfifferlinge: 2,10

7. Champignons: 1,90

8. Rinderleber: 1,70

9. Käse (Gouda, 45% F. i. Tr.): 1,30

10. Butter: 1,20

Was ist Vitamin D?

Im Unterschied zu anderen Vitaminen kann der menschliche Körper Vitamin D selbst bilden, und zwar in der Haut. Dort werden die bereits vorhandenen Vorstufen mithilfe von Sonnenlicht - oder genauer von UV-B-Strahlung - in Vitamin D umgewandelt. Bei ausreichend Sonnenbestrahlung kann der Mensch dadurch 80 bis 90 % seines Bedarfs decken. Den Rest (also etwa 10 bis 20 %) nimmt er über die Nahrung auf.

Wie hoch ist mein Vitamin-D-Tagesbedarf?

Um den Vitamin-D-Status eines Menschen festzustellen, messen Mediziner den Gehalt an 25-Hydroxyvitamin-D (Speicherform) im Blut. Dieser sollte mindestens 50 Nanomol pro Liter (nmol/l) Blut betragen - ein Wert, der als optimal für die Gesundheit der Knochen gilt. Liegt er bei 30 nmol/l oder darunter, sprechen Mediziner von einem Mangel.

Welche Folgen hat ein Vitamin-D-Mangel?

Ein Mangel kann verschiedene Ursachen haben. Er entsteht, wenn die Haut zu wenig Sonnenlicht abbekommt oder wenn im Winterhalbjahr die Sonnenstrahlung zu schwach ist, damit der Körper ausreichend Vitamin D produzieren kann.
Das Sonnenvitamin spielt für verschiedene Vorgänge im Körper eine wichtige Rolle:

Es kontrolliert den Kalzium- und Phosphatstoffwechsel und unterstützt die Aufnahme von Kalzium aus dem Darm. Diesen Mineralstoff kann der Körper anschließend in die Zähne und Knochen einbauen. Das macht sie stabil und fest.

Es wirkt sich positiv auf die Muskelkraft aus.

Es unterstützt das Immunsystem und ist an weiteren Stoffwechselvorgängen beteiligt.

Eine langfristig schlechte Versorgung kann schwere Folgen haben:

Vitamin-D-Mangel bei Babys:
Bei Säuglingen und Kindern führt ein Mangel an dem Sonnenvitamin zum Beispiel dazu, dass nicht ausreichend Mineralstoffe in die Knochen eingelagert werden: Sie bleiben weich und können sich dadurch dauerhaft verformen. Mediziner bezeichnen dieses Krankheitsbild als „Rachitis".

Vitamin-D-Mangel bei Erwachsenen:
Auch bei Erwachsenen kann eine Störung des Knochenstoffwechsels auftreten und die Knochen weich werden lassen (Osteomalazie). Das ist oft mit großen Schmerzen und Muskelschwäche verbunden. Bei älteren Menschen steigt durch einen Vitamin-D-Mangel zudem das Risiko, an Osteoporose (Knochenschwund) zu erkranken.

Möglicherweise hat die Versorgung mit Vitamin D auch einen Einfluss auf verschiedene andere Krankheiten wie Bluthochdruck, Diabetes mellitus Typ 2, Herz-Kreislauf-Beschwerden oder Krebs. Dafür gibt es aber lediglich Hinweise, ein wissenschaftlicher Nachweis fehlt bislang.

Vitamin-D-Bedarf über die Ernährung decken

In welcher Form kommt Vitamin D in Lebensmitteln vor?

In der Gruppe der Calciferole sind zwei 2 besonders wichtig für den Körper:

Vitamin D2 (Ergocalciferol) kommt ausschließlich in pflanzlicher Nahrung vor. Der Körper kann dieses Molekül in Cholecalciferol umwandeln.

Vitamin D3 (Cholecalciferol) vor allem in Lebensmitteln enthalten, die aus tierischen Quellen stammen. In der Niere wandelt der Körper Cholecalciferol in das biologisch aktive Calcitriol um.

So viel Vitamin D ist in Nahrungsmitteln enthalten

Zu den Nahrungsmitteln, die besonders viel Vitamin D enthalten, gehören vor allem

fetter Fisch (wie z.B. Hering, Makrele, Aal, Lachs etc.),

Innereien wie Leber,

Eigelb und

bestimmte Speisepilze.

Vitamin D: Lebensmittel richtig lagern und zubereiten

Im Gegensatz zu vielen anderen Vitaminen ist Vitamin D relativ stabil. Das bedeutet, dass es nicht empfindlich auf äußere Einflüsse wie Licht, Sauerstoff oder Temperatur reagiert und sich zersetzt. Lebensmittel mit Vitamin D kann man daher ganz normal lagern, ohne einen großen Verlust befürchten zu müssen. Auch Kochen schadet ihm nicht, da es Temperaturen bis zu 180° C ohne Probleme übersteht.

Vitamin-D-Präparate: Wann sind sie sinnvoll?

Für gesunde, aktive Erwachsene ist der Nutzen von Vitamin-D-Präparaten sehr gering. In bestimmten Fällen können sie aber durchaus sinnvoll sein. Es gibt mehrere Risikofaktoren, die eine Unterversorgung begünstigen:

Lebensalter: Je älter ein Mensch ist, desto mehr verliert die Haut die Fähigkeit, Vitamin D zu bilden. Säuglinge dagegen sollten im ersten Lebensjahr keiner direkten Sonnenstrahlung ausgesetzt werden, sodass auch hier ein Mangel entstehen kann.

Pflegebedürftigkeit: Bettlägerige oder anderweitig in ihrer Mobilität eingeschränkte Personen können sich nur sehr selten im Freien aufhalten.

Religiöse oder kulturelle Gründe: Wenn ein Großteil der Haut im Freien bedeckt ist, kann das zur Produktion von Vitamin D nötige Sonnenlicht nicht auf die Haut gelangen.

Hautfarbe: Dunkle Haut hat einen höheren Gehalt an Melanin und bildet daher weniger Vitamin D als helle Haut.

Chronische Krankheiten: Bestimmte Erkrankungen (z. B. des Dünndarms, der Leber, der Nieren) können die Vitamin-D-Produktion stören.

Medikamente: Auch Medikamente (z. B. gegen Epilepsie) können die Vitamin-D-Bildung hemmen.

Wichtig: Die Einnahme von Vitamin-D-Präparaten sollte man unbedingt mit seinem Arzt absprechen. Er kann feststellen, ob tatsächlich ein Mangel vorliegt und ob eine entsprechende Therapie nötig ist.

Wer auf Verdacht Vitamin-D-Pillen schluckt, riskiert nicht nur eine Überdosierung mit unangenehmen Nebenwirkungen wie Kopfschmerzen, Übelkeit oder sogar Nierensteinen. Diese Präparate können auch die Wirkung anderer Medikamente beeinflussen. Das kann zum Teil gefährliche Folgen wie zum Beispiel Herzrhythmusstörungen haben.

Häufige Fragen zu Vitamin-D-Lebensmitteln

Durch Sonneneinstrahlung kann der menschliche Körper Vitamin D selbst bilden. Nur ein geringer Anteil (etwa 10-20 %) wird über die Ernährung aufgenommen. Lebensmittel mit viel Vitamin D sind meist tierischen Ursprungs (wie fetter Fisch, Eigelb oder bestimmte Innereien). Zu den wenigen pflanzlichen Quellen zählen vor allem bestimmte Speisepilze.

Die deutsche Gesellschaft für Ernährung empfiehlt, maximal 20 Mikrogramm Vitamin D pro Tag zu sich zu nehmen. Das gilt allerdings nur, wenn die körpereigene Produktion nicht stattfindet. Grundsätzlich ist es für gesunde, aktive Menschen nicht sinnvoll, Nahrungsergänzungsmittel mit Vitamin D zu schlucken. Denn eine Unterversorgung tritt in der Regel nur in bestimmten Fällen (z. B. Krankheit) auf.

Welche Symptome entstehen bei Vitamin-D-Mangel?

Bei einem echten Mangel leiden vor allem die Knochen. Verformungen, Schmerzen oder Muskelschwäche sind die Folgen. Auch das Risiko, an Osteoporose (Knochenschwund) zu erkranken, ist erhöht.

Quellen:

Deutsche Gesellschaft für Ernährung e.V. (2018), D-A-CH-Referenzwerte für die Nährstoffzufuhr, 2. Auflage, 4. aktualisierte Ausgabe, Bonn.

Deutsche Gesellschaft für Ernährung e.V. (2012), Ausgewählte Fragen und Antworten zu Vitamin D, https://www.dge.de/wissenschaft/weitere-publikationen/faqs/vitamin-d/, aufgerufen am 24.04.2020.

Robert Koch-Institut (2019), Antworten des Robert Koch-Instituts auf häufig gestellte Fragen zu Vitamin D, https://www.rki.de/SharedDocs/FAQ/Vitamin_D/Vitamin_D_FAQ-Liste.html,

. (2015), Die große GU Nährwert Kalorien Tabelle, Gräfe und Unzer Verlag, 2. Auflage , München.

Psychrembel Online (2018), Wiesenauer, Markus: Vitamin D, https://www.pschyrembel.de/Vitamin%20D/H00DT, aufgerufen am 28.04.2020.

Bundesinstitut für Risikobewertung (2014), Ausgewählte Fragen und Antworten zu Vitamin D, https://www.bfr.bund.de/de/ausgewaehlte_fragen_und_antworten_zu_vitamin_d-131898.html, aufgerufen am 28.04.2020.

Bundesinstitut für Risikobewertung (2017), Vitamin D - aus Sicht der Risikobewertung, https://mobil.bfr.bund.de/cm/343/vitamin-d-aus-sicht-der-risikobewertung.pdf, aufgerufen am 28.04.2020.

Bundesamt für Verbraucherschutz und Lebensmittelsicherheit (2017), Stellungnahme zur Bewertung von Vitamin- D-haltigen Produkten, https://www.bvl.bund.de/SharedDocs/Downloads/01_Lebensmittel/expertenkommission/Zweite_Stellungnahme_VitaminD_Revision1.1.html, aufgerufen am 28.04.2020.

Berufsverband Deutscher Internisten e.V. (2018), Vitamin-D-Mangel - ein Hype?, https://www.internisten-im-netz.de/aktuelle-meldungen/aktuell/vitamin-d-mangel-ein-hype.html,

# data[].attributes.attachment_link.title
Vitamin-D-Lebensmittel: Die Top 10 mit hohem Gehalt | eatbetter: gesunde, einfache Rezepte & Tipps für jeden Tag

# data[].attributes.attachment_link.description
Inhaltsverzeichnis Eine genaue Übersicht über die top 10 Lebensmittel gibt die folgende Auflistung: Gehalt an Vitamin D (Mikrogramm pro 100 Gramm): Hering aus dem Atlantik: 25,00 Lachs: 16,00 Eigelb (Huhn): 5,60 Makrele: 4,00 Hühnerei, gesamt: 2,90 Pfifferlinge: 2,10 Champignons: 1,90 Rinderleber: 1,70 Käse (Gouda, 45% F. i.

# data[].attributes.body
Nur etwa 10-20% des benötigten Vitamin Ds werden mit Nahrungsmitteln aufgenommen. Der Rest stammt aus endogener Synthese unter Sonneneinstrahlung.
Eine Bestimmung des Vitamin D Statuses über eine Ernährungsanamnese ist in dem Fall also nicht sinnvoll.

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Wie viel wissen Sie über Vitamine & Mineralstoffe?

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Wie viel wissen Sie über Vitamine & Mineralstoffe?

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3.Which micronutrient can help our bodies absorb iron better?

Answer: B. Vitamin C. Eating vitamin C-rich food sources C (like bell peppers, citrus fruit, etc.) together with iron-rich meals can help our body better absorb iron, especially non-haem iron found in plant-based foods. However, this effect is dependent on other factors such as one's iron levels and the make-up of the meal (e.g. the presence of nutrients with the opposite effect).

That is not the right answer. Try again!

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3.Which micronutrient can help our bodies absorb iron better? Answer: B. Vitamin C. Eating vitamin C-rich food sources C (like bell peppers, citrus fruit, etc.) together with iron-rich meals can help our body better absorb iron, especially non-haem iron found in plant-based foods.

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Pregnancy | Eufic
Iron: foods, functions, how much do you need & more | Eufic

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The European Food Information Council : Food facts for healthy choices

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EUFIC is a non-profit organisation that provides clear, practical information on food and health, based on sound science. We believe in a world where people choose to live healthily because they know how to.

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empfohlene Eisenzufuhr für Schwangere: 30mg/Tag
Stillende: 20mg/Tag
Sehr viel!

erhöhter Bedarf: wird für den heranwachsenden Fetus, Plazenta und vermehrtes Blutvolumen benötigt.

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Eisenhaltige Lebensmittel: Die 60 besten Eisenquellen

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Es gibt 5 hemmende Faktoren die den Körper daran hindern, Eisen aus Lebensmitteln aufzunehmen. Wie stark der Einfluss dieser Hemmer (Eiseninhibitoren) ist, wird wissenschaftlich noch diskutiert und leider bringen diese Fakten teilweise Widersprüche mit sich, weil auch Lebensmittel mit viel Eisen gleichzeitig Hemmer enthalten.

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Richtige Ernährung in der Schwangerschaft ist nicht nur für das Baby wichtig, sondern auch für die Mutter. Hier erhalten Sie alle Infos rund ums Thema.

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Inhalte: Vitamin D S. 363, Folsäure S. 363f, Eisen S.364

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Ernährung fürs Leben: Ein Seminar über Ernährung in der Schwangerschaft und Stillzeit

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Schwangere und Stillende Personen befinden sich in einer Phase, bei dem der Körper andere Bedürfnisse hat, um die gesunde Entwicklung eines neuen Lebens sicherzustellen. Der Energiebedarf erhöht sich, zudem steigt auch der Bedarf einzelner Nährstoffe um ein Vielfaches. In diesem Seminar wird praxisbezogen über die Ernährungsbedürfnisse von Schwangeren und Stillenden aufgeklärt.

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Dieses Seminar richtet sich an Schwangere und Stillende, sowie Menschen mit Kinderwunsch, als auch an jene, die Personen in diesen Phasen unterstützen möchten.

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Energiebedarf für Schwangere und Stillende

Nährstoffbedarf für Schwangere und Stillende (bei Interesse auch bei vegetarischer und veganer Ernährung)

Flüssigkeitsbedarf für Schwangere und Stillende

Fokus auf die Vitamine/ Mineralstoffe: Eisen, Folsäure & Vitamin D in der Schwangerschaft und Stillzeit, ...

Nährstoffsupplemente/ Präperate in der Schwangerschaft

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Kritische Nährstoffe für Schwangere und Stillende kennen
K1.1
Die kritischen Nährstoffe für Schwangere/Stillende benennen können
K1.2
Lebensmittel bzw. Speisenbeispiele zu den kritischen Nährstoffen kennen.

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Die Kritischen Nährstoffe für Stillende/Schwangere den Lebensmitteln zuordnen können
K2.1
Auf einer Lebensmittelliste relevante Lebensmittel herausheben können

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Überlegungen über Speisen anstellen, die auf die Bedürfnisse von Schwangeren und Stilenden angepasst sind und diese umsetzen können.
P1.1
Speisen und Beilagen mit den relevanten Nährstoffen auflisten können

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Anhand des Gelernten, Präperate nach Relevanz  bewerten können.
P2.1
In einer Apotheke geeignete Präperate auswählen können.

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Die Teilnehmer*innen wissen über den Nährstoff- und Energiebedarf von Schwangeren und Stillenden bescheid.

Die Teilnehmer*innen wissen  auf welche Nährstoffe in der Schwangerschaft und Stillzeit besonders geachtet werden muss.

Die Teilnehmer*innen können gelerntes anwenden und wissen wie sie den Nährstoff- und Energiebedarf im Alltag erreichen können.

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Take the quiz

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Dive into the world of vitamins and minerals and find out how micronutrients work in our bodies and how we can get them from our diet!

