top of page
  • Clare Backhouse

The Vitamin A Controversy: or, why carrots and kale may not be for everyone

The trouble with being a nutritionist: no sooner do you get used to one health ‘rule’, than it’s reinvestigated!

Once we were told to avoid all kinds of fats. Now this theory has been largely debunked (Ramsden et al, 2016).

My own father was put on a very low fat diet to combat high cholesterol several years ago. Tragically, this very regime may actually have contributed to his development of Alzheimer’s.

The stakes are pretty high.

Today I'm going to question whether Vitamin A is really a ‘vital nutrient’ for all of us. And whether carrots and kale are really a good thing for everyone.

For me, the question is very much a work in progress. But I hope it will be an intriguing story, inspire you to hold lightly to the health headlines – and encourage you to investigate fearlessly what your own body is telling you.

Plus. I bet you haven’t heard this story before.

Being a rather nerdier post than usual, I’ve summarised it (for those of you in a hurry) in a few numbered points under ‘The Low Down’ at the bottom of the page.

For those of you sitting comfortably: well, then, let us begin.....

What is Vitamin A?

There are two kinds of Vitamin A:

1. ‘provitamin A carotenoids’ from vegetables and fruit, which the body converts into useable vitamin A.

2. ‘retinol’ from animal products, especially liver meat, which the body can use more quickly and easily.

Both kinds can convert to ‘retinoic acid’ in the body, which is the active form of vitamin A.

According to most research, vitamin A is crucial for our metabolism, vision, gene transcription, immunity, and skin health (Chapman, 2012).

So what on earth could be the problem? Well. Let’s have a look at some of the paradoxical claims.

The NHS recommends a good regular intake of vitamin A for all the above reasons, but also warns not to eat liver more than once per week, because of osteoporosis risk (NHS, 2017).

Vitamin A is believed to be essential for healthy hair growth, and yet, too much of the stuff will actually trigger hair loss (Guo and Katta, 2017).

It’s described as vital for the formation of normal embryo organs and tissues (Oliveira, 2015) but yet a danger to the normal development of babies in utero (Olson and Shah, 2018).

It’s been called an important antioxidant (cell protector), but yet at high concentrations it promotes oxidation, causing cell damage, cell death and inflammation (Oliveira, 2015)

Vitamin A is used for anti-ageing face creams, but yet it’s also found to cause skin burning, scaling and eczema (Kong et al, 2016).

It’s all pretty strange. As one article puts it, there is ‘a narrow margin between the population reference intake of vitamin A and adverse effects associated with preformed vitamin A’ (Grune et al, 2010).

So what about all those fish oil supplements we are supposed to be taking, which are rich sources of vitamin A?

What about carrots, which contain more than a day’s recommended amount of pro-vitamin A in a single cupful? Or kale, almost as potent? Shouldn’t we be warned off?

Well might we ask!

Questioning the Vitamin ‘Canon’

I’ve been intrigued by this conundrum ever since a nutritionist colleague mentioned it last year. Jenny Jones is a research scientist who found that a catalogue of odd symptoms began to disappear when she adopted a very low-vitamin-A diet. Her own research then backed up the changes she was observing. Her comments prodded me to question some of my own symptoms, which also mysteriously appeared (I now realise) after taking a lot of vitamin A.

And indeed there is a tranche of research which is pretty ambivalent about the nutrient. Various dangers have been identified.

While its risk to embryo formation has long been known (Parr et al, 2018), excess vitamin A also interferes with child and adult bone health, causing pain, fracture osteoporosis and abnormalities in bone marrow, even alongside high calcium intake (UK Scientific Advisory Committee, 2005; Penniston and Tanumihardjo, 2006; Hu et al, 2010; Lind et al, 2013; Baineni, 2017; Lind et al, 2018).

Vitamin A has been found to accumulate in the lungs of children whose mothers consumed a lot of it in pregnancy, causing asthma symptoms at school age (Parr, 2018).

Both animal and human studies have found it to reduce or suppress thyroid stimulating hormone, causing hypothyroidism (Sherman et al, 1999; Beibinger, 2007; Graeppi-Dulac, 2014).

