Vitamin A & Thyroid Function

Taking your thyroid meds, have “normal” looking thyroid hormones, but your TSH just won’t come down? You could be dealing with insufficient Vitamin A levels!

We’ve been told that if we eat enough carrots and sweet potatoes we’ll get enough beta-carotene to meet our Vitamin A needs, but that’s actually not completely accurate. In this post, I will dive into the specifics of the different “types” of vitamin A, the best food sources, how an insufficiency can manifest, whether you should be worried about toxicity, signs of toxicity, and how to pick up signs of Vitamin A deficiency on labs (because it isn’t as straightforward as you might think).

What is Vitamin A

Vitamin A is a powerful fat-soluble vitamin that wears many hats inside the body. The great demand for Vitamin A in the body isn’t always met due to a variety of factors including lack of animal rich foods, increased demands due to inflammation, and other cofactor deficiencies. 

There are two main categories of Vitamin A:

• Preformed Vitamin A (retinol, retinal, retinoic acid)
• Pro-Vitamin A Carotenoids (beta-carotene)

We often hear about foods like pumpkin, carrots, and sweet potatoes as being a good source of Vitamin A, which is true in part, but what they’re really rich in is beta-carotene (and other carotenoids). Beta-carotene is a precursor to Vitamin A that humans must convert inactive “active” Vitamin A (retinol) inside the body.

Beta-Carotene

Forms of preformed Vitamin A are found predominantly in animal foods including eggs, liver, organ meats, ghee, salmon, herring, milk and cheese. Therefore, those who follow a vegan or vegetarian diet tend to be at greater risk for Vitamin A deficiency because of their lack of/low intake of preformed Vitamin A rich foods in their diets.

The conversion of beta-carotene happens primarily in the liver and bowels at a rate of 12 mcg beta-carotene to 1 mcg of active Vitamin A. So while beta-carotene is an important antioxidant that helps to combat inflammation, support detoxification, and stabilize the immune response, beta-carotene isn’t adequate enough in typical amounts eaten to provide the amount of Active Vitamin A that the human body needs to function optimally– especially since the average conversion is anywhere from 10-25%. 

Preformed Vitamin A

Animal food products provides preformed Vitamin A (aka the form of Vitamin A we most efficiently use):

• Retinyl Esters
  • Retinol (from animal foods)
    • Supports reproduction
    • Major transport and storage form of Vitamin A
    • Can convert to retinal
  • Retinal
    • Participates in vision
    • Intermediate in the conversion of retinol to retinoic acid
    • Can convert to retinoic acid or back to retinol
  • Retinoic acid (produced from retinol, beta-carotene, and/or retinal)
    • Aids in growth and development
    • Acts like a hormone
    • Regulates cell differentiation, growth, and embryonic development
    • Retinoic acid cannot back-convert to retinal, so while animals can grow with only retinoic acid, they’ll be blind!

Role of Vitamin A in the Body

Vitamin A has many jobs in the body ranging from immune system support, to eye health, reproductive support, growth and development, gut health integrity, and yes, even thyroid health! (Keep reading for more specifics on thyroid function & Vitamin A)

Deficiency and Insufficiency of Vitamin A:

Vitamin A deficiency proper is not as common in developed countries, but Vitamin A insufficiency is rather epidemic. Determining adequate Vitamin A status can be a little tricky sometimes given that 90% of Vitamin A is stored in the liver. However, food recalls and certain blood values can be helpful to provide insight into whether a sub-optimal level of Vitamin A is contributing to many of the symptoms you’re experiencing. 

The status of Vitamin A is largely dependent on protein status in the body because Vitamin A is carried and delivered throughout the body on carrier proteins like RBC (retinol binding protein) and transthyretin. This is a big reason why vegan, vegetarians, and those who follow a low calorie and/or low-fat diet  are at higher risk of Vitamin A deficiency and insufficiency: lack of protein for carrier proteins, lack of fat for proper Vitamin A absorption, and lack of pre-formed Vitamin A. It can take 1-2 years before symptoms of low levels of Vitamin A show up because Vitamin A is fat-soluble (meaning it gets stored in fat cells). It can show up sooner in children and those who are actively growing (think pregnant women and nursing mothers) because the demand for Vitamin A is higher. 

