Vitamin A Zoomed In

Debunking Vitamin A On Your Prenatal to Postnatal Journey (Complete Guide)

Vitamin A is an incredibly important vitamin to humans and is even more important to consume adequate amounts during your prenatal to postnatal journey and beyond. However, despire the importance of this vitamin, there seems to be alot of scarcity or fear around its use during this important time. This fear seems to stem from a study conducted in 1995 which showed that synthetic vitamin A caused an increase in birth defects.

However, this study had many flaws and many studies following it have disproven and even shown contradictory evidence. Is this article we will go over the distinction you should make between synthetic vitamin A and natural vitamin A, the flaws of this 1995 study, the risks with not getting enough vitamin A during pregnancy and solutions.

Understanding Vitamin A

There is often a lot of confusion when it comes to Vitamin A. It is an essential fat soluble vitamin which means that it is often best absorbed in the presence of fat.

Your body gets vitamin A in two main ways. The first is by consuming preformed vitamin A (retinol) which is the most bioavailable form. You will find this exclusively in wholefood animal products like beef liver, eggs and fish. The second way is through provitamin A (carotenoids like beta carotene). You will find this mostly in fruits and vegetables. Beta Carotene needs to be converted in the body to form Vitamin A. 

It is important to note that many people on a plant based diet think they can get an adequate amount of vitamin A through eating enough plants and fruits rich in beta carotene. However, while this might be true for a large percentage of people, this is not the case for everyone. This is because up to 42% of people carry the BCMO1 gene mutation which makes it difficult to convert beta carotene into active vitamin A (1)(2). This is why many plant based eaters can be deficient in vitamin A without knowing why. 

Regardless of your dietary pattern of eating, the population in general seems to be largely deficient in this essential fat soluble vitamin. For instance, it is estimated that over 124 million children are vitamin A deficient (3). Globally, this might equate to 30% of children (4). Vitamin A deficiency is not just a concern for children but also adults with statistics suggesting adults consume less vitamin A than young children (5).

Synthetic Vitamin A v Natural Vitamin A

The difference between natural vitamin A and synthetic vitamin A is one of the biggest oversights that health professionals overlook. Synthetic vitamin A and natural vitamin A are not the same and close to 95% of research has studied only synthetic forms.

As already mentioned, you can get natural vitamin A through two ways. By consuming either preformed vitamin A from animals products like beef liver, organ meats, eggs and fish or by converting beta carotene from fruits and vegetables into active vitamin A. 

Synthetic vitamin A on the other hand is usually a vinyl or coal tar at one stage during processing. You will typically find it as reinyl acetate or retinyl palmitate in supplements. You might also find synthetic beta carotene in certain supplements. It is manufactured from benzene, which is often extracted crude oil.

The Risks of Not Getting Adequate Vitamin A For Pregnant Women

Oftentimes, many women will be told of the risks associated with supplementing with too much vitamin A but will rarely be advised about the risks of not getting enough vitamin A during this important period. This can have the effect where women come to fear vitamin A consumption entirely and consume less of it. The other overlooked part of vitamin intake during pregnancy is that the vitamin A requirements for mothers go up during this time, specifically in the third trimester where stores are being transferred to baby (6). Low consumption can not only increase your babies risk of health complications but can also impact a mums health.

Increased Maternal Mortality & Night Blindness

In fact, a vitamin A deficiency (VAD) during pregnancy is associated with an increase in maternal mortaility (7). In severe cases of VAD which is often seen in low income families or families in developing countries, maternal night blindness was associated with a 3-fold excess risk of maternal death (8).

Increased Maternal Mortality & Maternal Anaemia

However, one of the biggest risk factors for pregnant mums has to do with maternal anemia, which is a common consequence of VAD. According to statistics, maternal anaemia impacts 41.8% of women globally and increases (9) (10). Even subclinical levels of vitamin A have been associated with maternal anemia, particularly in the third trimester (11). Subclinical just means that your levels are on the low end of normal. This would make sense because nutrient stores in mums are depleted most during the third trimester and levels on the low-normal end will typically fall into the deficient zone.