In a stressed gut environment, vitamin A metabolites can enhance inflammatory cellular and humoral responses to ingested toxins (DePaolo, 2011) also creating high risk of celiac disease (Samsel and Seneff, 2013).

Excess vitamin A is associated with inflammation of the brain and spinal cord, oxidative stress (associated with cell damage) and mitochondrial dysfunction (associated with impaired energy production in our cells) (Oliverio, 2015).

Vitamin A has caused death in children who over-consumed it (Nordic Council of Ministers, 2003) and a retinoid cream study was halted six months early due to the number of deaths among the participants (Weinstock et al, 2009). A review of vitamin trials found that Vitamin A and its precursor betacarotene increased mortality (Bjelakovic et al, 2007).

Even previously fit American army veterans appear to have been poisoned by excess vitamin A accumulating in their bodies (Mawson and Croft, 2019).

If you’re anything like me, that collection of research leaves you wondering: why haven’t we heard about all this before?

Perhaps it’s because most vitamin A research has, historically, always focussed on deficiency. This perspective has in turn underpinned large western supplementation regimes in developing countries, lucrative for some (Latham, 2010; Wirth et al, 2017). Within such a bias, concerns about vitamin A intake outside of pregnancy may have seemed redundant.

Real-life experiments

Another reason for the lack of research has been proposed by a non-specialist researcher, who successfully self-treated his chronic severe eczema as vitamin A toxicity. Grant Genereux has written three highly personal, accessible ebooks about the subject, available freely on his blog

Genereux argues that the reason for the strangely narrow margin between vitamin A deficiency and excess (or ‘hypervitaminosis’) is that the foundational, early twentieth-century studies which observed disastrous consequences for vitamin A deficiency, were in fact unintentionally measuring the consequences of its excess, or even symptoms caused by different deficiencies altogether (such as fat).

As we know, remembering the ‘fat hypothesis’ I mentioned at the beginning, ‘scientific facts’ are slow to change, even with research.

While ‘acute’ hypervitaminosis A has long been medically established, Genereux argues that ‘chronic’ hypervitaminosis A – where the build-up is much slower – is in fact more widespread, and equally as serious.

This opinion is shared by various Scandinavian authors who found that their native diets caused occurrences of ‘chronic’ hypervitaminosis A, which resulted in a variety of pathologies such as osteoporosis (Nordic Council of Ministers, 2003), and by more recent studies that describe its symptoms in adults as dry, broken skin, eczema, brittle nails, hair loss, gingivitis, anorexia, and fatigue (García-Muñoz, 2019).

American naturopathic doctor Garrett Smith took inspiration from Genereux’s work and, after his own discovery that vitamin A seemed to harm his clients, he now devotes part of his practice to dealing with chronic hypervitaminosis A. He also takes pains to make current research on the subject accessible to the general reader; his website contains a wealth of collated research and lively comment:

Dr Smith usefully summarises how the body moves into hypervitaminosis A: the liver protects the body from the effects of retinoic acid by producing Retinol Binding Protein (RBP), which itself requires various nutrients. But, if the liver fills with retinol while lacking the RBP to get rid of it, excess retinol enters the body, causing a variety of diseases.

Well, I can hear my readers cry! - what is the real risk of overdosing vitamin A? Are my carrots and kale really going to get me into trouble?


First of all, I should explain that hypervitaminosis A is difficult to diagnose, because blood tests don’t tell the whole story. After all, one’s liver may be almost full of it, even while keeping it out of the blood (Mawson and Croft, 2019). Excess Vitamin A can therefore be ‘hidden’; it is also stored in the lungs (Parr, 2018). So, finding out just how much vitamin A resides in the body is not fully possible until a person dies.

Live diagnosis relies on the history of vitamin A intake, absence of other potential causes of liver disease, and a liver biopsy (García-Muñoz, 2019). One rather spooky study on human cadaver livers found that a third of the 27 bodies examined had hypervitaminosis A, concluding with an urgent call to diagnose it better in living people (Olsen, 2018).

So: could we be be overdosing?

