Vitamin A for allergies has been a popular topic lately with numerous unrelated articles popping up for each variation of “Vitamin a toxicity”. The amount of research supporting Vitamin A as a cure-all vitamin is widely debated. This article will explain the top therapeutic uses of Vitamin A and how it could potentially be toxic. Vitamin A benefits is one of the most important topic in today’s health world. People are dying because of lack of vitamin A…
Vitamin A For Allergies
Vitamins A and D are able to modulate innate and adaptive immune responses and may therefore influence the development and the course of allergic diseases.
Materials and methods
This article reviews the current evidence for the experimental effects of vitamins A and D in vivo in animal models and on immune cells in vitro, and discusses their translational implication. A systematic literature search over the last 10 years was performed using MEDLINE and PubMed databases.
Results
Deficiencies of vitamin A or vitamin D in mouse models of allergic asthma seem to exacerbate allergic symptoms along with enhanced lung inflammation and Th2 cytokine production. In contrast, supplementation regimes especially with vitamin D were able to attenuate symptoms in therapeutic mouse models.
The active metabolites retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (VD3) induced tolerogenic dendritic cells (DCs) and up-regulated T‑regulatory cells in the allergic sensitization phase, which likely contributes to tolerance induction.
Additionally, RA and VD3 maintained the stability of eosinophils and mast cells in the effector phase, thereby reducing allergic mediator release. Thus, both active vitamin metabolites RA and VD3 are able to influence allergic immune responses at several immunological sites.
Conclusion
Animal studies predict that vitamin A and D may also be attractive players in the control of allergy in humans. Whether these experimental observations can be translated to the human situation remains open, as results from clinical trials are controversial.
Vitamin A Toxicity
Introduction
Vitamins and their metabolites regulate tissue growth, differentiation and embryonic development and have an important control function in the immune homeostasis by influencing both innate and adaptive immune responses.
Vitamins A and D are distinct from other vitamins as their metabolites, retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (VD3), are synthesized from precursors by different body tissues and they exert their effects on target cells by binding to nuclear hormone receptors.
Vitamin A
is essential for pre- and postnatal development, eyesight and reproduction, but it also has an important role in the maintenance of the immune system. Vitamin A is taken up in form of retinol or retinyl esters from animal-derived food sources (e. g. fish, liver, milk, eggs) or in form of precursors such as carotenoids from plant food (e. g. carrots, red peppers, lettuce).
Vitamin A is stored mainly in the liver. In liver cells, retinol is oxidized to retinal by alcohol dehydrogenases and metabolized to its main active metabolite RA. In the target tissue, the two isoforms all-trans-RA and 9‑cis-RA bind to nuclear retinoic acid receptors and/or retinoid X receptors (RXR), regulating over 500 retinoid-responsive genes.
Formation of RA is catalysed by enzymes called retinal dehydrogenases (RALDH), which are expressed in epithelial cells and in immune cells such as macrophages and dendritic cells (DCs). Recent work has revealed that these enzymes are present not only in gut-associated cells but also in the lung, which has prominent extrahepatic stores of vitamin A.
Vitamin D
promotes calcium absorption in the gut and helps maintain calcium and phosphate levels to promote bone health. Apart from having neuromuscular and cardiovascular effects it is known to regulate immune cell functions. Vitamin D is acquired via the diet (especially contained in fatty fish) and large amounts are synthesized in the skin from 7‑dehydrocholesterol after exposure to UVB light.
After hydroxylation in the liver, the resulting 25-hydroxyvitamin D3 is further hydroxylated in the kidneys by the enzyme 1‑α-hydroxylase resulting in VD3, which is the physiologically active metabolite.
VD3 in the target tissue binds to the nuclear vitamin D receptor (VDR), which heterodimerizes with nuclear receptors of the retinoic X receptor family, and binds to VD3 response elements in the promoters of VD3-responsive genes.
Both rate-limiting enzymes 1‑α-hydroxylase and the vitamin D receptor are expressed in many tissues, including the lungs, colon, skin, lymph nodes and cells of the immune system. Macrophages, DCs and T and B cells are therefore able to produce VD3 locally, which can act on immune cells in an autocrine or paracrine manner by binding to the vitamin D receptor:
The immunomodulatory role of vitamin A/RA and VD3
The immunomodulatory potential of RA and VD3 was investigated since long and recently their general influence on immune cells was reviewed in detail. Here we review reports on the innate and adaptive immune cells which are key players in allergic diseases.
