Obesity
Received Questions:
Responses:
17th May 1999
Obesity is rapidly becoming prevalent in some populations, particularly in affluent countries with consumerist values (Fumento, 1997). Changes in lifestyle have included a preference for highly processed foods rich in fat, sugar, and salt, together with a reduction in physical activity as more time is spent sitting in cars or in front of the television. This leads to the common-sense view that obesity is the result of gluttony and sloth (Gibbs, 1996). Obesity occurs when the intake of energy in the diet exceeds the expenditure of energy by the body through metabolism over a prolonged period. It is believed that evolution has favoured a regulatory system that allows energy storage during times of plenty to carry the animal through the times when food is scarce (Friedman, 1997). The surplus is stored as fat (adipose tissue). In modern societies, there are no food shortages to balance out the overconsumption.
However, the gluttony-sloth explanation is not complete - not everyone in an affluent society becomes obese, so research is being conducted into why some people are more susceptible to obesity than others (Friedman and Halaas, 1998). It seems likely that the tendency to become obese is established early in the lifecycle, perhaps even during the prenatal period of development. Obesity is a consequence of a network of genetic and environmental factors - it is multifactorial with genes and environment contributing approximately equal shares of influence.
Paradoxically, as obesity becomes more prevalent, more value is placed on being thin. This creates powerful conflicts in some people, particularly the young. They are bombarded with mixed messages from the media, advertisers, the food industry, the slimming industry, and the ‘happy to be fat’ lobby. For many people, obesity leads to a fall in self-esteem, to discimination against them, and to depression.
The distinction between not-obese and obese is an arbitrary one. A commonly used measure is the Body Mass Index, which is calculated by dividing the person’s weight (in kilograms) by their height (in metres) squared. The dotted line between not-obese and obese is often drawn at an index value of 25 - above this value the health risks begin to increase rapidly. Approximately 60% of Americans have an index of 25 or more.
Studies in mice have revealed that at least 5 genes have links with weight control and obesity:
Obese gene - codes for leptin, a hormone produced predominantly by white adipose tissue but also found in the stomach wall and placenta. Discovered 5 years ago, leptin is considered to be an important feedback signal from adipose cells to the weight-regulating region in the hypothalamus. Here it inhibits the secretion of neuropeptide Y, a substance that is a potent stimulator of appetite
Diabetes gene - this codes for a receptor protein that responds to leptin, and triggering a reduction in appetite and increase in metabolism
Fat gene - codes for an enzyme that processes insulin
Tubby gene - function currently unknown
Agouti - function currently unknown.
Diagram showing feedback effect of leptin on the hypothalamus
Comparable genes have been found in the human genome, but their role in humans is unclear. Research is being carried out into leptin in the human context to see whether it might be possible to use it in the treatment of obesity. Leptin levels in obese people tend to be high, so it is possible that the regulatory centres in their brains have become insensitive to its action. Thus it is unlikely that administration of additional leptin will have a weight-reducing effect. Contrasting with this, two obese children have been described in whom there is a deficiency of leptin (Montague et al, 1997), but these are considered to be exceptional cases. It is possible that leptin levels influence the onset of puberty, since on average obese children enter puberty earlier than thin children.
Obesity increases the risk of a variety of serious health problems: cardiovascular disease (hyperlipidaemia, hypertension, ischaemic heart disease), non-insulin dependent diabetes mellitus, osteoarthritis, gallstones, cancer, and stroke. These contribute to an increased risk of premature death for the obese person and put a heavy burden on the health care system. However, although obesity generates medical problems, the solution does not necessarily have to be a medical one. It would seem to be more appropriate to tackle the social and economic pressures on people to overconsume. Clearly, the pharmaceutical industry can see considerable financial advantages in producing a pharmacological fix for obesity and several approaches are being tried, from non-absorbable fats and sugars to drugs that influence the appetite and activity control centres of the brain. Appetite suppressants such as fenfluramine and dexfenfluramine have been tried, but worries about harmful side effects have led to their withdrawal. The intestinal lipase inhibitor orlistat reduces the uptake of fat from the diet. Sibutramine acts on the weight control systems in the brain - it is a serotonin and noradrenaline re-uptake inhibitor. Surgical reduction of the size of the stomach - gastroplasty - has become popular in some countries, but although it is effective in producing weight loss and reducing the occurrence of diabetes, the procedure carries with it the risk of surgical complications.
