The importance of beta-carotene as vitamin A source

“There are many diet-related and host-related factors that may affect vitamin A equi- valency of beta-carotene (VEB). The main diet-related factors that influence VEB in humans are the food matrix in which beta-carotene is incorporated, the amount in- gested and the habitual diet type. The rupture of the food matrix by heating and homo- genizing promotes the release of beta-carotene from plant cells before and during digestion, and therefore it facilitates solubilization into mixed lipid micelles in the lumen and cellular uptake by intestinal mucosal cells. Cell wall structure in fruits is usually weaker than that in leaves, and therefore VEB for fruits deviates from that for vegetables. VEB may be regarded as constant as long as the consumption of beta-carotene is within physiological ranges and the host is in good health..With high (pharmaceutical) doses of beta-carotene, serum beta-carotene levels increase, and VEB can decrease when an oral dose of beta-carotene increases. The habitual diet type determines the composition of the diet, and various nutrient-to-nutrient interactions affect the absorption of beta-carotene to a greater or lesser extent. For example, beta-carotene absorption can be inhibited by lutein, when a minimum amount of about 5 g dietary fat is consumed simultaneously in a meal to ensure intestinal beta-carotene uptake. Also, absorp- tion of beta-carotene is reduced when dietary fiber content increases. Fiber interacts with bile acids, resulting in decreased absorption of fats and fat-soluble substances such as beta-carotene.

Host-related factors, such as age, pregnancy, health status, immune status and diarrhea, can also affect VEB. They could have more influence on populations in developing countries than on populations in Western countries, where public health care is well organized and, in general, persons are in good health. Another host-related factor is the recently described polymorphism in the BCMO1 gene coding for the enzyme res- ponsible for beta-carotene conversion into vitamin A. Studies have identified low responders who showed little or no response to plasma vitamin A concentration after a labelled dose of beta-carotene (1). The large inter-individual differences for estimates of VEB might be due to reduced enzymatic activity as a conse- quence of down-regulated activity of BCMO1 or polymorphisms in the BCMO1 gene. However, in none of the studies discussed were the genetic polymorphisms analyzed, as the importance of BCMO1 was only recently realized; therefore, VEB may be more efficient than currently proposed.The currently used VEB in a mixed diet and in oil are applicable only for individuals in general good health.

In the Western diet, which is relatively high in animal-derived foods (meat and dairy products), about 66 to 80% of the habitual intake for vitamin A is preformed vitamin A in the diet, with milk and dairy products contributing 15 to 20% to total vitamin A intake. On the other hand, 20 to 34% of vitamin A intake is based on intakes of provitamin A carotenoids. By assuming that at least 50% of provitamin A carotenoids are beta-carotene, dietary beta-carotene contributes at least 10 to 17% to daily dietary vitamin A activity in the Western diet. In contrast, the diet for most people living in developing countries contains only about 12 to 22% of preformed vitamin A, and consequently, they require 78 to 88% of provitamin A carotenoids in the diet. By assuming that at least 50% of provitamin A carotenoids are beta-carotene, dietary beta-carotene contributes at least 39 to 44% to daily dietary vitamin A activity in the diet in developing countries. Many people residing in developing countries consume the ‘prudent’ diet type, which is high in fresh fruits and vegetables and whole grains (e.g. rice, maize), and low in meat.

The present review focuses on the influence of the food matrix on VEB and distinguishes the results by the different types of dietary food matrices of beta-carotene, which are the oil matrix, the complex mixed diet matrix with various vegetables and fruits, and the single vegetable or fruit matrix. The majority of the data that the US Institute of Medicine reconsidered in 2001 were obtained from children and adults in developing countries with an inadequate nutritional status and their own habitual dietary patterns (2). The minority of the studies that the IOM reviewed were obtained from subjects in developed countries with an adequate nutri- tional status, consuming a Western diet.

The current review shows:

• For humans consuming beta-carotene dissolved in oil, a VEB between 2:1 – i.e. 2 micrograms beta-caro- tene dissolved in oil are required in the diet to produce 1 microgram vitamin A (retinol) in the human body – and 4:1 is feasible in a Western diet as well as in a ‘prudent’ (i.e. non-Western) diet. Fortified foods and dietary supplements are available, which contain physiological doses of beta-carotene in oil to complete an inadequate diet pattern. The down-regulation mechanism of the expression of BCMO1 by high doses and genetic polymorphisms in the BCMO1 gene might explain the observed variations in VEB in oil. The VEB is currently estimated by the IOM as 2:1 in oil (2).

• A VEB of approximately 4:1 is applicable for biofortified cassava, yellow maize and Golden Rice, which are specially bred for human consumption in developing countries.

• A range for VEB in a mixed diet of 9:1 to 16:1 is realistic for a Western diet and Western conditions. This range includes the VEB of 12:1 recommended by the IOM (2). For a ‘prudent’ diet including a variety of commonly consumed vegetables, a VEB in a mixed diet could range from 9:1 to 28:1. Large inter-individual variations in the estimates of VEB are reported, possibly due to genetic polymorphisms in the BCMO1 gene and the degree of regulation of the expression of BCMO1 in response to vitamin A status.

In future studies, as much data as possible should be collected to identify the impact of the three main factors that influence VEB in healthy human subjects: the amount ingested; the habitual diet type; the food matrix in which beta-carotene is incorporated. Furthermore, the known polymorphisms in the BCMO1 gene should be measured in the participants for clarification of possible variations in estimates for VEB.”

Based on: Van Loo-Bouwman C. A. et al. A review of vitamin A equivalency of b-carotene in various food matrices for human consumption. British Journal of Nutrition. 2014; 111:2153–2166.

1. Lietz G. et al. Single nucleotide polymorphisms upstream from the beta-carotene 15,15’-monoxygenase gene influence provitamin A conversion efficiency in female volunteers. J Nutr. 2012; 142:161S–165S.
2. US Institute of Medicine. Vitamin A. In Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. 2001; pp. 82–161. Washington, DC: National Academy Press.