One of the most common questions I get asked at some point of a consultation is “Doctor, with my condition, what kind of food should I avoid?”. This is a question I tend to get since I started practicing in the East. I think for the older generation of Asians, especially Chinese, they believe certain food stuff are ‘heaty’, ‘too cooling’ and may be ‘poisonous’ to certain conditions. For example, you will be assiduously warned to avoid prawns and crabs after an operation because consumption of such seafood can lead to pus formation in the wound. Another oft quoted statement is “You have to eat less! This will starve the cancer in your body and will cause it to grow more slowly!”.

Albumin is a key component of the total protein circulating in the body. The blood albumin level is a good indicator of ones nutritional status. A quick way to cause the albumin level in your body to drop is to starve yourself or stop consuming meat and protein containing foods. A low albumin level is associated with increased retention of fluid in the body tissue leading to oedema (swelling). This is associated with an increased risk of infection. In those who have had recent surgery, a low albumin level is associated with an increased risk of poor wound healing and wound related problems.

It has been shown in animal studies that protein restriction can lead to compromised immunity (a body’s defense mechanism), decreased clearance of influenza virus from the lungs of infected animals and increased death from the infection. Protein energy malnutrition (PEM, also known as protein-calorie malnutrition occurs when the consumption of protein and energy, measured in calories, is insufficient to satisfy the body’s nutritional needs) is the most common cause of immunosupression worldwide. PEM is characterized by a lymphopenia (a reduced amount of the white blood cell lymphocytes), reduced lymphocyte proliferation in response to antigenic (a foreign protein is an antigen, thus a bacteria or a cancer cell can be the antigen) stimulation, decreased cytotoxic (‘cell killing’) T lymphocyte activity and reduced antibody response to vaccination (Am J Clin Nutr 1997; 66: 464S–77S; J Nutr Health Aging 2004; 8: 28–37).

The body’s response to an infection, be it bacteria or viral in origin, is to mount a defense against the organism with the eventual aim of eliminating it from the body. To mount this response, the body requires energy quickly. This is achieved by the breakdown of protein in the body to produce glucose. If the body mounts a response with immune cells (called cell-mediated immune response) rather than antibody (secreted protein molecules), then the T lymphocytes will need increased glucose uptake and protein synthesis in order to support proliferation, differentiation (to change form), cytokine (special protein molecule) production and eventual direct encounter with and destruction of the offending organism or cell (Trends Immunol 2004; 25: 193–200). (The body tends to mount an antibody response to bacterial infection and a cell-mediated response to viral infection and cancer.) Thus, restriction of food intake can have an adverse effect on your body’s response to an infection or an underlying growth.

It is well known that patients with a viral infection or an underlying cancer condition will have reduced appetite. Patients who have had recent surgery may also feel full after eating only a small amount of food. For these individuals, they should be encouraged to eat a smaller portion each time but to eat many times through out the day. Unless you have an allergy to a particular food, it should be part of your diet. Of course, if you are diabetic then you need to watch your total sugar intake. If you have elevated cholesterol then you should stick to lean meat and avoid oily foods. A sensible balanced diet consisting of meat, fish, vegetable and fruits is the best.

Should you be taking vitamin supplements, nutritional supplements and herbal remedies? Ah, that’s a different kettle of fish! It would be true to say “Nothing beats a wholesome and nutritious meal!”.

Colorectal cancer (CRC) is a common cancer both in the East as well as in the West. CRC is the third most commonly diagnosed cancer and the second most common cause of cancer deaths in North America. In Singapore, CRC is the second most common cause of cancer deaths in both men and women. The American College of Gastroenterology has recommended colonoscopy as the preferred initial screening test for the average-risk individual in the population.

In the general population, if you do not have a family history of CRC or other colon conditions such as inflammatory bowel disease which predispose you to the development of CRC, how often do you need to have a colonoscopy after an initial negative colonoscopy? Once you have embarked on a programme of screening colonoscopy, when can you stop having another colonoscopy? When you reach 70, or 80, or never?

A recent report (JAMA 2006; 295: 2366 – 2373) from Manitoba, Canada looked at the risk of developing CRC in those individuals who had had an initial negative colonoscopy. A total of 35,975 individuals had an initial negative colonoscopy. The risk of these individuals developing CRC subsequently was found to be only 60-70% of the risk of developing CRC as found in the unscreened general population. This 30% reduction in the risk of developing CRC persisted for more than 10 years. (Thus this finding seems to confirm the present recommendation that colonoscopy need only be repeated 10 years after the initial negative colonoscopy.) One interesting finding from the study was that slightly more of these screened individuals were found to have developed right sided colon cancer within 2 years of the initial colonoscopy. The authors thought that this could be due to the possibility that the initial colonoscopy did not actually reach the caecum, thus resulting in some ‘missed’ CRC. Previous studies have shown that endoscopists who spend more time examining the bowel during colonoscopy withdrawal and have a more meticulous colonoscopic withdrawal technique will detect more colon polyps and thus tend to ‘miss’ less lesions in the colon. Clearly a situation where speed does not equate with excellence!

