(pic: bmj.com)

Many companies have clearly shared that fantasy or vision. Billions of dollars are at stake to be the one to discover the ultimate pill. The Ultimate Pill™ will have the following characteristics:

1. Help burn fat

2. Allow you to eat normally without putting on fat

3. Have no side effects

4. Be cheap and easily available

5. Reverse obesity-related changes (this is perhaps taking things too far)

Obviously, we are nearly talking science fiction here.

The various drugs that have been used in the past are now mere footnotes in the history of obesity medicine. Heard of fenfluramine? A few years back, rimonabant was said to be the wonder drug, working through some mysterious cannabinoid receptors in the brain (how exotic it sounds!). That fell through, because people were getting depressed enough to commit suicide.

Sibutramine and Orlistat have been heavily prescribed by physicians around the world to effect weight loss short of bariatric surgery. Sibutramine causes appetite suppression, while orlistat affects fat absorption and allows unhealthy eating without the fear of weight gain. So they said.

We have said it before that orlistat can cause liver problems, and is a candidate for withdrawal. Now the world is told that sibutramine has been withdrawn in the US, Canada and Europe because of heart attacks (the SCOUT study).

The BMJ says:

The therapeutic cupboard containing antiobesity drugs has never been well stocked. The European Medicines Agency (EMA) recently decided that sibutramine must follow the example of rimonabant, withdrawn last year because of safety concerns. This leaves just one drug—orlistat—to face the rising tide of obesity across the continent. The demise of sibutramine carries both irony and wider messages for the management of obesity.

Sibutramine fell at the crucial hurdle of cardiovascular risk. Arterial disease—which leads ultimately to myocardial ischaemia, heart failure, and stroke—affects most obese people to some degree and is their major cause of death. Much evidence suggests that weight loss decreases morbidity and mortality associated with cardiovascular disease,3 and this is an important justification for all antiobesity measures, including drugs. Unfortunately for sibutramine, an interim analysis of the SCOUT (Sibutramine Cardiovascular Outcome Trial) study found that the drug increased morbidity from cardiovascular disease. The odds were always stacked against sibutramine, because cardiovascular risk is embedded in its mechanism of action. Sibutramine acts centrally to reduce food intake; it inhibits the presynaptic reuptake and degradation of serotonin and noradrenaline, thus enhancing the appetite suppressing actions of both neurotransmitters.

Why drugs have not yet worked for weight loss in obese patients may be due to the fact that obesity is a heterogeneous disease with multiple factors, whereas the drug tends to be focal in its mechanism of action.

So, sadly, another drug has failed. The role of bariatric surgery is as crucial as ever. It is now the only scientifically proven method of weight loss. What is more, it is safe and effective. As study after study keeps showing us. But will the naysayers hear the truth?

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We have all heard of this saying, and all of us agree. A skilled laparoscopic surgeon plots to take out huge tumors and cysts through the keyhole method, while the dinosaur surgeon tends to think of employing his hands to remove organs (like the appendix) that may have been better left alone.

Let me tell you a small story about myself. Not too long ago, at a Bariatric Surgery conference three or some years back, I had a chat with a renowned endocrinologist who was known for his work in obesity and diabetes. At that time, I was 86 kgs heavy, and most of it was fat. A hard-working surgeon, I was in the peak of physical un-fitness and a heart attack waiting to happen. My resting heart rate was always around 100 and my blood glucose was similarly poised over the century mark. I asked this gentleman how I could improve my markers and lose my fat. I also didn’t want to become a diabetic, I said.

He told me what anyone in his position would have: take a metformin pill, and do some walking. If your sugar levels go up, we will add another drug, he said.

I thought long and hard over what he said. I embarked on a new journey in life: a life of health and fitness. I trained hard and started IF (Intermittent Fasting). After an year of blundering along, I found my groove and results came in: resting heart rate down to 6o, blood glucose and lipid levels normal, and body fat well down (BW now 75 kgs).

To come back to the point, the doctor I asked hit my problem with the drug hammer he was holding by default. I did the smart thing by trying something different. I now firmly believe that everyone should try healthy eating and exercise in order to improve health and reduce body fat. As bariatric surgeons, we should not use the surgery hammer to hit every obese patient. When there is clear burden of disease (diabetes, hypertension, sleep apnea, gallstone disease, etc.) and the level of obesity is such that it is statistically unlikely to come off with lifestyle regulation, we recommend bariatric surgery. Not otherwise.

In other words, as specialists dealing with obesity and related diseases, we should have a broad perspective. We are always in danger of using a narrow knife-wielder’s perspective and eyeing every patient as a potential victim. We must be very careful. At BMI, we never stop telling each other this.

In clinical practice, the psyche of the patient is very important. But a more important factor (and an often unrecognized one) is the psyche of the doctor.

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