For an obese person, a sustained reduction in weight produces a sharp increase in life expectancy. However, at present only a small minority of people are able to achieve this. Although many people try weight-reducing diets, the long-term success rate is extremely small. The homeostatic control systems that regulate our weight are extremely difficult to influence by conscious effort.
References
Friedman,, J.M. (1997) The alphabet of weight control. Nature, 385, 119-120.
Friedman, J.M., and Halaas, J.L. (1998) Leptin and the regulation of body weight in mammals. Nature, 395, 763-770.
Fumento, M. (1997) The fat of the land: the obesity epidemic and how overweight Americans can help themselves. Viking.
Gibbs, W.W. (1996) Gaining on fat. Scientific American, 70-76 (Aug).
Montague, C.T. et al (1997) Congenital leptin deficiency is associated with severe early onset obesity in humans. Nature, 387, 903-908.
Nearly three years ago I developed M.E. which as you will be able to gather has dramatically changed my life. From being a very fit & healthy night duty carer, I now find myself to be 'the cared for'..... I am only 55 years of age, and not quite ready for the Knackers Yard yet, but because of the effects of M.E. I have put on nearly SIX Stone! From being a 20-mile a day walker, I have now become a female whom can only walk a few steps at a time & this is one factor of why the weight has piled on me.
My doctor has now said that because of all this weight, the M.E., the falls I have had, and the general slowness of me that I am now very obese (and yes, he is quite right) and I do know this fact does put my life in danger, so, he has to-day put me on Diabetic Tablets to help ensure I don't get that...He say's I have to have no fat at all, and to have a 600 calories a day diet. Could you PLEASE work out a decent 600 a day calorie menu for me. I like all fruits & vegetables, fish, chicken, etc. I know it is going to be hard to accomplish this reduction in weight because I am so inactive, but I do hope to get well one day, but if that's not to be, I certainly cannot afford to put on any more weight as I am just a little over five feet tall, so am looking as fat as I am tall! I don't want to die from a heart attack, etc.
24th December 2004
With regard to a suitable low calorie diet, your doctor should be able to put you in contact with a nurse locally who has a special knowledge of nutrition - there will be one associated with most NHS hospitals. The thing about changes in diet is that they must be managed carefully, over a period of time, and we are not in the position to help in that way.
In the last 3 years you have experienced a significant change in lifestyle, with a much-reduced level of activity. However, eating patterns are deeply ingrained, and perhaps you have continued to eat in a similar way to when you were more active. If so, that would be why you have put on weight – your energy intake has exceeded the diminished energy output. Now, even if all the symptoms of ME clear up, you will still feel lethargic due to the burden of the extra body weight. The extra weight plus the effects of ME mean that exercise will become steadily more difficult and the problem progressively worse unless the energy balance can be shifted in the other direction.
You sound determined to make that change now, so my advice would be to begin the process of recovery gradually, aiming to get back to your former self over the next 3 years. Gradually increase your level of activity, gradually reduce your calorie intake, and in time you will see the effects and enjoy the health benefits. Personally, I am not a fan of crash diets, because for most people they are followed by a significant rebound, but this is something you can discuss with a nutritionist. I have seen people make significant weight losses with the Lipotrim programme, for example, but then regain most if not all the weight in the months that follow. In my experience, one of the keys to weight control is to find a form of exercise that you enjoy, whether it is walking the dog, gardening, or dancing. That way, we are more likely to sustain the activity over a period of months and years rather than signing up with a gym and going only twice. You have glimpsed the medical risks, suffering, and loss of independence that await you on your current path, and now is the time to move in a different direction. Try and break those habits that you have that may be preventing you from changing. Your body can still remember the time when it was slim and active, and after a bit of a struggle at first it will appreciate going back to that state.