Energy balance

Energy balance is the difference between energy intake and energy expenditure. Weight gain or loss is a simple, but accurate, way of indicating differences in energy balance.

Energy requirements

There are two approaches to assessing energy requirements for subjects who are weight stable and close to energy balance:

Energy expenditure

Daily energy expenditure (Fig. 5.2) is the sum of:

The basal metabolic rate (BMR)

The thermic effect of food eaten

Occupational activities

Non-occupational activities.

Figure 5.2 Daily energy expenditure in an active and a sedentary 70 kg adult. BMR, basal metabolic rate; DIT, dietary induced thermogenesis; PAR, physical activity ratio.

Total energy expenditure can be measured using a double-labelled water technique. Water containing the stable isotopes ²H and ¹⁸O is given orally. As energy is expended carbon dioxide and water are produced. The difference between the rates of loss of the two isotopes is used to calculate the carbon dioxide production, which is then used to calculate energy expenditure. This can be done on urine samples over a 2–3-week period with the subject ambulatory. The technique is accurate, but it is expensive and requires the availability of a mass spectrometer. An alternative tracer technique for measuring total energy expenditure is to estimate CO₂ production by isotopic dilution. A subcutaneous infusion of labelled bicarbonate is administered continuously by a minipump, and urine is collected to measure isotopic dilution by urea, which is formed from CO₂. Other methods for estimating energy expenditure, such as heart rate monitors or activity monitors, are also available but are less accurate.

Basal metabolic rate. The BMR can be calculated by measuring oxygen consumption and CO₂ production, but it is more usually taken from standardized tables (Table 5.1) that only require knowledge of the subject’s age, weight and sex.

Table 5.1 Equations for the prediction of basal metabolic rate (in MJ/day)

Age range (years)	Equation for predicting BMRa	95% confidence limits
Men
10–17	0.0740 × (wt) + 2.754	±0.88
18–29	0.0630 × (wt) + 2.896	±1.28
30–59	0.0480 × (wt) + 3.653	±1.40
60–74	0.0499 × (wt) + 2.930	N/A
75+	0.0350 × (wt) + 3.434	N/A
Women
10–17	0.0560 × (wt) + 2.898	±0.94
18–29	0.0620 × (wt) + 2.036	±1.00
30–59	0.0340 × (wt) + 3.538	±0.94
60–74	0.0386 × (wt) + 2.875	N/A
75+	0.0410 × (wt) + 2.610	N/A

Data from Department of Health, 1991. BMR, basal metabolic rate. ^aBodyweight (wt) in kg.

Physical activity. The physical activity ratio (PAR) is expressed as multiples of the BMR for both occupational and non-occupational activities of varying intensities (Table 5.2).

Table 5.2 Physical activity ratio (PAR) for various activities (expressed as multiples of BMR)

	PAR
Occupational activity
Professional/housewife	1.7
Domestic helper/sales person	2.7
Labourer	3.0
Non-occupational activity
Reading/eating	1.2
Household/cooking	2.1
Gardening/golf	3.7
Jogging/swimming/football	6.9

Total daily energy expenditure = BMR × [Time in bed + (Time at work × PAR) + (Non-occupational time × PAR)].

Thus, for example, to determine the daily energy expenditure of a 69-year-old, 50 kg female doctor, with a BMR of 4805 kJ/day spending one-third of a day sleeping, working and engaged in non-occupational activities, the latter at a PAR of 2.1, the following calculation ensues:

In the UK, the estimated ‘average’ daily energy requirement is:

for a 55-year-old female – 8100 kJ (1940 kcal)

for a 55-year-old male – 10 600 kJ (2550 kcal).

This is at present made up of about 50% carbohydrate, 35% fat, 15% protein ± 5% alcohol. In developing countries, however, carbohydrate may be >75% of the total energy input, and fat <15% of the total energy input.

Energy requirements increase during the growing period, with pregnancy and lactation, and sometimes following infection or trauma. In general, the increased BMR associated with inflammatory or traumatic conditions is counteracted or more than counteracted by a decrease in physical activity, so that total energy requirements are not increased.

In the basal state, energy demands for resting muscle are 20% of the total energy required, abdominal viscera 35–40%, brain 20% and heart 10%. There can be more than a 50-fold increase in muscle energy demands during exercise.

