Carrots are a good source of beta-carotene, which is a precursor of vitamin A. But to receive the full health benefits of this superfood, you want an active enzyme to produce this vitamin, propose the findings of a novel study.
Beta-carotene is the bioactive compound that gives carrots their orange colour. Studies with humans and mice show the conversion of beta-carotene to vitamin A reduces “poor” cholesterol in the blood. Thus, beta-carotene can help give protection to against atherosclerosis development, which results in the accumulation of fats and cholesterol in our arteries. Atherosclerosis cardiovascular disease is the primary cause of death worldwide, says Jaume Amengual, assistant professor of personalized nutrition in the Branch of Food Science and Human Nutrition at the University of Illinois.
Amengual and his colleagues conducted two studies to further understand the effects of beta-carotene on cardiovascular health. They confirmed its importance but identified a critical step in the process.
Beta-carotene converts to vitamin A with the assistance of an enzyme called beta-carotene oxygenase 1 (BCO1). A genetic variation determines when you’ve got a kind of active version of BCO1. People with a less active enzyme could need other sources for vitamin A in their diet, Amengual says.
The first study, published in the Publication of Nutrition, analyzed blood and DNA samples from 767 healthy young adults aged 18 to 25. As expected the researchers found a correlation between BCO1 activity and poor cholesterol level.
“People who had a genetic variant associated with making the enzyme BCO1 more active had lower cholesterol in their blood. That used to be our first commentary,” Amengual paper money.
To follow up on these findings, Amengual and his colleagues conducted a second study, published in the Publication of Lipid Research, the usage of mice.
“In the human study, we saw that cholesterol used to be higher in people who do not produce much vitamin A. To realize whether that commentary has an effect, ultimately, we must wait 70 years to see whether they develop cardiovascularly. In real life, that isn’t doable. That’s why we use animals for sure studies, so we will speed up the process,” he explains.
“The main findings of the mice study reproduce what we found in humans. We saw that when we give beta-carotene to mice, they have got lower cholesterol levels. These mice develop smaller atherosclerosis lesions, or plaques, in their arteries. Which means that mice fed beta-carotene are more safe against atherosclerosis than those fed a diet without this bioactive compound,” Amengual states.
In the second one study, the researchers also investigated the biochemical pathways of these processes, determining where in the body the effect occurs.
“We narrow it down to the liver as the organ in charge of producing and secreting lipoproteins to the bloodstream, including those lipoproteins referred to as poor cholesterol. We observed that in mice with high levels of vitamin A, the secretion of lipids into the bloodstream slows down,” Amengual paper money.
Understanding how the BCO1 enzyme relates to cholesterol has important implications. In most cases, high beta-carotene levels in the blood are associated with health benefits. But it may be a signal of a less active BCO1 enzyme that isn’t converting the beta-carotene we eat into vitamin A.
Up to 50 per cent of the population have the less-active variant of the enzyme, Amengual paper money. That means their body is slower at producing vitamin A from a plant source, and they could wish to get this nutrient directly from an animal source such as milk, or cheese, as an example.
(This story has been published from a wire agency feed without modifications to the text.)
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