Explore all vitamins & minerals

Discover more information on individual vitamins and minerals.

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Take the quiz Dive into the world of vitamins and minerals and find out how micronutrients work in our bodies and how we can get them from our diet! Discover more information on individual vitamins and minerals.

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Mo, 22.5.2023 08:45 - 10:00
Einführungsvortrag zum Thema Energiebedarf und allgemeine Informationen über den Nährstoffbedarf

Di, 23.5.2023 10:00 - 11:15
Vitamin A, Vitamin B 12, Jod

Mi, 24.5.2013 08:45 - 10:00
Eisen, Folsäure, Vitamin D

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Sich den kritischen Nährstoffen für Schwangere/Stillende bewusst werden
A1.1
Die kritischen Nährstoffe in einzelnen Lebensmitteln wiedererkennen können
A1.2
Quantität der besagten Nährstoffe in Lebensmitteln wahrnehmen

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Das Seminar findet in den Räumlichkeiten der FH Campus Wien statt. (C.Z.13)

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Das Seminar wird kostenlos angeboten und ist für alle zugänglich, die an dem Thema interessiert sind.

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An der Auseinandersetzung mit der Ernährung für Schwangere gefallen finden
A2.1
An weiteren Informationen zum Thema Ernährung in der Schwangerschaft interessiert sein

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Dieses Seminar wird von Studierenden im zweiten Semester des Studiengangs Diätologie der FH Campus Wien durchgeführt.

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This is the place to be if you're trying to participate in a live poll

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Kevin D Cashman, 3, 4,* Kirsten G Dowling, ³ Zuzana Škrabáková, ³ Marcela Gonzalez-Gross, 6, ⁷ Jara Valtueña, ⁶ Stefaan De Henauw, ⁸ Luis Moreno, ⁹ Camilla T Damsgaard, ¹⁰ Kim F Michaelsen, ¹⁰ Christian Mølgaard, ¹⁰ Rolf Jorde, ¹¹ Guri Grimnes, ¹¹ George Moschonis, ¹² Christina Mavrogianni, ¹² Yannis Manios, ¹² Michael Thamm, ¹³ Gert BM Mensink, ¹³ Martina Rabenberg, ¹³ Markus A Busch, ¹³ Lorna Cox, ¹⁴ Sarah Meadows, ¹⁴ Gail Goldberg, ¹⁴ Ann Prentice, ¹⁴ Jacqueline M Dekker, ¹⁵ Giel Nijpels, ¹⁶ Stefan Pilz, ¹⁸ Karin M Swart, ¹⁵ Natasja M van Schoor, ¹⁵ Paul Lips, ¹⁷ Gudny Eiriksdottir, ¹⁹ Vilmundur Gudnason, 19, ²⁰ Mary Frances Cotch, ²¹ Seppo Koskinen, ²³ Christel Lamberg-Allardt, ²⁴ Ramon A Durazo-Arvizu, ²⁵ Christopher T Sempos, ²² and Mairead Kiely 3, ⁵

Abstract

Background: Vitamin D deficiency has been described as being pandemic, but serum 25-hydroxyvitamin D [25(OH)D] distribution data for the European Union are of very variable quality. The NIH-led international Vitamin D Standardization Program (VDSP) has developed protocols for standardizing existing 25(OH)D values from national health/nutrition surveys.

Objective: This study applied VDSP protocols to serum 25(OH)D data from representative childhood/teenage and adult/older adult European populations, representing a sizable geographical footprint, to better quantify the prevalence of vitamin D deficiency in Europe.

Design: The VDSP protocols were applied in 14 population studies [reanalysis of subsets of serum 25(OH)D in 11 studies and complete analysis of all samples from 3 studies that had not previously measured it] by using certified liquid chromatography-tandem mass spectrometry on biobanked sera. These data were combined with standardized serum 25(OH)D data from 4 previously standardized studies (for a total n = 55,844). Prevalence estimates of vitamin D deficiency [using various serum 25(OH)D thresholds] were generated on the basis of standardized 25(OH)D data.

Results: An overall pooled estimate, irrespective of age group, ethnic mix, and latitude of study populations, showed that 13.0% of the 55,844 European individuals had serum 25(OH)D concentrations <30 nmol/L on average in the year, with 17.7% and 8.3% in those sampled during the extended winter (October-March) and summer (April-November) periods, respectively. According to an alternate suggested definition of vitamin D deficiency (<50 nmol/L), the prevalence was 40.4%. Dark-skinned ethnic subgroups had much higher (3- to 71-fold) prevalence of serum 25(OH)D <30 nmol/L than did white populations.

Conclusions: Vitamin D deficiency is evident throughout the European population at prevalence rates that are concerning and that require action from a public health perspective. What direction these strategies take will depend on European policy but should aim to ensure vitamin D intakes that are protective against vitamin D deficiency in the majority of the European population.

Keywords: vitamin D deficiency, prevalence, 25(OH)D, standardized, Europe

See corresponding editorial on page 957.

INTRODUCTION

Vitamin D is the nutrient that has captured the attention of the scientific and medical communities, regulatory agencies, the food industry, and the public alike over the past 15 y. This is evidenced by the explosion of scientific literature, a dramatic increase in physician-requested tests for patient vitamin D status in some countries, a number of authoritative re-evaluations of dietary recommendations, and sales of vitamin D supplements and the increased number of vitamin D-fortified food products coming on the market. Vitamin D deficiency has been described as being pandemic ( 1), with associated direct and indirect costs for Europe estimated to be running at hundreds of billion Euro ( 2).

Vitamin D deficiency has been variably defined as possessing a serum 25-hydroxyvitamin D [25(OH)D,26 the biochemical index of vitamin D status ( 3)] concentration <25 to <75 nmol/L ( 4). Knowledge of the distributions of serum 25(OH)D concentrations in representative populations, with appropriate consideration of sex, life stage, ethnicity, and seasonality, is critical for the quantification of vitamin D deficiency as well as for devising effective strategies for its prevention ( 4, 5). However, serum 25(OH)D distribution data for the European Union are of variable quality, making it difficult to estimate the prevalence of vitamin D deficiency across member states. For example, a recent systematic review of vitamin D status in populations worldwide clearly showed that the variability in mean serum 25(OH)D concentrations across European countries was large, and even within a country, the variability from different studies ranged from 10% to 300% ( 6). Although there are many likely contributory reasons for differences in vitamin D deficiency prevalence estimates between populations, differences in analytic method for serum 25(OH)D are likely to contribute ( 4). In addition, several reports have shown that available 25(OH)D assays can yield markedly differing results ( 7- 10).

Calls have been made to use centralized laboratories to make an international comparison of serum 25(OH)D and vitamin D deficiency prevalence estimates more reliable ( 11), but this approach might not be feasible, given existing national structures and systems. As a consequence of these widespread, method-related differences in results of serum 25(OH)D ( 7- 10), the NIH-led international Vitamin D Standardization Program (VDSP) developed protocols for standardizing 25(OH)D measurement in national health/nutrition surveys around the world, as have been described in detail elsewhere ( 4, 12). Their recent application to serum 25(OH)D data from the Irish National Adult Nutrition Survey showed that the yearly prevalence of serum 25(OH)D <30 nmol/L [the US Institute of Medicine's definition of vitamin D deficiency ( 13)] increased from 6.5% (via the original immunoassay measurement) to a projected 11.4% ( 14). Importantly, reanalysis of all serums in the survey ( n = 1118) by our certified liquid chromatography-tandem mass spectrometry (LC-MS/MS) method confirmed the true prevalence estimate as 11.2%, which was almost twice as high as the immunoassay-based estimate and almost identical to the VDSP projection ( 14).

Thus, the VDSP approach, if coupled with key representative population studies, provides the potential for generation of prevalence estimates of vitamin D deficiency in Europe by using standardized serum 25(OH)D data. This would permit quantification of the magnitude of the public health problem and a solid platform on which to build public health policy aimed at preventing vitamin D deficiency in Europe. Accordingly, our objective was to apply the VDSP protocols to existing serum 25(OH)D data from 18 key (identified nationally or regionally) representative studies of European children, teenagers, adults, and older adults ( n = 55,844 individuals).

METHODS

Studies included and categorizations applied

Within the VDSP, nationally representative nutrition and health surveys are prioritized; however, some member states in Europe do not have such surveys with nationally representative data on serum 25(OH)D concentrations. Thus, in the absence of such data, well-curated samples from regionally representative health surveys can also achieve some degree of population coverage. Our present work is part of the European Commission-funded integrated project, Food-based solutions for optimal vitamin D nutrition and health through the life cycle (ODIN; www.odin-vitd.eu). One of the primary aims of ODIN was to quantify the prevalence of vitamin D deficiency in European populations by using standardized serum 25(OH)D values as a key prioritized existing knowledge gap. The project included a number of identifiable nationally representative nutrition and health surveys in addition to regionally representative health surveys from various European member states and of different life stage groups, which were of strategic importance for European coverage (a brief description of each of the studies, including their full names, acronyms, and country of origin, is provided in the Supplemental Material). The 14 European childhood and teenage as well as adult and older adult study populations, identified as a priority to obtain data on standardized serum 25(OH)D data, are as follows:

1. Healthy Lifestyle in Europe by Nutrition in Adolescence study (9 European countries) ( 15, 16)

2. Optimal well-being, development and health for Danish children through a healthy New Nordic Diet School Meal Study (Denmark) ( 17, 18)

3. Tromsø Study: Fit Futures (Norway) ( 19- 21)

4. Healthy Growth Study (Greece) ( 22)

5. Infant's Nourishment and Nutritional Status study (Greece) ( 23)

6. Cork BASELINE Birth Cohort Study (Ireland) ( 24)

7. German Health Interview and Examination Survey for Children and Adolescents (Germany) ( 25)

8. National Diet and Nutrition Survey (NDNS): Years 1-4 (combined) of the Rolling Program (2008/2009-2011/12) (United Kingdom) ( 26)

9. German Health Interview and Examination Survey for Adults (Germany) ( 27, 28)

10. Tromsø Study-6th Survey (Tromsø 6) (Norway) ( 19, 29- 31)

11. New Hoorn Study (Netherlands) ( 32)

12. Longitudinal Aging Study Amsterdam (Netherlands) ( 33)

13. Age, Gene/Environment Susceptibility-Reykjavik study (Iceland) ( 34)

14. Finnish Migrant Health and Wellbeing Study (Maamu) (Finland) ( 35, 36)

The key summary demographic characteristics (age, sex distribution, ethnicity, and season of blood sampling) of these 14 studies are shown in Table 1 . We also had vitamin D deficiency prevalence data from 4 additional European studies, on which we had previously standardized serum 25(OH)D data by using the same VDSP approach ( 14, 37), and we combined these data with data from the 14 new studies in generating a pooled estimate in the present work. The descriptions of these other 4 studies [National Adult Nutrition Survey, Ireland; Health 2011, Finland; HUBRO (Oslo Health Study), Oslo, Norway; and Health2006, Copenhagen, Denmark] have been reported in detail elsewhere ( 14, 37). None of the 18 studies included pregnant women or older adults in care homes.

TABLE 1

Study [year(s) of study] (ref)

Region/country (latitude)
N
Age, y

Sex, female:male, %

Ethnicity, white:nonwhite, %

Season of sampling, %

Original 25(OH)D method

HELENA [2006-2007] ( 15, 16)

10 EU Centres ² (35-59°N)

1006

14.7 ± 1.2 (12.5-17.4) ³

53.2:46.8

93.3:4.8 ⁴

Winter: 21.9

IDS ELISA

Spring: 45.6

Summer: 9.0

Autumn: 23.5

OPUS School Meal Study [2011-2012] ( 17, 18)

Eastern Denmark (54-55°N) (regionally representative)

779 ⁵

10.0 ± 0.6 (8.4-11.6) ⁵

47.8:52.2 ⁵

94.7:5.3 ⁵

Baseline visit ⁵

DiaSorin Liaison

Winter: 0.0

Spring: 2.7

Summer: 97.3

Autumn: 0.0

Tromsø Study: Fit Futures [2010-2011] ( 19- 21)

Tromsø/Norway (69°N) (regionally representative)

890

16.0 ± 1.0 (15.0-18.0)

46.6:53.4

97.1:1.9 ⁴

Winter: 45.7

LC-MS/MS

Spring: 24.2

Summer: 0.0

Autumn: 30.1

Spring: 51.1

Summer: 1.9

Autumn: 25.7

Spring: 36.5

Summer: 0.4

Autumn: 25.7

Spring: 24.7

Summer: 22.2

Autumn: 30.9

Spring: 21.9

Summer: 24.3

Autumn: 29.4

NDNS: Rolling Program Years 1-4 [2008-2012] ( 26)

United Kingdom (50-59°N) (nationally representative)

511 ⁶

11.6 ± 4.7 (1-18) ⁶

45.4:54.6 ⁶

87.7:12.3 ⁶

Winter: 25.4 ⁶

DiaSorin Liaison

Spring: 25.6

Summer: 23.7

Autumn: 25.2 ⁴

NDNS: Rolling Program Years 1-4 [2008-2012] ( 26)

United Kingdom (50-59°N) (nationally representative)

977 ⁶

50.5 ± 16.0 (19-91) ⁶

53.4:46.6 ⁶

93.2:6.8 ⁶

Winter: 24.1 ⁶

DiaSorin Liaison

Spring: 26.0

Summer: 25.3

Autumn: 24.7 ⁴

DEGS [2008-2011] ( 27, 28)

Germany (47-55°N) (nationally representative)

6995

50.6 ± 16.6 (18-79)

52.0:48.0

NA

Winter: 22.7

DiaSorin Liaison

Spring: 24.8

Summer: 20.9

Autumn: 31.6

Tromsø Study-6th Survey [2008] ( 29- 31)

Norway (69°N) (regionally representative)

12,817

57.5 ± 12.6 (30-87)

46.7:53.3

100.0:0.0

Winter: 24.6

Roche ECLIA

Spring: 21.4

Summer: 16.3

Autumn: 37.7

Spring: 14.2

Summer: 26.3

Autumn: 33.3

LASA [2009] ( 33)

Netherlands (52°N) (nationally representative)

915

71.4 ± 7.7 (61-99)

53.4:46.6

96.8:3.0 ⁴

Winter: 7.5

DiaSorin Liaison

Spring: 28.8

Summer: 40.2

Autumn: 22.8 ⁴

Spring: 26.5

Summer: 15.1

Autumn: 32.9

Finnish Migrant Health and Wellbeing Study (Maamu) [2010-2012] ( 35, 36)

Finland (60-63°N) (representative of the immigrant populations in 6 Finnish cities)

1310

37.0 ± 12.0 (18-64)

56.5:43.5

Ethnic ⁷

Winter: 32.2

Architect chemiluminscent

Spring: 32.5

Summer: 12.4

Autumn: 23.9

Winter and spring represent the seasons during which vitamin D status declines and reaches its nadir, typically in late winter/early spring ( 38). Thus, the present work applied a wider definition capturing an extended winter (i.e., November-March) and an extended summer period (i.e., April-October), where appropriate. In the present work, we classified population samples as being of young children if the participants were aged 1-6 y, older children as 7-14 y, and teenagers as 15-18 y, in line with that applied by the European Food Safety Agency in their Dietary Reference Values ( 39). Adult populations were those with participants aged ≥19 y.

Categories of ethnicity varied across the population samples, and thus in the present work, a "white" and "nonwhite" categorization was applied. The nonwhite category included those recorded as being black, Asian, or other, including mixed race. The exception to this categorization was within the ethnic Maamu sample, where the study, by design, included 3 Finnish ethnic immigrant groups: white Russian speaking, Kurdish, and Somali ( 36). Details of the method used for the original serum/plasma total 25(OH)D analysis are also shown in Table 1 .