Risk factors:

• Vegan & vegetarian
• Low-fat diet
• Low- protein diets
• Low calorie diets
• Intense amounts of exercise
• Gut infections & parasitic overgrowth
• Poor intake of Vitamin A rich foods 
• Pregnant and postpartum moms (I know there is controvery around HIGH doses of Vitamin A and pregnancy. Studies caution the intake of >10,000 IU/day of  preformed Vitamin A from supplements. If you’re taking more close to this from supplements, you definitely want to chat with your provider about the safety of this.)

Symptoms of deficiency:

• Infectious diseases: Due to Vitamin A’s role in supporting the immune system. When Vitamin A demand isn’t met, epithelial tissues in which the cells weaken defense and makes infection more likely. Without Vitamin A, the goblet cells diminish in number and activity which limits the secretion of mucus in the gut, vagina, ears, urinary tract, lungs which can predispose to higher rates of infection.
• Poor gut function: Vitamin A plays a powerful role in the lining of the gastrointestinal tract’s protective mucus layer that modulates the immune system, regulates inflammation, and prevents permeability of the gut (AKA leaky gut).
• Keratinization: The epithelial cells on the outside of the body (skin) begin to change shape and secrete keratin– hard inflexible protein and can lead to bumps on the skin
• Night blindness
• Blindness
• Macular degeneration
• Cancer occurrence 

Vitamin A Toxicity

As with any micronutrient, there is a Goldilocks situation at hand. While too little is problematic, too much Vitamin A, especially since it is fat-soluble (meaning we store a lot in the body) can post risks!

Symptoms of toxicity begin to occur when all binding proteins are saturated. A way to determine this would be to assess Retinol Binding Protein (RBP) on lab work. Toxicity is much more common in those taking high amounts of preformed Vitamin A. More often than not, toxicity from preformed Vitamin A is due to supplement use and not typically from food consumption as food is more self-limiting than supplements. That is, we get FULL from food way before we reach toxic levels. That said, if you go eat an entire polar bear liver in one sitting, you may get acute Vitamin A toxicity. Acute Vitamin A toxicity usually occurs days to weeks after ingestion (studies show ingestion of about 100 times the RDA) and include symptoms such as: headache, blurred vision, nausea, dizziness, aching muscles, and coordination problems.

Many studies have shown that there is not really a toxic level of beta-carotene that you can reach from food alone. However, taken in high amounts from supplements, beta-carotene can actually turn from an antioxidant into a pro-oxidant and promote cell division and destruction of. Vitamin A which can then lead to the Vitamin A deficiency symptoms. 

Symptoms of toxicity:

• Bone defects
• Birth defects
• Hair loss
• Nausea/vomiting
• Blurred vision
• Headache
• Dizziness
• Muscle aches
• Coordination problems

Safe Amounts of Vitamin A:

Labeling of Vitamin A on food and supplement packages can be a little confusing because there are a few different ways it can be reported:

• IU (international unites)
• RAE: retinol activity equivalents
• Mcg: micrograms

One does need to convert into the associated unit in order to determine if the amounts they’re ingesting is safe! 