Increased Risk For Multiple Health Concerns

Outside of pregnancy specific concerns, VAD generally has been connected with a host of health concerns including inflammatory conditions, skin issues, poor immune health, vision concerns, infertility, plus more (12)(13)(14)(15)(16). 

So do not overlook the importance of vitamin A for mums aswell as their baby as there are risk for not consuming enough vitamin A for both parties.

The Risks of Not Getting Adequate Vitamin A For Baby

Many people will point to birth defects as the main reason to be wary of vitamin A during pregnancy. While you should not be downing vitamin A like candy, there is more solid evidence that not getting enough vitamin A during pregnancy can lead to birth defects and developmental concerns in infants.

Congenital Diaphragmatic Hernia (CDH) 

While vitamin A deficiency has been linked to a number of birth defects, the one which has been studied the most and is not often talked about is Congenital diaphragmatic Hernia (CDH). CDH occurs when the diaphragm fails to close during the prenatal period, allowing the contents of the abdomen to migrate into the chest, preventing the growth and development of the respiratory system. CDH is the greatest cause of respiratory failure in infants and accounts for 8% of congenital anomalies (17)(18).  

The connection began in the early 2000s when researchers coined the retinoid hypothesis for CDH which was based on circumstantial and direct experience evidence (19). Since then, several studies have found and continue to find evidence that a Vitamin A deficiency might be the primary driver of this congenital defect.  

Most recently, a 2022 animal study found that pregnant mice fed a low vitamin A diet over a 3 month period, lead to an increased incidence of CDH in mice, providing evidence for the retinoid hypothesis (20). This was the first study which showed that manipulating dietary intake of vitamin A strongly induced CDH in offspring.

This study supports two recent epidemiological studies in humans which have found that a low dietary intake of vitamin A during pregnancy was strongly correlated with CDH in humans (21)(22). Infants with CDH have also been shown to have low circulating levels of vitamin A (23)(24). Other studies also provide evidence for the link between vitamin A and CDH (25)(26).  

CDH is not the only birth defect associated with a VAD. There are also many developmental concerns linked with not getting enough vitamin A. 

Abnormal Pancreas Development Risk 

Outside of CDH, VAD has also been connected with multiple variations of other birth defects. For example, animal studies have shown that VAD during pregnancy can impact the development of the pancreas in rats, potentially connecting VAD to the onset of diabetes in infants, adulthood and beyond (27)(28).

Abnormal Auditory Development Risk

Likewise, other animal studies have also shown that a VAD during pregnancy may lead to the abnormal development of the inner ear in infants (29)(30)(31). Based on these findings, researchers believe that adequate levels of vitamin a during pregnancy might offset the risk of sensorineural hearing loss in humans (32).

Abnormal Kidney Development Risk

VAD also has links with poor kidney development. In study, it was found that mild VAD led to a decrease in kidney weight and nephron numbers in newborns (33). Another study conducted on 16 mothers with VAD and 64 mothers with sufficient Vitamin A found that infants born to VAD mothers had smaller kidneys compared to infants born to mums with sufficient vitamin A (34). A systematic review also found an association between VAD during pregnancy and poor kidney function and structure in children (35).

Abnormal Congenital Spinal Deformities Risk

In one animal study where they manipulate dietary intake of vitamin A from preconception to birth, it was found that a VAD led to an increased risk of congenital scoliosis by 13.79% compared to the 0% risk in control group who were fed a normal diet during this time (36). The researchers concluded that a VAD impacted retinoid signalling pathways leading to defects.

Abnormal Anorectal Malformation Risk

In other animal studies looking at VAD, researchers have found that inadequate vitamin A during pregnancy may lead to embryonic development of anaorectal malformations in offspring (37).

Aside from VAD risk and birth defects, not getting enough vitamin A has also been connected with other conditions.

Increased Risk Of Childhood Schizophrenia

VAD, especially during the second trimester, was found to be connected with a 3x increase in the risk of developing a schizophrenia spectrum disorder in a large study looking at 19,044 births (38).