Applying the VDSP protocol for standardization of serum 25(OH)D data from past surveys to the study populations

The VDSP protocol for standardization of serum 25(OH)D data from past surveys, as used by some of us previously on the Irish national serum 25(OH)D data ( n = 1118) ( 14) and that of Finnish white adults ( n = 4102) ( 37), as well as regionally representative adult samples in Copenhagen, Denmark ( n = 3409), and Oslo, Norway ( n = 1042) ( 37), and again in this study, are outlined in detail elsewhere ( 4, 12) but can be briefly summarized as follows: the protocols conduct a within-quartile uniform sampling procedure of the serum 25(OH)D data from the entire survey sample ( 40) to select a subset of 100-175 biobanked serum samples for reanalysis of 25(OH)D by a standardized and certified LC-MS/MS method, which is traceable to the National Institute of Standards and Technology higher-order Reference Measurement Procedure ( 4, 12). The results are used to develop master regression equations, which then recalibrate the existing 25(OH)D data set for the entire survey sample.

The LC-MS/MS method at University College Cork used in this study for all samples, except those from the United Kingdom's NDNS, is certified by the CDC's Vitamin D Standardization Certification Program ( 41). Because the LC-MS/MS method at the NDNS laboratory at the Medical Research Council Human Nutrition Research Unit, Cambridge, was also standardized against the National Institute of Standards and Technology higher-order Reference Measurement Procedure through the VDSP, this was used for their sample reanalysis to use the biobanked samples as efficiently as possible [ R ² = 0.997; University College Cork measured (25[OH]D) = 0.968 × Human Nutrition Research Unit measured (25[OH]D) + 0.806; n = 50 (VDSP Seattle sera [ 4])].

In addition to the 11 studies for which the existing serum 25(OH)D data were standardized, the biobanked sera from 3 study populations (Infant's Nourishment and Nutritional Status, BASELINE, and New Hoorn Study) were analyzed de novo by the certified LC-MS/MS method and thus did not require a calibration equation. The standardized data from 14 studies included in the present work ( n = 46,173) plus the 4 studies previously standardized by us with the VDSP approach ( n = 9671) ( 14, 37) were used in estimating prevalence. In both human serum and plasma, 25(OH)D metabolites have been shown to be stable when stored frozen ( 42) and when subjected to multiple freeze-thaw cycles ( 43). In addition, Hollis ( 44) has reported that long-term (>10-y) storage of pooled human 25(OH)D internal controls at −20°C led to no detectable degradation of 25(OH)D.

Serum 25(OH)D thresholds

Original and standardized serum 25(OH)D concentrations were compared with cutoffs for 25(OH)D as per the US Institute of Medicine Dietary Reference Intake committee's definitions: persons are at risk of deficiency at serum 25(OH)D concentrations <30 nmol/L, whereas 40 and 50 nmol/L are consistent with that needed by 50% and 97.5% of individuals aged >1 y, respectively, in terms of bone health ( 13). In addition, a serum 25(OH)D concentration <25 nmol/L has also been a traditional cutoff used in Europe to define vitamin D deficiency on the basis of metabolic bone disease ( 45, 46) and thus was also included. Because the Task Force for the Clinical Guidelines Subcommittee of The Endocrine Society has suggested that to maximize the effect of vitamin D on calcium, bone, and muscle metabolism, serum 25(OH)D concentration should exceed 75 nmol/L ( 47), we also used this cutoff for comparison purposes. The same task force suggests <50 nmol/L as vitamin D deficiency ( 47).

Data and statistical analysis

Data and statistical analysis was conducted by using STATA 12 (StataCorp LP) and CBStat5 (Kristian Linnet). A statistical algorithm, developed within the VDSP and published recently ( 40), for estimating the number of stored samples that need to be reanalyzed was used. The maximum projected sample size of stored serum samples required for the VDSP protocol and with this collection of population studies was calculated by using procedures for the estimation of the predicted LC-MS/MS-based 25(OH)D value for a given serum 25(OH)D value from the original method of analysis (e.g., immunoassay or LC-MS/MS) with a predefined precision of a 95% CI, as has been described elsewhere ( 14, 37). At the beginning of the work, once preliminary data on the current collection of population samples were available [e.g., CV of assays and spread within distribution of original serum 25(OH)D data], a projected maximum sample size of 175 sera was estimated as being sufficient to meet and, indeed, exceed the needs of the study with the highest number of sera required for standardization. Thus, for logistical considerations in dealing with multiple partner laboratories and groups within the project, all groups were requested to supply 175 stored serum samples. However, this projected maximum was confirmed as being more than sufficient for each individual study on receipt of their full existing serum 25(OH)D data files (post hoc analysis showed that sample size ranged from 60 to 155 sera being required). Regression models [ordinary least squares and Deming (weighted and unweighted) and piecewise] were used to establish the relation between the originally measured and the LC-MS/MS reanalyzed serum 25(OH)D in the subsets, as described elsewhere ( 14, 37). Piecewise regression is a method in regression analysis in which the independent variable is partitioned into intervals and a separate line segment is fit to each interval. A Deming regression model is an errors-in-variables model that tries to find the line of best fit for a 2-dimensional data set. It differs from the simple linear regression, such as the ordinary least squares models, in that it accounts for errors in observations on the x and y axes. We report prevalence as a yearly mean (i.e., arising from blood sampling of participants that has occurred throughout the year), as well as by extended winter and summer season, as appropriate.

RESULTS

The relation between serum 25(OH)D in the statistical algorithm-defined subsets of serum samples from the 11 study populations, as measured by their original methods and reanalyzed by a certified LC-MS/MS method, is shown in Table 2 and Supplemental Figures 1 and 2. Seven study populations (which included the NDNS "old" and "new" assay formulation subsets separately; see Supplemental Material) required a piecewise regression fit between the previously measured and LC-MS/MS remeasured serum 25(OH)D concentrations. A further 6 study populations (which included the Tromsø 6 smoker and nonsmoker subsets separately) required a Deming (unweighted or weighted) regression fit between the previously measured and LC-MS/MS remeasured serum 25(OH)D concentrations. These calibration equations were applied to the entire 25(OH)D data set for the respective studies producing the standardized serum 25(OH)D data sets.

TABLE 2

If Rval ≤ value ³

If Rval > value ³

Study ( n) ² (ref)

Model type

Value

Intercept 1

X 1

Value

Intercept 2

X 2
R ²

NDNS (Old) (91) ⁴ ( 26)

Piecewise

62.1396

4.3376

0.9719

62.1396

28.0068

0.5910

0.82

NDNS (New) (115) ⁴ ( 26)

Piecewise

83.5082

1.2955

1.0380

83.5082

30.3591

0.6900

0.95

Weighted Deming

-

12.5531

0.9547

-

-

-

0.81

Unweighted Deming

-

−0.7299

0.9047

-

-

-

0.75

That 13.0% of the 55,844 young and adult European individuals had a yearly mean standardized serum 25(OH)D <30 nmol/L [the US Institute of Medicine's definition of vitamin D deficiency ( 13)] was highlighted by the present overall pooled estimate of 18 studies [i.e., 14 standardized in the present work plus the 4 previously standardized ( 14, 37)], irrespective of age group, ethnic mix, and latitude of study populations. Among those tested in the extended winter and summer periods, it was 17.7% and 8.2%, respectively. Using the alternately suggested definition of vitamin D deficiency of <50 nmol/L, as per the US Endocrine Society ( 47), the yearly prevalence was 40.4%.

The mean, SD, median, and 5th, 25th, 75th, and 95th percentiles of serum 25(OH)D concentration using standardized serum 25(OH)D data in the childhood and teenage as well as adult and older adult study samples separately are shown in Table 3 . The equivalent data [but based on originally analyzed serum 25(OH)D data for the 11 studies standardized in the present work] are also shown in Table 3 . The prevalence estimates for serum 25(OH)D concentration below the variously proposed public health-relevant thresholds, using standardized and unstandardized serum 25(OH)D data in the childhood and teenage as well as adult and older adult study samples separately, are shown in Table 4 . These findings highlight population subgroups within Europe at higher risk of vitamin D deficiency. Within the Finnish Maamu sample, the prevalence of serum 25(OH)D <30 nmol/L was 4.5%, 28.0%, and 50.4% for white Russian-speaking, Somali, and Kurdish immigrant subgroups ( n = 446, 364, and 50), respectively. Likewise, although with more limited numbers, the prevalence among the ∼12% nonwhite participants in the United Kingdom's NDNS (subset aged 1-18 y) was much higher (42.9%; n = 63) compared with that in the equivalently aged white young individuals (15.0%, n = 448). Because the nonwhite proportion of the populations in all other studies was <7%, the prevalence estimates by ethnicity were not reported, but in all cases, estimates for nonwhite adult and older adults were higher compared with that of the equivalently aged white individuals within a study population (data not shown).

TABLE 3

Percentile

Study (country) (ref)
N
Serum 25(OH)D, nmol/L, via

Mean

SD

Median

5th

25th

75th

95th

1006

Original

58.3

22.6

56.0

24.9

43.3

70.6

98.0

VDSP-Calibrated

49.2 (46.8, 51.6) ³

15.3 (15.3, 15.4)

50.2 (48.1, 52.2)

22.0 (18.9, 25.1)

38.5 (36.7, 40.4)

61.2 (58.5, 63.8)

71.2 (68.8, 73.6)

KiGGS ⁴ (Germany) ( 25)

10,015

Original

47.8

27.5

42.5

14.4

29.3

61.4

97.8

NDNS (1-18 y) ⁴,⁵ (United Kingdom) ( 26)

511

Original

47.1

22.0

45.1

15.1

30.7

61.9

87.9

NDNS (≥19 y) ⁴,⁵ (United Kingdom) ( 26)

977

Original

44.8

22.6

41.4

14.1

26.7

59.8

86.5

6995

Original

46.3

24.6

43.0

14.0

28.0

60.0

90.0

TABLE 4

Percentage below thresholds, nmol/L

Study (country) (ref)
N
Serum 25(OH)D, nmol/L

<25

<30

<40

<50

<75

1006

Original

4.7

9.1

17.9

37.3

79.7

VDSP-Calibrated

7.9 (4.7, 9.6) ³

12.2 (9.5, 14.7)

28.3 (24.2, 31.8)

49.4 (45.0, 53.6)

97.3 (95.7, 98.3)

NDNS (1-18 y) ⁴,⁵ (United Kingdom) ( 26)

511

Original

15.9

23.3

41.5

58.3

88.8

NDNS (≥19 y) ⁴,⁵ (United Kingdom) ( 26)

977

Original

21.8

30.7

48.2

61.4

88.6

6995

Original

19.4

28.0

44.4

60.8

88.3

NANS ⁴,⁶ (Ireland) ( 14)

1118

VDSP-LC-MS/MS

7.0

12.3

29.1

45.9

81.0

In general, sex differences in prevalence of serum 25(OH)D <30 nmol/L within the entire collection of studies were not evident (13.1% compared with 12.9%, on average, for males and females, respectively). The prevalence of vitamin D deficiency by age group, and irrespective of latitude of study populations, suggests that teenagers may have higher risk on average. The range of deficiency in the various teenage study populations (age range: 15-18 y) was 12-40%, whereas childhood samples (age ranges: 1-6 and 7-14 y), older adult samples (>61 y), and adult samples were 4-7%, 1-8%, and 9-24%, respectively ( Table 4 ). Such comparisons need to be interpreted cautiously, because differences in latitude of sample population, ethnic mix, and season of blood sampling differed for these populations (see Table 1 ).

The importance of using standardized serum 25(OH)D values for comparisons of the prevalence of vitamin D deficiency is clearly illustrated by the data from 2 of the nationally representative surveys, both of which reside in a latitude band of 47-55°N. In the case of the German adult survey (German Health Interview and Examination Survey for Adults; 18-79 y), the prestandardization prevalence estimate [serum 25(OH)D <30 nmol/L] of 25.9% decreased after standardization to 15.2%. For the Irish survey (National Adult Nutrition Survey), the prevalence of deficiency in adults (aged 18-84 y) increased from 6.6% (prestandardization) to 12.3% after standardization. Thus, the prevalence of vitamin D deficiency for these relatively cognate, predominantly white adult population samples, which were originally extremely disparate (25.9% compared with 6.6%), became close after standardization (15.2% compared with 12.3%) ( Table 4 ). The prevalence estimates for standardized serum 25(OH)D concentrations <30 and <50 nmol/L in the 4 nationally representative survey by extended winter and summer are also shown in Table 5 .

TABLE 5

% Serum 25(OH)D <30 nmol/L

% Serum 25(OH)D <50 nmol/L

Study (country; n) (ref)

Yearly

Extended winter

Extended summer

Yearly

Extended winter

Extended summer

KiGGS (Germany; n = 10,015) ( 25)

12.5

21.1

5.7

45.6

64.3

30.7

DEGS (Germany; n = 6995) ( 27, 28)

15.2

25.5

6.9

56.0

74.9

40.7

NDNS: Rolling Program Year 1-4 (United Kingdom; n = 1488) ( 26)

22.1

31.8

15.3

55.4

69.3

45.7

NANS (Ireland; n = 1118) ( 14)

12.4

19.7

6.6

46.0

61.2

35.4

DISCUSSION

In the absence of global consensus on the concentration of 25(OH)D that defines vitamin D deficiency, the ODIN project consortium chose to use that assigned by the US Institute of Medicine [i.e., <30 nmol/L ( 13)], which is based on risk of metabolic bone disease. A serum 25(OH)D <25 nmol/L has been a traditional cutoff used in Europe for several decades ( 45, 46). There is universal agreement that we do not wish to have individuals in the populations with circulating concentrations <25-30 nmol/L. On this basis, the present work, which is the first to report to our knowledge the prevalence estimates of vitamin D deficiency based on standardized serum 25(OH)D data, suggests that vitamin D deficiency is widespread across Europe and at prevalence rates that meet the criteria of a pandemic (definition of a pandemic: "an epidemic occurring worldwide, or over a very wide area, crossing international boundaries and usually affecting a large number of people" ( 48). Although there was considerable variation dependent on age group, ethnic mix, and latitude of study populations, overall 13% of our combined sample of childhood, teenage, adult, and older adult population studies across Europe ( n = 55,844), ranging from southern to mid to northern European member states (35-69°N), had vitamin D deficiency (i.e., <30 nmol/L) at the time of sampling. That 13 in 100 European citizens have serum 25(OH)D concentrations <30 nmol/L, using even this relatively conservative definition of vitamin D deficiency, translates into enormous numbers of individuals and highlights the need to devise strategies for prevention of vitamin D deficiency in Europe. For example, taking the vitamin D deficiency estimates of 12.5-15.2%, 12.3%, and 22.0% from the nationally representative nutrition/health surveys for Germany, Ireland, and the United Kingdom included in the present work would relate to 10.9, 0.6, and 14.1 million individuals, respectively, in these member states alone based on their recent census data. It is also worth noting that other expert bodies have suggested vitamin D deficiency is defined by a higher serum 25(OH)D threshold of 50 nmol/L ( 47). Using serum 25(OH)D <50 nmol/L in the same surveys would translate to 44.9, 2.1, and 32.6 million individuals in Germany, Ireland, and the United Kingdom, respectively, having deficiency as defined by this threshold.

The importance of using standardized serum 25(OH)D data in the present assessment of the prevalence of vitamin D deficiency in Europe was exemplified in the upward and downward revision of prevalence estimates after standardization in some studies. For example, 10.4 million fewer German adults and 267,000 more Irish adults had vitamin D deficiency by using the estimates based on standardized compared with the corresponding nonstandardized serum 25(OH)D data from these surveys. It should be stressed that standardization had very little impact on serum 25(OH)D data from a minority of population samples included in this work, which relates to the types of 25(OH)D assays used in these studies as these perform comparably to LC-MS/MS from an analytic perspective.

