ARTICLE In the UK in 2005, 35% of all adults were
overweight, and another 24% were actually obese; by 2013 the total had increased to 65%. In 2003, WHO declared obesity to be a global pandemic, and being overweight is now the ‘norm’ for the UK adult population.
CONSEQUENCES OF OBESITY Obesity has significant effects on mental and physical health, as well as life expectancy. Standardised mortality ratio increases exponentially with increasing BMI, being 1.5 at 30 kg/m2
, 2 at a BMI of 32.5 kg/m2 and 2.5 at a BMI of 35 kg/m2. Despite such linkages,
the loss of life expectancy associated with even ‘minor’ degrees of obesity has received little media attention, nor indeed attention from healthcare planners in general. Being obese at the age of 40 years is associated with a reduction in life expectancy of approximately seven years for non-smoking women and six years for non-smoking men. Risk of death increases by 7% every two years for the obese patient. Being obese carries the same risk for myocardial infarction as a diagnosis of diabetes or hypertension, or a smoking habit, and yet only a fraction of the resources devoted to addressing these ‘classical’ risk factors is available for the treatment of obesity. The two key co-morbidities associated with obesity that attract most attention in terms of healthcare are cancer and diabetes. Obesity is associated with significant increases in a wide range of malignancies, particularly in women. In 2001, obesity accounted for 30,000 deaths per year in the UK, and it is likely to have increased significantly since then. The association of obesity with type 2 diabetes (mature onset) is particularly striking, many would say causal. There is general agreement that the vast majority of cases of type 2 diabetes are associated with, if not caused by, obesity. This is particularly true in the Western world and for individuals of Indian and South-East Asian extraction where the ‘Western norms’ of BMI are probably overly generous in terms of health risk associated with excess weight.
PATHOLOGY OF OBESITY Obesity is not merely a social or cosmetic problem. As mentioned above, it is associated with significant reduction in life expectancy and significant morbidity for those affected. Although BMI is widely used to indicate the presence of obesity, it is a relatively crude index as the distribution of body fat is also important in terms of health impact for any given weight. A waist circumference of 32 inches for women and 35 inches for men has also significant predictive value in terms of long-term health, as it is abdominal obesity or visceral fat that is particularly associated with premature mortality and excess morbidity. Many physically active individuals have
apparent excess weight due to muscle rather than fat mass. In general, physically active individuals have approximately one-third of
700 THE BIOMEDICAL SCIENTIST
7.5 7.0 6.5 6.0 5.5 5.0 4.5 4.0
1990
Diabetes Mean body weight
78 77 76 75 74 73 72
1992 1994 Year
the mortality of physically inactive individuals of the same weight, and the ‘fatness versus fitness’ debate is ongoing. The excessive accumulation of abdominal
fat results in excess risk of a range of metabolic and physical conditions, many of which have been alluded to above. The common assertion by patients that they are obese because of their ‘slow metabolism’ does not seem to be borne out by objective analysis of the evidence. A small minority of obese individuals have undetected hypothyroidism, are on steroid therapy or have other identifiable causes of obesity, and a full clinical, biochemical and physical examination should be undertaken prior to writing off such claims by patients. Abdominal obesity results in increased
cardiac output and reduced lung capacity that can compromise cardiac and lung function. Excess abdominal fat is also associated with fatty infiltration of the liver, often a precursor to cirrhosis, and the metabolic effects of excess fat are a major contributor to diabetes, dyslipidaemia and abnormal biochemical liver function tests.
50
Multivariate adjusted relative risk of type 2 diabetes
40 30 21.3 20 11.6 10 1.0 0 1.0 1.5 2.2 6.7 4.4
<23 23–23.9 24–24.9 25–26.9 27–28.9 29–30.9 31–32.9 33–34.9 BMI
Obesity is a risk factor for type 2 diabetes in men.4 DECEMBER 2013 ≥35 42.1 1996 The growing epidemic of type 2 diabetes in relation to obesity.1–3
For most patients, the biochemistry of obesity can be reduced to an evaluation of the metabolic consequences of excess calorie storage on either the calorie sources in blood, glucose and triglycerides, the effects of excess calories on organ function, γ-glutamyl transferase, brain natriuretic peptide, and alanine transaminase, or a search for the common secondary causes of obesity such as thyroid function or excess steroid production. The First Law of Thermodynamics has
already been alluded to above. Humans, as most animals, store excess calories as fat as a reserve energy source. This ‘reserve’ is ideal when it is drawn on periodically during times of shortage and is ‘maintained’ within certain limits, but in economically developed human societies these times of shortage do not occur, and the capacity of the abdominal store can be exceeded, resulting in the appearance of calorie sources (ie glucose and triglycerides) in the fasting blood, from which they are normally removed in the post- prandial state by insulin secretion. When the stores are already filled to capacity, higher and higher concentrations of insulin in the
1998 2000
kg
Age
Prevalence
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