Approximately 81 million adults (>18 years of age) in the United States are obese or smoke. Of these, 9 million (4.5%) smoke and are obese. In China, it is estimated that there are 350 million smokers! While obesity among Chinese has not been a problem, the incidence of obesity will most likely increase with increasing affluence.

Obesity and smoking are primary risk factors for several chronic conditions and early death for a large number of people worldwide. Obesity is associated with diabetes, high blood pressure, high cholesterol, fatty liver, arthritis, uterine cancer and colon cancer. Smoking is associated with ischaemic heart disease, peripheral vascular disease, chronic bronchitis, emphysema and lung cancer. Many, if not all, of the health problems seen in people who are obese or who are smokers occur as a consequence of a lifestyle choice. For these individuals, and for the public in general, should the society as a whole look at preventive health care or providing a health care that aims to cure?

Traditionally, the healthcare industry has concentrated on cure rather than prevention, ameliorating disease instead of mitigating its onset. In 1997 the estimated total smoking-related healthcare cost was $89.2 billion in the United States. If one could halve the number of people smoking, the healthcare savings from reducing the incidence of smoking-related healthcare problems would run into the billions! The desire to find a cure is no more compelling than in our quest to find a cure for cancer. From 1971 to 2004, the government of the United States poured about 200 billion dollars into cancer research. Despite this massive amount of investment, our ability to cure has remained pretty poor for cancers of the lungs, colon, stomach and pancreas, to name a few. This abysmal performance is in no small measures due to our inability to detect the cancer at an early stage. If we can detect the cancer early enough and remove it completely, then we have a very high rate of cure. (Fortune magazine had a special article titled ‘Why we are losing the war on cancer’ in its March 22nd 2004 issue and the archived online article can be accessed here)

For lung cancer, most patients are discovered late. Would the more logical solution not be preventing the person from developing lung cancer? In USA, there is an effective preventive service for tobacco users. The service screens adults for tobacco use, provides brief counseling and offers pharmacotherapy to quit smoking. However, only about 35% of smokers availed themselves of the service. It is estimated that in a cohort of 4 million smokers, and if the current 35% receiving the service were to be increased to 90%, this would lead to an additional 1.3 million QALYs (quality-adjusted life years) saved.

In 1998, obesity-related health problems accounted for 9.1% of the total annual medical expenditure in the United States. What is interesting news to me is a recent report from Boston (Radiology 2006; 240: 435 -439) which reported that from 1989 to 2003, there has been a progressive increase in the number of cases where the obese state has interfered with the quality of the images obtained by the various imaging methods. The imaging modality most affected is abdominal ultrasound. In some instances, the patient’s habitus has prevented the use of CT and MRI scanners because the patient could not pass through the tubular tunnel of the machine. The poor quality images or an inability to use a certain imaging modality will directly impact on the doctor’s ability to diagnose a condition, let alone treat it.

In the case of smoking and obesity, we, as individuals, have a say in the matter. We can choose to be a smoker or a non-smoker. We can choose to eat more than we need or eat appropriately. While the health professionals have a responsibility to inform and to educate, the ultimate responsibility rests with each and every one of us. To prevent or to hope for a cure, it’s up to you. For me, I choose to heed the age-old saying “Prevention is better than cure!”.

A recent review article on “Bioavailability of selenium from foods” (Nutrition Reviews 2006; 64: 146-151) made me look at what’s new about the role of selenium in our health and in cancer. My interest in selenium is linked to the fact that selenium deficiency may play a role in the development of primary liver cancer or hepatocellular carcinoma (HCC). For example, a recent study from Taiwan (Biol Trace Elem Res 2006; 109: 15 – 24) found that the blood level of selenium in patients with HCC, on a background of hepatitis B virus infection, was significantly lower than in individuals without HCC, thus, confirming earlier similar findings. As such, would selenium supplementation protect an at risk individual from developing HCC or other cancers?

The major source of dietary selenium is plant foods. Wheat, broccoli, brazil nuts, oatmeal, white and brown rice are just a few examples. Animal products such as beef, turkey, chicken, egg, cod and tuna also provide dietary selenium. The content of selenium in the   food is however dependent on the selenium soil content where the crop is grown or animals are raised. In United States, people living in northern Nebraska and the Dakotas have the highest selenium intakes because the soils contain very high levels of selenium. In some parts of Russia and China, the soils contain very low levels of selenium. Consequently, selenium deficiency is common there because the food consumed is locally grown.

Selenium is a micronutrient essential to normal and healthy bodily function. During protein synthesis, selenium, in the form of selenomethionine, is incorporated to make selenoproteins which are important antioxidant enzymes. Antioxidants play an important role in mopping up free radicals (very reactive molecules) which can cause damage to DNA, lipids and proteins in cells. The cumulative effects of such damage can lead to heart disease and cancer. There are 3 diseases specifically linked with selenium deficiency. Keshan disease, first described in the early 1930s in China, occurs in selenium-deficient children. These children develop an enlarged heart with poor heart function.  Kashin-Beck disease, which results in bone and joint problems (osteoarthropathy), and myxedematous endemic cretinism, a consequence of associated poor thyroid function resulting in mental retardation, are the other two conditions.

How is selenium linked to thyroid disease? The 3 enzymes, called deiodinases, which convert thyroxine (T4, thyroid hormone) into triiodothyronine (T3, the active form of thyroid hormone) contain selenocysteine. The production of active thyroid hormone is thus dependent on the body’s selenium status. The selenoenzymes, with their antioxidant properties, also protect the thyrocytes (thyroid cells) from oxidative damage. There is evidence that selenium supplementation in patients with autoimmune thyroiditis (inflammation of the thyroid gland) seems to modify the immune response and reduce the oxidative damage to the thyroid gland.