As expected, there was considerable variation in prevalence of vitamin D deficiency among the European Union countries, which appeared to be dependent on age group. In studies of adult and older adult populations, the prevalence of vitamin D deficiency was much less in the more northerly latitude countries such as Norway, Iceland, and Finland, whereas more mid-latitude countries such as the United Kingdom, Ireland, Netherlands, and Germany had a higher prevalence, even accounting for ethnicity. The amplitude of an increase in prevalence in vitamin D deficiency in extended winter compared with extended summer was also much lower in the northerly latitude countries, which is likely attributable to higher rates of vitamin D supplement and/or food fortification use in these countries ( 49- 51). In the case of the childhood population studies, the relatively mid-latitude countries (47-60°N) had a higher prevalence range (5-20%) than did southern countries (<41°N) at 4.2-6.9%.

The present findings may also be of importance to risk managers in the European Commission and the various member states within Europe as they highlight population subgroups within Europe that may be at increased risk of vitamin D deficiency and that may require a specific focus on devising public health strategies for the prevention of deficiency. Nonwhite populations in Europe are at higher risk of vitamin D deficiency than their white counterparts. For example, compared with white populations in the United Kingdom, Norway, and Finland, the nonwhite population subgroups have 3- to 71-fold higher yearly prevalence of vitamin D deficiency. Differences also exist within different nonwhite ethnic groups residing in the same country. For example, within the Finnish Maamu representative sample, the Kurdish immigrant subgroup ( n = 500) had a much higher prevalence of yearly serum 25(OH)D <30 nmol/L (50.4%) than the Somali immigrant subgroup (28.0%; n = 364), and both were much higher than either the Russian-speaking white immigrant subgroup (4.5%; n = 446) in Maamu or the general Finnish native white adult population as studied in the representative Health 2011 survey ( 37) (0.4%; n = 4102). Although not assessed in the present analysis, the subjects of Kurdish origin (born in Iraq or Iran) in the present study generally have, on average, a lighter skin pigmentation than those of Somali origin, highlighting that skin color is only part of the reason for lower vitamin D status in certain ethnic groups and that other (dietary, cultural, and biologic) factors influence the prevalence of vitamin D deficiency. As an additional insight, although cognizant of the fact that the numbers were low and thus caution is needed in their interpretation, the current analysis of standardized serum 25(OH)D from the United Kingdom's NDNS (all subjects) showed that the prevalence of vitamin D deficiency was 35.7% and 59.6% in black ( n = 28) and Asian participants ( n = 52), respectively, compared with 19.6% in white participants ( n = 1359). Standardized serum 25(OH)D data for South Asian (Pakistani) immigrants in Oslo, Norway, also highlight an extremely high prevalence of vitamin D deficiency (64.8%, n = 176) relative to that in the white native adult population (1.3%, n = 866) ( 37). European teenagers, aged 15-18 y, seemed to exhibit a higher prevalence of vitamin D deficiency (range: 12.2-39.6%) than did other age groups (range: 0.9-19.6%), a phenomenon observed previously ( 52- 54). It is worth noting that none of the studies included pregnant women or older adults in care homes, both life-stage groups that are considered vulnerable to vitamin D deficiency. In general, sex differences in the prevalence of vitamin D deficiency within the collection of population studies were not very pronounced compared with ethnic and some age-grouping differences. Thus, risk of vitamin D deficiency was largely similar in males and females of both young and older European populations.

The key strengths of this study were the inclusion of the 18 representative European population studies of children, teenagers, adults, and older adults, representing a sizable geographical footprint with 55,844 total participants, and our ability to standardize their serum 25(OH)D data so as to better quantify the prevalence of vitamin D deficiency in Europe and inform development of prevention policies. In terms of limitations of this study, it is worth noting that some of the studies were 7-11 y old, and vitamin D supplement and/or fortified food usage patterns and formulations as well as adherence to sun awareness campaigns since that time may have altered, which would affect these estimates.

In conclusion, vitamin D deficiency is evident throughout the European population at prevalence rates that are a matter of concern and that require action both from a public health and a clinical perspective. What direction these strategies take will depend on risk managers. Although there have been some guidelines on sun exposure ( 55), the question of whether a minimal-risk approach to UV-B exposure would enable vitamin D production without increasing the risk of skin cancer is still outstanding. It is the view of this consortium that these factors re-emphasize the need for public health strategies to explore food-based solutions for prevention of vitamin D deficiency. The pros and cons of vitamin D supplementation and/or food fortification have been well documented in recent times ( 49, 56- 58). Finally, assessment of the prevalence of vitamin D deficiency within and between populations is enormously enhanced by use of standardized serum 25(OH)D data.

Supplementary Material

Online Supporting Material:

Acknowledgments

The following authors were the link and designated principal investigators within the ODIN project consortium and who provided sera and required data on each of their various population studies, as follows: Healthy Lifestyle in Europe by Nutrition in Adolescence: M Gonzalez-Gross, J Valtueña, S De Henauw, and L Moreno; Optimal well-being, development and health for Danish children through a healthy New Nordic Diet: CT Damsgaard, KF Michaelsen, and C Mølgaard; Tromsø 6 and Fit Futures: R Jorde and G Grimnes Infant's Nourishment and Nutritional Status and Healthy Growth Study: G Moschonis, C Mavrogianni, and Y Manios; German Health Interview and Examination Survey for Children and Adolescents and German Health Interview and Examination Survey for Adults: M Thamm, GBM Mensink, M Rabenberg, and MA Busch; NDNS: L Cox, S Meadows, G Goldberg, and A Prentice; New Hoorn Study: JM Dekker, G Nijpels, and S Pilz; Longitudinal Aging Study Amsterdam: KM Swart, NM van Schoor, and P Lips; Age, Gene/Environment Susceptibility-Reykjavik: G Eiriksdottir, V Gudnason, and MF Cotch; Maamu: S Koskinen and C Lamberg-Allardt; Cork BASELINE: M Kiely.

We thank Nida Ziauddeen from the MRC Human Nutrition Research Unit and Elsie Widdowson Laboratory, Cambridge, United Kingdom, for her help with calculating the weighted estimates for the NDNS data.

The authors' responsibilities were as follows-MG-G, JV, SDH, LM, CTD, KFM, C Mølgaard, RJ, G Grimnes, GM, C Mavrogianni, YM, MT, GBMM, MR, MAB, LC, SM, G Goldberg, AP, JMD, GN, SP, KMS, NMvS, PL, GE, VG, MFC, SK, CL-A, and MK: supplied sera and data on the population studies to allow standardization of serum 25(OH)D; KGD, ZŠ, and SM: undertook the LC-MS/MS analysis and associated data analysis; KDC, RAD-A, and CTS: performed regression modeling and statistical analysis; KDC and MK: were ODIN project coordinators; and KDC: drafted the manuscript. The authors declared no conflicts of interest.

Footnotes

²⁶ Abbreviations used: LC-MS/MS, liquid chromatography-tandem mass spectrometry; NDNS, National Diet and Nutrition Survey; ODIN, Food-based solutions for optimal vitamin D nutrition and health through the life cycle; VDSP, Vitamin D Standardization Program; 25(OH)D, 25-hydroxyvitamin D.

REFERENCES

13. Institute of Medicine Food and Nutrition Board. Dietary reference intakes for calcium and vitamin D. Washington (DC): National Academies Press; 2011. [ Google Scholar]

19. The Tromsø Study [Internet]. [cited 2013 Oct 22]. Tromsø (Norway): UiT The Artic University of Norway; 2015. Available from: http://www.tromsostudy.com.

24. O'Donovan SM, Murray DM, Hourihane JO, Kenny LC, Irvine AD, Kiely M. Cohort profile: The Cork BASELINE Birth Cohort Study: Babies after SCOPE: Evaluating the Longitudinal Impact on Neurological and Nutritional Endpoints. Int J Epidemiol 2015. [[ PubMed] Google Scholar]

39. EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA). Scientific opinion on principles for deriving and applying Dietary Reference Values. EFSA J 2010;8:1458. [ Google Scholar]

41. Rahmani YE, Botelho JC & Vesper HW. CDC Vitamin D Standardization Certification Program. [ Endocr Rev 2013; 34:SUN-277. Google Scholar]

45. Department of Health. Dietary reference values for food energy and nutrients for the United Kingdom. London: Her Majesty's Stationery Office; 1991. (Report on Health and Social Subjects 41.) [ Google Scholar]

46. Commission of the European Communities. Vitamin D. In: Nutrient and energy intakes of the European Community: report of the Scientific Committee for Food. 31st series. Brussels (Luxembourg): Office of Official Publications of the European Communities; 1993. p. 132-9. [ Google Scholar]

48. Last J. A dictionary of epidemiology. 4th ed. Oxford (United Kingdom): Oxford University Press; 2001. [ Google Scholar]

50. Norwegian Directorate of Health, Norwegian Food Safety Authority and University of Oslo. Norkost 3: a nationwide dietary survey among men and women in Norway aged 18-70 years. Oslo: Norwegian Directorate of Health; June 2012. (Report IS-2000.).

51. Helldán A, Raulio S, Kosola M, Tapanainen H, Ovaskainen M-L, Virtanen S. Finravinto 2012-tutkimus-The National FINDIET 2012 Survey. Raportti 16/2013. Helsinki (Finland): National Institute for Health and Welfare; 2013. [ Google Scholar]

Articles from The American Journal of Clinical Nutrition are provided here courtesy of American Society for Nutrition

# data[].attributes.attachment_link.title
Vitamin D deficiency in Europe: pandemic?

# data[].attributes.attachment_link.description
Kevin D Cashman, 3, 4, * Kirsten G Dowling, 3 Zuzana Škrabáková, 3 Marcela Gonzalez-Gross, 6, 7 Jara Valtueña, 6 Stefaan De Henauw, 8 Luis Moreno, 9 Camilla T Damsgaard, 10 Kim F Michaelsen, 10 Christian Mølgaard, 10 Rolf Jorde, 11 Guri Grimnes, 11 George Moschonis, 12 Christina Mavrogianni, 12

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Links: allgemein zu Schwangerschaft/ Stillzeit +Ernährung

# data[].attributes.subject
Links: allgemein zu Schwangerschaft/ Stillzeit +Ernährung

# data[].attributes.body
Folsäure - Gehalte in Lebensmitteln

# data[].attributes.body
Alternative zu Femibion 0 bzw. 1

# data[].attributes.attachment_link.readable_text
SCHWANGERSCHAFT PHASE 0 RedCare

Mit Folsäure und weiteren Vitaminen

Nahrungsergänzung bei Kinderwunsch

Vegan und glutenfrei

Was ist drin in den SCHWANGERSCHAFT PHASE 0 Kapseln?
SCHWANGERSCHAFT PHASE 0 RedCare enthält Vitamine und Mineralstoffe zur Nahrungsergänzung während der Babyplanung. Die Kapseln enthalten den lizensierten Inhaltsstoff Quatrefolic® - eine aktive Form von Folat, dass besonders gut vom Körper aufgenommen werden kann.
Die ergänzende Aufnahme von Folsäure erhöht bei Schwangeren den Folatspiegel. Das ist wichtig, denn ein niedriger Folatspiegel bei Schwangeren ist ein Risikofaktor für die Entstehung von Neuralrohrdefekten beim heranwachsenden Fötus. Die positive Wirkung stellt sich bei einer ergänzenden Aufnahme von 400 µg täglich ein. Die Deutsche Gesellschaft für Ernährung empfiehlt die Einnahme eines Folsäurepräparats mindestens einem Monat vor und bis zu drei Monaten nach der Empfängnis.

Zudem trägt Folat zum Wachstum des mütterlichen Gewebes während der Schwangerschaft und zu einer normalen Blutbildung bei.

Neben Folsäure enthalten die Kapseln Jod sowie fünf weitere wichtige Vitamine, die den Körper bei der Vorbereitung auf die Schwangerschaft unterstützen:

Vitamin D und Vitamin B12 haben eine Funktion bei der Zellteilung.

Vitamin B12 und Vitamin B6 tragen zu einer normalen Bildung roter Blutkörperchen bei.

Vitamin B6 leisten einen Beitrag zur Regulierung der Hormontätigkeit.

Vitamin D, Vitamin B6 und Vitamin B12 tragen zu einer normalen Funktion des Immunsystems bei.

Vitamin B2 und Vitamin B12 leisten einen Beitrag zur Verringerung von Müdigkeit und Ermüdung.

Jod, Vitamin B2 und Vitamin B12 tragen zu einer normalen Funktion des Nervensystems bei.

Zudem sind die RedCare Schwangerschaftsvitamine vegan, glutenfrei und frei von Farb- und Konservierungsstoffen.

Wie nimmt man die SCHWANGERSCHAFT PHASE 0 RedCare Kapseln ein?
Eine Kapsel pro Tag genügt. Diese sollte man zu einer Mahlzeit mit einem Glas Wasser (200 ml) einnehmen.

Zutaten:
Reismehl, Überzugsmittel: Hydroxypropylmethylcellulose Cholecalciferol, DL-alpha-Tocopherylacetat, Cyanocobalamin, Pyridoxinhydrochlorid, Riboflavin, (6S)-5-Methyltetrahydrofolsäure, Glucosaminsalz, Pteroylmonoglutaminsäure, Kaliumiodid
Nährwerte:
*angegebene tägliche Verzehrmenge
**Anteil an der Nährstoffreferenzmenge
***Folat aus 400 µg (6S)-5-Methyltetrahydrofolsäure, Glucosaminsalz (Quatrefolic®) und 400µg Pteroylmonoglutaminsäure

Verzehrempfehlung:
Eine Kapsel pro Tag genügt. Diese sollte man zu einer Mahlzeit mit einem Glas Wasser (200 ml) einnehmen.

Hinweis:
Die angegebene empfohlene Tagesmenge darf nicht überschritten werden.

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Kühl (6-25 °C) und lichtgeschützt lagern. Außerhalb der Reichweite von Kindern aufbewahren.

Nettofüllmenge:
60 Kapseln

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Shop-Apotheke B.V.
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SCHWANGERSCHAFT PHASE 0 RedCare 60 St - shop-apotheke.at

# data[].attributes.attachment_link.description
SCHWANGERSCHAFT PHASE 0 RedCare Mit Folsäure und weiteren Vitaminen Nahrungsergänzung bei Kinderwunsch Vegan und glutenfrei Was ist drin in den SCHWANGERSCHAFT PHASE 0 Kapseln? SCHWANGERSCHAFT PHASE 0 RedCare enthält Vitamine und Mineralstoffe zur Nahrungsergänzung während der Babyplanung. Die Kapseln enthalten den lizensierten Inhaltsstoff Quatrefolic® - eine aktive Form von Folat, dass besonders gut vom Körper aufgenommen werden kann.

# data[].attributes.attachment_link.readable_text
*Femibion®-Produkte enthalten Folsäure Plus (eine Kombination aus Folsäure und Metafolin®) sowie ausgewählte Nährstoffe. Femibion® 3 enthält außerdem DHA (mehrfach ungesättigte Omega-3-Fettsäure).

Die ergänzende Aufnahme von Folsäure erhöht bei Schwangeren den Folatspiegel. Ein niedriger Folatspiegel bei Schwangeren ist ein Risikofaktor für die Entstehung von Neuralrohrdefekten beim heranwachsenden Fötus. Dafür sollten zusätzlich täglich 400 μg Folsäure über einen Zeitraum von mindestens einem Monat vor und bis zu drei Monaten nach der Empfängnis eingenommen werden. Ein Neuralrohrdefekt ist durch mehrere Risikofaktoren bedingt. Die Veränderung eines Risikofaktors kann eine positive Wirkung haben oder auch nicht. Folat trägt zum Wachstum des mütterlichen Gewebes während der Schwangerschaft bei, einschließlich der Entwicklung der Plazenta. Die Einnahme von DHA durch die Mutter trägt zur normalen Entwicklung des Gehirns und der Augen des Fötus und gestillten Säuglings bei. Die positive Wirkung von DHA tritt ein, wenn zusätzlich zu der für Erwachsene empfohlenen Tagesdosis an Omega-3-Fettsäuren (d.h. 250 mg DHA und EPA) täglich 200 mg DHA eingenommen werden.

Femibion® ist ein Nahrungsergänzungsmittel und kein Ersatz für eine ausgewogene, abwechslungsreiche Ernährung und gesunde Lebensweise.