• RAE = retinol activity equivalents; the amount of retinol that the body will derive from a food containing preformed retinol or precursor beta-carotene
• 1 mcg retinol = 1 RAE
• 12 mcg beta-carotene = 1 RAE
• 1 IU retinol = 0.3 mcg retinol or 0.3 RAE
• 1 IU beta-carotene = 0.5 IU retinol or 0.15 mcg RAE
• 1 IU beta-carotene (dietary) = 0.165 IU retinol or 0.05 mcg RAE
• 1 IU other Vitamin A precursor carotenoids = 0.025 mcg RAE

RDA for Vitamin A 

(Recommended Daily Allowance: the amount needed to prevent disease… AKA it is set pretty low)

• Adult females: 700 mcg RAE → 2333 IU daily

• Adult males: 900 mcg RAE → 3000 IU daily

This RDA is also equivalent to 18,000 IU beta-carotene from food

Upper Limits (UL) for Preformed Vitamin A:

• These ULs apply only to products from animal sources and supplements whose vitamin A comes entirely from retinol or its ester forms, such as retinyl palmitate. However, many dietary supplements (such as multivitamins) do not provide all of their vitamin A in retinol or its ester forms. For example, the vitamin A in some supplements consists partly or entirely of beta-carotene. In such cases, the percentage of retinol or retinyl ester in the supplement should be used to determine whether an individual’s vitamin A intake exceeds the UL. For example, a supplement whose label indicates that the product contains 3,000 mcg RAE vitamin A and that 60% of this vitamin A comes from beta-carotene (and therefore 40% comes from retinol or retinyl ester) provides 1,200 mcg RAE of preformed vitamin A.

Adult Male: 3000 mcg or 10,000 IU retinol

Adult Female: 3000 mcg or 10,000 IU retinol 

The Link Between Vitamin A & Thyroid Status

• Vitamin A deficiency is tightly correlated with structural and functional impairment of the thyroid gland and it often associated with iodine deficiency
• Increase iodine uptake and sodium-iodine symporter activity in human thyroid cells
• Works with retinol binding protein (RBP) and transthyretin (TTR) to transport thyroid hormones through the blood
• Retinol influences the TSH-secreting pituitary function 
• Vitamin A deficiency is frequently associated with iodine deficiency
• Low Vitamin A =
  • low iodine uptake into the cells
  • Impaired coupling of iodothyronines (which influences the T4 and T3 conversion)
  • Reduced thyroglobulin synthesis (which is the building block of thyroid hormones)
  • Thyroid hypertrophy & goiter (which would show up as an enlarged thyroid upon exam)
  • Decreased pool of T4 and T3 (which meals your cells are starved of the energy and metabolism enhancing effects of thyroid hormones)
  • Studies (in mice) showed that Vitamin A deficiency caused TSH levels that increased 2x as much despite increases in levothyroxine. A high TSH is a marker of hypothyroidism and that the thyroid hormones aren’t getting into the cells.
    • In animal studies of those with iodine deficiency and Vitamin A deficiency, administration of Vitamin A alone helped to reduce thyroid volume and TSH serum levels and increase iodine uptake
  • Vitamin A deficiency reduces binding of T3 and uptake by the tissues
  • Vitamin A deficiency decreases T4 to T3 conversion
    • Labs shown elevated levels of total T4 and T3 with lower levels of Free T4 and T3

Best ways to assess Vitamin A status:

• Liver biopsy (HA! This obviously isn’t totally realistic): 90% stored in liver
• Hemoglobin: low levels can suggest low Vitamin A due to the relationship between Vitamin A and iron
• Copper: we need Vitamin A to make copper bioavailable. High or low copper can suggest low Vitamin A
• Ceruloplasmin: Vitamin A helps to produce ceruloplasmin to transport copper throughout the body. A low ceruloplasmin can suggested low Vitamin A
• Zinc

• Reqiured for protein synthesis including the hepatic synthesis and secretion of retinol binding protein (RBP) and transthyretin
• Zinc deficiency influences the mobilization of Vitamin A from the liver and transport into circulation 
• Low zinc = low hepatic Vitamin A

• Retinol binding protein
• Retinol, serum or plasma
• Retinol, WBC
• Iron & Ferritin: retinol levels were positively correlated with serum iron & Vitamin A status

HTMA Test:

• Copper (high or low)
• Calcium (high or low)
• Chromium (high)

GI Map:

• Secretory IgA

Do you want to take a deeper look into your nutritional numbers to see how you stack up? Here are some ways I can help:

