Blaming food for causing obesity is like blaming water intake for edema or blaming the glucose bolus for diabetes. An individual with an impairment in energy balance will find it easier to gain weight on energy-dense food than another individual eating the same food who does not have an impairment in energy balance.
Although obesity has many causes, as we’ll discuss below, its current treatment involves creating an energy deficit by reducing food intake. The fact that reducing food intake may produce weight loss is often considered proof that obesity is caused by food. However, that does not demonstrate its role in causing obesity. Often, cause and treatment are not two sides of the same coin. Excessive exposure to UV radiation may contribute to skin cancer, but its treatment does not involve placing a person in a dark room, away from sunlight.
‘Obesity Is a Choice’
A popular and simplistic assumption is that energy balance is completely under volitional control, which stems from the observation that individuals control their food intake and physical activity. However, the numerous controls up- and downstream that collectively determine energy balance are ignored.
There are numerous physiologic factors beyond volitional control that influence energy balance and keep energy storage within a reasonable range. Such nonvolitional controls may explain why some individuals eat seemingly huge amounts of food but have lean body weight.
Factors that regulate energy balance include acute, medium, and long-term control of energy intake and expenditure, and may have some overlapping functions.
Besides the executive function by higher brain centers, satiety hormones such as GLP-1 (glucagon-like peptide 1) and PYY (peptide tyrosine tyrosine), and the hunger hormones, such as ghrelin, help regulate food intake acutely. As blood ghrelin levels rise, hunger sets in. As food intake proceeds, ghrelin levels start dropping and the satiety hormones GLP1 and PYY start rising, signaling satiety and enabling meal termination.
Leptin, a protein made by adipocytes, gives the brain a biochemical estimate of the amount of adipose tissue in the body and allows the brain to take longer-term actions to increase or decrease adipose tissue over time. Recent studies raise the possibility that gut microbe composition influences the extraction of additional calories from food. Brown adipose tissue, which consumes energy instead of storing it, influences energy expenditure over the medium term.
An example of long-term regulation of energy deposition is suggested by the seasonal regulation of the enzyme lipoprotein lipase (LPL), which is present on adipose tissue and skeletal muscle cells, and which facilitates the entry of triglycerides into those cells. Typically, the entry of triglycerides into skeletal muscle cells leads to its “burning” for energy production, and entry into adipocytes indicates storage.
It appears that in winter, adipose tissue LPL activity increases, suggesting that energy storage is favored in winter, perhaps to provide insulating fat for protection. The potential for adipose tissue LPL activity to increase or the skeletal muscle LPL to decrease in response to a meal predicts weight gain over time.