Early studies from China suggested a link between low selenium levels and liver cancer. In China, high rates of hepatitis B virus (HBV) infection and primary liver cancer (PLC) are present in Qidong county. Epidemiological surveys demonstrated an inverse association between selenium level and regional cancer incidence, as well as HBV infection. Four-year animal studies showed that dietary supplement of selenium reduced the HBV infection by 77.2% and liver precancerous lesion by 75.8% of ducks, caused by exposure to natural environmental etiologic factors.
In 1991, Yu et al. reported on an on-going liver cancer study. (57) The researchers found a significantly reduced risk for liver cancer in those who used selenium supplements for two years. In the 2-year intervention trial the incidence of primary liver cancer was significantly less (p<0.05) in selenium supplemented subjects (10 of 1444; 0.69%) compared to control subjects (13 of 1030; 1.26%).
In 1997, Yu et al. published the results of their intervention trial among the general population of 130,471 residents of Qidong. (96) Individuals in five townships were involved for observation of the preventive effect of selenium. The 8-year follow-up data showed reduced PLC incidence by 35.1% in selenized table salt supplemented vs. the nonsupplemented population. On withdrawal of selenium from the treated group, PLC incidence rate began to increase. However, the inhibitory response to HBV was sustained during the 3-yr cessation of treatment. The clinical study among 226 Hepatitis B Surface Antigen (HBsAg)-positive persons provided either 200 micrograms of selenium in the form of selenized yeast tablet or an identical placebo of yeast tablet daily for 4 years showed that 7 of 113 subjects were diagnosed as having PLC in the placebo group, whereas no incidence of PLC was found in 113 subjects supplemented with selenium. Again on cessation of treatment, PLC developed at a rate comparable to that in the control group, demonstrating that a continuous intake of selenium is essential to sustain the chemopreventive effect.
In 1999, Yu et al. published a “nested” case-control study which determined that there was a significant inverse relationship between selenium levels in stored plasma and later development of liver cancer in 7,000 Taiwanese men. (43)
In an intervention trial published in 2000, Li et al. measured the preventive effects of selenium on primary liver cancer. (98) According to the English language abstract, after screening of blood samples in 18,000 males from 20 to 65 years-old in Qidong, Jiangsu province, 2,065 cases of HBsAg positive, AFP negative and normal liver function (normal ALT values) were found. The subjects were randomly divided into two groups; 1,112 subjects (experimental group) received one tablet of sodium selenite (0.5 mg Se) every day and 953 subjects (control group) received one placebo tablet every day. During three years of intervention and follow up, the blood selenium concentration and glutathione peroxidase activity of the subjects in the experimental group were increased and had significant difference as compared with those of the control group (P < 0.01). At the same time, the prevalence rate of micronucleus cells in peripheral blood lymphocytes in the experimental group was significantly lower than that of the control group (P < 0.01), and the incidence of new liver cancer in the experimental group (3 057.55/10(6), 34 cases out of 1,112 subjects) was significantly lower than the control group (5 981.11/10(6); 57 cases out of 953 subjects) (P < 0.01).
The researchers concluded that, “the results confirms that selenium supplementation in general populations lived in high risk is effective in the prevention of liver cancer and the using of selenium tablets is simple and feasible.”
Thus, there is credible evidence from four intervention trials that selenium decreases the risk of developing liver cancer.