Energy stores

Although virtually all body fat and glycogen are available for oxidation, less than half the protein is available for oxidation. Figure 5.3 shows that fat accounts for the largest reserves of energy in both lean and obese subjects. The size of the stores determines survival during starvation.

Figure 5.3 Available energy reserves from different fuels expressed in MJ (upper) and as a percentage of total (lower) in a lean hypothetical 70 kg adult and an obese 140 kg adult.

Bodyweight

Bodyweight depends on energy balance. Intake depends not only on food availability but also on a number of complex interrelationships that include the stimulus of good food, the role of hunger, metabolic changes (e.g. hypoglycaemia), and the pleasure and habit of eating. Some people are able to keep their bodyweight constant within a few kilograms for many years, but most gradually increase their weight owing to a small but continuous increase of intake over expenditure. A gain or loss of energy of 25–29 MJ (6000–7000 kcal) would respectively increase or decrease bodyweight by approximately 1 kg.

Trans fats (partly hydrogenated fatty acids)

Increased consumption of hydrogenated vegetable and fish oils in margarines has led to increased trans fatty acid consumption. Trans fatty acids (also called trans fats) behave as if they were saturated fatty acids, increasing circulating LDL and decreasing HDL cholesterol concentrations, which in turn increase the risk of cardiovascular disease. In most countries, nutrition labels for all conventional foods and supplements must indicate the trans fatty acid content. The usage of trans fatty acids from partially hydrogenated oils has now been banned in many countries.

Polyunsaturated fatty acids

The n-6 polyunsaturated fatty acids (PUFA) are components of membrane phospholipids, influencing membrane fluidity and ion transport. They also have antiarrhythmic, antithrombotic and anti-inflammatory properties, all of which are potentially helpful in preventing cardiovascular disease.

The n-3 PUFA increase circulating high-density lipoprotein (HDL) cholesterol and lower triglycerides, both of which might reduce cardiovascular risk. Some of the actions of n-3 PUFA are mediated by a range of leukotrienes and eicosanoids, which differ in pattern and functions from those produced from n-6 PUFA.

Epidemiological studies and clinical intervention studies suggest that n-3 PUFA may have effects in the secondary prevention of cardiovascular disease and ‘all-cause mortality’ (e.g. 20–30% reduction in mortality from cardiovascular disease according to some studies). The benefits, which have been noted as early as 4 months after intervention, have been largely attributed to the antiarrhythmic effects of n-3 PUFA, but some work suggests that n-3 PUFA, administered as capsules, can be rapidly incorporated into atheromatous plaques, stabilizing them and preventing rupture. Whether these effects are due directly to n-3 PUFA or other changes in the diet is still debated.

The GISSI Prevention Trial, which followed over 11 000 patients for 3.5 years after a myocardial infarction, administered fish oils (eicosapentaenoic acid, EPA and docosahexaenoic acid, DHA) in the form of capsules and demonstrated a striking benefit in reducing mortality. The effects of vitamin E (300 mg α-tocopherol/day) were also studied, but no benefit was found.

Recommendations for fat intake

The British Nutrition Foundation and the American Heart Association presently recommend a two-fold increase of the current intake of total n-3 PUFA (several fold increase in the intake of fish oils, and a 50% increase in the intake of α-linolenic acid). Implementing this recommendation will mean either a major change in the dietary habits of populations that eat little fish, or ingestion of capsules containing fish oils. Some government agencies have warned of the hazards of eating certain types of fish, which increase the risk of mercury poisoning and possibly other toxicities.

The current recommendations for fat intake for the UK are shown in Box 5.2.

Cholesterol

Cholesterol is found in all animal products. Eggs are particularly rich in cholesterol, which is virtually absent from plants. The average daily intake in the UK is 300–500 mg. Cholesterol is also synthesized (see p. 306) and only very high or low dietary intakes will significantly affect blood levels.

Essential fatty acid deficiency

Essential fatty acid deficiency may accompany protein-energy malnutrition (PEM), but it has been clearly defined as a clinical entity only in patients on long-term parenteral nutrition given glucose, protein and no fat. Alopecia, thrombocytopenia, anaemia and dermatitis occur within weeks with an increased ratio of triene (n-9) to tetraene (n-6) in plasma fatty acids.

Dietary fibre

Dietary fibre, which is largely non-starch polysaccharide (NSP) (entirely NSP according to some authorities), is often removed in the processing of food. This leaves highly refined carbohydrates such as sucrose which contribute to the development of dental caries and obesity. Lignin is included in dietary fibre in some classification systems, but it is not a polysaccharide. It is only a minor component of the human diet.