Metafolin® ist eine eingetragene Marke der Merck KGaA, Darmstadt, Deutschland, und wird unter Lizenz verwendet.

# data[].attributes.attachment_link.description
Femibion®-Produkte enthalten Folsäure Plus (eine Kombination aus Folsäure und Metafolin®) sowie ausgewählte Nährstoffe. Femibion® 3 enthält außerdem DHA (mehrfach ungesättigte Omega-3-Fettsäure). Die ergänzende Aufnahme von Folsäure erhöht bei Schwangeren den Folatspiegel. Ein niedriger Folatspiegel bei Schwangeren ist ein Risikofaktor für die Entstehung von Neuralrohrdefekten beim heranwachsenden Fötus.

# data[].attributes.headline
Vitamin D Supplementation für Schwangere

# data[].attributes.subject
Vitamin D Supplementation für Schwangere

# data[].attributes.attachment_link.readable_text
J Clin Endocrinol Metab. 2016 Feb; 101(2): 394-415.

Consensus Statement

Craig F. Munns, Nick Shaw, Mairead Kiely, Bonny L. Specker, Tom D. Thacher, Keiichi Ozono, Toshimi Michigami, Dov Tiosano, M. Zulf Mughal, Outi Mäkitie, Lorna Ramos-Abad, Leanne Ward, Linda A. DiMeglio, Navoda Atapattu, Hamilton Cassinelli, Christian Braegger, John M. Pettifor, Anju Seth, Hafsatu Wasagu Idris, Vijayalakshmi Bhatia, Junfen Fu, Gail Goldberg, Lars Sävendahl, Rajesh Khadgawat, Pawel Pludowski, Jane Maddock, Elina Hyppönen, Abiola Oduwole, Emma Frew, Magda Aguiar, Ted Tulchinsky, Gary Butler, and Wolfgang Högler *

Abstract

Background:

Vitamin D and calcium deficiencies are common worldwide, causing nutritional rickets and osteomalacia, which have a major impact on health, growth, and development of infants, children, and adolescents; the consequences can be lethal or can last into adulthood. The goals of this evidence-based consensus document are to provide health care professionals with guidance for prevention, diagnosis, and management of nutritional rickets and to provide policy makers with a framework to work toward its eradication.

Evidence:

A systematic literature search examining the definition, diagnosis, treatment, and prevention of nutritional rickets in children was conducted. Evidence-based recommendations were developed using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) system that describe the strength of the recommendation and the quality of supporting evidence.

Process:

Thirty-three nominated experts in pediatric endocrinology, pediatrics, nutrition, epidemiology, public health, and health economics evaluated the evidence on specific questions within five working groups. The consensus group, representing 11 international scientific organizations, participated in a multiday conference in May 2014 to reach a global evidence-based consensus.

Results:

This consensus document defines nutritional rickets and its diagnostic criteria and describes the clinical management of rickets and osteomalacia. Risk factors, particularly in mothers and infants, are ranked, and specific prevention recommendations including food fortification and supplementation are offered for both the clinical and public health contexts.

Conclusion:

Rickets, osteomalacia, and vitamin D and calcium deficiencies are preventable global public health problems in infants, children, and adolescents. Implementation of international rickets prevention programs, including supplementation and food fortification, is urgently required.

Summary of Consensus Recommendations¹

Section 1: Defining nutritional rickets and the interplay between vitamin D status and calcium intake

1.4. Dietary calcium intake to prevent rickets

For infants 0-6 and 6-12 months of age, the adequate calcium intake is 200 and 260 mg/d, respectively. (1⊕⊕⊕)

For children over 12 months of age, dietary calcium intake of <300 mg/d increases the risk of rickets independent of serum 25OHD levels. (1⊕⊕○)

Section 2: Prevention and treatment of nutritional rickets and osteomalacia

2.3. Candidates for preventative vitamin D supplementation beyond 12 months of age

In the absence of food fortification, vitamin D supplementation should be given to:

Children with a history of symptomatic vitamin D deficiency requiring treatment. (1⊕⊕⊕)

Children and adults at high risk of vitamin D deficiency, with factors or conditions that reduce synthesis or intake of vitamin D. (1⊕⊕⊕)

Pregnant women (see Section 3.1).

2.5. Appropriate route of administration and duration of therapy

We recommend oral treatment, which more rapidly restores 25OHD levels than IM treatment. (1⊕⊕⊕)

For daily treatment, both D ₂ and D ₃ are equally effective. (1⊕⊕⊕)

When single large doses are used, D ₃ appears to be preferable compared to D ₂ because the former has a longer half-life. (1⊕⊕⊕)

Vitamin D treatment is recommended for a minimum of 12 weeks, recognizing that some children may require longer treatment duration. (1⊕⊕⊕)

Section 3: Prevention of nutritional rickets/osteomalacia: identification of risk factors

3.3. Association of sunlight exposure to nutritional rickets

Because UVB rays trigger epidermal synthesis of pre-vitamin D ₃, restricted exposure to sun increases the risk of vitamin D deficiency and nutritional rickets. (1⊕⊕⊕)

Environmental factors, such as latitude, season, time of day, cloud cover, and pollution affect availability of UVB, whereas personal factors, such as time spent outdoors, skin pigmentation, skin coverage, age, body composition, and genetics affect the dose-response of UVB exposure and circulating 25OHD. (2⊕⊕○)

No safe threshold of UV exposure allows for sufficient vitamin D synthesis across the population without increasing skin cancer risk. (2⊕⊕○)

Section 4: Prevention of osteomalacia during pregnancy and lactation and congenital rickets

Section 5: Assessing the burden of nutritional rickets and public health strategies for prevention

5.2. Public health strategies for rickets prevention

Universally supplement all infants with vitamin D from birth to 12 months of age, independent of their mode of feeding. Beyond 12 months, supplement all groups at risk and pregnant women. Vitamin D supplements should be incorporated into childhood primary health care programs along with other essential micronutrients and immunizations (1⊕⊕⊕), and into antenatal care programs along with other recommended micronutrients. (2⊕⊕○)

Recognize nutritional rickets, osteomalacia, and vitamin D and calcium deficiencies as preventable global public health problems in infants, children, and adolescents. (1⊕⊕⊕)

Implement rickets prevention programs in populations with a high prevalence of vitamin D deficiency and limited vitamin D and/or calcium intakes, and in groups of infants and children at risk of rickets. (1⊕⊕⊕)

Monitor adherence to recommended vitamin D and calcium intakes and implement surveillance for nutritional rickets. (1⊕⊕⊕)

Fortify staple foods with vitamin D and calcium, as appropriate, based on dietary patterns. Food fortification can prevent rickets and improve vitamin D status of infants, children, and adolescents if appropriate foods are used and sufficient fortification is provided, if fortification is supported by relevant legislation, and if the process is adequately monitored. Indigenous food sources of calcium should be promoted or subsidized in children. (1⊕⊕⊕)

Promote addressing the public health impact of vitamin D deficiency as both a clinical and a public health issue. (1⊕⊕⊕)

5.3. Economic cost/benefits of prevention programs

The cost-effectiveness of supplementation and food fortification programs needs further study. (1⊕⊕○)

Nutritional rickets (NR), secondary to vitamin D deficiency and/or dietary calcium deficiency, remains a significant global, public health problem despite the availability of supplementation and numerous published guidelines for its prevention ( 1, -8). This is concerning because NR can have a major impact on the health of infants, children, and adolescents, with ramifications that persist into adulthood. The morbidity and mortality associated with NR can be devastating, with substantial but poorly recognized consequences for society and health economics. Features of NR and osteomalacia include: 1) hypocalcemic seizures and tetanic spasms; 2) life-threatening hypocalcemic cardiomyopathy; 3) bone pain and muscle weakness; 4) limb and pelvic deformities; 5) failure to thrive; 6) developmental delay; and 7) dental anomalies ( 9, 10). Alarmingly, NR can also lead to death from heart failure caused by hypocalcemic cardiomyopathy, even in developed countries ( 11). In addition, narrowing of the pelvic outlet after NR in childhood can result in obstructed labor and maternal and fetal death ( 12).

Despite intense focus around the role of vitamin D status in health and disease, there has been a worldwide failure to implement public health guidance and eradicate the most severe manifestations of vitamin D and calcium deficiency in our most vulnerable population-NR and osteomalacia of childhood. Therefore, the goal of this Consensus Statement is to provide clinicians with clarity and recommendations on the recognition, societal burden, and treatment of NR and osteomalacia, and to enable clinicians and health policy leaders to establish appropriate clinical and public health interventions to prevent this debilitating, costly, and under-recognized global health problem.

Methods

In recognition of the considerable variation in the definition, diagnosis, and management of NR worldwide, the European Society for Pediatric Endocrinology decided to examine current best practice in NR and to formulate evidence-based recommendations. Experts were assembled from the following societies: the Pediatric Endocrine Society (PES), the Asia Pacific Pediatric Endocrine Society (APPES), the Japanese Society for Pediatric Endocrinology (JSPE), the Sociedad Latino-Americana de Endocrinología Pediátrica (SLEP), the Australasian Pediatric Endocrine Group (APEG), the Indian Society for Pediatric and Adolescent Endocrinology (ISPAE), the African Society for Pediatric and Adolescent Endocrinology (ASPAE), the Chinese Society of Pediatric Endocrinology and Metabolism (CSPEM), the British Nutrition Society, and the European Society for Pediatric Gastroenterology Hepatology and Nutrition (ESPGHAN). This consensus paper includes the cumulative evidence up to the end of 2014.

Participants included individuals from Europe, North America (United States and Canada), Latin America, Asia, Africa, and Australia, with a balanced spectrum of professional seniority and expertise. In addition, an expert on the development of evidence-based guidelines served in an advisory capacity. Panel members declared any potential conflict of interest at the initial meeting of the group. Thirty-three participants were assigned to one of five groups to which topics 1-5 were allocated, and a chairperson was designated for each group. Each participant prepared an evidence-based summary of the literature relating to a particular question distributed before the conference (which was held over 3 days in May 2014).

Each group presented the revised summaries for discussion to the full conference. This report is based on the questions addressed. A detailed description of the GRADE classification has been published elsewhere ( 13). Recommendations were based on published findings and on expert opinion when appropriate.

The best available research evidence was used to develop recommendations. Preference was given to articles written in English, identified by PubMed searches with MeSH terms. For each point, recommendations and evidence are described, with a modification in the grading evidence as follows: 1 = strong recommendation (applies to most patients in most circumstances, benefits clearly outweigh the risk); and 2 = weak recommendation (consensus opinion of working group or should be considered; the best action may depend on circumstances or patient values, benefits, and risks closely balanced or uncertain). Quality of evidence is indicated as follows: ⊕⊕⊕, high quality (prospective cohort studies or randomized controlled trials [RCTs] at low risk of bias); ⊕⊕○, moderate quality (observational studies or trials with methodological flaws, inconsistent or indirect evidence); and ⊕○○, low quality (case series or nonsystematic clinical observations) ( 13).

The target audience for these guidelines includes general and specialist pediatricians, other professionals providing care for patients with NR, and health policy makers, particularly in countries with developing economies.

1.0. Defining Nutritional Rickets and the Interplay between Vitamin D Status and Calcium Intake

1.1. Definition and diagnosis of nutritional rickets

1.1.2. Evidence

Bone mineralization requires sufficient supply of the essential mineral ions, calcium and phosphate, with vitamin D optimizing their absorption from the gut. With insufficient serum calcium concentration caused by either vitamin D deficiency or inadequate dietary calcium intake, PTH will stimulate osteoclastic bone resorption to release stored bone minerals into the bloodstream and maintain normal serum calcium ( 14). Bone disease (rickets and osteomalacia) develops once elevated PTH has led to low serum phosphate levels, as a result of impaired renal phosphate conservation ( 15).

NR is a disorder of defective growth plate chondrocyte apoptosis and matrix mineralization in children. Osteomalacia is abnormal matrix mineralization in established bone, and although present in children with rickets, it is used to describe bone mineralization defects after completion of growth. Children with an underlying disease such as fat malabsorption, liver disease, renal insufficiency, and illnesses necessitating total parenteral nutrition can also develop NR and are briefly discussed in this review. NR does not include rickets associated with heritable disorders of vitamin D metabolism, including 1-α-hydroxylase deficiency and vitamin D receptor defects, or congenital or acquired hypophosphatemic rickets.

The clinical features and consequences of NR are broad and potentially severe ( Table 1 ) ( 8). Defective mineralization leads to radiographic growth plate widening as well as metaphyseal cupping and fraying, which confirm the diagnosis of NR.

Table 1.

Osseous signs and symptoms

Swelling wrists and ankles

Delayed fontanelle closure (normally closed by age 2 y)

Delayed tooth eruption (no incisors by age 10 mo, no molars by age 18 mo)

Leg deformity (genu varum, genu valgum, windswept deformity)

Rachitic rosary (enlarged costochondral joints-felt anteriorly, lateral to the nipple line)

Frontal bossing

Craniotabes (softening of skull bones, usually evident on palpation of cranial sutures in first 3 mo)

Bone pain, restlessness, and irritability

Radiographic features

Splaying, fraying, cupping, and coarse trabecular pattern of metaphyses

Widening of the growth plate

Osteopenia

Pelvic deformities including outlet narrowing (risk of obstructed labor and death)

Long-term deformities in keeping with clinical deformities

Minimal trauma fracture

Non-osseous features

Hypocalcemic seizure and tetany

Hypocalcemic dilated cardiomyopathy (heart failure, arrhythmia, cardiac arrest, death)

Failure to thrive and poor linear growth

Delayed gross motor development with muscle weakness

Raised intracranial pressure

Biochemical testing alone is not sufficient to diagnose NR and may not differentiate whether the primary cause of NR is vitamin D or dietary calcium deficiency because combined deficiencies are common. Typical laboratory findings in NR are decreases in 25OHD, serum phosphorus, serum calcium, and urinary calcium. Conversely, serum PTH, ALP, and urinary phosphorus levels are invariably elevated ( 10, 16).

Vitamin D status is assessed by measuring blood levels of total 25OHD. Total 25OHD is used, assuming that 25OHD ₂ and 25OHD ₃ are of equal biological value ( 16). There is considerable variability between laboratory methods for measuring serum 25OHD concentrations ( 17). Immunoassays are popular due to their convenience and high sample throughput; however, cross-reactivity between vitamin D metabolites (25OHD ₂, 25OHD ₃, and 24,25(OH) ₂D) and high levels of estimated bias in several automated assays cast doubt on their reliability, particularly at high and low concentrations of 25OHD ( 18). Higher-order reference measurement procedures for serum 25OHD have been established by the National Institute of Standards and Technology (NIST) ( 19) and Ghent University ( 20) based on isotope dilution liquid chromatography-tandem mass spectrometry. In recent years, the accuracy of 25OHD assays has improved, including through activities of the Vitamin D Standardization Program ( 21), which aims to standardize the results of different measurement techniques to those of the reference measurement procedures ( 22). Significant reductions in interlaboratory variation in serum 25OHD are observed using liquid chromatography-tandem mass spectrometry with the application of NIST standard reference materials ( 23).

Dietary calcium deficiency is diagnosed by obtaining a calcium intake history. Because the sources of calcium will vary by country and region, we recommend that clinicians develop a dietary calcium intake questionnaire specific to their country/region.

1.3. Vitamin D toxicity

1.3.1. Recommendation

Toxicity is defined as hypercalcemia and serum 25OHD > 250 nmol/L with hypercalciuria and suppressed PTH2. (1⊕⊕⊕)

1.3.2. Evidence

Intoxication is predominantly seen in infants and young children after exposure to high doses of vitamin D (240 000 to 4 500 000 IU) ( 32, -37). High 25OHD concentrations can cause hypercalcemia, hypercalciuria, and if prolonged, nephrocalcinosis and renal failure. To allow a large safety margin, the consensus group felt it prudent to use the concentration of 250 nmol/L as the recommended upper limit of serum 25OHD-even if symptomatic toxicity from RCTs has only been reported at levels >500 nmol/L ( 32). In otherwise healthy infants, hypercalcemia and hypercalciuria in the absence of elevated 25OHD concentrations have been reported and may be related to genetic variation in vitamin D metabolism ( 38, 39).