Vitamin A/RA
B cells
The major influence on RA signalling in B cells concerns immunoglobulin class switching [1]. RA from intestinal DCs promotes generation of IgA+ producing B cells and potentiates memory B cell differentiation Consequently, vitamin A deficiency leads to a severe decrease in intestinal and serum IgA levels
APCs, T cells/Treg cells
On the T cellular level RA influences the homing of both CD4+ and CD8+ T cells by enhancing the expression of the gut-homing molecules α4ß7 and CCR9, promoting preferential migration to the gut-associated lymphoid tissue (GALT).
Most importantly, local production of RA by mucosal DCs together with TGF-ß can induce naive T cells to differentiate into FOXP3+ regulatory T cells (Tregs), thereby maintaining immune tolerance. This phenomenon is not restricted to the gut-associated lymphoid tissue.
Alveolar macrophages in the lung were found to promote the induction of FOXP3+ Tregs, which then again mediate respiratory tolerance through the production of RA and TGF-ß. A reciprocal regulatory effect of RA is seen in the suppression of Th27 and Th2 cell differentiation.
While under steady-state conditions RA maintains tolerance at mucosal surfaces inducing tolerogenic DCs and Tregs, RA can also induce inflammatory DCs and differentially affect T cell responses in already polarized T cells during infection or autoimmunity.
ILCs
In innate lymphocytes RA promotes the generation of ILC3s and antagonizes ILC2 function, highlighting the multiple functions of RA in immune cells.
Vitamin D/VD3
APCs
VD3 has a stimulatory effect on monocytes and macrophages, enhancing chemotaxis and activating the cathelicidin antimicrobial peptide. VD3 can also inhibit the differentiation and maturation of DCs, leading to a tolerogenic state with lower antigen presentation but increased production of IL-10. As DCs express 1‑α-hydroxylase they can acquire high local concentrations of VD3. This notion is supported by studies in VDR/1-α-hydroxylase knockout mice, which show a large increase in mature DCs.
B cells
In B cells, which express 1‑α-hydroxylase and VDR upon activation, VD3 has an antiproliferative effect. This effect is mediated by T helper cells but recent studies have shown that VD3 directly inhibits IgG secretion and the generation of memory and plasma cells, and promotes the apoptosis of B cells.
T cells/Treg cells
VD3 inhibits the expression of the Th2 (IFN-y, TNF-α), Th9 (IL-9), Th27 (IL-17) and Th22 (IL-22) cytokines in T cells, but has been described to up-regulate Th2 (IL-4, IL-10) cytokines and to induce FOXP3+ regulatory T cells.
A recent study on human CD4+ T cells showed a significant increase in the frequency of FOXP3+ regulatory T cells after stimulation with physiologically relevant levels of VD3 in combination with TGF-ß. Interestingly, Th2 cell differentiation can also be inhibited by VD3.
ILCs
In innate lymphoid cells VD3 seems to inhibit ILC2 activation and the expression of gut homing integrin.
Taken together, both active vitamin A and D metabolites seem to have a major influence on effector Th2/Th2/Th27 cell differentiation and regulatory T cell induction, which could also have implications for allergic disease development.
Correlation of vitamin A/D deficiency with allergic immune responses in vivo
In recent decades animal models have significantly contributed to the understanding of pathophysiologic mechanisms of allergic diseases such as asthma, anaphylaxis or food allergy.
Here we will concentrate on animal models of vitamin deficiency or supplementation that operate with and reflect on vitamin A or vitamin D contents that are taken up via the diet.
In neonate mice vitamin A deficiency (VAD) resulted in impairment of oral tolerance induction with insufficient Treg cell activation by DCs in mesenteric lymph nodes as possible underlying mechanism.
Interestingly, feeding of a single dose of vitamin A in adult mice could amplify the tolerogenic properties of mesenteric lymph node DCs.
Several studies reported that VAD in adult mice leads to increased airway hyperresponsiveness, lung inflammation and Th2 cytokine production;.
These mice were also prone to develop skin allergy upon oral antigen administration due to strong, IL-13 dependent IgE response. Earlier observations on VAD found a dose-dependent alteration of asthma symptoms, with low-level VAD decreasing airway inflammation and hyperresponsiveness while high-level dietary vitamin A increased disease severity.
The resulting hypothesis that excessive vitamin A intake in industrialized countries induces a Th2 bias and atopy prevalence is still very much under discussion.