The principal classes of NSP are:

None of these are digested by gut enzymes. However, NSP is partly broken down in the gastrointestinal tract, mainly by colonic bacteria, producing gas and volatile fatty acids, e.g. butyrate.

All plant food, when unprocessed, contains NSP, so that all unprocessed food eaten will increase the NSP content of the diet. Bran, the fibre from wheat, provides an easy way of adding additional fibre to the diet: it increases faecal bulk and is helpful in the treatment of constipation.

The average daily intake of NSP in the diet is approximately 16 g. NSP deficiency is accepted as an entity by many authorities and it is suggested that the total NSP be increased to up to 30 g daily. This could be achieved by increased consumption of bread, potatoes, fruit and vegetables, with a reduction in sugar intake in order not to increase total calories. Each extra gram of fibre daily adds approximately 3–5 g to the daily stool weight. Pectins and gums have also been added to food to slow down monosaccharide absorption, particularly useful in type 2 diabetes.

Eating a diet rich in plant foods (fruits, vegetables, cereals and whole grain – the main sources of dietary fibre) is generally recommended for general health promotion, including protection against ischaemic heart disease, stroke and certain types of cancers. This has been attributed to a lipid lowering effect, the presence of protective substances, such as vitamin and non-vitamin antioxidants and other vitamins such as folic acid, which is linked to homocysteine metabolism, a risk factor for cardiovascular disease. Fermentation of fibre in the colon may protect against development of colonic cancer. However, associated lifestyle factors such as low physical activity may also help explain some of those associations.

Fortification of foods

Fortification of foods with specific nutrients is common. In the UK, margarine and milk are fortified with vitamins A and D, flour with calcium, iron, thiamin and niacin and breakfast cereals with several vitamins and iron. Not all substances used in fortification have nutritive value. For example, Olestra is a polymer of sucrose and six or more triglycerides which has been introduced to combat obesity. It is not absorbed and is therefore used particularly in savoury snack foods (where it has FDA approval) as a ‘fake fat’. Therefore, it results in a reduction in total calories. It has side-effects, e.g. loose stools, abdominal cramps, and its use is being carefully monitored.

Nutrient goals and dietary guidelines

The interests of the individual are often different from those associated with government policy. A distinction needs to be made between nutrient goals and dietary guidelines:

Since dietary habits in different countries vary, dietary guidelines may also differ, even when the nutrient goals are the same. Nutrient goals are based on scientific information that links nutrient intake to disease. Although the information is incomplete, it includes evidence from a wide range of sources, including experimental animal studies, clinical studies and both short-term and long-term epidemiological studies.

Pathophysiology of starvation (Fig. 5.4)

In the first 24 h following low dietary intake, the body relies for energy on the breakdown of hepatic glycogen to glucose. Hepatic glycogen stores are small and therefore gluconeogenesis is soon necessary to maintain glucose levels. Gluconeogenesis takes place mainly from pyruvate, lactate, glycerol and amino acids, especially alanine and glutamine. The majority of protein breakdown takes place in muscle, with eventual loss of muscle bulk.

Figure 5.4 Metabolism in (a) the fed and (b) the fasted state. NEFA, non-esterified fatty acids.

Lipolysis, the breakdown of the body’s fat stores, also occurs. It is inhibited by insulin, but the level of this hormone falls off as starvation continues. The stored triglyceride is hydrolysed by lipase to glycerol, which is used for gluconeogenesis, and also to non-esterified fatty acids that can be used directly as a fuel or oxidized in the liver to ketone bodies.

Adaptive processes take place as starvation continues, to prevent the body’s available protein being completely utilized. There is a decrease in metabolic rate and total body energy expenditure. Central nervous metabolism changes from glucose as a substrate to ketone bodies. Gluconeogenesis in the liver decreases as does protein breakdown in muscle, both of these processes being inhibited directly by ketone bodies. Most of the energy at this stage comes from adipose tissue, with some gluconeogenesis from amino acids, particularly from alanine in the liver, and glutamine in the kidney.