As one grows older, the incidence of developing cancer increases. In the case of CRC, the time lag from the development of an adenomatous polyp to a frank cancer of the colon is long. Hence the benefit of removing a polyp years earlier to prevent it from becoming a frank cancer may well be negligible when you reach a certain age. This is because you may die from other natural causes before the polyp can turn into a colon cancer which kills you. A recent North American study (JAMA 2006; 295: 2357 – 2365) looked at the estimated life-years saved with screening colonoscopy in very old and younger patients. The authors found that the prevalence of colorectal neoplasia (new growth) increased with age; 13.8% in the 50-54 year-old group, 26.5% in the 75-79 year-old group and 28.6% in the ≥ 80 year-old group. Despite this increased prevalence of neoplasia in the older population, screening colonoscopy in those aged ≥ 80 years resulted in only 15% of the expected gain in life expectancy in the 50-54 year-old group. The much reduced gain in life expectancy is a direct result of other natural causes of death among the elderly. Bearing in mind also that colonoscopy in the elderly is associated with (1) a higher failure rate of being able to perform a complete colon examination, (2) a longer time to perform, (3) higher risk of perforating the colon during the procedure and (4) a higher rate of suboptimal bowel preparation before the procedure, a standard policy of performing screening colonoscopy in all elderly individuals should be re-examined. Perhaps a more prudent approach would be one based on individual assessment by the family practitioner to determine if there are suspicious symptoms which would warrant a colonoscopy.

At present the British and American consensus is that screening colonoscopy should begin at age 50 for all individuals who are not at high risk of developing CRC. However, there is no consensus as to when colonoscopy can be dispensed with. Colonoscopy is not the only way to screen for CRC. Other methods include faecal occult blood testing (testing the stool for invisible blood), double contrast barium enema (an X-ray examination of the colon) and flexible sigmoidoscopy (a short telescope examination of the left side of the colon). You can read a succinct article on CRC screening at the American College of Gastroenterology web site.

“Your symptoms suggest that you may be suffering from a peptic ulcer”. What is peptic ulcer disease? Peptic ulcer is a collective term referring to gastric ulcer (also called stomach ulcer) and / or duodenal ulcer. The symptoms of PUD include epigastric pain or discomfort, uncomfortable bloatedness, early satiety (all 3 symptoms are collectively known as dyspepsia), heartburn and acid regurgitation (both are known as gastro-esophageal reflux symptoms), nausea and vomiting. It is possible to have PUD without any symptoms at all. The common risk factors associated with PUD include Helicobacter pylori infection, ingestion of aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) and smoking.

In population based studies, up to a third of adults in the Western world report dyspeptic symptoms. In Scandinavian studies of primary care patients with dyspepsia, PUD was found in 13% of them. In secondary care patients, the prevalence was 13% in USA and 31% in Italy. As the prevalence in the general population is difficult to determine, a recent study (Am J Epidemiol 2006; 163: 1025 – 1034) was performed in randomly selected adults from two communities in northern Sweden as an attempt to look at the prevalence of PUD in the general population. Gastric ulcer was detected in 2% of the studied population and another 2.1% were found to have duodenal ulceration. The symptoms which were significant predictors of PUD were nausea and gastro-esophageal reflux, while epigastric pain and /or discomfort were not. Smoking, obesity and aspirin intake were independent risk factors for the development of gastric ulcer. For duodenal ulcer development, the independent risk factors were smoking, aspirin intake and H. pylori infection. One quarter of the patients with gastric ulcer and 20% of the patients with duodenal ulcer had idiopathic PUD. That means the cause of the ulcers cannot be linked to the use of aspirin, NSAIDs or an underlying H. pylori infection.

Aspirin

Aspirin is invaluable to patients with a history of vascular disease, such as blockage of the blood vessels in the heart treated by by-pass heart surgery or a narrowed heart artery being kept open with a stent. These patients are given daily low doses of aspirin to help reduce the risk of renewed blockage of the stent or the new blood vessels. However, aspirin can lead to peptic ulceration. A recent study (Aliment Pharmacol Ther 2005; 22: 795 -801) looked at the prevalence of peptic ulceration in patients taking protective doses of aspirin. It was found that 11% of the studied population developed PUD. Only 20% of the patients had dyspeptic symptoms. H. pylori infection increased the risk of developing duodenal ulcer and those over 70 years of age also had increased risk of stomach and duodenal ulcers. This is NOT to say that we should not prescribe aspirin to patients with a history of vascular disease; this knowledge is important to doctors so that they can advise and inform their patients about the risk benefit ratio. Every form of treatment is associated with potential side-effects and risks, it is the duty of a responsible doctor to guide his / her patients to make the right choice. Only two kinds of doctor can promise a ‘no risk policy’ from the treatment they prescribed; a doctor who is the Almighty in disguise and a doctor who is economical with the truth.

Helicobacter pylori
For the most part of the 20th century, the idea that stomach ulcers are caused by a bacteria was unheard of. For quite some time, stomach ulcers were believed to be caused by stress and dietary factors. Treatment strategies consisted of hospitalization, bed rest and prescription of a bland diet! Subsequently, gastric acid was blamed. As a result, the correct treatment became more scientific with the use of antacids to neutralize the acid and medicine to block acid production. Despite this, the ulcers tended to recur.

In 1982, Drs Barry J. Marshall, a microbiologist, and J. Robin Warren, a pathologist, of Perth, Western Australia announced their findings that a bacterium was the culprit in patients with PUD. The organism was initially named Campylobacter pyloridis. It was only in 1989 that the name of the bacterium was changed to Helicobacter pylori. It took the medical community a long time before they accepted the fact that a bacterium is the cause of PUD. In 1994, a National Institute of Health Consensus Development Conference concluded that there is a strong association between H. pylori and ulcer disease. It recommended that ulcer patients with H. pylori infection be treated with antibiotics. From then onwards, the controversy about the role of H. pylori in PUD became history. In 2005, Drs Barry Marshall and Robin Warren were honoured with the Nobel Prize in Medicine for their work on H. pylori.

Peptic ulcer disease is a major and common health problem worldwide. It can affect the young as well as the old. It is easy to diagnose and can be treated effectively. While some can be related to drugs and others related to H. pylori infection, there are some who will have no obvious cause for their PUD. In some, the symptoms of PUD may have nothing to do with an underlying ulcer. The symptoms are actually due to the presence of stone(s) in the gall-bladder!