Table 1
Effects of vitamin A and D in mouse models of airway inflammation associated with allergic asthma/rhinitis
| Treatment protocol | Results | Reference |
|---|---|---|
| Vitamin A/RA | ||
| Murine asthma model—ovalbumin (OVA) sensitization and challenge | Vitamin A deficiency exacerbates OVA-induced lung inflammation and type 2 cytokine production | |
| Murine asthma model—OVA sensitization and challenge | Vitamin A deficiency decreases eosinophils, IL-4, IL-5 in lung together with hyperreactivity | |
| Murine asthma model—OVA sensitization and challenge | RA administration leads to reduced airway inflammation by inhibiting Th2/Th27 differentiation | |
| Murine house dust mice (HDM) induced allergic rhinitis | RA administration leads to reduced allergic rhinitis by inhibiting Th2 response and induction of Treg cells | |
| Vitamin D/VD3 | ||
| HDM-induced airway hyperresponsiveness | Vitamin D deficiency results in increased airway eosinophilia and Th2 cells | |
| Murine asthma model—OVA sensitization and challenge | Vitamin D deficiency is associated with airway hyperresponsiveness, high eosinophilia and proinflammatory cytokines in lungs of challenged mice | |
| Murine asthma model—OVA sensitization and challenge | VD3 treatment is able to reduce chronic lung inflammation together with goblet cell hyperplasia and subepithelial collagen deposition | |
| Murine asthma model—OVA sensitization and challenge | Transfer of VD3-treated CD8+ T cells is able to prevent airway hyperresponsiveness and inflammation in OVA-challenged recipient mice |
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HDM House dust mite, OVA Ovalbumin
Vitamin D deficiency in neonate mice seems to contribute to allergic disease severity with high eosinophilia and airway remodelling, which could be improved by vitamin D supplementation.
Similarly, supplementation of vitamin D reduced airway hyperresponsiveness and lung inflammation in mouse models of allergic asthma.
In this respect, it was reported that eosinophils in vitamin D deficient mice seem to produce higher levels of mediator substances and are prone to spontaneous mediator release. Effects could be demonstrated not only in asthma-related studies, but also in models of food allergy.
In this experimental set-up vitamin D deficiency led to exacerbation of symptoms, possibly mediated by increased expression of IL-4 in mesenteric lymph nodes.
In allergen-specific immunotherapy (AIT), the only curative treatment for type I allergies, supplementation with 25-hydroxyvitamin D3 (inactive precursor of VD3) was able to enhance the beneficial effects in sensitized, vitamin D deficient mice.
This could have major implications for AIT in human allergic patients who often show a prevalence for vitamin D deficiency, especially in northern latitudes during wintertime which is exactly the time when pollen-specific AIT is initiated.
Thus, a recent study demonstrated enhanced efficacy of sublingual AIT (SLIT) in combination with vitamin D supplementation in grass pollen allergic children.
In vivo treatment with RA or VD3 as reference to underlying mechanisms of immunomodulation
There are a number of studies that focus on the in vivo administration of the major vitamin metabolites RA and VD3 and the effects of such treatment on immune cells of the innate as well as adaptive immune system.
Repeated antigen challenge in the presence of 9‑cis-RA reduced specific IgE responses and increased specific IgA responses in mice, probably via B cell derived IL-10. At the same time, it was reported that the IgE-repressive activity of RA was mediated mainly through the RA receptor alpha (RARα) by down-regulating IgE class-switching recombination.
Interestingly, by using lecithin:retinol acetyltransferase-deficient mice that are more susceptible to vitamin A deficiency elevated serum levels of mouse mast cell protease-1 together with significantly reduced numbers of intestinal Treg cells were also found.
DCs at the borderline between the innate and adaptive immune system play a major role in tolerance induction and their phenotypic differentiation can be regulated by vitamin metabolites.
In this respect, DCs when differentiated under RA stimulation were able to prevent anaphylactic responses to oral peanut allergen challenge in mice. The RA-generated DCs in this model displayed a tolerogenic mature phenotype expressing IL-10, TGF-ß and IL-27.
Overall, in vivo administration of RA in murine models of allergic rhinitis or asthma was able to attenuate airway inflammation and hyperreactivity due to induction of FOXP3+ r.