It is interesting to note that the Food and Drug Administration (FDA) of United States has determined that there is sufficient evidence to warrant a qualified health claim for selenium and cancer. Like HCC, a low blood level of selenium has also been associated with increased risk of thyroid cancer. A research group in United States, using a special strain of mice which develop prostate cancer, looked at the influence of different levels of selenium-containing proteins on prostate cancer development. They found that the selenoprotein-deficient mice showed accelerated development of lesions associated with prostate cancer progression (Proc Natl Acad Sci U S A 2006; 103: 8179 – 8184).

Will selenium supplementation be effective in preventing cancer and heart disease? The jury is still out. Two long term studies are awaited with interest. The French study, SU.VI.MAX, is a prevention trial looking at the effects of antioxidant vitamins and minerals (including a daily supplement of 100 μg selenium) on chronic diseases such as cancer and cardiovascular disease. The Selenium and Vitamin E Cancer Prevention Trial (SELECT), a United States study, is sponsored by the NIH. This is a long-term study on whether supplemental selenium and / or vitamin E can decrease the risk of prostate cancer in healthy men. Until we know, a balanced diet is the best!

The Cacao (pronounced kahkow) tree, from which chocolate is derived, was worshipped by the Mayans of Central America. Cacao is a Mayan word meaning ‘God food’ and the word was corrupted by the early European explorers into the more familiar word ‘cocoa’. Although Columbus was given some cacao beans to take back to Spain in 1492, he did not know how to process them. It was Cortez who finally learnt how to process the beans and introduced chocolate to Spain in 1528. Up till the Industrial Revolution, chocolate was expensive to produce and remained a drink for the rich and powerful.

Cadbury, Van Houten, Lindt, Nestle are names of individuals who are intimately linked to one word – chocolate!  In 1815 Van Houten, the Dutch chemist, added alkaline salts to powdered chocolate to help it mix better with water and give it a darker colour and milder flavour. Thirteen years later, he invented the cocoa press to squeeze out the cocoa butter and leave the cocoa powder behind. This led to a more consistent cocoa powder and was much cheaper to produce. In 1875, Daniel Peter and Henri Nestle introduced condensed milk to chocolate leading to the birth of the popular creamy milk chocolate.

Flavonoids are micronutrients derived from plants, primarily fruits and vegetables. There are more than 5000 flavonoids and six flavonoid categories, namely, flavanols, flavanones, flavones, isoflavones, flavonols and anthocyanidins. Chocolate is in the flavanols category together with tea, red wine, beans, apricot, cherry, grape, peach, blackberry and apple. (The falvanols molecules are catechin and epicatechin.)

Dietary flavonoids are of interest to the scientific and medical communities because of their antioxidant properties. Flavonoids have the ability to scavenge (mop up) reactive oxygen species (ROS) and reactive nitrogen species. Excessive production of ROS gives rise to oxidative stress and is associated with a number of cardiovascular risk factors such as hypertension, dyslipidaemias (abnormal lipids / cholesterol profile in the body), diabetes and smoking. The protein molecules, lipid (fat) molecules and DNA of cells are susceptible to ROS damage and this can result in damage to cell membranes and organelles (cellular machinery). These damages lead to increased vascular (blood vessel) cell death and tissue damage. Endothelial (inner lining of blood vessels) dysfunction and atherosclerosis (hardening of blood vessels and formation of plaques) eventually ensue. Oxidative stress can also modify the low-density lipoproteins (LDL, the ‘bad’ cholesterol) and this modification is thought to be a major contributing factor in atherosclerosis.

The cocoa and chocolate flavonoids, (-)-epicatechin, decrease LDL modification by oxidative stress. Two hours after chocolate consumption, the plasma level of epicatechin was significantly increased. Endothelial dysfunction is an early event in the development of atherosclerosis. This is associated with a decreased availability of the vasodilator (factors causing blood vessel dilatation) nitric oxide (NO). In animal blood vessel studies, cocoa extracts induced endothelium-dependent relaxation and activated endothelial nitric oxide synthase. (Nitric oxide synthase helps with NO production.) Recent studies in healthy subjects found that after 4 days to 2 weeks of daily consumption of a cocoa beverage or flavonoid-rich dark chocolate bar, there was increased vasodilatation and improved endothelial function in these individuals. Another study, involving individuals with at least one cardiovascular risk factor such as hypertension, hyperlipidaemia, diabetes, smoking or a history of coronary heart disease, found that a single dose of a cocoa beverage led to a demonstrable reversal of endothelial dysfunction. These researchers also found increased NO bioactivity in these individuals. The cocoa and chocolate flavonoids also have anti-platelet effects. This effect may be due to increased production of NO which not only causes vasodilatation but also inhibits platelet aggregation. (Platelet aggregation can cause clot formation and blockage of blood vessels. Platelets also play a role in atherosclerosis.)

Inclusion of flavonoid-rich foods in one’s diet is essential. Indeed a ‘polymeal’ combining seven food components, including dark chocolate, wine, fish, fruits, vegetables, garlic and almonds, has been proposed as a strategy to reduce cardiovascular events by 76% and increase total life expectancy by 4.8 to 6.6 years (BMJ 2004; 329: 1447 – 1450). One could not and should not survive on chocolate alone! One more thing before you rush to the nearest local convenience store to empty its shelf of your favourite milk chocolate, remember this – dark chocolate typically contains two to three times as many cocoa flavonoids as milk chocolate. Yum, yum!