The prevailing view is that one can overdose on retinol from animal products and supplements, but not on provitamin A carotenoids from vegetables. However, this has been questioned, both in older studies which implicated beta-carotene in higher risk of lung cancer, and in more recent animal studies (Albanes et al, 1996; Omenn et al, 1996; Arreguín, 2018).

But I think the important thing to realise is that Vitamin A can build up in our bodies gradually, and that it can do so from a variety of non-food sources, such as:

- via fish or cod liver oil supplements

- through the skin in anti-ageing creams

- in some sun screens

- in most multivitamin supplements

- in treatments for acne

- in cancer therapies

(Lunder, 2011; Oliveira, 2015).

Another factor may be the Pill. Less than a decade after the contraceptive pill was introduced, various studies found increased levels of vitamin A in the blood of women who took it (cited in Wild, 1974).

One final reason why we may all be more at risk of excess vitamin A, is that the common plant pesticide glyphosate can cause vitamin A to accumulate in our bodies, possibly by disrupting the enzymes responsible for breaking it down (Paganelli, 2010; Samsel and Seneff, 2013).

So there is my summary of possible problems with vitamin A. As I said, it’s a work in progress, and I haven’t even attempted a ‘balanced and rounded’ view!

But I hope you’ve gained an insight into just why I am so keen to focus on individuals' needs, rather than rely on ‘set programmes’ for health. We’re each biochemically unique, and our personal histories can make things even more complicated.

Even the most well-founded research can’t always relate to all. Careful analysis of the individual, and tailor-made plans for health, are essential. Carrots and kale are definitely not for everyone all the time!

The Low Down

1. Vitamin A is highly controversial. It can be both beneficial, in limited amounts, AND highly toxic in excess.

2. All conceiving and pregnant women should avoid concentrated sources totally.

3. Accumulating toxic levels of Vitamin A in the body can occur suddenly, or build up gradually.

4. The highest everyday ‘retinol’ sources are vitamin supplements, liver meat, and fish oils. These are most potent forms.

5. The highest ‘provitamin A carotenoid’ sources are sweet potato, carrot, kale and spinach.

6. You can also accumulate vitamin A from beauty creams, some sunscreens, certain cancer therapies, and acne treatments.

7. Some factors can heighten vitamin A’s impact, eg glyphosate pesticides used on grains and legumes.

8. If you have a history of high vitamin A intake as well as ‘unexplained’ symptoms, particularly autoimmunity, skin or gut issues, it may be worth reducing your overall consumption.

Finally, if you're looking for some professional support for your health, have a look at the rest of my website, eg for how I work, and some encouraging testimonials. And do get in touch with me via my contact page - we can even set up a quick conversation so that you can find out more without obligation.

To your best of health, Clare

Clare Backhouse, dipION, Registered Nutritionist MBANT, Registered Nutritional Therapist CNHC

Consultations in London, in West Sussex, and online

References and sources

Albanes, D., Heinonen, O.P., Taylor, P.R., Virtamo, J., Edwards, B.K., Rautalahti, M., Hartman, A.M., Palmgren, J., Freedman, L.S., Haapakoski, J., Barrett, M.J., Pietinen, P., Malila, N., Tala, E., Liippo, K., Salomaa, E.-R., Tangrea, J.A., Teppo, L., Askin, F.B., Taskinen, E., Erozan, Y., Greenwald, P., Huttunen, J.K., 1996. α-Tocopherol and β-Carotene Supplements and Lung Cancer Incidence in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study: Effects of Base-line Characteristics and Study Compliance. J Natl Cancer Inst 88, 1560–1570.

Arreguín, A., Ribot, J., Mušinović, H., von Lintig, J., Palou, A., Bonet, M.L., 2018. Dietary vitamin A impacts DNA methylation patterns of adipogenesis-related genes in suckling rats. Arch. Biochem. Biophys. 650, 75–84.

Baineni, R., Gulati, R., Delhi, C.K., 2017. Vitamin A toxicity presenting as bone pain. Archives of Disease in Childhood 102, 556–558.