Concerning VD3, intraperitoneal administration at the time of airway antigen challenge led to reduced airway inflammation and remodeling in murine models of OVA-induced asthma. The protective role of VD3 in the lung of treated mice may be caused by inhibition of NF-kB activation, but also suppression of TGFß/SMAD signalling pathways was reported. Together with activation of the Nrf2/HO-1 pathway VD3 may be able to protect mice from antigen-induced oxidative injury and could be effective in the control of asthma.
Another recent report showed that VD3 could prevent the conversion of CD8+ T cells to IL-13 producing pathogenic effector cells in the lungs of antigen challenged mice. The authors argue that vitamin D could therefore be beneficial for asthmatics, but restricted to a subpopulation of steroid-refractory asthmatics with increased numbers of CD8+IL-13+ T cells.
In mouse—and human—mast cells, key proinflammatory effector cells of allergic response, VD3 was able to inhibit mediator release in a vitamin D receptor-mediated manner. These data are in line with a recent publication from Liu et al.
They reported that VD3 is important to maintain the stability of mast cell by increasing vitamin D receptor expression together with inhibition of IgE-sensitized mast cell activation.
In this respect, VD3 seems to interfere with two major key components of mast cell activation, the adaptor protein Myd88 and the FcεR1ß subunit of the high-affinity IgE receptor.
Thus, both active vitamin metabolites RA and VD3 are able to influence allergic immune responses at several immunological sites (Fig. 1).
Vitamin A and vitamin D impact immune cells relevant in the control of allergy. In mouse models of allergic disease vitamin A and D, and their major metabolites retinoic acid (RA) and vitamin D 3 (VD3), down-regulate Th2 and IgE immune responses.
Vitamin metabolite-treated dendritic cells (DCs) are prone to adapt a tolerogenic phenotype, leading to up-regulation of T‑regulatory cells (Tregs). Both vitamins also modulate T and B cell responses as well as mediator release from mast cells and eosinophils. (Copyrights from ©motifolio.com, and Fotolia.com©Anastasia Anisenko)
Can data from in vivo animal studies be correlated to the human situation?
The findings from in vivo animal studies suggest that vitamin A and D seem to have a major impact on immune cells as well as on the development, and in the case of vitamin D even on the treatment of allergic Th2-dominated diseases. The question remains whether these findings can be translated to the human situation, especially concerning the dosage of vitamin supplementation in connection with adequate vitamin status.
Nonetheless, in some of the studies conducted in mice the doses of vitamins were comparable to those applied in humans.
Studies in neonate mice predict that there could exist a “window of opportunity” for prevention of allergic diseases by vitamins A and D. This is reflected in human studies concentrating on the maternal vitamin A or D status that can be of importance for reducing the development of allergic diseases in children.
On the other hand, application of vitamin A as aerosol to asthmatic children was of no benefit, and no association between serum carotenoids and risk of asthma in young children could be established in a recently published longitudinal study.
Therefore, primary randomized controlled trials of the use of vitamin A to prevent or treat asthma that could elucidate the role of this vitamin in the human allergic disease are still missing.
Earlier studies reported that the vitamin D status in human allergic patients shows a nonlinear relationship with immune parameters relevant for allergic and asthmatic disease (e. g. serum IgE levels).
Nevertheless, vitamin D supplementation trials in asthmatic and/or pollen allergic children gave positive results with regard to asthma exacerbations and improvement of immunotherapy, similarly seen in case reports from adult asthmatics.
Funding
This work was supported by grant SFB F4606-B28 of the Austrian Science Fund FWF to EJJ.Go to:
Abbreviations
| AIT | Allergen-specific immunotherapy |
| APC | Antigen-presenting cell |
| DC | Dendritic cell |
| GALT | Gut-associated lymphoid tissue |
| HDM | House dust mite |
| IL | Interleukin |
| ILC | Innate lymphoid cell |
| OVA | Ovalbumin |
| RA | Retinoic acid |
| Treg | T-regulatory cell |
| VA | Vitamin A |
| VAD | Vitamin A deficiency |
| VDR | Vitamin D receptor |
| VD3 | 1,25-dihydroxyvitamin D3 |
vitamin a allergy skin rash
If you want a healthy body and beautiful skin, you need vitamins. However, excessive amounts of certain vitamins caused by overuse of supplements, or a deficiency caused by a poor diet or other conditions, may have an adverse effect on your skin. Try to maintain the recommended intake to avoid skin-related problems, like rashes that result from taking too much or not enough of certain vitamins.
