If you want to wage battle against cholesterol and other lipids (fat) that can contribute to vascular disease, then make tomatoes a big part of your diet. Scientists say this popular fruit contains a nutrient that can fight vascular disease such as stroke and arteriosclerosis.
Tomatoes fight more than cholesterol and fat
Excessive levels of lipids, such as cholesterol and triglycerides in the bloodstream, a condition known as dyslipidemia, can lead to potentially deadly diseases such as arteriosclerosis, cirrhosis, and stroke. Scientists from Kyoto University and New Bio-industry Initiatives, Japan, report that a compound called 9-oxo-octadecadienoic extracted from tomatoes can boost oxidation of fatty acids and contribute to the regulation of lipid metabolism by the liver. These qualities indicate that 9-oxo-octadecadienoic acid can fight cholesterol and other lipids and therefore help prevent vascular diseases.
Vascular disease is a general term used to describe diseases that affect the blood vessels. The Vascular Disease Foundation offers information on nearly two dozen different conditions that fit this category, including abdominal aortic aneurysm, carotid artery disease, deep vein thrombosis, lymphedema, peripheral artery disease, and stroke.
Tomatoes are also valued for other health benefits. Much research has been dedicated to a potent antioxidant in tomatoes, lycopene, and its potential in the fight against various types of cancer, and especially prostate cancer. Tomatoes also contain excellent levels of other nutrients, including niacin, which helps lower cholesterol; and potassium, which reduces blood pressure and the risk of heart disease.
Dr. Teruo Kawada, who is from Kyoto University and who led the study, noted that “Finding a compound which helps the prevention of obesity-related chronic diseases in foodstuffs is a great advantage to tackling these diseases. It means that the tomato allows people to easily manage the onset of dyslipidemia through their daily diet.” To help the fight against cholesterol and other fats that contribute to vascular disease, enjoy more tomatoes.
Kim YI et al. Molecular Nutrition & Food Research doi:10.1002/mnfr.201000264
The factors instrumental in triggering latent tuberculosis (TB) infection to progress into active disease have long remained elusive to researchers. New insight into the mystery is provided by Professor David Russell, speaking at the Society for General Microbiology's spring meeting in Edinburgh today. His work could help develop innovative strategies for treating the disease.
Professor Russell and his group at Cornell University in New York, USA, have demonstrated that TB-causing bacteria are able to hijack fat metabolism in the host to drive the progression of the disease. The team's research shows that Mycobacterium tuberculosis (Mtb) is able to stimulate macrophages – the immune cells the bacterium infects – to accumulate fat droplets, turning them into “foamy” cells. This cellular transformation can trigger a reawakening of the TB infection from its latent state.
Following initial infection by Mtb, the infected immune cells in the body can clump together in the lungs in a cellular mass that is surrounded by a fibrous cuff. This containing structure, called a
tubercle, physically protects the bacteria from being destroyed by the immune system. This allows them to persist inside the host for years during a latent period in which the host shows no symptoms. The respiratory infection is reactivated only in a small percentage of individuals (often those who are immunosuppressed) in whom it progressively destroys lung tissue. Very little is known about the exact causes of reactivation and the relative roles of the host and the pathogen.
Professor Russell's group discovered that inside the tubercle, surface molecules of Mtb prompted host macrophage cells to take up vast quantities of cholesterol-type lipids from the surrounding blood
vessels. “We think that the lipids in the newly-formed foamy cell are then expelled into the cellular environment, which contributes to the collapse of the tubercle,” he said.
Once freed from their containing structure, the infectious bacteria are able to leak out into the airways where they can progressively destroy lung tissue. “If our model is correct, it has huge implications for
vaccines and chemotherapy programmes. A more detailed knowledge of the bacterium's life cycle and its host interactions will allow us to spot new targets for drugs – opening up new possibilities for treatment,” said Professor Russell.