1. Private 1:1 work– this is a 16 week retainer in which we collaborate closely together to really dive into your unique story, hear your symptoms, and get a LOT of lab testing. This is the most comprehensive approach to optimizing your health with regular bi-weekly meetings, multiple lab tests, and daily accountability checks through food logging surveillance. You also get between session support via private chat and access to the Thyroid Bootcamp Course & Resource Library.
2. Thyroid Bootcamp + Lab Hybrid: this is a go-at-your-own speed course and lab testing hybrid. If you’re great at the implementation piece of the puzzle, Thyroid Bootcamp is perfect for those who are seeking Information (Thyroid Bootcamp Course) and Investigation (lab testing). The labs included are: HTMA test and blood testing (including assessing nutrients like Vitamin A via the blood). The Hybrid includes a detailed personal health history questionnaire that I use to properly interpret your labs. You receive a comprehensive video-recorded lab review along with a written assessment of labs, interventions, and 7 days of private chat access with me regarding your lab results.
3. HTMA + Food Foundations course bundle: this includes the HTMA (hair tissue mineral analysis) and a mini virtual Food Foundations course that teaches you: What to Eat, When to Eat, What NOT to Eat, and more. This bundle also features a video recorded lab interpretation from me, written assessment of your lab findings, therapeutic interventions (foods, supplements), and 7 days of private chat support

Disclaimer: Please note that “Thyroid School” emails and blogs from and written by Chews Food Wisely, LLC (and Nicole Fennell, RD) are not intended to create any physician-patient relationship or supplant any in-person medical consultation or examination. Always seek the advice of a trained health professional with any questions you may have regarding a medical condition and before seeking any treatment. Proper medical attention should always be sought for specific ailments. Never disregard professional medical advice or delay in seeking medical treatment due to information obtained in “Thyroid School” emails. Any information received from these emails is not intended to diagnose, treat, or cure. These emails, websites, and social media accounts are for information and educational purposes only. The information in these emails, websites, and social media accounts is not intended to replace proper medical care.

References: 

​​https://ods.od.nih.gov/factsheets/VitaminA-Consumer/

https://doi.org/10.1080/07315724.2012.10720431

https://doi.org/10.1093/ajcn/86.4.1040

Carazo A, Macáková K, Matoušová K, Krčmová LK, Protti M, Mladěnka P. Vitamin A Update: Forms, Sources, Kinetics, Detection, Function, Deficiency, Therapeutic Use and Toxicity. Nutrients. 2021 May 18;13(5):1703. doi: 10.3390/nu13051703. PMID: 34069881; PMCID: PMC8157347.

Tang G. Bioconversion of dietary provitamin A carotenoids to vitamin A in humans. Am J Clin Nutr. 2010 May;91(5):1468S-1473S. doi: 10.3945/ajcn.2010.28674G. Epub 2010 Mar 3. PMID: 20200262; PMCID: PMC2854912.

Dwyer J, Saldanha L, Haggans C, Potischman N, Gahche J, Thomas P, Bailen R, Costello R, Betz JM, Andrews K, Gusev P, Pehrsson P, Savarala S, Tey P, Harnly J. Conversions of β-Carotene as Vitamin A in IU to Vitamin A in RAE. J Nutr. 2020 May 1;150(5):1337. doi: 10.1093/jn/nxz334. PMID: 32367133; PMCID: PMC7373782.

Pino-Lagos K, Benson MJ, Noelle RJ. Retinoic acid in the immune system. Ann N Y Acad Sci. 2008 Nov;1143:170-87. doi: 10.1196/annals.1443.017. PMID: 19076350; PMCID: PMC3826166.

Higueret P, Pailler I, Garcin H. Vitamin A deficiency and tri-iodothyronine action at the cellular level in the rat. J Endocrinol. 1989 Apr;121(1):75-9. doi: 10.1677/joe.0.1210075. PMID: 2715762.