Niacin Can Cause Dermatitis
Excessive niacin (vitamin B3) can be toxic with the most common symptom being flushing, signaled by the skin turning red and feeling warm on the face and neck. Other side effects include hives, nausea, vomiting and chronic itchy skin. With a severe allergic reaction to niacin, chest pain, difficulty breathing or jaundice can develop, which requires medical attention.
While excessive niacin can cause skin irritation, so can a lack of it says Healthy Skin Care. Niacin deficiency is often associated with malnutrition and causes symptoms involving the skin as well as the digestive and nervous systems. Sun exposure with a vitamin B3 deficiency may trigger a thick and scaly, dark-pigmented rash.
Other symptoms include inflammation of the mouth, causing an enlarged bright red tongue, vomiting, constipation, abdominal pain and diarrhea. The late stage of severe niacin deficiency is known as pellagra, with one symptom being dermatitis, according to Oregon State University.
Vitamin A Toxicity
Antioxidant properties of vitamin A are essential for maintenance and repair of cells, tissue and skin. However, excessive vitamin A in your body could lead to a condition called hypervitaminosis A. Vitamin A, in combination with medications for skin conditions, such as retinoids may cause toxicity, as could accidental overdose, which sometimes happens with children.
Symptoms of chronic vitamin A toxicity that affect the skin include dry, rough skin; itchy or peeling skin; skin sensitivity to light; cracked fingernails; mouth ulcers; and skin cracks around your mouth.
Beta carotene is a precursor of vitamin A. Although a high intake of foods or supplements containing beta carotene does not induce dangerous toxic effects, the telltale sign of excessive carotene is yellow-orange skin, most often concentrated on the palms and soles of the feet. Topical tanning products make use of carotene to create the skin discoloration called carotenodermia, which simulates a suntan.
If you’re pregnant, avoid high intake of vitamin A, and don’t use skin creams containing retinoid. Excessive vitamin A can cause birth defects in babies, including cleft palate and heart defects, according to the book “Prescription For Nutritional Healing.”
Although vitamin A deficiency is rare in the United States, it can cause an eye condition, especially in young children and pregnant women, called xerophthalmia, which hinders the ability to see in low light. If left untreated, it can lead to blindness, warns the National Institutes of Health. Vitamin A can react with certain drugs, such as warfarin, that could induce skin bruising and bleeding.
A Rare B7 Deficiency
In addition to the potential problems with niacin, other B vitamins can be responsible for skin eruptions. One such example is the connection between biotin and skin rash.
A report in Medical News Today said a rare inherited disorder called biotinidase deficiency, where the body cannot effectively use biotin, is the most common cause of biotin deficiency. Babies with the disorder often show symptoms of dermatoses in the first weeks of life, including eczema, hair loss, psoriasis, dermatitis or scaling skin that may be very thin or thickened.
Zinc for Healthy Skin
Zinc is necessary for maintaining the health of your skin. Used as a cream, zinc has anti-inflammatory properties that are beneficial for acne. Zinc deficiency that results in dermatitis-like skin changes can occur as a result of a poor diet or medical conditions that cause malabsorption, such as celiac disease.
Skin may be cracked, especially around the mouth and the hands. Other symptoms of a zinc deficiency may include hair loss, nail changes and skin infections. Skin irritations from a zinc deficiency are difficult to treat since they generally don’t respond to topical steroids and moisturizers, says the Australasian College of Dermatologists.
Vitamin C: Reducing Skin Irritations
Vitamin C helps fight skin infections and promotes healing of wounds and production of collagen. In fact, vitamin C is useful to help reduce skin irritations, such as dermatitis, due to allergic reactions. Vitamin C acts as a natural antihistamine by preventing the secretion of histamine in blood cells, according to a study in Alternative Medicine Review.
Since vitamin C is water soluble, an overabundance in your body is rare if your source is coming from your diet. However, a lack of vitamin C can cause skin disorders as a result of impairments in collagen production.
If you’re deficient in vitamin C you may experience symptoms of rough, dry, bumpy skin, easy bruising, spoon-shaped fingernails with red spots, bright red spots on skin around hair follicles, bleeding gums and wounds that won’t heal. In severe deficiencies, scurvy may result, causing swollen gums, poor wound healing and bruising.
Concluding remarks
The manifold impact of vitamin A and D on immune cell responses and profound evidence from animal studies provide hope that these molecules can help control allergy. More randomized controlled human studies are needed to underpin the potential of these vitamins and their metabolites in prevention or therapy of Th2-dominant allergic diseases including asthma.