1.4. Dietary calcium intake to prevent rickets

1.4.1. Recommendations

For infants 0-6 and 6-12 months of age, the adequate calcium intake is 200 and 260 mg/d, respectively. (1⊕⊕⊕)

For children over 12 months of age, dietary calcium intake of <300 mg/d increases the risk of rickets independent of serum 25OHD levels. (1⊕⊕○)

1.4.2. Evidence

In developing countries where calcium intake is characteristically very low, with few or no dairy products, dietary calcium deficiency is the main cause of NR among children outside the infant age group.

In 2011, the IOM recommended adequate intakes of calcium for infants, children, and adults ( 16). The adequate intake for infants was based on breast milk calcium content, which is 200 mg/d and 260 mg/d for babies from 0-6 and 6-12 months of age, respectively. For children 1-18 years of age, the IOM set the daily calcium requirement at 700-1300 mg/d, depending on age ( 28). There is, however, no true definition of dietary calcium deficiency without a reliable biomarker of calcium intake status, and there are little data to indicate what the lowest calcium intake is that prevents NR. Reports from Nigeria, India, and Bangladesh ( 6, 30, 40, -43) highlighted the role of low dietary calcium intake in the pathogenesis of NR among children. Although some of these children also had suboptimal 25OHD, others had values >50 nmol/L, which points to the interplay between calcium and vitamin D in the pathogenesis of NR ( Figure 1 ). These studies suggest that in children >12 months of age, a dietary calcium intake of <300 mg/d significantly increases the risk of NR independent of serum 25OHD levels, and that at a daily intake of >500 mg, no NR was seen.

1.5. Vitamin D deficiency and fractures

1.5.2. Evidence

Based on evidence from available observational studies and case reports, children with clinical, biochemical, and radiographic evidence of NR are at increased risk of fracture. A retrospective study found that fractures occurred in seven of 45 (17.5%) infants and toddlers with NR, aged between 2 and 14 months ( 44). However, fractures only occurred in those who were mobile and had severe radiographic evidence of rickets. Although none of the fractures were considered to be characteristic of nonaccidental injury (child abuse), two infants had lateral or anterior-lateral rib fractures. In a national survey in Canada, 11 of 108 cases of NR (11%) had suffered fractures, although details on the bone sites and numbers of fractures were not provided ( 1). Fractures also have been reported in cases or case series of NR in toddlers and adolescents ( 45, -50), but details about the number, site, and type of fracture were absent.

It has been suggested that radiographic features of rickets may be mistaken for those characteristic of nonaccidental injury ( 51, 52), but the necessary biochemical and radiographic data on the cases for validation of the authors' conclusions were absent. In addition, serum 25OHD levels are similar in infants with accidental and nonaccidental injuries ( 53). Thus, simple vitamin D deficiency, that is, vitamin D deficiency without biochemical or radiological signs of rickets, has not been associated with increased fracture risk in infants and children.

2.0. Prevention and Treatment of Nutritional Rickets and Osteomalacia

2.1. Vitamin D supplementation for the prevention of rickets and osteomalacia

2.1.2. Evidence

Few published studies have included the prevention of radiographic or clinical signs of rickets as an outcome. Consequently, we also reviewed studies that assessed the effect of different vitamin D supplementation regimens3 on 25OHD levels and other bone parameters (such as bone mineral density) with the goal of preventing NR by maintaining levels above the rachitic range, ie, >30 nmol/L ( 54).

In infants and children, 400 IU/d of vitamin D given as a supplement during infancy is sufficient to prevent radiographic signs of rickets in the short term (up to 12 mo) ( 54). Specifically, an RCT demonstrated that a vitamin D supplement of 400 IU/d was sufficient to prevent radiographic signs of rickets at 6 months of age, even among infants born with vitamin D deficiency ( 25). Similarly, no cases of radiographically confirmed rickets were seen after administration of 400 IU/d of vitamin D for 12 months, whereas the incidence was 3.8% in Turkish infants and young children who did not receive supplementation ( 55). In addition, no incident cases of radiographically confirmed rickets were reported in a 2-year surveillance study of Canadian infants who received 400 IU/d of vitamin D ( 1). Worldwide, there have been no reports of radiographically confirmed rickets in infants or children receiving 400 IU on a regular, daily basis. Furthermore, this dose has been shown in RCTs to achieve 25OHD levels more frequently above the rachitic (severe deficiency) range compared to 100 or 200 IU/d ( 25).

The prevention of vitamin D deficiency in the absence of NR was also briefly reviewed. In a double-blind RCT of infants without vitamin D deficiency (25OHD > 50 nmol/L), the impact of 400, 800, 1200, and 1600 IU of vitamin D ₃ per day was assessed ( 54). Doses of 400 IU/d maintained 25OHD levels > 50 nmol/L in 97% of infants after 12 months; doses of 800 and 1200 IU/d were of no added benefit to bone mineral density parameters, and 1600 IU/d raised concerns about potential toxicity. A study in infants with vitamin D deficiency (25OHD < 25 nmol/L) found that a single dose of 100 000 IU maintained 25OHD levels above 37.5 nmol/L for 3 months without hypercalcemia, whereas higher doses led to unacceptably high 25OHD levels ( 56).

Among infants and toddlers with 25OHD levels < 50 nmol/L for whom daily vitamin D supplementation may not be ideal, intermittent bolus doses of 50 to 100 000 IU every 3 months hold promise, although a comprehensive understanding of the safety and efficacy of this approach remains to be studied.

2.2. Target for vitamin D supplementation

2.2.2. Evidence

No studies have specifically examined the best monitoring approach once supplementation has been given to prevent vitamin D deficiency rickets. 25OHD is a reasonable monitoring parameter to ensure levels > 30-34 nmol/L for prevention of NR. Biochemically, a fall in 25OHD concentration < 34 nmol/L is associated with rising PTH levels, but this intersection point depends on the prevailing calcium intake ( 7).

The frequent coexistence of dietary calcium deficiency and vitamin D deficiency alters the threshold for rickets development ( 57). Similarly, monitoring 25OHD concentrations as a public health policy for all individuals is impractical; fortunately, high-risk groups can easily be identified based on clinical profile ( Table 2 ).

Table 2.

Maternal factors

Vitamin D deficiency

Dark skin pigmentation

Full body clothing cover

High latitude during winter/spring season

Other causes of restricted sun (UVB) exposure, eg, predominant indoor living, disability, pollution, cloud cover

Low vitamin D diet

Low calcium diet

Poverty, malnutrition, special diets

Infant/childhood factors

Neonatal vitamin D deficiency secondary to maternal deficiency/vitamin D deficiency

Lack of infant supplementation with vitamin D

Prolonged breast-feeding without appropriate complementary feeding from 6 mo

High latitude during winter/spring season

Dark skin pigmentation and/or restricted sun (UVB) exposure, eg, predominant indoor living, disability, pollution, cloud cover

Low vitamin D diet

Low calcium diet

Poverty, malnutrition, special diets

Risk factors are prevented by:

Sun exposure (UVB content of sunlight depends on latitude and season)

Vitamin D supplementation

Strategic fortification of the habitual food supply

Normal calcium intake

2.3. Candidates for preventative vitamin D supplementation beyond 12 months of age

2.3.1. Recommendations

In the absence of food fortification, vitamin D supplementation should be given to:

Children with a history of symptomatic vitamin D deficiency requiring treatment. (1⊕⊕⊕)

Children and adults at high risk of vitamin D deficiency with factors or conditions that reduce synthesis or intake of vitamin D. (1⊕⊕⊕)

Pregnant women (see Section 3.1).

2.3.2. Evidence

Supplementation is a feasible and acceptable way to ensure adequate vitamin D intake independent of nutrition ( 58). Consensus guidelines for vitamin D supplementation have been drafted from a variety of pediatric/endocrine groups ( 16, 59, -62). Although there are numerous studies regarding vitamin D deficiency in pediatric populations and primary evaluations of the efficacy of various programs for supplementation of pregnant women, breast-feeding mothers, infants, children, and adolescents, there is more opinion than evidence on many aspects of this topic. However, there is strong, high-quality evidence that vitamin D supplementation should be provided for at-risk groups. All at-risk groups ( Table 2 ) are specifically vulnerable and, in the absence of food fortification, require supplementation.

Vitamin D fortification of infant formula is well established and recommended by all European countries, Australia, New Zealand, and the American Academy of Pediatrics ( 60). Vitamin D fortification of milk is mandated in Canada, and "enriched milk" is voluntarily fortified in the United States ( 63).

Children with chronic illnesses and conditions affecting vitamin D synthesis/absorption/metabolism may also benefit from supplementation and may require higher doses ( 58) but are not in the remit of this consensus on NR.

2.4. Dose of vitamin D and calcium for the treatment of nutritional rickets

2.4.2. Evidence

Most studies claim that the different doses commonly employed to treat vitamin D deficiency are safe, with hypercalcemia and/or hypercalciuria observed as a side effect only in a few individuals and usually seen in the 300 000 to 600 000 IU range ( 64). In a small study of children with NR (n = 17), doses of 1700 to 4000 IU of vitamin D ₂ rapidly increased 25OHD concentrations within 1 week and normalized calcium, phosphate, and ALP levels at 10 weeks ( 65). In another study in children aged 2-36 months with NR (n = 19), 5000 to 10 000 IU of oral vitamin D ₃ and calcium 0.5 to 1.0 g daily normalized serum PTH, calcium, and phosphate within 3 weeks, although ALP levels remained elevated ( 66).

2.5. Appropriate route of administration and duration of therapy

2.5.1. Recommendations

We recommend oral treatment, which more rapidly restores 25OHD levels than IM treatment. (1⊕⊕⊕)

For daily treatment, both D ₂ and D ₃ are equally effective. (1⊕⊕⊕)

When single large doses are used, D ₃ appears to be preferable compared to D ₂ because the former has a longer half-life. (1⊕⊕⊕)

Vitamin D treatment is recommended for a minimum of 12 weeks, recognizing that some children may require longer treatment duration. (1⊕⊕⊕)

2.5.2. Evidence

Some studies compared IM and oral administration of vitamin D, but most were conducted in adults and, therefore, may not be entirely relevant for children with NR. Oral or IM vitamin D was given to 24 normal volunteers (age, 50-78 y) in a dose of 600 000 IU of D ₂ or D ₃ ( 70). Peak levels of 25OHD were seen at 30 and 120 days in those given oral and IM treatment, respectively. Another study in 92 adults with 25OHD < 75 nmol/L compared 300 000 IU vitamin D ₃ IM to 50 000 IU D ₃ orally given on six occasions over 3 months ( 71). A higher proportion of subjects receiving oral treatment had 25OHD > 75 nmol/L at 3 and 6 months than IM subjects.

One RCT in 61 children with NR compared a single IM dose of 600 000 IU vitamin D ₃ to a weekly oral dose of 60 000 IU D ₃ for 10 weeks ( 72). There were no differences at 1, 4, and 12 weeks between groups in bone profiles, 25OHD concentrations, or side effects. A meta-analysis of studies comparing the administration of vitamin D ₂ and D ₃ concluded that, when given as bolus doses, vitamin D ₃ was more effective at raising 25OHD concentrations, but no significant differences were seen with daily doses ( 73).

Several studies explored the concept of "stoss therapy," ie, the administration of a large dose given as a single dose or in divided doses over several days. This approach has been advocated for ease of use and compliance with therapy. Three different single oral doses (150 000, 300 000, or 600 000 IU) in 56 Turkish children aged 3-36 months with NR did not affect the rate of improvement of rickets at 30 days ( 64).

However, eight subjects (two in the 300 000-IU group, six in the 600 000-IU group) developed hypercalcemia. A recent study in India compared single oral doses of 300 000 vs 600 000 IU of vitamin D ₃ in 76 rachitic children aged 6 months to 5 years ( 78). At 12 weeks, all children demonstrated radiographic healing with comparable decreases in ALP and PTH. However, hypercalcemia occurred in five children (6.5%)-two receiving 300 000 IU and three receiving 600 000 IU. Several review articles advocate different recommendations with stoss therapy that are not supported by evidence ( 75, -77). The few studies comparing daily treatment to stoss therapy contained groups with different subject characteristics. Although we recommend daily treatment as the first line of management, we recognize that in some situations, stoss therapy may be more practical. Therefore, we provide vitamin D dose recommendations for both treatment options ( Table 3 ). Any treatment needs to be followed by supplementation (see Sections 2.1 and 2.3).

Table 3.

Age

Daily Dose for 90 Days, IU

Single Dose, IU

Maintenance Daily Dose, IU

<3 mo

2000

N/A

400

3-12 mo

2000

50 000

400

>12 mo to 12 y

3000-6000

150 000

600

>12 y

6000

300 000

600

3.0. Prevention of Nutritional Rickets/Osteomalacia: Identification of Risk Factors

3.1. Dietary practices and nutrient intakes among mothers associated with nutritional rickets in infants

3.1.2. Evidence

Maternal diet and nutrient intake as a predictor of infantile rickets have not been addressed in the literature as an a priori hypothesis. However, available data have been collected during vitamin D intervention studies, case studies, or case series in women during pregnancy.

Many cases of NR included data on maternal 25OHD and, in some cases, dietary information ( 79, -81). Neonatal vitamin D deficiency is always caused by maternal deficiency and can have life-threatening consequences such as hypocalcemic seizures and dilated cardiomyopathy in unsupplemented infants ( 11). Hypocalcemia (see Section 4.1.2) or other early biochemical signs of rickets (such as elevated ALP and PTH) are present before radiographic signs of NR occur in unsupplemented neonates and infants ( 82, 83). A high percentage of mothers of infants with symptomatic vitamin D deficiency are from high-risk groups who are vitamin D deficient and exclusively breast-feeding ( 11, 24, 83, -85).

In a Canadian case series, six First Nation infants presented with hypocalcemic seizures within the first 30 days of life, with suspected or confirmed maternal vitamin D deficiency and a lack of supplementation during pregnancy ( 86). All were formula fed, which suggests that although their intake of vitamin D would have been sufficient in normal circumstances, in these infants the oral vitamin D supply via formula milk was insufficient to treat their pre-existing severe neonatal deficiency.

Prevention of maternal deficiency is critical, and all mothers should meet their nutritional requirement for vitamin D, which is currently set at 600 IU/d, although this value is not based on direct evidence from RCTs of vitamin D supplementation in pregnant women ( 28). Potentially, a higher intake of vitamin D may be required to prevent both maternal and neonatal deficiency ( 87). Prevention of congenital vitamin D deficiency is described in Section 4.4.

3.2. Early feeding, supplementation, complementary feeding, and nutrient intake associated with NR in infants

3.3. Association of sunlight exposure to nutritional rickets

3.3.1. Recommendations

Because UVB rays trigger epidermal synthesis of previtamin D ₃, restricted exposure to sun increases the risk of vitamin D deficiency and nutritional rickets. (1⊕⊕⊕)

Environmental factors such as latitude, season, time of day, cloud cover, and pollution affect availability of UVB, whereas personal factors such as time spent outdoors, skin pigmentation, skin coverage, age, body composition, and genetics affect the dose-response to UVB exposure and circulating 25OHD. (2⊕⊕○)

No safe threshold of UV exposure allows for sufficient vitamin D synthesis across the population without increasing skin cancer risk. (2⊕⊕○)

4.0. Prevention of Osteomalacia During Pregnancy and Lactation and Congenital Rickets

4.1. The relationship between vitamin D during pregnancy and infant growth and bone mass

4.1.2. Evidence

There are conflicting data about the association between maternal vitamin D status during pregnancy and birth anthropometry. Three RCTs of moderate to high quality using daily dose or single high-dose regimens did not find an association ( 151, -153), whereas two controlled trials of moderate-grade evidence found a positive association ( 146, 147). Three low- to high-quality RCTs did not find any difference in birth anthropometry in offspring of mothers supplemented with 400, 2000, or 4000 IU/d; none of the studies had a placebo group ( 87, 154, 155).

