According to The Guardian (8september 2014) Professor Sir Stephen Bloom is developing an “intelligent microchip” which will send signals to the brain that will stop the urge to eat. Bloom is head of the diabetes, endocrinology and metabolism at Imperial College London in Hammersmith Hospital. He believes that this will reduce appetite and therefore act as a means of overcoming obesity. In the interview Bloom says that obesity increases blood pressure and therefore increases the risk of having a stroke. He mentions that higher cholesterol means a person is more likely to have a heart attack, presumably also linked to obesity. Furthermore the incidence of Alzheimer’s Disease is one third higher in people who are obese. He goes on to state that most diabetes is caused by people being slightly overweight. So he concludes that if:

“….you could get rid of obesity, diabetes would fall to about a third or maybe a quarter”.

In my opinion Professor Bloom has made a number of assumptions in developing his strategy, which do not stand up to rigorous examination. As a consequence it is extremely doubtful if he can achieve his objectives.

First of all, if we consider those who are “overweight” as determined by BMI, we find that they actually have a greater life expectancy than those with a “normal” BMI, which is regarded as the ideal    (Table 1) (1). Although there is a small increase in the number of deaths due to kidney diseases and diabetes, this is more than offset by the reductions in deaths attributed to other causes.While it is true that those who are in the “obese” category have higher death rates, this only applies to those who are severely obese with a BMI >35 (2). Even then it is crucial to recognise this does not allow us to conclude that the cause is the excess weight.

TABLE 1 RELATIONSHIP BETWEEN BMI AND EXCESS DEATHS (1000s)

                                                                 BMI
Cause of death <18.5 18.5-25 25-30 >30
Coronary heart disease +3 0 -12 +6
Other   cardiovascular +8 0 -5 +36
Lung   cancer 0 0 -10 -7
Obesity   related cancer 0 0 -3 +20
All   other cancers +3 0 +3 +2
Diabetes/kidney   disease 0 0 +15 +34
Chronic   respiratory +16 0 -30 -6
Acute   respiratory/infectious +8 0 -8 -3
Injury +2 0 -32 -13
Other   causes +6 0 -52 +13
ALL +46 0 -134 +82

 

The nutrition literature is littered with examples of confusing cause and effect, which can be simply illustrated by this example. In an area of high crime it is likely that there will be frequent observations of police cars, while low crime localities will rarely have a visit from a police car. This does not mean that the police cars are the cause of the crime rate and it certainly does not follow that crime will be reduced if police cars are kept away!

We really do need to be much more critical in our thinking. It could well be that diabetes is one cause of obesity. However the most likely explanation is that there is a common cause for both. Our main concern is diabetes Type2 (T2D). This is raised blood glucose which stimulates the production of insulin by the pancreas. The insulin directs the glucose to the liver where it is converted into fat and then stored, which can ultimately result in obesity. The high levels of insulin in the body damage many of the organs, which can lead to heart disease and cancers. The obvious answer is to reduce the amount of glucose coming into the blood by cutting back on the consumption of sugar and refined carbohydrates.

There is a growing volume of evidence that this approach can overcome T2D (3,4,5). Invariably those who successfully reduce their blood glucose also find that they lose weight and the risk factors for heart disease are also lowered.

By contrast, the results for those who focus on weight loss alone are not encouraging. For example, in the Honolulu Heart Study, 6537 Japanese-American men aged 45 to 68 in 1965 and living in Hawaii, were monitored from 1973 to 1988 during which time there were 1217 deaths. The results are shown in Table 2. It is quite clear that there has been a notable increase in the death rate of those who lost weight. On the other hand, those who gained up to 4.5kg had a reduced death rate while those who gained more than that did not experience any increase in mortality rate when compared with those whose weight did not vary (6). Similar results have been observed in other investigations (7).

TABLE 2 RELATIVE DEATHS AND CHANGE IN BODY WEIGHT

  ALL-CAUSE MORTALITY  RELATIVE   RISK
Weight loss >4.5 kg 1.21
Weight loss 2.6-4.5 kg 1.29
No change 1.00
Weight gain 2.5-4.5 kg 0.83
Weight gain >4.5 kg 0.99

 

The hard reality is that T2D is not confined to those who are overweight or obese. A recent study conducted in the USA compared the death rates between those with T2D who were normal weight (BMI 18.5-25) and those who were overweight and obese (BMI>25). It was found that the death rates for those with normal weight was more than double that of those who were in the heavier categories (8). This paper also noted that overweight and obese patients with end-stage renal disease have better health outcomes than those who are lean. Furthermore, lean people with raised blood pressure and those with heart failure have worse health outcomes than their heavier counterparts.

So any strategy which focuses on weight loss per se is unlikely to be effective and may well do more harm than good. In addition, many diabetics are not overweight so weight loss is clearly not the solution.

CONCLUSION

It is virtually certain that this project is doomed to failure. There is ample evidence to demonstrate that weight loss by calorie control is very difficult to achieve and even when successful is rarely maintained. Even then, the chances are that there will not be any benefit to health. The real danger is that it diverts attention from the methods that are effective, especially making changes to food consumption patterns by limiting sugar and refined carbohydrates.

REFERENCES

  1. http://jama.jamanetwork.com/article.aspx?articleid=209359
  2. http://vernerwheelock.com/?p=132
  3. http://vernerwheelock.com/?p=226
  4. http://vernerwheelock.com/?p=405
  5. http://vernerwheelock.com/?p=422
  6. http://www.nejm.org/doi/full/10.1056/NEJM199509143331102
  7. http://vernerwheelock.com/?p=221
  8. http://jama.jamanetwork.com/article.aspx?articleid=1309174