A cup of camomile tea could help ward off cancer, researchers say.
The tea contains a chemical, apigenin, which takes away some of the ‘superpowers’ of cancer cells.
Scientists at Ohio State University found apigenin can block the ability of breast cancer cells to live far longer than normal cells, halting their spread and making them more sensitive to drug therapy.
Camomile tea, parsley and celery are the most abundant sources of apigenin but it is also found in many fruit and vegetables common in a Mediterranean diet.
The chemical, which has also been shown to act as an anti-inflammatory, works in a way that suggests other nutrients could have similar effects in warding off cancer.
It helps proteins correct the abnormalities in RNA – molecules carrying genetic information – that are responsible for about 80 per cent of cancers.
Molecular geneticist Professor Andrea Doseff, of Ohio State University, said: ‘We know we need to eat healthfully, but in most cases we do not know the actual mechanistic reasons for why we need to do that.’We see here the beneficial effect on health is attributed to this dietary nutrient affecting many proteins.
‘In its relationship with a set of specific proteins, apigenin re-establishes the normal profile in cancer cells. We think this can have great value clinically as a potential cancer-prevention strategy.’
Cancer cells thrive by inhibiting a process that would cause them to die on a regular cycle subject to strict programming. The researchers found apigenin could stop breast cancer cells from inhibiting their own death.
Much of what is known about the health benefits of nutrients is based on epidemiological studies that show strong positive relationships between eating specific foods and better health outcomes, especially reduced heart disease.
But how the actual molecules within these healthy foods work in the body is still a mystery in many cases, and especially with those linked to lower risk for cancer.
The researchers also showed apigenin binds with an estimated 160 proteins in the human body, suggesting other nutrients linked to health benefits called ‘nutraceuticals’ might have similar far reaching effects. In contrast, most pharmaceutical drugs target a single molecule.
The researchers, whose findings are published online in the Proceedings of the National Academy of Sciences, likened their technique to ‘fishing’ for the human proteins in cells that interact with small molecules available in the diet.
Prof Doseff said: ‘You can imagine all the potentially affected proteins as tiny fishes in a big bowl.
‘We introduce this molecule to the bowl and effectively lure only the truly affected proteins based on structural characteristics that form an attraction.
‘We know this is a real partnership because we can see that the proteins and apigenin bind to each other.’
Experiments established apigenin had relationships with proteins that have three specific functions. Among the most important was one known as hnRNPA2 which influences tiny bits of DNA called mRNA containing the instructions needed to produce a specific protein.
Abnormalities in these are responsible for about 80 percent of all cancers.
The researchers observed apigenin’s connection to the hnRNPA2 protein restored the function of mRNA to breast cancer cells, suggesting when they are normal cells die in a programmed way, or become more sensitive to chemotherapeutic drugs.
Added Prof Doseff: ‘So by applying this nutrient, we can activate that killing machinery.’
The beneficial effects of nutraceuticals are not limited to cancer, as the investigators previously showed that apigenin has anti-inflammatory activities. The scientists noted that with its multiple cellular targets, apigenin potentially offers a variety of additional benefits that may even occur over time. The researchers are now testing whether food modified to contain proper doses of the nutrient can prevent cancer in mice.
Source: Dailymail
This is the compilation of questions and answers during our Session with the founder of House of Healin Dato’ Dr Hassan Yaacob on 29th of April 2012.