OKAY, But Doesn’t Excessive Vitamin A Also Cause Birth Defects? 

The vast majority of fear and caution comes from a study conducted in 1995. Since then, this study has left a lasting imprint on vitamin A guidelines and how health professionals choose to navigate vitamin A recommendations during pregnancy.

The 1995 Study Summary:

In this study, the researchers main conclusion was that infants were at an increased risk of birth defects when the pregnant woman's intake exceeded more than 10,000IU per day in supplemental Vitamin A (39). This study had a few flaws however and since its publication, multiple other studies have shown conflicting results, with some even showing that 10,000IU daily is not just safe but may even be indicated for preventing birth defects.

Issue 1: ‘Normal’ Birth Defects Normally Occur At 3%

The conclusion of this study was that “high dietary intake of preformed vitamin A appears to be teratogenic. Among the babies born to women who took more than 10,000 IU of preformed vitamin A per day in the form of supplements, we estimate that about 1 infant in 57 had a malformation attributable to the supplement”. However, according to the CDC, 3% of births, which is around 1 in 33 births, are likely to result in a birth defect (40). Technically, you could say that the study had a protective effect based on ‘normal’ defect rates and the studies' conclusion.

Issue 2: The Conclusion Was Based Off Synthetic Vitamin A Intake 

The conclusion surrounding the 10,000IU threshold was based purely on the synthetic form of vitamin A, not the natural food complex vitamin A. The majority of studies looking at vitamin A toxicity usually research the synthetic form and not food based vitamin A. They are not the same. Synthetic vitamin A is an isolated compound devoid of cofactors, minerals and other compounds which assist in the utilisation and biocompatibility of natural vitamin A. While this study did consider food based vitamin A and did see an increased prevalence in birth defects, the amount of women consuming above 10,000IU was so few, that it made “birth defect estimates from food imprecise” and some prevalence ratios “statistically unstable”.

Issue 3: No Distinction Made Between Synthetic A, Fortified A and Natural A

The study also failed to distinguish between fortified foods which contained synthetic vitamin A and wholefood sources of vitamin A like liver, eggs and fish. Given fortified food cereals are full of sugar, pesticide residues, artificial colours, additives and preservatives, it would make sense that you might see an increase in birth defects for people consuming large amounts of these foods. For instance, certain diets like the western or vegetarian diet have been connected with an increased risk for birth defects (41)(42).

Issue 4: Vitamin A Status Was Determined By Questionnaire

This study also used food based questionnaires for measuring vitamin A consumption, rather than doing blood work and testing vitamin A status. For example, what did you eat last Monday? In questionnaire or survey based studies, there is the potential for both demand and recall bias where participants change their behaviour by simply being in the study or cannot accurately recall information. 

Issue 5: A 1990 Study Found The Opposite

Before we jump into the post 1995 studies, one study with similar methods found that daily supplementation up to 40,000IU actually reduced the risk of birth defects by 50% compared to no supplementation. While amounts over 40,000IU increased the risk of birth defects by 2.7% (43). So yes, there might be a risk, but at levels greater than 10,000IU as concluded by the study.

What Has Research Post 1995 Shown?

Since the publication of the 1995 study, several studies have provided evidence contradicting the results. Again, it is important to note that these studies mainly looked at synthetic vitamin A and not food based.

1998 Study: “Periconceptional vitamin A use: how much is teratogenic?”

In this study, the researchers stated that no human epidemiological studies establish at what level vitamin A becomes teratogenic (44). However, the study did present data based on blood tests that showed that women taking 30,000IU of preformed vitamin A daily, were not greater than the retinoid blood levels in pregnant women during the first trimester who delivered healthy babies. The researchers also reference non human primate data showing no teratogenicity of vitamin A at doses of 30,000 IU/d. They state that if periconceptual levels up to 30,000IU occur unintentionally, animal studies support only a very low risk of teratogenicity.  Based on this study, it seems that vitamin A consumption at doses up to 30,000IU present only a low risk of causing issues.