Biebinger, R., Arnold, M., Langhans, W., Hurrell, R.F., Zimmermann, M.B., 2007. Vitamin A Repletion in Rats with Concurrent Vitamin A and Iodine Deficiency Affects Pituitary TSHβ Gene Expression and Reduces Thyroid Hyperstimulation and Thyroid Size. J Nutr 137, 573–577.

Bjelakovic, G., Nikolova, D., Gluud, L.L., Simonetti, R.G., Gluud, C., 2007. Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis. JAMA 297, 842–857.

Chapman, M.S., 2012. Vitamin A: history, current uses, and controversies. Semin Cutan Med Surg 31, 11–16.

de Oliveira, M.R., 2015. Vitamin A and Retinoids as Mitochondrial Toxicants. Oxid Med Cell Longev 2015.

DePaolo, R.W., Abadie, V., Tang, F., Fehlner-Peach, H., Hall, J.A., Wang, W., Marietta, E.V., Kasarda, D.D., Waldmann, T.A., Murray, J.A., Semrad, C., Kupfer, S., Belkaid, Y., Guandalini, S., Jabri, B., 2011. Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens. Nature 471, 220–224.

García-Muñoz, P., Bernal-Bellido, C., Marchal-Santiago, A., Cepeda-Franco, C., Álamo-Martínez, J.M., Marín-Gómez, L.M., Suárez-Artacho, G., Castillo-Tuñón, J.M., Navarro-Morales, L., Padillo-Ruíz, F.J., Gómez-Bravo, M.A., 2019. Liver Cirrhosis From Chronic Hypervitaminosis A Resulting in Liver Transplantation: A Case Report. Transplantation Proceedings 51, 90–91.

Graeppi-Dulac, J., Vlaeminck-Guillem, V., Perier-Muzet, M., Dalle, S., Orgiazzi, J., 2014. Endocrine side-effects of anti-cancer drugs: The impact of retinoids on the thyroid axis. European Journal of Endocrinology 170, R253–R262.

Grune, T., Lietz, G., Palou, A., Ross, A.C., Stahl, W., Tang, G., Thurnham, D., Yin, S., Biesalski, H.K., 2010. β-Carotene Is an Important Vitamin A Source for Humans. J Nutr 140, 2268S-2285S.

Guo, E.L., Katta, R., 2017a. Diet and hair loss: effects of nutrient deficiency and supplement use. Dermatol Pract Concept 7, 1–10.

Hu, L., Lind, T., Sundqvist, A., Jacobson, A., Melhus, H., 2010. Retinoic Acid Increases Proliferation of Human Osteoclast Progenitors and Inhibits RANKL-Stimulated Osteoclast Differentiation by Suppressing RANK. PLoS One 5.

Kong, R., Cui, Y., Fisher, G.J., Wang, X., Chen, Y., Schneider, L.M., Majmudar, G., 2016. A comparative study of the effects of retinol and retinoic acid on histological, molecular, and clinical properties of human skin. Journal of Cosmetic Dermatology 15, 49–57.

Latham, M., 2010. The great vitamin A fiasco. World Nutrition. 1, 1.

Lind, T., Lugano, R., Gustafson, A.-M., Norgård, M., van Haeringen, A., Dimberg, A., Melhus, H., Robertson, S.P., Andersson, G., 2018. Bones in human CYP26B1 deficiency and rats with hypervitaminosis A phenocopy Vegfa overexpression. Bone Rep 9, 27–36.

Lind, T., Sundqvist, A., Hu, L., Pejler, G., Andersson, G., Jacobson, A., Melhus, H., 2013. Vitamin a is a negative regulator of osteoblast mineralization. PLoS ONE 8, e82388.

Lunder, S., 2011. What Scientists Say About Vitamin A in Sunscreen. Environmental Working Group.

Manickavasagar, B., McArdle, A.J., Yadav, P., Shaw, V., Dixon, M., Blomhoff, R., Connor, G.O., Rees, L., Ledermann, S., van’t Hoff, W., Shroff, R., 2015. Hypervitaminosis A is prevalent in children with CKD and contributes to hypercalcemia. Pediatr Nephrol 30, 317–325.