4.2. The effect of calcium supplementation during pregnancy on infant bone mass

4.2.2. Evidence

Calcium supplementation studies in pregnancy have not had congenital or neonatal rickets as an outcome, but three RCTs of maternal calcium supplementation during pregnancy measured neonatal bone ( 165, -167). These RCTs were conducted in West Africa where typical dietary calcium intakes are 250-300 mg/d ( 165), in the United States with an average intake of about 2000 mg/d ( 166), and in a multicenter World Health Organization study in populations with dietary calcium intake of approximately 600 mg/d (Argentina, Peru, India, Egypt, Vietnam, South Africa) ( 167). Maternal calcium supplementation had no effect on neonatal bone mineral assessed by dual-energy x-ray absorptiometry in the Gambian and US studies, except in the latter study in offspring of women in the lowest quintile of dietary calcium intake (<600 mg/d). There was no effect of maternal calcium supplementation on neonatal or infant anthropometry, a finding consistent with observational studies.

4.3. Influence of calcium or vitamin D supplementation in pregnancy or lactation on breast milk calcium or vitamin D

4.3.2. Evidence

Maternal vitamin D intake during lactation correlates with milk vitamin D activity. Several double-blind RCTs found that high maternal intakes of vitamin D (2000, 4000, and 6400 IU/d) were associated with higher breast milk vitamin D concentration ( Figure 2 ) ( 168, -171).

Supplementing mothers with high amounts of vitamin D has been suggested as a means of increasing both maternal ( Figure 3 ) and infant serum 25OHD concentrations ( 172, -175). Maternal vitamin D intakes up to 4000 IU/d are likely safe during pregnancy and lactation ( 16). However, the finding that infants of mothers supplemented with 2000 IU/d or more have similar serum 25OHD concentrations as infants receiving 400 IU/d ( Figure 4 ), as well as safety concerns, and our own recommendation that all infants receive 400 IU vitamin D per day lead us to advise that mothers should take recommended amounts (600 IU/d) rather than higher doses of vitamin D.

Maternal calcium intake during pregnancy or lactation does not influence breast milk calcium concentrations. Only one observational study found a weak association between maternal calcium intakes during pregnancy and breast milk calcium level at day 40 (mature milk) ( 176). Numerous studies, including two RCTs ( 177, 178) and two observational studies ( 179, 180) have not found a relationship between maternal calcium intake and breast milk calcium concentrations.

No studies have investigated the effect of maternal vitamin D intake during pregnancy on either milk calcium or vitamin D concentrations. Two double-blind RCTs found that maternal serum 25OHD concentration or maternal intake of vitamin D (up to 4000 IU/d) during lactation was not associated with milk calcium concentrations ( 181, 182).

4.4. Causes and therapy of congenital rickets

5.0. Assessing the Burden of Nutritional Rickets and Public Health Strategies for Prevention

5.1. Assessment of disease burden

5.2. Public health strategies for rickets prevention

5.2.1. Recommendation

Universally supplement all infants with vitamin D from birth to 12 months of age, independent of their mode of feeding. Beyond 12 months, supplement all groups at risk and pregnant women. Vitamin D supplements should be incorporated into childhood primary health care programs along with other essential micronutrients and immunizations (1⊕⊕⊕), and into antenatal care programs along with other recommended micronutrients. (2⊕⊕○)

Recognize nutritional rickets, osteomalacia, and vitamin D and calcium deficiencies as preventable global public health problems in infants, children, and adolescents. (1⊕⊕⊕)

Implement rickets prevention programs in populations with a high prevalence of vitamin D deficiency or limited vitamin D and/or calcium intakes and in groups of infants and children at risk of rickets. (1⊕⊕⊕)

Monitor adherence to recommended vitamin D and calcium intakes and implement surveillance for nutritional rickets. (1⊕⊕⊕)

Fortify staple foods with vitamin D and calcium, as appropriate, based on dietary patterns. Food fortification can prevent rickets and improve vitamin D status of infants, children, and adolescents if appropriate foods are used and sufficient fortification is provided, if fortification is supported by relevant legislation, and if the process is adequately monitored. Indigenous food sources of calcium should be promoted or subsidized in children. (1⊕⊕⊕)

Promote addressing the public health impact of vitamin D deficiency as both a clinical and a public health issue. (1⊕⊕⊕)

5.2.2. Evidence

Vitamin D supplementation

Infants aged 0-12 months and adolescents are at increased risk of NR and osteomalacia from vitamin D deficiency due to rapid growth. Vitamin D is found in a limited number of foods, and dietary intakes apart from fortified foods have little impact on overall vitamin D status. Programs that deliver micronutrient supplements provide the fastest improvement in micronutrient status of individuals or targeted populations ( 227, 228).

Food fortification with vitamin D

Although several studies have assessed the effectiveness of vitamin D fortification of food to increase 25OHD concentrations in different age groups and communities, relatively few fortification studies have targeted children. A systematic review and meta-analysis concluded from food-based RCTs that vitamin D-fortified foods increase serum 25OHD and reduce the prevalence of deficiency (<30 nmol/L) in adults, provided appropriate vehicles are chosen based on analysis of habitual diet ( 234). Fortification of chupatty flour (6000 IU/kg) raised 25OHD from approximately 12.5 nmol/L to approximately 48 nmol/L in children over a 6-month period ( 235). Fortification of fluid milk and margarine was estimated to increase vitamin D intake in 4-year-old children from 176 to 360 IU/d (4.4 to 9 μg/d) and 25OHD concentrations from 55 to 65 nmol/L ( 236). Milk fortification has also been a successful strategy to improve the vitamin D status of schoolchildren in India ( 237). Fortification and supplementation requirements may vary with population exposure to sunshine (see Section 3) ( 238).

Food fortification with calcium

Inadequate dietary calcium intake is a risk factor for NR in children over the age of 12 months with low dairy product intake, a common situation in low-income countries. The IOM recommends a calcium intake of 500 mg/d in children ages 1-3 years when children are at the greatest risk of NR, based on calcium retention in absorption studies ( 16). In populations with low dairy intake such as in Africa and parts of Asia, indigenous food sources of calcium or fortification of staple foods with calcium can provide adequate calcium intake in children ( 213, 239). Calcium salts can be used to fortify infant formulas, complementary foods, and staple food in areas where dairy intake is low. Calcium carbonate for food fortification is available at very low cost ( 227).

Food fortification effectively increased dietary calcium intakes by using calcium-fortified laddoos in the diet of underprivileged Indian toddlers ( 240) and by calcium fortification of cereal for 7- to 12-year-old children ( 241). More than 1100 foods are calcium fortified in the United States, yet dairy food makes up more than 65% of adolescents' calcium intake ( 242). In the United Kingdom, calcium fortification of flour is an important source of calcium intake (16% of total) for young adolescent girls ( 243). There are limited data from studies on calcium fortification or the acceptability of dietary diversification to include locally available and affordable calcium-rich foods in developing countries. Periodic monitoring for NR is important to determine the effectiveness of fortification and/or supplementation programs in preventing NR.

Health promotion

Education of medical providers and organizations, health insurers, policy makers, governments, public health officials, and the general public is vital to address the public health issue of NR and vitamin D deficiency. They should be provided with guidelines on the importance of adequate vitamin D and calcium intakes in children, adolescents, and pregnant and lactating women ( 244). National and global public health promotion strategies are essential to raise professional and community awareness, and global action to protect all children from vitamin D and calcium deficiency is imperative.

5.3. Economic cost/benefits of prevention programs

5.3.2. Evidence

Very weak evidence supports a policy of providing vitamin D supplementation to Asian children in the United Kingdom for the first 2 years of life ( 245). However, this report had methodological limitations that preclude any conclusions.

Urgent research is required to model the cost-effectiveness of alternative vitamin D supplementation strategies and food fortification programs. Future economic models should include:

Resources associated with different supplementation strategies

Indirect costs of treatment and complications

Resource use of current practice

Effectiveness of different approaches

Outcomes such as quality of life associated with 25OHD levels, and

Health care costs of disease caused by both skeletal and extraskeletal effects of vitamin D deficiency.

Costs of vitamin D supplementation and/or fortification programs will differ depending on the target 25OHD level and population characteristics. Subgroup analyses targeting high-risk groups, such as people with darkly pigmented skin, limited sun exposure, and low calcium intakes, should be conducted.

Conclusion

Vitamin D deficiency should be considered a major global public health priority. NR can have severe consequences, including death from cardiomyopathy or obstructed labor, myopathy, seizures, pneumonia, lifelong deformity and disability, impaired growth, and pain. NR is the "the tip of the iceberg," and its resurgence indicates widespread vitamin D deficiency with important public health implications. NR and osteomalacia are fully preventable disorders that are on the rise worldwide and should be regarded as a global epidemic. We advocate for the eradication of NR and osteomalacia through vitamin D supplementation of all infants, pregnant women, and individuals from high-risk groups and the implementation of international food fortification programs to ensure nutritional sufficiency of vitamin D and calcium for the whole population. This consensus document provides policy makers with a reference framework to work toward the global eradication of rickets.

Acknowledgments

Editorial support was provided by Sally Farrand. This guideline was produced by by ESPE, PES, SLEP, ASPAE, ISPAE, CSPEM, JSPE, APEG, APPES, ESPGHAN, and other expert participants. The consensus was financially supported by the above societies and an educational grant (non-participatory) by Danone Nutricia.

Disclosure Summary: M.Z.M. has received honoraria and lecture fees from Nutricia and Alexion. T.D.T. is a consultant for Biomedical Systems. W.H. has received honoraria and lecture fees from Internis and Alexion. No other author has anything to disclose.

Appendix A: Affiliations of Consensus Group Members

Magda Aguiar, Health Economics Unit, University of Birmingham, Birmingham, United Kingdom

Navoda Atapattu, Lady Ridgeway Hospital, Colombo, Sri Lanka

Vijayalakshmi Bhatia, Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Uttar Pradesh, India

Christian Braegger, Division of Gastroenterology and Nutrition and Children's Research Center, University Children's Hospital, Zurich, Switzerland

Gary Butler, Department of Paediatric and Adolescent Endocrinology, University College London Hospital, London, United Kingdom

Hamilton Cassinelli, Endocrinology Division, Ricardo Gutierrez Children's Hospital, Buenos Aires, Argentina

Linda A. DiMeglio, Section of Pediatric Endocrinology/Diabetology, Riley Hospital for Children at Indiana University Health, Indianapolis, Indiana, USA

Emma Frew, Health Economics Unit, University of Birmingham, Birmingham, United Kingdom

Junfen Fu, Division of Endocrinology, Children's Hospital of Zhejiang University School of Medicine, Hangzhou, China

Gail Goldberg, Nutrition and Bone Health Research Group, Medical Research Council Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, United Kingdom

Wolfgang Högler, Department of Endocrinology and Diabetes, Birmingham Children's Hospital; Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, United Kingdom

Elina Hyppönen, School of Population Health and Sansom Research Institute, University of South Australia; South Australian Health and Medical Research Institute, Adelaide, Australia; Population Policy and Practice, University College London Institute of Child Health, London, United Kingdom

Hafsatu Wasagu Idris, Endocrinology and Gastroenterology Unit, Department of Paediatrics, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria

Rajesh Khadgawat, Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India

Mairead Kiely, Vitamin D Research Group, School of Food and Nutritional Sciences; Irish Centre for Fetal and Neonatal Translational Research [INFANT], University College Cork, Cork, Ireland

Jane Maddock, University College London, Institute of Child Health, London, United Kingdom

Outi Mäkitie, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

Toshimi Michigami, Department of Bone and Mineral Research, Research Institute, Osaka Medical Center for Maternal and Child Health, Osaka, Japan

M. Zulf Mughal, Department of Paediatric Endocrinology, Royal Manchester Children's Hospital, Manchester, United Kingdom

Craig F. Munns, Department of Endocrinology and Diabetes, The Children's Hospital at Westmead, Sydney, Australia

Abiola Oduwole, College of Medicine University of Lagos, Lagos, Nigeria

Keiichi Ozono, Osaka University Graduate School of Medicine, Department of Pediatrics, Osaka, Japan

John M. Pettifor, Medical Research Council/Wits Developmental Pathways for Health Research Unit, Department of Paediatrics, University of the Witwatersrand, Johannesburg, South Africa

Pawel Pludowski, Department of Biochemistry, Radioimmunology, and Experimental Medicine, The Children's Memorial Health Institute, Warsaw, Poland

Lorna Ramos-Abad, University of the Philippines, College of Medicine, Manila, The Philippines

Lars Sävendahl, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden

Anju Seth, Division of Pediatric Endocrinology, Lady Hardinge Medical College & Kalawati Saran Children's Hospital, New Delhi, India

Nick Shaw, Department of Endocrinology and Diabetes, Birmingham Children's Hospital, Birmingham, United Kingdom

Bonny L. Specker, Ethel Austin Martin Program, South Dakota State University, Brookings, South Dakota, USA

Tom D. Thacher, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA

Dov Tiosano, Department of Pediatrics, Rambam Medical Center, Haifa, Israel

Ted Tulchinsky, Braun School Public Health, Hebrew University-Hadassah, Jerusalem, Israel; Public Health Reviews, Brussels, Belgium

Leanne Ward, Department of Pediatrics, University of Ottawa and Division of Endocrinology and Metabolism, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada

² In areas where 25OHD assays are not readily available, suppression of PTH in the presence of hypercalcemia and pharmacological doses of vitamin D may support the diagnosis of vitamin D toxicity. When PTH assay is also unavailable, the possibility of toxicity should be considered in the presence of symptomatic hypercalcemia in association with pharmacological doses of vitamin D.

³ Note that the term "supplementation" may be interpreted to mean additional vitamin D provided from supplements, general multivitamins, or food fortification. In the context of this article, vitamin D supplementation refers to vitamin D above that which is found in standard dietary sources, with the exception of fortified infant formula.

Abbreviations:

ALP

alkaline phosphatase

DXA

dual-energy x-ray absorptiometry

NR

nutritional rickets

25OHD

25-hydroxyvitamin D₂ and/or D₃ or 25-hydroxycholecalciferol D₂ and/or D₃

1,25(OH)₂D

1,25-dihydroxyvitamin D₂ and/or D₃ or 1,25-dihydroxycholecalciferol D₂ and/or D₃ (calcitriol)

PTH

parathyroid hormone

RCT

randomized controlled trial

UVB

ultraviolet B

Vitamin D₂

ergocalciferol

Vitamin D₃

cholecalciferol.

References

9. Pettifor JM. Vitamin D deficiency and nutritional rickets in children. In: Feldman D, Pike JW, Adams J, eds. Vitamin D. 3rd ed London: Elsevier Inc; 2011:1107-1128. [ Google Scholar]

10. Pettifor JM. Nutritional rickets. In: Glorieux FH, Pettifor JM, Juppner H, eds. Pediatric Bone: Biology and Diseases. 2nd ed Amsterdam, The Netherlands: Elsevier; 2012:625-654. [ Google Scholar]

16. Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: The National Academies Press; 2011. [ Google Scholar]

110. Strand MA, Peng G, Zhang P, Lee G. Preventing rickets in locally appropriate ways: a case report from north China. Int Q Community Health Educ. 2003;21:297-322. [ Google Scholar]

227. World Health Organization. Guidelines on food fortification with micronutrients. Geneva, Switzerland: World Health Organization; 2006. [ Google Scholar]

229. Flynn M. Recommendations for a national policy on vitamin D supplementation for infants in Ireland. Dublin, Ireland: Food Safety Authority of Ireland; 2007. [ Google Scholar]

Articles from The Journal of Clinical Endocrinology and Metabolism are provided here courtesy of The Endocrine Society

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Consensus Statement: Global Consensus Recommendations on Prevention and Management of Nutritional Rickets

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J Clin Endocrinol Metab. 2016 Feb; 101(2): 394-415. Consensus Statement Craig F. Munns, Nick Shaw, Mairead Kiely, Bonny L. Specker, Tom D. Thacher, Keiichi Ozono, Toshimi Michigami, Dov Tiosano, M. Zulf Mughal, Outi Mäkitie, Lorna Ramos-Abad, Leanne Ward, Linda A. DiMeglio, Navoda Atapattu, Hamilton Cassinelli, Christian Braegger, John M.

