A.2.1 Compare the energy content per 100g fat, carbohydrate and protein.
Various units of energy can be used on food labels, but we use the unit kJ (kilojoules).
Notice that fats contain more than double the energy per unit mass than carbohydrates or proteins.
Some food labels use Calories, which is the more common term in public science.
One calorie is the energy required to raise the temperature of 1kg water by 1oC.
One food Calorie is actually 1000 calories (1kcal). One food Calorie is equivalent to 4.18kJ.
Students might like to consider what the link is between the energy content of fats and their metabolism in respiration? Refer to the role of CoA.
Sources: (1) (17)
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A.2.2 Compare the main dietary sources of energy in different ethnic groups.
Dietary energy can come from various sources, carbohydrates, proteins or fats, depending on the foods available to a population. These staples make up the bulk of a population’s diet, and are generally crops.
This map shows some of the main staple crops around the world
Sources: (21) (22) (4)
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A.2.3 Explain the possible health consequences of diets rich in carbohydrates, fats and proteins.
Sources: (17) (6) (23) (8)
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A.2.4 Outline the function of the appetite control centre of the brain.
Link to 6.5
Appetite is controlled in the hypothalamus of the brain. Control is both nervous and hormonal: some hormones trigger appetite-stimulating neurons, others trigger appetite-inhibiting neurons.
An empty stomach releases the hormone gherin, which triggers appetite-stimulating hormones, leading to hunger. When food enters the stomach, gherin production is stopped, reducing hunger.
Appetite is also inhibited when:
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Food entering the intestine stimulates release of PYY3-36 hormone.
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Carbohydrate and protein digestion stimulate release of insulin hormone from the pancreas.
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Fat storage stimulates release of leptin hormone from the pancreas. This is enhanced by insulin.
These three hormones trigger appetite-inhibiting neurons in the appetite control centre.
There are strong links to malfunction of any of these pathways and obesity, as the individual eats more than is required.
Sources: (24)
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A.2.5 Calculate body mass index (BMI) from the body mass and height of a person.
e.g. 1: 70kg man, 1.8m tall. BMI = 70 / 1.8 = 21.6
A.2.6 Distinguish, using the body mass index, between being underweight, normal weight, overweight and obese.
Limitations of the BMI using this table:
Examples:
Source for A.2.5 and A.2.6: (1) (8)
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A.2.7 Outline reasons for increasing rates of clinical obesity in some countries, including availability of cheap high-energy foods, large portion sizes, increasing use of vehicles for transport, and a change from active to sedentary occupations.
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Clinical obesity is an excess of body fat. Generally it is caused by consuming more energy than is used in activity, with the excess stored as body fat.
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Obesity carries a reduced life expectancy, high risks of CHD, diabetes, heart attacks and strokes.
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The obesity epidemic is on the increase globally, in developed nations in particular.
There are many contributing factors:
Sources: (25) (24)
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A.2.8 Outline the consequences of anorexia nervosa.
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Anorexia nervosa is an eating disorder in which the patient severely limits food intake.
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It is a medical condition with mental and physiological causes.
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It is closely associated with body image and meeting aest-hetic standards imposed by culture.
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It is most common in females, but does occur in males.
Health consequences include:
Sources: (26) (image from the same source)
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