Mawson, A.R., Croft, A.M., 2019. Gulf War Illness: Unifying Hypothesis for a Continuing Health Problem. International Journal of Environmental Research and Public Health 16, 111.

Nordic Council of Ministers, 2003. Health Risks Related to High Intake of Preformed Retinol (vitamin A) in the Nordic Countries. Nordic Council of Ministers.

Oliveira, M.R.D., 2015. The neurotoxic effects of vitamin A and retinoids. Anais da Academia Brasileira de Ciências 87, 1361–1373.

Olsen, K., Suri, D.J., Davis, C., Sheftel, J., Nishimoto, K., Yamaoka, Y., Toya, Y., Welham, N.V., Tanumihardjo, S.A., 2018. Serum retinyl esters are positively correlated with analyzed total liver vitamin A reserves collected from US adults at time of death. Am J Clin Nutr 108, 997–1005.

Olson, J.M., Shah, N.A., 2018. Vitamin A Toxicity, in: StatPearls. StatPearls Publishing, Treasure Island (FL).

Omenn, G.S., Goodman, G.E., Thornquist, M.D., Balmes, J., Cullen, M.R., Glass, A., Keogh, J.P., Meyskens, F.L., Valanis, B., Williams, J.H., Barnhart, S., Cherniack, M.G., Brodkin, C.A., Hammar, S., 1996. Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial. J. Natl. Cancer Inst. 88, 1550–1559.

Paganelli, A., Gnazzo, V., Acosta, H., López, S.L., Carrasco, A.E., 2010. Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling. Chem. Res. Toxicol. 23, 1586–1595.

Parr, C.L., Magnus, M.C., Karlstad, Ø., Holvik, K., Lund-Blix, N.A., Haugen, M., Page, C.M., Nafstad, P., Ueland, P.M., London, S.J., Håberg, S.E., Nystad, W., 2018a. Vitamin A and D intake in pregnancy, infant supplementation, and asthma development: the Norwegian Mother and Child Cohort. Am J Clin Nutr 107, 789–798.

Pasantes-Morales, H., Wright, C.E., Gaull, G.E., 1984. Protective Effect of Taurine, Zinc and Tocopherol on Retinol-Induced Damage in Human Lymphoblastoid Cells. J Nutr 114, 2256–2261.

Penniston, K.L., Tanumihardjo, S.A., 2006. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr 83, 191–201.

Ramsden, C.E., Zamora, D., Majchrzak-Hong, S., Faurot, K.R., Broste, S.K., Frantz, R.P., Davis, J.M., Ringel, A., Suchindran, C.M., Hibbeln, J.R., 2016. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 353, i1246.

Samsel, A., Seneff, S., 2013. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdiscip Toxicol 6, 159–184.

Sherman, S.I. et al, 1999. Central Hypothyroidism Associated with Retinoid X Receptor–Selective Ligands. New England Journal of Medicine 340, 1075–1079.

UK Scientific Advisory Committe on Nutrition, 2005. Review of Dietary Advice on Vitamin A

Van der Auwera, I., Wera, S., Van Leuven, F., Henderson, S.T., 2005. A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer’s disease. Nutrition & Metabolism 2, 28.

Weinstock, M.A., Bingham, S.F., Lew, R.A., Hall, R., Eilers, D., Kirsner, R., Naylor, M., Kalivas, J., Cole, G., Marcolivio, K., Collins, J., Digiovanna, J.J., Vertrees, J.E., Veterans Affairs Topical Tretinoin Chemoprevention (VATTC) Trial Group, 2009. Topical tretinoin therapy and all-cause mortality. Arch Dermatol 145, 18–24.

Wild, J., Schorah, C.J., Smithells, R.W., 1974. Vitamin A, Pregnancy, and Oral Contraceptives. Br Med J 1, 57–59.

Wirth, J.P., Petry, N., Tanumihardjo, S.A., Rogers, L.M., McLean, E., Greig, A., Garrett, G.S., Klemm, R.D.W., Rohner, F., 2017a. Vitamin A Supplementation Programs and Country-Level Evidence of Vitamin A Deficiency. Nutrients 9, 190.

bottom of page