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Du musst nicht für Zwei essen, dennoch spielt die richtige Ernährung in der Schwangerschaft eine große Rolle. Wir erklären dir, welche Nahrungsmittel besonders empfehlenswert sind und worauf du lieber verzichten solltest.

Weiterlesen Stärkende Getränke für Schwangerschaft, Wochenbett und Stillzeit

Weiterlesen Ernährung in der Schwangerschaft

Weiterlesen Ernährung im ersten Trimester

Weiterlesen Ernährung bei Schwangerschaftsdiabetes

Weiterlesen Lebensmittelinfektionen vorbeugen & Hygienetipps für Schwangere

Weiterlesen Tees in der Schwangerschaft - Was du beachten solltest

Weiterlesen
Melde dich zum Schwanger.at Newsletter an - dich erwarten spannende Artikel, Produkttests und Gewinnspiele!

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Du musst nicht für Zwei essen, dennoch spielt die richtige Ernährung in der Schwangerschaft eine große Rolle. Wir erklären dir, welche Nahrungsmittel besonders empfehlenswert sind und worauf du lieber verzichten solltest.

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Warum Folsäure auch für Väter relevant ist

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Unser Leitfaden bietet hilfreiche Tipps zur Einordnung von Forschungsergebnissen und soll dazu beitragen, gezielt nachfragen zu können, wenn allzu plakative Formulierungen verwendet werden. ZUM DOWNLOAD

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Ernährung in der Schwangerschaft Archive

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Wie sieht die perfekte Ernährung in der Schwangerschaft aus? Und worauf solltests Du jetzt verzichten? Entdecke hier alle unsere Beiträge zum Thema

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Eisen ist ein Spurenelement mit wichtigen Funktion

Erhöhter Bedarf an Eisen für Schwangere/ Stillende

Große Vielfalt an eisenhaltigen Lebensmitteln

Empfehlung ist mit der Ernährung schwer zu erreichen

Möglichkeit des Einsatzes von Präperaten & (Supplementierung) nach medizinischer Beratung

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Viele Menschen glauben, dass schwangere Frauen „für zwei" essen sollen, also doppelt so viel wie normal. Das stimmt aber nicht!

Viel wichtiger ist eine gesunde Ernährung mit viel frischem Obst und Gemüse, Fisch, Milch, Milchprodukten und hochwertigen Fetten. Trinken Sie viel, am besten Wasser oder ungesüßten Tee. Machen Sie keine Diäten und fasten Sie nicht, auch nicht aus religiösen Gründen. Diäten und Fastenkuren sind für Schwangere ungesund.

Wichtig für die gesunde Entwicklung Ihres Babys sind:

Folsäure: in Spinat, Brokkoli, Eigelb, Tomaten, Bananen

Eisen: in Fleisch, schwarzem Pfeffer, Zimt, Petersilie, Bohnen, Erbsen, Linsen, Sesam, Mohn, Nüssen

Jod: Verwenden Sie jodiertes Speisesalz!

Kalzium: in Milch, Milchprodukten, Kohl, Brokkoli, Lauch, Fenchel

Besprechen Sie alle Ihre Fragen mit Ihrer Ärztin oder Ihrem Arzt, und lesen Sie hier weitere Informationen:

Risiko-Lebensmittel und Tabus in der Schwangerschaft

In der Schwangerschaft verändert sich der gesamte Körper der Frau. Das Immunsystem, also die Abwehrkraft, kann dadurch geschwächt werden. Daher verlaufen Infektionen in dieser Zeit manchmal komplizierter als sonst und können die Gesundheit von Mutter und ungeborenem Kind gefährden.

Beugen Sie daher vor, indem Sie beim Kochen und Essen zwei Dinge beachten:

Achten Sie bei der Zubereitung und bei der Lagerung von Lebensmitteln auf höchst sorgfältige Hygiene.

Verzichten Sie auf so genannte Risiko-Lebensmittel.

Zu den Risiko-Lebensmitteln zählen:

Rohmilch & Rohmilch-Produkte
Rohmilch ist Milch von Tieren, die nicht behandelt wurde. Verzichten Sie auf Rohmilch oder kochen Sie sie vorher ab.
Verzichten Sie auf Produkte aus Rohmilch. Sie erkennen diese an der Kennzeichnung „mit Rohmilch hergestellt". Entfernen Sie bei Käse die Rinde und essen Sie keinen geschmierten Käse (beispielsweise Tilsiter, Quargel) oder Weichkäse (zum Beispiel Camembert).

Fisch, Fleisch & Eier
ACHTUNG! Meiden Sie fettreiche Raubfische wie Thunfisch, Schwertfisch, Heilbutt und Hecht. Diese Fische sind oft mit Schwermetallen belastet. Schwermetalle kommen auch in Innereien vor. Auch auf Innereien sollten Sie daher verzichten.
Verzichten Sie auf rohe und halbrohe Fische und Meeresfrüchte, etwa Sushi, Austern und ähnliches. Vermeiden Sie auch geräucherten und gebeizten Fisch, etwa Räucherlachs, Graved Lachs. Essen Sie kein Fleisch, keine Wurst und keine Eier, die roh oder nicht ganz durchgegart sind. Dazu zählen beispielsweise Carpaccio, Beef Tartar, Steak rare und medium, Salami, Kantwurt, Landjäger, Rohschinken, Selchfleisch, Schinkenspeck, weich gekochte Eier, Spiegeleier oder Speisen mit rohen Eiern wie selbst gemachtes Tiramisu und ähnliches.

Verzichten Sie auf Alkohol. Bisher konnte keine wissenschaftliche Studie beweisen, dass selbst kleine Mengen Alkohol in der Schwangerschaft ungefährlich sind. Daher gilt: Finger weg von Alkohol! Beachten Sie, dass auch Mehlspeisen, Süßigkeiten oder gekochte Soßen (Rest-)Alkohol enthalten können! Trinken Sie zur Vorsicht auch nur wenig koffeinhaltige Getränke. Höchstens 2 bis 3 Tassen Kaffee oder 4 Tassen grüner oder schwarzer Tee sind erlaubt. Achtung: Auch Eistee, Cola-Getränke, Eiskaffee, Getränke mit Guarana, viele Energy Drinks und ähnliches enthalten Koffein!
Vermeiden Sie zur Sicherheit frisch gepresste und nicht erhitzte Säfte aus Obst und Gemüse an Saftständen und in der Gastronomie. Trinken Sie keine Getränke, die den Bitterstoff Chinin enthalten, zum Beispiel Tonic Water, Bitter Lemon und ähnliches.

Besprechen Sie alle Ihre Fragen mit Ihrer Ärztin oder Ihrem Arzt, und lesen Sie hier weitere Informationen:

Suchtmittel

Verzichten Sie in der Schwangerschaft auf jede Art von Alkohol, Rauchen und Drogen!

Alkohol
Trinken Sie in der Schwangerschaft keinen Alkohol! Schon kleine Mengen können das ungeborene Kind auf Dauer schädigen. Alkohol wirkt wie Gift auf die Nerven und das Gehirn und ist damit eine der häufigsten Gründe für Fehlbildungen bei Kindern.

Besprechen Sie alle Ihre Fragen mit Ihrer Ärztin oder Ihrem Arzt, und lesen Sie hier weitere Informationen:

Rauchen
Rauchen Sie in der Schwangerschaft nicht und vermeiden Sie Räume, wo geraucht wird! Zigaretten enthalten Nikotin und fast 5.000 Chemikalien. All diese Inhaltsstoffe können bei Ihrem Baby schwere Schäden verursachen. Oft kommt es bei Schwangeren, die rauchen, zu Frühgeburten und Fehlgeburten. Kinder von rauchenden Müttern bekommen häufiger Asthma, Allergien, Lungenentzündung, Bronchitis und andere Krankheiten. Auch die Gefahr von plötzlichem Kindstod ist größer.

Besprechen Sie alle Ihre Fragen mit Ihrer Ärztin oder Ihrem Arzt, und lesen Sie hier weitere Informationen:

Drogen
Nehmen Sie in der Schwangerschaft keine Drogen und Rauschmittel! (Rauschmittel sind alle Mittel, die das Bewusstsein verändern.) Drogen und Rauschmittel können die Entwicklung Ihres Kindes schwer schädigen und im schlimmsten Fall zu Fehlgeburten und Totgeburten führen. Wenn Sie Suchtprobleme haben, schämen Sie sich nicht, sondern sprechen Sie mit Ihrer Ärztin oder Ihrem Arzt. Sie können sich auch direkt an Stellen wenden, die sich auf Suchtberatung spezialisiert haben.

Besprechen Sie alle Ihre Fragen mit Ihrer Ärztin oder Ihrem Arzt, und lesen Sie hier weitere Informationen:

Medikamente

Manche Medikamente sind für Schwangere und ihre Babys gefährlich. Wenn Sie regelmäßig Medikamente nehmen müssen, sagen Sie unbedingt Ihrer Ärztin oder Ihrem Arzt, dass Sie schwanger sind. Auch wenn sie jetzt krank werden und Medikamente nehmen sollen, informieren Sie die Ärztin oder den Arzt über Ihre Schwangerschaft. Sagen Sie auch in der Apotheke immer dazu, dass Sie schwanger sind, wenn Sie dort Medikamente kaufen.

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Viele Menschen glauben, dass schwangere Frauen „für zwei" essen sollen, also doppelt so viel wie normal. Das stimmt aber nicht! Viel wichtiger ist eine gesunde Ernährung mit viel frischem Obst und Gemüse, Fisch, Milch, Milchprodukten und hochwertigen Fetten. Trinken Sie viel, am besten Wasser oder ungesüßten Tee.

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Folate and pregnancy go hand in hand. This vitamin - also referred to as folic acid - is a key player in the healthy development of the baby.

What is folate?

Folate is the generic name used for a group of water-soluble compounds that belong to the family of B-vitamins.

Folate and folic acid are often used interchangeably, but they're actually two different forms of the same vitamin. Folate is the natural form of the vitamin found in foods and in the body; while folic acid is its synthetic form, used in supplements or fortified foods. Our bodies absorb folic acid from fortified foods or supplements significantly better than folate from foods.

What are the functions of folate?

Folate is needed to help our cells grow and multiply, which makes it a key vitamin in periods of rapid growth and development, such as pregnancy and infancy. Folate is particularly important to help develop the baby's skull and spinal cord, which is why low levels of this vitamin, before and during pregnancy, can lead severe birth defects, called neural tube defects.

Folate and vitamin B12 share many functions in the body. For example, they both work together to create our genetic material (DNA), form healthy red blood cells and support the normal functioning of our brain and nervous system. Both vitamins, alongside vitamin B6, also collaborate in the breaking down of homocysteine, an amino acid that can put us at higher risk of cardiovascular disease, when present in high amounts.

How much folate do I need per day?

How much folate you need per day changes according to your age, sex and life-stage.

Folate recommendations are measured in μg of folate equivalents (DFE), a unit that takes into account the fact that we absorb folic acid better than folate from foods.

1 μg of DFE is equivalent to:

1 μg of folate from foods

0.6 μg of folic acid from fortified foods

0.6 μg folic acid supplement taken with food

0.5 μg folic acid supplement taken on an empty stomach

The dietary reference value (DRV)* for healthy adults (over the age of 18) is 330 μg DFE per day. During pregnancy and lactation, needs can go up to 600 μg and 500 μg DFE per day, respectively.

Following your country's dietary guidelines on a healthy and balanced diet will help you meet your needs for folate. However, those who wish to become pregnant are advised to take 400 μg of folic acid daily from fortified foods, supplements, or both, starting up to a month prior to conception, to lower the risk of neural tube defects in the baby.
* These values are based on the adequate intake (AI) and population reference intakes (PRI) estimates from the European Food Safety Authority (EFSA). They should not be interpreted as nutrient goals. To know more about DRVs in Europe .
What foods contain folate?

dark green vegetables,

legumes

orange and grapefruit juice

peanuts and almonds.

We can find folate in small amounts in a variety of foods, but some of its richest sources include:

Meat is usually low in folate, but kidney and liver are two good animal sources of this vitamin.

In some countries, folic acid is added to foods, which helps people get more of this vitamin by eating grain and cereal products (such as bread and breakfast cereals) and some fat spreads.

Does folate interact with other nutrients?

Folate and vitamin B12 share many important tasks in the body, which support the healthy function of our cells and the nervous system. If we don't get enough folate or vitamin B12 for a long period, their common functions become compromised and our health can be affected in the long-term.

Besides, folate (together with vitamin B12 and vitamin B6) and choline help our bodies break down an excess of homocysteine, through two different processes. Meeting the recommended amounts for these micronutrients is important to help our bodies maintain safe levels of homocysteine, which can put us at higher risk of cardiovascular disease, when present in high amounts. In some cases, mainly affecting people with a genetic predisposition, low levels of folate could make our bodies compensate by using more choline in this process.

What happens if I have too little folate?

Folate deficiency is not common in healthy adults with a healthy and balanced diet. Nevertheless, it can affect people who have higher needs for this vitamin, or those with specific health conditions that impair the absorption of nutrients by our bodies (such as celiac disease, inflammatory bowel disease or chronic alcohol abuse). It can also affect people who have a specific mutation in the MTHFR gene, which prevents the body from converting folate to its active (functional) form.

Folate deficiency is particularly harmful during the early stages of pregnancy as it increases the risk of pregnancy complications. For example, low levels of folate before or during pregnancy increase the risk of babies having neural tube defects (NTDs), such as spina bifida, which are severe malformations of the spinal cord and brain.

Folate deficiency can cause us to become irritable and forgetful. In the long-term, it can lead to megaloblastic anaemia, a disease that causes our bodies to form unusually large red blood cells in lower amounts. The few misshaped red blood cells then have difficulties delivering enough oxygen around the body, leading to constant fatigue and shortness of breath. This condition can also be caused by vitamin B12 deficiency.

What happens if I have too much folate?

It is highly unlikely to get harmful amounts of folate through foods alone. Even if we exceed our daily needs, our bodies remove the folate surplus through urine.

Nevertheless, adults are advised not to have more than 1 mg of folic acid (from fortified foods or supplementation) per day.

Supplementation of folic acid is not harmful per se, but it can mask the symptoms of vitamin B12 deficiency (if there's one) which if it's not diagnosed in time, can cause serious harm to the function of our nervous system.

Before taking folate supplements, check with your doctor or a registered dietitian/nutritionist or consult your national dietary guidelines.

When should I pay extra attention to a folate deficiency?

People who are, or want to become pregnant, need to pay extra attention to their folate intake, as their needs for this vitamin are higher to support a healthy pregnancy. Up to a month before pregnancy, it's advised to have 400 μg of folic acid per day from supplements, fortified foods, or both on top of a healthy diet.

If you are or want to become pregnant, make sure to get professional advice on folic acid supplementation or consult your national dietary guidelines.

1. European Food Safety Authority. 2014. Scientific Opinion on Dietary Reference Values for folate. EFSA Journal 2014;12(11):3893

2. World Health Organization (WHO). 2004. Vitamin and mineral requirements in human nutrition. 2nd edition. Geneva, Switzerland: WHO.

3. Public Health England. 2019. McCance and Widdowson's Composition of Foods Integrated Dataset.

References

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Folate: foods, functions, how much do you need & more

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Folate and pregnancy go hand in hand. This vitamin - also referred to as folic acid - is a key player in the healthy development of the baby. Folate is the generic name used for a group of water-soluble compounds that belong to the family of B-vitamins.