Vitamin A deficiency happens when your body consistently gets too little vitamin A from food, can’t absorb it properly, or can’t store and use what it takes in. In much of the world, the primary cause is simply not eating enough foods that contain it. But even in countries with abundant food, certain medical conditions, genetic variations, and lifestyle factors can quietly drain your vitamin A levels.
Not Enough Vitamin A in the Diet
The most straightforward cause is dietary. Your body gets vitamin A from two types of food sources: preformed vitamin A (found in animal products) and provitamin A carotenoids (found in plants). Preformed vitamin A comes from dairy, eggs, fish, and organ meats like liver. The plant-based form comes from leafy greens, orange and yellow vegetables, tomatoes, and fruits. Your body converts these plant pigments into usable vitamin A, but the conversion isn’t as efficient as getting it directly from animal sources.
In many developing countries, deficiency remains widespread because poverty and traditional diets limit access to both animal-based foods and carotenoid-rich produce. But restrictive diets in wealthier countries can cause the same problem. People following very low-fat diets, highly processed diets with few vegetables, or poorly planned vegan diets without adequate carotenoid-rich foods are also at risk. Because vitamin A is fat-soluble, you need some dietary fat to absorb it, so an extremely low-fat diet can undermine absorption even when intake looks adequate on paper.
Conditions That Block Absorption
Even if your diet provides plenty of vitamin A, your body may not absorb it. Because vitamin A dissolves in fat rather than water, any condition that impairs fat absorption will reduce how much vitamin A reaches your bloodstream. This is called secondary deficiency, and it’s the more common cause in developed countries.
Celiac disease, Crohn’s disease, and other inflammatory bowel conditions damage or inflame the intestinal lining, reducing the gut’s ability to pull fat-soluble nutrients from food. Cystic fibrosis affects the pancreas, which produces the enzymes needed to digest fat in the first place. Without those enzymes working properly, fat and the vitamins dissolved in it pass through largely unabsorbed. Chronic pancreatitis causes similar problems. Surgical removal of part of the small intestine, such as after bariatric surgery, physically reduces the surface area available for absorption.
Liver disease is a particularly important culprit. Your liver is your body’s primary vitamin A warehouse, storing roughly 80% of the vitamin A in your body. When liver injury progresses to fibrosis or cirrhosis, the specialized storage cells in the liver (called hepatic stellate cells) transform into scar-producing cells and lose their vitamin A reserves in the process. So liver disease doesn’t just impair absorption; it destroys the body’s existing stockpile. Children with liver disease are especially vulnerable to deficiency of all fat-soluble vitamins, including A, D, E, and K.
How Alcohol Depletes Vitamin A
Chronic alcohol use attacks vitamin A levels from multiple directions. Ethanol directly competes with vitamin A for the same enzyme, alcohol dehydrogenase, that converts stored vitamin A into its active form in the eye. This competition is one reason heavy drinkers often develop problems with night vision, sometimes before other signs of deficiency appear.
Alcohol also accelerates the breakdown of retinoic acid, the form of vitamin A your cells use for growth, immune function, and gene regulation. Ethanol activates a liver enzyme system that degrades retinoic acid into inactive byproducts at a faster-than-normal rate. The result is that even when a heavy drinker consumes enough vitamin A, their body chews through it more quickly than it should. Combined with the poor dietary habits and liver damage that often accompany alcohol use disorder, this creates a perfect storm for deficiency.
Genetic Differences in Conversion
Some people are genetically less efficient at converting beta-carotene from plants into usable vitamin A. The key enzyme responsible for this conversion is encoded by the BCO1 gene, and common variants of this gene significantly reduce its activity. Two well-studied variants, present in more than 1% of the general population, lower the body’s ability to convert beta-carotene into retinol.
This matters most for people who rely primarily on plant sources for their vitamin A. If you carry these variants and eat little to no animal-based food, you could be getting far less usable vitamin A than your diet suggests. The effect varies across ethnic groups, meaning some populations may face higher genetic risk for deficiency than others. Most people never get tested for these variants, so they may not realize their colorful vegetable intake isn’t translating into adequate vitamin A levels.
Zinc Deficiency and the Connection to Vitamin A
Vitamin A doesn’t work in isolation. Zinc plays a critical supporting role in vitamin A metabolism at nearly every stage: absorption, transport through the bloodstream, and conversion into its active forms. Your liver needs zinc to produce the transport protein that carries vitamin A from storage to the tissues that need it. Without enough zinc, vitamin A can get trapped in the liver, unable to reach your eyes, skin, and immune cells.
Zinc is also required for the enzyme that converts retinol into retinal, the form of vitamin A your eyes use for vision. This means a person could have reasonable vitamin A stores but still show symptoms of deficiency if their zinc levels are too low. The two deficiencies frequently overlap because they share common dietary sources and risk factors, and each one makes the other worse. Correcting vitamin A status without addressing zinc often produces disappointing results.
Who Faces the Highest Risk
Certain groups are more vulnerable to vitamin A deficiency than others. Young children are at the top of the list because they have smaller liver stores, higher nutrient demands relative to body size, and are more susceptible to infections that further deplete vitamin A. Pregnant and breastfeeding women have increased requirements and can become deficient even on diets that would be adequate otherwise.
People with chronic digestive conditions, anyone who has had gastrointestinal surgery, and those with liver disease all face ongoing risk. Heavy drinkers and people taking certain medications that interfere with fat absorption should also pay attention. In wealthier countries, deficiency tends to fly under the radar because it develops gradually. Early signs like difficulty seeing in dim light, dry skin, and frequent infections are easy to attribute to other causes, so the underlying deficiency can go unrecognized for months or years.
How Deficiency Is Identified
The standard marker is the level of retinol circulating in your blood. A concentration below 0.70 micromoles per liter is the established threshold for deficiency. However, blood levels don’t drop until your liver stores are substantially depleted, so by the time a blood test confirms deficiency, the shortage has typically been building for a while. Night blindness, one of the earliest functional signs, can appear before blood levels look abnormal on standard testing. If you have risk factors, a combination of symptoms and dietary history is often more revealing than a single lab value.