The U.S. researchers say that evidence shows that the zinc reduces the chance of diarrhoea and pneumonia without any risk of worsening the HIV infection.
The use of zinc has been questioned in the past because HIV thrives on zinc for its structure and to help it penetrate immune cells and reproduce, and zinc also activates the body cells that are targeted by HIV, the T lymphocytes.
Lead researcher Dr William Moss says that zinc supplementation could be a simple and cost-effective intervention to reduce morbidity and mortality in children with HIV-1 infection, and any safety fears are unfounded.
Dr William Moss and colleagues at Johns Hopkins School of Public Health, in Baltimore, recruited 96 children, aged between 6 months and five years, from Grey's Hospital in Pietermaritzburg, South Africa, and randomly assigned the children to receive zinc supplements or a dummy drug each day for six months.
The researchers say that zinc supplements did not result in an increase in blood HIV viral load, a measure of HIV severity, but the children receiving zinc did have less diarrhoea.
According to Dr Moss there are few interventions available to reduce morbidity in children with HIV-1 infection in resource-poor countries.
Dr Moss says that although UNAIDS, the World Health Organisation and their partners are committed to providing antiretroviral therapy to 3 million people by the end of 2005, many children still do not have access to this treatment or drugs to prevent opportunistic infections.
A spokeswoman from the HIV charity AVERT says further studies would be desirable before any decision was made to recommend zinc supplementation as standard practice.
As more than half the children die before the age of three years, usually of respiratory tract infections and diarrhoeal diseases, zinc supplementation could be a simple and cost-effective intervention to reduce morbidity and mortality in children with HIV-1 infection.
People with a healthy, balanced diet should not normally be deficient in zinc.
Foods rich in zinc include fish, meat, cheese, some nuts and seeds and brown rice.
The report is published in the current edition of The Lancet.
Previously, researchers knew that NPY could cause acute narrowing of the vessel by contraction of its muscular wall. However, this study showed that it has even more profound effects when it its levels are elevated chronically. In stressed rats which underwent angioplasty, NPY stimulated growth of abnormal smooth muscle in the blood vessels and caused them to become blocked with lesions containing microphages, thrombus and lipid deposits. These lesions resembled plaques which develop in humans in a process of atherosclerosis and are the cause of vessel blocking after angioplasty. This process has never before been reproduced in normal laboratory animals, unless they were genetically manipulated or were fed a fat-rich diet.
Researchers also found that it was possible to reverse this process by giving rats a compound that prevented cells from reading the increased levels of NPY. This compound, called the Y1 receptor antagonist, completely prevented the NPY-induced changes, allowing rats to undergo stress without increasing risk for atherosclerosis.
"This research has great potential for clinical applications in the future," said Zukowska. "Although this needs more study, if this same phenomenon occurs in humans, it is possible that Y1 antagonist could be used as a therapy for at-risk individuals."
Zukowska noted that if validated in humans, the research could be particularly applicable to men, whose bodies release more NPY during stress and who are generally more susceptible to heart attacks than pre-menopausal women. The findings also may prove helpful for individuals with mutations in the NPY gene, which occurs in some ethnic populations in as high as 9 percent of people, and which causes nerves to release the neurotransmitter in elevated levels.
gumc.georgetown/ and atvb.ahajournals/cgi/content/abstract/25/10/2075