A study accepted for publication in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism and published on-line ahead of publication on Feb. 25, highlights the importance of avoiding becoming deficient in vitamin D. The study showed older individuals who are vitamin D deficient also tend to have compromised immune function.
It is well known that vitamin D plays a role in helping the body absorb the calcium needed to maintain healthy bones. The skin naturally produces vitamin D when it is exposed to sunlight. People also obtain smaller amounts of the vitamin through foods, such as fortified milk.
In the United States, studies by both the Institute of Medicine and the Centers for Disease Control and Prevention show many consumers have adequate levels of vitamin D. But more than 1 billion people worldwide are estimated to have deficient levels due to limited exposure to the sun, according to the United Nations.
“Our data suggest vitamin D may be involved in maintaining the health of the immune system as well as the skeletal system,” said Mary Ward, Ph.D., of the University of Ulster in Coleraine, the United Kingdom. “This study is the first to find a connection between vitamin D levels and inflammation in a large sample of older individuals.”
The observational study of 957 Irish adults who were at least 60 years old examined vitamin D levels as well as biomarkers of inflammation. Participants who were vitamin D deficient were more likely to have high levels of the biomarkers, which are linked to cardiovascular disease and inflammatory conditions such as multiple sclerosis and rheumatoid arthritis.
“The results indicate immune function may be compromised in older individuals with vitamin D deficiency,” Dr. Ward said.
Vitamin A and fighting infections
In findings published in the March 1 issue of the Journal of Immunology, University of California at Los Angeles (U.C.L.A.) researchers investigating the role of nutrients in helping the immune system fight against major infections show vitamin A may play a role combating tuberculosis.
The U.C.L.A. research team said for the first time the mechanism by which vitamin A and a specific gene assist the immune system by reducing the level of cholesterol in cells infected with tuberculosis had been identified. Cholesterol may be used by tuberculosis bacteria for nutrition and other needs, the researchers said.
“If we can reduce the amount of cholesterol in a cell infected with tuberculosis, we may be able to aid the immune system in better responding to the infection,” said Philip Liu, an assistant professor of medicine in the divisions of dermatology and orthopedic surgery at U.C.L.A.’s David Geffen School of Medicine and Orthopaedic Hospital Research Center and senior author of the study.
Although vitamin A circulates in the body in an inactive form known as retinol, it’s the active form — all-trans reinoic acid — that is responsible for activating the immune system.
To investigate the role of the active form of vitamin A in immune defense, the U.C.L.A. team first compared its effects on cells to the effects of vitamin D, which the group previously had studied. The researchers thought the two vitamins may use the same mechanism to aid the immune system, but it wasn’t the case. They found when the vitamins were added to human blood cells infected with tuberculosis, only vitamin A decreased the cells’ cholesterol levels.
The researchers also discovered that the action of vitamin A was dependent on the expression of a gene called NPC2. Further experiments in the lab showed that even if an infected blood cell was stimulated with vitamin A, it would not be able to fight the tuberculosis bacteria if the cell couldn’t express the NPC2 gene.
Vitamin A induces the cell to express NPC2, which helps the cell remove cholesterol from the lysosomes, which are “compartments” in a cell that also play a role in fighting infections, so the bacteria can’t access it.
“We may be able to target these pathways that regulate cholesterol within a cell to help the immune system respond to infection,” said Matthew Wheelwright, a medical and doctoral student at the University of Minnesota who was an undergraduate research assistant in Dr. Liu’s lab when the research was conducted and is a co-author of the study. “The cells need vitamin A to trigger this defense process and NPC2 to carry it out.”
Mr. Wheelwright noted this is an early study and more research needs to be done before recommending vitamin A supplementation to combat tuberculosis or other infections.