1998 Study: “Safety of vitamin A: recent results”

Again, the researchers in this study stated that the available data (1995 study) cannot convincingly define an upper safe limit for periconceptional vitamin A intake (45). In this study, researchers who evaluated blood levels of vitamin A in pregnant women found that doses of 30,000IU per day resulted in healthy blood levels of vitamin A and had no association with teratogenicity.  

1999 Study: “High vitamin A intake in early pregnancy and major malformations”

In this study, 311 mothers consumed between 10,000IU-300,000IU of vitamin A during the first trimester of pregnancy with the median dose being 50,000IU (46). This study found no congenital malformations among the 120 infants exposed to more than 50,000IU of vitamin A per day.

What Can We Learn From These Studies?

Based on the overall research it seems that evidence supports intake of vitamin A of 10,000IU for protective benefit against birth defects. Of course, best practice is to always consult with your health care professional and even request to test your vitamin A status. From there, you can tailor your diet to suit your needs. 

From the evidence we also know that any birth defects related to excess vitamin A, relate mainly to the synthetic form of the vitamin and not the natural food based vitamin A (not including fortified foods made with synthetic vitamin A).

Why Is Food Based Vitamin A Supreme?

The problem with nutritional studies is that they tend to study specific vitamins and nutrients in isolation and in the absence of other nutrients and cofactors. This is not just an issue with nutrition studies but medicine generally. For example, vitamin A is never found in isolation in foods like liver, eggs and fish. It is always found alongside other nutrients which help absorption, utilisation and minimise the risk of toxicity.

For example, Vitamin E, Taurine, cholestrol and Vitamin K have been shown to reduce vitamin A toxicity (47) (48) (49) (50).

However, when we study nutrients like vitamin A in isolation and disconnect them from nature, it makes sense that we might find adverse results. Humans were never supposed to consume single forms of nutrients from artificial sources.

Of course, this is not to say that you cannot overdo it with vitamin A from food because you definitely can but as is with any food, balance and moderation is key.

Vitamin A Trade Off: A Summary

Based on the research, there is far more ‘good evidence’ that consuming too little natural vitamin A can increase your baby's risk of birth defects than consuming too much vitamin A.

In Vitamin A deficiency studies, they directly manipulated vitamin A intake (e.g. they gave rats low vitamin A to see the impact versus a normal diet).

In comparison, it is not ethically feasible to manipulate vitamin A intake in humans which is why vitamin A toxicity studies mostly look at observational studies or make inferences from blood tests. 

Always consult with your health care professional when making any dietary changes during your pre to postnatal period. They can help dial in a nutritional plan optimal to your unique situation and health situation.