The metabolic response to prolonged starvation differs between lean and obese individuals. One of the major differences concerns the proportion of energy derived from protein oxidation, which determines the proportion of weight loss from lean tissues. This proportion may be up to three times smaller in obese subjects than lean subjects. It can be regarded as an adaptation which depends on the composition of the initial reserves (Fig. 5.3). This means that deterioration in body function is more rapid in lean subjects. Furthermore, survival time is much less in lean subjects (~2 months), compared to the obese (can be at least several months).

Following trauma or shock, some of the adaptive changes do not take place. Glucocorticoids and cytokines (see below) stimulate the ubiquitin-proteasome pathway in muscle, which is responsible for accelerated proteolysis in muscle in many catabolic illnesses. In starvation, there is a decrease in BMR, while in inflammatory and traumatic disease the BMR is often increased. These changes all result in continuing gluconeogenesis with massive muscle breakdown, and further reduction in survival time.

Regulation of metabolism

Tissue metabolism is regulated by multiple coordinated processes. Some are rapid involving nerves, whilst others are slower involving circulating substrates and hormones. Factors include:

Insulin/glucagon ratios in the fed and fasted state

In the fed state, insulin/glucagon ratios are high. Insulin promotes synthesis of glycogen, protein and fat, and inhibits lipolysis and gluconeogenesis.

In the fasted state, insulin/glucagon ratios are low. Glucagon acts mainly on the liver and has no action on muscle. It increases glycogenolysis and gluconeogenesis, as well as increasing ketone body production from fatty acids. It also stimulates lipolysis in adipose tissue. Catecholamines have a similar action to glucagon but also affect muscle metabolism. These agents both act via cyclic adenosine monophosphate (cAMP) to stimulate lipolysis, producing free fatty acids that can then act as a major source of energy.

Proportion of lean to fat tissue

During weight loss uncomplicated by disease, the proportion of lean to fat tissue loss (or proportion of energy derived from protein metabolism) is greater in lean than overweight/obese individuals.

During acute disease, loss of lean tissue, which is associated with protein oxidation, can be particularly rapid. Hormones such as corticosteroids, proinflammatory cytokines and insulin resistance are all involved.

Role of cytokines

The metabolic response to trauma, injury and inflammation depends on the balance between proinflammatory (e.g. tumour necrosis factor, TNF; interleukin-2, IL-2) and anti-inflammatory cytokines (e.g. IL-10), and the production of many of these cytokines is influenced by genetic polymorphisms. Since many chronic diseases, including atherosclerosis, have an inflammatory component, these changes have wide-reaching metabolic implications.

Cytokines such as IL-1, IL-6 and TNF play a significant role in regulating metabolism. In acute diseases they contribute to the catabolic process, glycogenolysis, and acute-phase protein synthesis. TNF, which inhibits lipoprotein lipase, is one of a number of ‘cachexia factors’ in patients with cancer.

It is unclear how these cytokines interact with central feeding pathways to cause anorexia. However, in animal models of both cancer and inflammatory bowel disease, many peripheral and central mediators of appetite are involved. For example, neuropeptide Y levels in the hypothalamus are often inappropriately low, so there is a reduced drive to feeding.

Function

Retinol is stored in the liver and is transported in plasma bound to an α-globulin, retinol-binding protein (RBP). Vitamin A has several metabolic roles:

Vitamin A deficiency

Worldwide, vitamin A deficiency and xerophthalmia (see below) is the major cause of blindness in young children despite intensive preventative programmes.

Xerophthalmia has been classified by the WHO (Table 5.10). Impaired adaptation followed by night blindness is the first effect. There is dryness and thickening of the conjunctiva and the cornea (xerophthalmia occurs as a result of keratinization). Bitot’s spots – white plaques of keratinized epithelial cells – are found on the conjunctiva of young children with vitamin A deficiency. These spots can, however, be seen without vitamin A deficiency, possibly caused by exposure. Corneal softening, ulceration and dissolution (keratomalacia) eventually occur, superimposed infection is a frequent accompaniment and both lead to blindness. In PEM, retinol-binding protein along with other proteins is reduced. This suggests vitamin A deficiency, although body stores are not necessarily reduced.

Table 5.10 Classification of xerophthalmia by ocular signs

Vitamin A deficiency. Blindness due to vitamin A deficiency and corneal scarring.

(Courtesy of Ehrnstrom P. In: Bolognia J, Jorrizzo J, Rapini R (eds). Dermatology, 2nd edn. St Louis: Mosby; 2008: Fig. 51.6.)

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