Biebinger R, Arnold M, Koss M, Kloeckener-Gruissem B, Langhans W, Hurrell RF, Zimmermann MB. Effect of concurrent vitamin A and iodine deficiencies on the thyroid-pituitary axis in rats. Thyroid. 2006 Oct;16(10):961-5. doi: 10.1089/thy.2006.16.961. PMID: 17042680.

Capriello S, Stramazzo I, Bagaglini MF, Brusca N, Virili C, Centanni M. The relationship between thyroid disorders and vitamin A.: A narrative minireview. Front Endocrinol (Lausanne). 2022 Oct 11;13:968215. doi: 10.3389/fendo.2022.968215. PMID: 36303869; PMCID: PMC9592814.

Smolle J, Wawschinek O, Hayn H, Eber O. Vitamin A und Carotin bei Schilddrüsenkrankheiten [Vitamin A and carotene in thyroid diseases]. Acta Med Austriaca. 1983;10(2-3):71-3. German. PMID: 6880574.

Aktuna D, Buchinger W, Langsteger W, Meister E, Sternad H, Lorenz O, Eber O. Beta-Carotin, Vitamin A und seine Trägerproteine bei Schilddrüsenerkrankungen [Beta-carotene, vitamin A and carrier proteins in thyroid diseases]. Acta Med Austriaca. 1993;20(1-2):17-20. German. PMID: 8475673.

Woźniak D, Drzymała S, Przysławski J, Drzymała-Czyż S. Dietary supplements in hypothyroidism. Acta Sci Pol Technol Aliment. 2021 Oct-Dec;20(4):375-381. doi: 10.17306/J.AFS.0985. PMID: 34724363.

Hinako Homma, Mikio Watanabe, Naoya Inoue, Moeko Isono, Yoh Hidaka, and Yoshinori Iwatani.

Polymorphisms in Vitamin A-Related Genes and Their Functions in Autoimmune Thyroid Disease. Thyroid.Nov 2021.1749-1756.http://doi.org/10.1089/thy.2021.0312

Farasati Far B, Broomand Lomer N, Gharedaghi H, Sahrai H, Mahmoudvand G, Karimi Rouzbahani A. Is beta-carotene consumption associated with thyroid hormone levels? Front Endocrinol (Lausanne). 2023 May 26;14:1089315. doi: 10.3389/fendo.2023.1089315. PMID: 37305054; PMCID: PMC10250628.

Triggiani Vincenzo, Tafaro Emilio, Giagulli Angelo Vito, Sabba Carlo, Resta Francesco, Licchelli Brunella and Guastamacchia Edoardo, Role of Iodine, Selenium and Other Micronutrients in Thyroid Function and Disorders, Endocrine, Metabolic & Immune Disorders – Drug Targets 2009; 9 (3) . https://dx.doi.org/10.2174/187153009789044392

Ihnatowicz P, Drywień M, Wątor P, Wojsiat J. The importance of nutritional factors and dietary management of Hashimoto’s thyroiditis. Ann Agric Environ Med. 2020;27(2):184-193. doi:10.26444/aaem/112331.

Zimmermann MB. Interactions of vitamin A and iodine deficiencies: effects on the pituitary-thyroid axis. Int J Vitam Nutr Res. 2007 May;77(3):236-40. doi: 10.1024/0300-9831.77.3.236. PMID: 18214025.

Rabbani, E., Golgiri, F., Janani, L. et al. Randomized Study of the Effects of Zinc, Vitamin A, and Magnesium Co-supplementation on Thyroid Function, Oxidative Stress, and hs-CRP in Patients with Hypothyroidism. Biol Trace Elem Res 199, 4074–4083 (2021). https://doi.org/10.1007/s12011-020-02548-3

Capriello S, Stramazzo I, Bagaglini MF, Brusca N, Virili C, Centanni M. The relationship between thyroid disorders and vitamin A.: A narrative minireview. Front Endocrinol (Lausanne). 2022 Oct 11;13:968215. doi: 10.3389/fendo.2022.968215. PMID: 36303869; PMCID: PMC9592814.

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