  1. Lietz, G., Lange, J., & Rimbach, G. (2010). Molecular and dietary regulation of beta,beta-carotene 15,15'-monooxygenase 1 (BCMO1). Archives of biochemistry and biophysics, 502(1), 8–16.
  2. van Helden, Y. G., Heil, S. G., van Schooten, F. J., Kramer, E., Hessel, S., Amengual, J., Ribot, J., Teerds, K., Wyss, A., Lietz, G., Bonet, M. L., von Lintig, J., Godschalk, R. W., & Keijer, J. (2010). Knockout of the Bcmo1 gene results in an inflammatory response in female lung, which is suppressed by dietary beta-carotene. Cellular and molecular life sciences : CMLS, 67(12), 2039–2056.
  3. Humphrey, J. H., West, K. P., Jr, & Sommer, A. (1992). Vitamin A deficiency and attributable mortality among under-5-year-olds. Bulletin of the World Health Organization, 70(2), 225–232.
  4. Stevens, G. A., Bennett, J. E., Hennocq, Q., Lu, Y., De-Regil, L. M., Rogers, L., Danaei, G., Li, G., White, R. A., Flaxman, S. R., Oehrle, S. P., Finucane, M. M., Guerrero, R., Bhutta, Z. A., Then-Paulino, A., Fawzi, W., Black, R. E., & Ezzati, M. (2015). Trends and mortality effects of vitamin A deficiency in children in 138 low-income and middle-income countries between 1991 and 2013: a pooled analysis of population-based surveys. The Lancet. Global health, 3(9), e528–e536.
  5. Messina, A. E., Hambridge, T. L., & Mackerras, D. (2019). Change in Australian Vitamin A Intakes over Time. Current developments in nutrition, 3(9), nzz081.
  6. James M. Tielsch, Lakshmi Rahmathullah, Joanne Katz, R. D. Thulasiraj, Christian Coles, S. Sheeladevi, Kartik Prakash, Maternal Night Blindness during Pregnancy Is Associated with Low Birthweight, Morbidity, and Poor Growth in South India, The Journal of Nutrition, Volume 138, Issue 4, April 2008, Pages 787–792,
  7. P. Christian, K. P. West Jr., S. K. Khatry et al., “Night blindness during pregnancy and subsequent mortality among women in Nepal: effects of vitamin A and β-carotene supplementation,” The American Journal of Epidemiology, vol. 152, no. 6, pp. 542–547, 2000.
  8. Christian P, West KP Jr, Khatry SK, Pradhan EK, LeClerq SC, Katz J, Shrestha SR, Dali SM, Sommer A. Night blindness during pregnancy and subsequent mortality among women in Nepal: effects of vitamin A and beta carotene supplementation. Am J Epidemiol. 2000;152:542–7; Christian P, West KP Jr, Khatry SK, LeClerq SC, Pradhan EK, Katz J, Shrestha SR. Maternal night blindness increases risk of mortality in the first 6 months of life among infants in Nepal. J Nutr. 2001;131:1510–2.
  9. B. Benoist, E. McLean, M. Cogswell, I. Egli, and D. Wojdyla, Worldwide Prevalence of Anemia 1993–2005, WHO Global Database on Anemia, World Health Organization, Geneva, Switzerland, 2008,
  10. K. Kalaivani, “Prevalence & consequences of anaemia in pregnancy,” Indian Journal of Medical Research, vol. 130, no. 5, pp. 627–633, 2009.
  11. Radhika, M. S., Bhaskaram, P., Balakrishna, N., Ramalakshmi, B. A., Devi, S., & Kumar, B. S. (2002). Effects of vitamin A deficiency during pregnancy on maternal and child health. BJOG : an international journal of obstetrics and gynaecology, 109(6), 689–693.
  12. Reifen R. (2002). Vitamin A as an anti-inflammatory agent. The Proceedings of the Nutrition Society, 61(3), 397–400.
  13. Ibid.
  14. Huang, Z., Liu, Y., Qi, G., Brand, D., & Zheng, S. G. (2018). Role of Vitamin A in the Immune System. Journal of clinical medicine, 7(9), 258.
  15. Faustino, J. F., Ribeiro-Silva, A., Dalto, R. F., Souza, M. M., Furtado, J. M., Rocha, G., Alves, M., & Rocha, E. M. (2016). Vitamin A and the eye: an old tale for modern times. Arquivos brasileiros de oftalmologia, 79(1), 56–61.