We propose that more emphasis should be put on the determination of the vitamin status of allergic patients and, especially for vitamin D, on prophylaxis in early life or during pregnancy.
Vitamin A Benefits
Health Benefits of Vitamin A, Backed by Science
Vitamin A is the generic term for a group of fat-soluble compounds highly important for human health.
They’re essential for many processes in your body, including maintaining healthy vision, ensuring the normal function of your immune system and organs and aiding the proper growth and development of babies in the womb.
It’s recommended that men get 900 mcg, women 700 mcg and children and adolescents 300–600 mcg of vitamin A per day
Vitamin A compounds are found in both animal and plant foods and come in two different forms: preformed vitamin A and provitamin A.
Preformed vitamin A is known as the active form of the vitamin, which your body can use just as it is. It’s found in animal products including meat, chicken, fish and dairy and includes the compounds retinol, retinal and retinoic acid.
Provitamin A carotenoids — alpha-carotene, beta-carotene and beta-cryptoxanthin — are the inactive form of the vitamin found in plants.
These compounds are converted to the active form in your body. For example, beta-carotene is converted to retinol (an active form of vitamin A) in your small intestine
1. Protects Your Eyes From Night Blindness and Age-Related Decline
Vitamin A is essential for preserving your eyesight.
The vitamin is needed to convert light that hits your eye into an electrical signal that can be sent to your brain.
In fact, one of the first symptoms of vitamin A deficiency can be night blindness, known as nyctalopia
Night blindness occurs in people with vitamin A deficiency, as the vitamin is a major component of the pigment rhodopsin.
Rhodopsin is found in the retina of your eye and extremely sensitive to light.
People with this condition can still see normally during the day, but have reduced vision in darkness as their eyes struggle to pick up light at lower levels.
In addition to preventing night blindness, eating adequate amounts of beta-carotene may help slow the decline in eyesight that some people experience as they age
Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. Though its exact cause is unknown, it’s thought to be the result of cellular damage to the retina, attributable to oxidative stress
The Age-Related Eye Disease Study found that giving people over the age of 50 with some eyesight degeneration an antioxidant supplement (including beta-carotene) reduced their risk of developing advanced macular degeneration by 25%
However, a recent Cochrane review found that beta-carotene supplements alone won’t prevent or delay the decline in eyesight caused by AMD
SUMMARY
Eating adequate amounts of vitamin A prevents the development of night blindness and may help slow the age-related decline of your eyesight.
2. May Lower Your Risk of Certain Cancers
Cancer occurs when abnormal cells begin to grow or divide in an uncontrolled way.
As vitamin A plays an important role in the growth and development of your cells, its influence on cancer risk and role in cancer prevention is of interest to scientists
In observational studies, eating higher amounts of vitamin A in the form of beta-carotene has been linked to a decreased risk of certain types of cancer, including Hodgkin’s lymphoma, as well as cervical, lung and bladder cancer
Yet, though high intakes of vitamin A from plant foods have been associated with a reduced risk of cancer, animal foods which contain active forms of vitamin A aren’t linked in the same way
Similarly, vitamin A supplements haven’t shown the same beneficial effects
In fact, in some studies, smokers taking beta-carotene supplements experienced an increased risk of lung cancer (17Trusted Source, 18Trusted Source, 19Trusted Source).
At the moment, the relationship between vitamin A levels in your body and cancer risk is still not fully understood.
Still, current evidence suggests that getting adequate vitamin A, especially from plants, is important for healthy cell division and may reduce your risk of some types of cancer
SUMMARY
Adequate vitamin A intake from whole plant foods may reduce your risk of certain cancers, including Hodgkin’s lymphoma, as well as cervical, lung and bladder cancer. However, the relationship between vitamin A and cancer is not fully understood.
3. Supports a Healthy Immune System
Vitamin A plays a vital role in maintaining your body’s natural defenses.
This includes the mucous barriers in your eyes, lungs, gut and genitals which help trap bacteria and other infectious agents.
It’s also involved in the production and function of white blood cells, which help capture and clear bacteria and other pathogens from your bloodstream.
This means that a deficiency in vitamin A can increase your susceptibility to infections and delay your recovery when you get sick
In fact, in countries where infections like measles and malaria are common, correcting vitamin A deficiency in children has been shown to decrease the risk of dying from these diseases
SUMMARY
Having enough vitamin A in your diet helps keep your immune system healthy and function at its best.