Vitamin A and Your Gut

Many of us hear “vitamin A” and think “beta-carotene”, the orange-pigment in vegetables like carrots and butternut squash that we were all told as kids would help us see better. Although that’s an easy relationship to remember, the human body is never that simple. Vitamin A comes in many forms – carotenoids (like beta-carotene), retinol, retinal, and trans retinoic acid (RA). Each plays a different role in the body – from gut health to immunity to skin integrity to vision -  and the body converts one form into another based on what it needs.

If we’re “eating the rainbow” of fruits and vegetables we’re likely consuming carotenoids in that mix. Carotenoids are “provitamin A”, meaning they can get converted into active vitamin A (retinol) but they are not yet active themselves. Luckily, nature provided us with several foods that have retinol already formed in them, bypassing that first step. Unluckily, many of us no longer regularly eat these foods. Some examples are liver, certain types of fish, eggs, and dairy products like cheese and butter. Men need 900 mcg RAE daily, while women need 700 mcg (770mcg if pregnant and a whopping 1300 mcg if breastfeeding!) (1).

Food	Vitamin A content
Chicken liver	932 mcg RAE per ounce
Bluefin tuna	215 mcg RAE per ounce
Egg	75 mcg RAE per egg
Cheddar cheese	96 mcg RAE per ounce
Grass Fed Butter	97 mcg RAE per tablespoon
Baked sweet potato	1403 mcg RAE per whole sweet potato
Boiled frozen spinach	573 mcg RAE per ½ cup
Raw carrots	459 mcg RAE per ½ cup
Cantaloupe	135 mcg RAE per ½ cup

As you can see, most of us are probably not eating a daily ounce of chicken liver, or enough eggs and butter to reach the RDA without great intention. And although we can reach the RDA with a daily sweet potato or some creativity with carrots and boiled spinach, it may be more complicated than this. I’m going to get a bit technical for a second, so bear with me. The units above are in RAE, which is retinol activity equivalents. One mcg RAE is equivalent to 1mcg retinol, 12 mcg dietary beta-carotene, 24 mcg alpha-carotene, or 24 mcg beta-cryptoxanthin (the different types of carotenoids). So, it takes more carotenoids to equate to the active retinol, because we absorb each of these things at different rates. Where it gets tricky is that it now seems like the conversion rate can vary from person to person (2), so it’s possible we’re not getting all the benefit from our orange fruits and vegetables that we think we are. Bottom line, by eating animal sources of vitamin A that contain retinol in its active state, we are certain that we are getting that amount of active vitamin A.

Once we absorb the retinol, a couple of things can happen:

Retinol gets converted to retinal, which allows us to form rhodopsin.

Or

Retinol gets converted to retinal, which allows us to synthesize trans retinoic acid (RA).

Rhodopsin is what helps our vision. But RA is where the magic really happens. RA is used in DNA expression and regulates immune cells within the GI tract. It is essential for the cells involved in both innate and adaptive immunity (non-specific and specific immune responses), is anti-inflammatory, and can also promote proinflammatory signals during infection which signals the immune system to get to work (this is a good thing!).

When the intestinal cells convert retinal to RA, it tells the cells to produce inflammatory signals that trigger the shedding and elimination of infected intestinal cells (3). This is beneficial during the early stage of acute infection, as it assists the body in ridding itself of infection before it becomes widespread. Beyond maintaining the health of intestinal cells themselves, research by Wang and colleagues (2024) has also shown greater intestinal permeability (ie, “leaky gut”) and significantly increased inflammatory cytokines in vitamin A deficient groups (4). Considering a higher degree of intestinal permeability could allow more undigested food particles as well as bacteria and viruses to bypass the intestinal cells and go straight to the blood stream, it makes sense that greater levels of inflammation would be present. The measure of inflammatory signals between vitamin A “normal” and “supplemented” groups was not significantly different, possibly showing that supplementation beyond sufficient vitamin A levels is not necessary to maintain reduced inflammation levels. Unfortunately, as this is an animal study, actual measures of vitamin A intakes are not translatable to humans, so further research would need to be done to determine dosing recommendations, as well as determining if there is a significant difference in effect between supplemented synthetic vitamin A or whole food sources of vitamin A.

An additional animal study, by Yan and colleagues (2023) confirmed increased gut permeability in vitamin A deficient rats. Of note, it also caused increased gut permeability in the rats’ offspring (they were pregnant during the study) but this was alleviated by supplementing the offspring with vitamin A after birth. Vitamin A deficient rats also had significantly reduced diversity of gut microbiota, as well as reduced structure and richness of the microbiome (5). This is very important to the health of the intestinal cells of the offspring, as the change in the gut microbiome resulted in reduced production of short chain fatty acids (SCFAs). SCFAs are a main food source for our intestinal cells, and without them, these rats had worse degrees of gut permeability. As you can see, everything works together! Vitamin A impacts the health of the intestinal cells as well as the diversity of the gut microbiome, and the gut microbiome impacts the health of the intestinal wall, both of which greatly affect inflammation in the gut.

Even more so, researchers found that even short-term vitamin A deficiency has a significant effect on the gut microbiome, increasing and decreasing certain species of gut bacteria in periods of deficiency and normalizing after dietary intake of vitamin A improved (6).

Clearly, further human studies need to occur. We also need to know the effect of synthetic supplementation versus whole food supplementation as well as dosing requirements. However, it is undeniable that these studies make a case for including vitamin A-rich foods in our diet to support our overall health and wellness. My favorite way to get this vitamin into my diet? Chicken liver. It’s far milder than beef liver, and can be hidden really well! I do not like chicken liver straight up, so I boil it with meat stock, blend it into a pate, and freeze it in some silicone ice cube trays. Whenever I’m making ground meat, I pop a few cubes in. Blended soups? A cube of chicken liver. Tomato sauce? Add a cube of chicken liver! I’ve even thawed one out and mixed it in with salsa to eat with chips or put over chicken. Truly, it is doable, and adding it in just a few times per week even is a huge boost to the nutritional depth of your diet.

References

1.      Office of dietary supplements - vitamin A and carotenoids. (2025). https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/

2.     Tang, G. (2010). Bioconversion of dietary provitamin A carotenoids to vitamin A in humans. https://pmc.ncbi.nlm.nih.gov/articles/PMC2854912/

3.     Iyer, N., Grizotte-Lake, M., Duncan, K., Gordon, S. R., Palmer, A. C. S., Calvin, C., … Vaishnava, S. (2020). Epithelium intrinsic vitamin A signaling co-ordinates pathogen clearance in the gut via IL-18. https://pmc.ncbi.nlm.nih.gov/articles/PMC7202665/

4.     Wang, Z.-L., Pang, S.-J., Zhang, K.-W., Li, P.-Y., Li, P.-G., & Yang, C. (2024). Dietary vitamin A modifies the gut microbiota and intestinal tissue transcriptome, impacting intestinal permeability and the release of inflammatory factors, thereby influencing AΒ pathology. https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2024.1367086/full

5.     Yan, J., Xiao, L., Feng, D., Chen, B., Yang, T., Tong, B., … Chen, J. (2023). Vitamin A deficiency suppresses CEACAM1 to impair colonic epithelial barrier function via downregulating microbial-derived short-chain fatty acids. https://pmc.ncbi.nlm.nih.gov/articles/PMC10491915/

6.     Hibberd, M. C., Wu, M., Rodionov, D. A., Li, X., Cheng, J., Griffin, N. W., … Gordon, J. I. (2017). The effects of micronutrient deficiencies on bacterial species from the human gut microbiota. https://pmc.ncbi.nlm.nih.gov/articles/PMC5524138/