From Ravussin et al. (1982).

From Ravussin et al. (1982).

Controls (open symbols) Obese (solid symbols)

Controls (open symbols) Obese (solid symbols)

35 45 55 65

35 45 55 65

Fat free mass (kg)

Fig. 11.5 Relationship between metabolic rate and fat free mass (FFM; a measure of lean body mass), in lean and obese women. The graph shows both basal metabolic rate (BMR) (circles), measured in a calorimeter, and total metabolic rate (TMR) (triangles), measured during normal life with double-labelled water (Box 11.3). Open symbols: lean subjects; solid symbols, obese. Note (1) the close relationship between BMR and FFM (or lean body mass) over a wide range (referred to in Section 11.3.2); (2) that the obese group have both greater FFM (i.e. lean tissue), and greater metabolic rate, than the lean. Regression lines for BMR and TMR against FFM are shown. Adapted from data in Prentice et al. (1986).

have accumulated excess lean body mass along with their excess fat. But, on the other hand, if they are now at a stable weight, the implication is that their rate of energy intake matches their rate of energy expenditure, and is therefore also greater than normal. Of course, these are not necessarily measurements made during the period of weight gain; but it is argued that if these people who are obese now have elevated rates of energy intake and energy expenditure, it seems highly unlikely that their obesity was brought about initially by a decreased rate of energy expenditure.

Thus, the message from such studies is clear: for the majority of obese people, the cause of the obesity is not a defect in energy expenditure but a rate of energy intake that is greater than normal. The same message is coming out of the single-gene defects discovered in markedly obese children: those discovered are all genes involved in the pathways of appetite regulation rather than of energy expenditure. Of course, if energy expenditure per unit of fat free mass is also lower than normal, perhaps because of lack of physical activity or because of subtle genetic changes affecting the basal metabolic rate, then the situation will be made worse.

Table 11.3 Health consequences of obesity.

Possible metabolic cause

Adverse consequences Cardiovascular disease

Hypertension (high blood pressure) Type 2 diabetes mellitus Gallstones

Reduced fertility (males), polycystic ovary syndrome (females) Breast and other cancers Obstructive sleep apnoea (pausing breathing, usually during sleep)

Osteoarthritis in weight-bearing joints

Accidents and suicides Benefits

Protection against postmenopausal osteoporosis

Elevated LDL-cholesterol, decreased HDL-cholesterol and elevated triacylglycerol concentrations in serum; high blood pressure (see Box 10.1, insulin resistance and Box 9.6, atherogenic lipoprotein phenotype) May result indirectly from insulin resistance Insulin resistance

Increased cholesterol flux into bile (? related to insulin resistance and high insulin concentrations) Decreased androgens, increased oestrogen production in adipose tissue*

Increased oestrogen production in adipose tissue* Not thought to be metabolic: more a mechanical effect of excess fat. But serious nonetheless as it makes people sleepy during the day so that they may fall asleep driving. It has also been shown that obstructive sleep apnoea is a risk marker for coronary heart disease Not metabolic: due to excess weight

Not metabolic: obesity and depression are closely linked

Increased oestrogen production in adipose tissue

Based on van Itallie (1985) and Garrow (1991).

"Increased oestrogen production occurs because adipose tissue contains the enzyme aromatase, which converts androgens (e.g. testosterone) into oestrogens.

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