  16. Simşek, M., Naziroğlu, M., Simşek, H., Cay, M., Aksakal, M., & Kumru, S. (1998). Blood plasma levels of lipoperoxides, glutathione peroxidase, beta carotene, vitamin A and E in women with habitual abortion. Cell biochemistry and function, 16(4), 227–231; Clagett-Dame, M., & Knutson, D. (2011). Vitamin A in reproduction and development. Nutrients, 3(4), 385–428.
  17. Stege, G., Fenton, A., & Jaffray, B. (2003). Nihilism in the 1990s: the true mortality of congenital diaphragmatic hernia. Pediatrics, 112(3 Pt 1), 532–535.
  18. Torfs, C. P., Curry, C. J., Bateson, T. F., & Honoré, L. H. (1992). A population-based study of congenital diaphragmatic hernia. Teratology, 46(6), 555–565.
  19. Greer, J. J., Babiuk, R. P., & Thebaud, B. (2003). Etiology of congenital diaphragmatic hernia: the retinoid hypothesis. Pediatric research, 53(5), 726–730.
  20. Rocke, A.W., Clarke, T.G., Dalmer, T.R.A. et al. Low maternal vitamin A intake increases the incidence of teratogen induced congenital diaphragmatic hernia in mice. Pediatr Res 91, 83–91 (2022).
  21. Michikawa, T. et al. Maternal dietary intake of vitamin A during pregnancy was inversely associated with congenital diaphragmatic hernia: the Japan Environment and Children’s Study. Br. J. Nutr. 122, 1295–1302 (2019).
  22. Beurskens, L. W. J. E. et al. Dietary vitamin A intake below the recommended daily intake during pregnancy and the risk of congenital diaphragmatic hernia in the offspring. Birth Defects Res. A Clin. Mol. Teratol. 97, 60–66 (2013).
  23. Beurskens, L. W., Tibboel, D., Lindemans, J., Duvekot, J. J., Cohen-Overbeek, T. E., Veenma, D. C., de Klein, A., Greer, J. J., & Steegers-Theunissen, R. P. (2010). Retinol status of newborn infants is associated with congenital diaphragmatic hernia. Pediatrics, 126(4), 712–720.
  24. Major, D. et al. Retinol status of newborn infants with congenital diaphragmatic hernia. Pediatr. Surg. Int. 13, 547–549 (1998).
  25. Babiuk, R. P., Thébaud, B. & Greer, J. J. Reductions in the incidence of nitrofen-induced diaphragmatic hernia by vitamin A and retinoic acid. Am. J. Physiol. Lung Cell. Mol. Physiol. 286, L970–L973 (2004).
  26. Coste, K. et al. Metabolic disturbances of the vitamin A pathway in human diaphragmatic hernia. Am. J. Physiol. Lung Cell. Mol. Physiol. 308, L147–L157 (2015).
  27. Matthews K.A., Rhoten W.B., Driscoll H.K., Chertow B.S. Vitamin A deficiency impairs fetal islet development and causes subsequent glucose intolerance in adult rats. J. Nutr. 2004;134:1958–1963. doi: 10.1093/jn/134.8.1958
  28. Chien C.Y., Lee H.S., Cho C.H., Lin K.I., Tosh D., Wu R.R., Mao W.Y., Shen C.N. Maternal vitamin A deficiency during pregnancy affects vascularized islet development. J. Nutr. Biochem. 2016;36:51–59. doi: 10.1016/j.jnutbio.2016.07.010.
  29. Frenz D.A., Liu W., Cvekl A., Xie Q., Wassef L., Quadro L., Niederreither K., Maconochie M., Shanske A. Retinoid signaling in inner ear development: A “Goldilocks” phenomenon. Am. J. Med. Genet. A. 2010;152:2947–2961. doi: 10.1002/ajmg.a.33670.
  30. Kil S.H., Streit A., Brown S.T., Agrawal N., Collazo A., Zile M.H., Groves A.K. Distinct roles for hindbrain and paraxial mesoderm in the induction and patterning of the inner ear revealed by a study of vitamin-A-deficient quail. Dev. Biol. 2005;285:252–271. doi: 10.1016/j.ydbio.2005.05.044.
  31. Romand R., Dollé P., Hashino E. Retinoid signaling in inner ear development. J. Neurobiol. 2006;66:687–704. doi: 10.1002/neu.20244.
  32. Emmett S.D., West K.P., Jr. Gestational vitamin A deficiency: A novel cause of sensorineural hearing loss in the developing world? Med. Hypotheses. 2014;82:6–10. doi: 10.1016/j.mehy.2013.09.028.
  33. Gilbert T., Merlet-Bénichou C. Retinoids and nephron mass control. Pediatr. Nephrol. 2000;14:1137–1144. doi: 10.1007/s004670000385.
