“I can’t help being fat, it’s in my genes!’ We hear this statement quite often but is it the whole truth?  Obesity is a major global health problem. In 2005, it was estimated that at least 400 million adults were obese (BMI > 30) world-wide. By 2015, it is estimated that the number will increase to about 700 million. Genome-wide studies have identified 12 alleles (an allele is a locus on a chromosome where the DNA is different) that are associated with increased BMI. Does the possession of one or more of these alleles sentence you to a life of obesity? Or could you influence this genetic predisposition to increased obesity risk by lifestyle changes?

Researchers from Cambridge University genotyped the 12 loci in a population-based sample of 20,430 adults from the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort and assessed the influence of a physically active lifestyle on the genetic predisposition to obesity in these individuals (PLoS Med 7(8): e1000332. doi:10.1371/journal.pmed.1000332). The study showed that, in a 1.70 metre tall person, every additional BMI-increasing allele was associated with an increase in BMI equivalent to 445 gm in body weight. In physically inactive individuals, the increase was 592 gm per allele. In physically active individuals, the increase was 36% lower at 379 gm per allele. In physically inactive individuals, possession of one of these obesity-susceptibility alleles increases the obesity risk by 15.8%. However, in physically active individuals the risk is 40% less at 9.5%.

While possession of the wrong genes can predispose an individual to weight gain, the trigger for weight gain is not purely genetic. We have to provide that trigger in the form of inappropriate lifestyle choices. Eating more than we need, eating foods that are high in fat and sugars, lack of physical activity due to increasingly sedentary lifestyles are all triggers to the worldwide obesity epidemic. Becoming obese not only affects self esteem and image, it also brings with it a slew of health problems such as heart disease, hypertension, diabetes, steatohepatitis, joint problems and cancer.

The next time you are about to blame your weight gain on mother nature, perhaps you might want to think again!

The recent wild fire in Moscow has caused much misery for its inhabitants. Fortunately, it is not a frequent occurrence. The smoke from wild fire carries particulate matter, which can cause or exacerbate respiratory problems. Every year around this time, large areas of Indonesia, Malaysia and Singapore are blanketed with smog due to the forest fires in Sumatra and on the Borneo island.  Acute and chronic exposure to smog causes or exacerbates respiratory illnesses such as asthma, emphysema and COPD in all age groups.  However, does particulate matter exposure cause other health problems?

A recent study from Taiwan investigated the association between asthma and suicide mortality in 162,766 high school students aged 11 to 16 years (Am J Psychiatry 2010; epub July 15). These students were classified into 3 groups at baseline – current asthma (symptoms present in the past year), previous asthma (history of asthma but no symptoms in the past year) and no asthma. Compared to non-asthmatics, the risk for suicide in the current asthma and previous asthma groups was increased 126% and 76%, respectively. The incidence rate of suicide death in those with current asthma was more than twice that of non-asthmatics.

Another study examined the relationship between exposure to ambient particulate matter (particulate matter ≤ 10 mum and ≤ 2.5 mum in aerodynamic diameter) and suicide in seven cities in the Republic of Korea (Am J Psychiatry 2010; epub July 15).  The study found a 9% increase in suicide risk related to an increase in particulate matter of ≤ 10 mum in aerodynamic diameter (average of 0 – 2 days prior to the day of suicide). For particulate matter of ≤ 2.5 mum in aerodynamic diameter (1 day prior to the day of suicide), the increased suicide risk was 10.1%. In those with cardiovascular disease, there was an 18.9% increase in suicide risk in relation to increase in particulate matter of ≤ 10 mum in aerodynamic diameter (average of 0 – 2 days prior to the day of suicide).

Smog from traffic pollution or from forest fires contains particulate matter. The particles are ≤ 10 mum and ≤ 2.5 mum in aerodynamic diameter. Thus, when cities in Malaysia, Singapore and Indonesia are covered in smog annually, people with asthma and cardiovascular disease are not only exposed to increased risk of exacerbation of their underlying conditions but also possibly to an increased risk of committing suicide. Citizens of these countries have reasons to embrace the idea of ‘Going Green’ and to encourage their respective governments to tackle the problem of annual forest fires.

It is known that smoking causes lung cancer and heart disease. Does smoking play a role in causing colorectal cancer (CRC)? While there are well known genetic causes for CRC, most CRCs in the general population are not genetically linked. Colonic adenomatous polyps are precursors to CRC; the larger the polyp, the higher the chance that it will have malignant potential. Colorectal polyps can be pedunculated or flat. Pedunculated polyps are easier to visualise and flat polyps can be missed easily during colonoscopy, especially when they are small. If adenomatous polyps are left untreated, they will turn into colon cancer with time. Recently, the American College of Gastroenterology published guidelines suggesting that smokers with a history of > 20 pack years may need screening for CRC earlier than their non-smoking counterparts. Are smokers at higher risk of developing colon polyps?

Researchers from Seoul National University Hospital studied 5254 asymptomatic subjects undergoing screening colonoscopy (J Gastroenterol Hepatol 2010; 25: 519 – 525). They were split into 3 groups aged 30 – 39 years, 40 – 49 years and 50 – 59 years. The prevalence of overall adenomas was 10.4% in the 30- 39 years age group, 22.2% in the 40 – 49 years age group and 32.8% in the 50 – 59 years age group. The prevalence of advanced adenoma was 0.7%, 2.7% and 4.1%, respectively. Male sex, current smoker and family history of CRC were independent predictors of advanced adenoma in the 40 - 49 years group. The risk of developing advanced adenoma in smokers is increased by 58%.

In another study from the University of Connecticut, 600 asymptomatic patients presenting for CRC screening were studied with high-definition colonoscope to detect flat adenomas (Gastrointest Endosc 2010; 71: 1234 – 1240). Of these 600 patients, 313 were non-smokers, 115 were heavy smokers (10 or more pack years and still smoking or had quit within 10 years) and 172 were low-exposure smokers (< 10 pack years or had quit more than 10 years ago). Heavy smoking increased the risk for flat adenomas of any size by 153%. The risk for flat adenomas of 6 mm or more was increased 284% in heavy smokers. Heavy smoking increased the risk of advanced flat adenomas by 181%. How heavy you smoke also increased the risk of developing flat adenomas. The risk was increased 128 % in those with > 30 pack years of smoking compared to those with < 30 pack years.

Smoking is known to cause many health problems. It is also considered to be an anti-social behaviour by many. Yet the number of smokers worldwide is increasing, especially in developing and under-developed countries. The mind boggles!