Regular physical exercise has cardioprotective effects but heavy physical exertion can trigger the onset of acute myocardial infarction (heart attacks). Thus, strenuous exercise has been called a “two-edged sword, both triggering and preventing myocardial infarction”. Marathon running has been shown to cause changes to the blood components within our body. It has been shown to increase white blood cell count, possibly due to increased blood flow or an inflammatory response caused by tissue injury such as rhabdomyolysis (muscle cell death). The dehydration leads to raised haematocrit, red blood cell count and haemoglobin level. As a result, in 2003 the International Marathon Medical Directors Association and USA Track and Field issued recommendations advising runners to drink ad libitum between 400 and 800 mL/h, as opposed to the previous "as much as possible" recommendations. Vigorous exercise is associated with a significant increase in the risk of acute myocardial infarction. It is estimated that 6% to 17% of all sudden deaths are associated with exertion. Platelet activation can have an important role in the acute coronary syndrome. Vigorous exercise such as marathon running can also induce haemolysis (breakdown of red blood cells). This is thought to be due to mechanical trauma to red blood cells during footstrike. Kratz and his coworkers of Harvard Medical School have used a modern cell counter to study the effects of a marathon on platelets and on RBC integrity and obtained evidence for in vivo platelet activation and for RBC fragmentation. They conclude by saying that further study is warranted to investigate the use of automated hematology systems to rapidly identify patients who may benefit from specific therapeutic interventions directed at counteracting platelet activation. They did not say that marathon is bad for health! Their article is published in American Journal of Clinical Pathology [2006;125(2):1-5].

A short article with that headline caught my attention the other day. The article mentioned that the bright red carotenoid pigment, called lycopene, in tomatoes is a powerful antioxidant. I ‘Googled’ the word lycopene and it returned 3.67 million hits for me to view!!

Lycopene is found in any red fruits or vegetables. In addition to tomato, lycopene is also found in watermelon, pink grapefruit, papaya and rosehip. It derives its name from the tomato’s species classification Solanum lycopersicum. Normally nutritional content such as Vitamin C is diminished by cooking. However, the process of cooking tomatoes actually increases the bioavailability of lycopene in food. There is evidence that regular intake of lycopene may help to reduce the risk of cardiovascular disease and prostate cancer.

Reddy and coworkers (Biol Chem 2006; 387: 87-93) published their findings recently on the protective effect of lycopene and beta-carotene on cells. When cells are exposed to aflatoxin B1 (AFB1), a fungal toxin that has been associated with primary liver cancer in man, they develop toxic damage to the cellular mechanisms and its DNA. When a new batch of cells, pre-treated with lycopene and beta-carotene, is exposed to AFB1, more of the cells survived the toxic effect of AFB1.

Perhaps the bottle of ketchup should be allowed to make its appearance on the dinner table more often?!

People with chronic hepatitis B and C viral infection have continuing inflammation in the liver. The liver responds by regenerating itself and this can lead to development of nodules within the liver. These nodules, called regenerating nodules, are usually benign and harmless in most instances. However, repeated inflammation and regeneration can lead to instability of the liver cells within the nodule and this can lead to abnormal cells (called dysplastic cells) which can assume a nasty growth behavior. The dysplasia can be high grade (HG, more severe) or low grade (LG, less severe). Nodules with these dysplastic cells are called dysplastic nodules. Dr Kobayashi and his coworkers in Tokyo recently published their study (CANCER 2006; 106: 636-647) on 154 patients with liver nodules and no evidence of primary liver cancer (hepatocellular carcinoma, HCC). Of these patients, 99 had regenerative nodules, 42 had LG dysplastic nodules and 13 had HG dysplastic nodules. Over a median observation period of 2.8 years, 29 of these nodules (18.8%) developed into HCC. The rate of developing HCC in these nodules is highest in HG dysplastic nodules and lowest in regenerative nodules. The annual development rate to HCC was estimated to be 20% for high grade dysplastic nodules and 10% for low grade dysplastic nodules. The cumulative HCC development rate at the fifth year is 80.8% for HG dysplastic nodules, 36.6% for LG dysplastic nodules and 12.4% for regenerative nodules.

Remember, if you are chronically infected with hepatitis B or C virus, you need to have six monthly check up with your doctor.