  34. El-Khashab E.K., Hamdy A.M., Maher K.M., Fouad M.A., Abbas G.Z. Effect of maternal vitamin A deficiency during pregnancy on neonatal kidney size. J. Perinat. Med. 2013;41:199–203. doi: 10.1515/jpm-2012-0026.
  35. Lee Y.Q., Collins C.E., Gordon A., Rae K.M., Pringle K.G. The relationship between maternal nutrition during pregnancy and offspring kidney structure and function in humans: A systematic review. Nutrients. 2018;10:E241. doi: 10.3390/nu10020241
  36. Li, Z., Shen, J., Wu, W. K., Wang, X., Liang, J., Qiu, G., & Liu, J. (2012). Vitamin A deficiency induces congenital spinal deformities in rats. PloS one, 7(10), e46565.
  37. Huang, Y., & Zheng, S. (2011). The effect of vitamin A deficiency during pregnancy on anorectal malformations. Journal of pediatric surgery, 46(7), 1400–1405.
  38. Bao Y., Ibram G., Blaner W.S., Quesenberry C.P., Shen L., McKeague I.W., Schaefer C.A., Susser E.S., Brown A.S. Low maternal retinol as a risk factor for schizophrenia in adult offspring. Schizophr. Res. 2012;137:159–165. doi: 10.1016/j.schres.2012.02.004.
  39. Rothman, K. J., Moore, L. L., Singer, M. R., Nguyen, U. S., Mannino, S., & Milunsky, A. (1995). Teratogenicity of high vitamin A intake. The New England journal of medicine, 333(21), 1369–1373.
  40. Centers for Disease Control and Prevention. (2008). Update on overall prevalence of major birth defects—Atlanta, Georgia, 1978–2005. MMWR Weekly Report, 57(1), 1–5. Retrieved February 7, 2017, from
  41. Yang, J., Kang, Y., Cheng, Y., Zeng, L., Yan, H., & Dang, S. (2019). Maternal Dietary Patterns during Pregnancy and Congenital Heart Defects: A Case-Control Study. International journal of environmental research and public health, 16(16), 2957.
  42. Vujkovic, M., Ocke, M. C., van der Spek, P. J., Yazdanpanah, N., Steegers, E. A., & Steegers-Theunissen, R. P. (2007). Maternal Western dietary patterns and the risk of developing a cleft lip with or without a cleft palate. Obstetrics and gynecology, 110(2 Pt 1), 378–384.
  43. Martínez-Frías, M. L., & Salvador, J. (1990). Epidemiological aspects of prenatal exposure to high doses of vitamin A in Spain. European journal of epidemiology, 6(2), 118–123.
  44. Miller, R. K., Hendrickx, A. G., Mills, J. L., Hummler, H., & Wiegand, U. W. (1998). Periconceptional vitamin A use: how much is teratogenic?. Reproductive toxicology (Elmsford, N.Y.), 12(1), 75–88.
  45. Wiegand, U. W., Hartmann, S., & Hummler, H. (1998). Safety of vitamin A: recent results. International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition, 68(6), 411–416.
  46. Mastroiacovo, P., Mazzone, T., Addis, A., Elephant, E., Carlier, P., Vial, T., Garbis, H., Robert, E., Bonati, M., Ornoy, A., Finardi, A., Schaffer, C., Caramelli, L., Rodríguez-Pinilla, E., & Clementi, M. (1999). High vitamin A intake in early pregnancy and major malformations: a multicenter prospective controlled study. Teratology, 59(1), 7–11.<7::AID-TERA4>3.0.CO;2-6
  47. St Claire, M. B., Kennett, M. J., & Besch-Williford, C. L. (2004). Vitamin A toxicity and vitamin E deficiency in a rabbit colony. Contemporary topics in laboratory animal science, 43(4), 26–30.
  48. Yen-Hung Yeh, Ya-Ting Lee, Hung-Sheng Hsieh, Deng-Fwu Hwang, Effect of taurine on toxicity of vitamin A in rats, Food Chemistry, Volume 106, Issue 1, 2008, Pages 260-268,
  49. eh, Y. H., Lee, Y. T., & Hsieh, Y. L. (2012). Effect of cholestin on toxicity of vitamin A in rats. Food chemistry, 132(1), 311–318.
  50. Walker, S. E., Eylenburg, E., & Moore, T. (1947). The action of vitamin K in hypervitaminosis A. The Biochemical journal, 41(4), 575–580.
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