DPT-607- Nutrition: Weight Management

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Weight Management and Eating Behaviours

The goal of weight management is to prevent the accumulation of excess body fat and for those who are already overweight, to reduce body fat to an acceptably safe level in order to prevent the health risks associated with obesity (Robinson et al, 1995). The ultimate answer to successfully managing your weight is eating according to your metabolism. Metabolism is dependent on many factors and variables which need to be understood in order to eat accordingly. Energy balance, insulin response, leptin control, activity levels, body size and genetics are some of the major factors involved in managing weight. Understanding how and why the body accumulates body fat helps in providing measures on body fat reduction or maintenance.

Adipose Tissue

Adipose tissue consists of individual fat cells or adipocytes, which function to store excess dietary fat and energy in the form of triglycerides. Circulating lipoproteins serve as transport vehicles for lipids within the bloodstream. Lipoprotein lipase (LPL) acts on lipid containing lipoproteins sent out to the adipose tissue from the liver, causing them to unload excess triglycerides into adipocytes.

Adipose tissue is also capable of storing excess energy from an over consumption of carbohydrate. If excess carbohydrate is consumed over several consecutive days leading to a positive energy balance, the result will be an increase in body fat (Acheson et al, 1988). Glucose enters the adipose tissue where under the influence of insulin, it is synthesised into fat and stored as triglycerides. It is more likely when insulin levels are elevated.

An increase in the size of adipocytes is usually what occurs when body fat is stored. Although an individual’s overall number of adipocytes is genetically predetermined, environmental factors can also exert an effect. Appetite is subject to a number of complex hormonal and nervous signals as well as behavioural responses and parental influence. Overfeeding during childhood stimulates an increase in the number of fat cells. This is especially the case during puberty (Malina and Bouchard 1991) and is of concern, since these fat cells remain for life and may exert a long-term influence on appetite. The goal therefore of effective weight management is to progressively reduce the size of the existing fat cells. 

Distribution of Body Fat

apple-pear obesity

The distribution of adipose tissue also has significance and is heavily influenced by genetics and gender. An excess of central or abdominal fat is more common within males and gives rise to an ‘android’ or ‘apple’ shape. Central obesity is associated with insulin resistance (Helmrich et al, 1991), and with an increased risk of disease including coronary heart disease (Seidell et al, 89). Peripherally distributed fatness is more common within females and gives rise to a ‘gynoid’ or ‘pear shape’, and represents less of a risk factor. 

The Release of Signalling Hormones

Adipose tissue has been found to produce several signalling proteins or hormones, which appear to have far reaching effects on metabolism. One such protein produced by the ob (obese) gene within fat cells is leptin, which is known to: 

  • reduce appetite
  • increase energy expenditure  

As fat cells increase in size they produce more leptin, and the levels of leptin are directly proportional to the levels of body fat or adipose tissue (Woods et al 1998). Fat loss will reduce leptin levels, whilst fat gain will cause a corresponding increase (Kolaczynski et al, 1996; Weigle et al, 1997). 

Proponents of the ‘set point’ theory claim that we possess a genetically determined level of body fat and that any attempt to alter this level will cause metabolic adjustments designed to regain the previous “set point”. Lipoprotein lipase (LPL) is the enzyme responsible for storing triglycerides into adipocytes. Increased activity will increase the size of those fat cells. This starvation response is thought to have originated from our hunter gatherer evolutionary ancestors. As the body often went for long periods without food when meat was scarce, it developed a way of preserving its most valuable energy store, body fat, in order to assure longer survival. It also reduced daily calorie needs by burning up ‘energy hungry’ muscle tissue, thereby lowering BMR. 

Typical dieting alone will likely bring about this response and often leads to weight cycling up and down, which has been linked with poor nutritional levels of health. Understanding this response can help so that we do not restrict calories too severely and bring about a fat storing environment. To reset your body’s “fat thermostat” requires a slower more sustainable rate of weight loss, accompanied by a gradual increase in physical activity.

Total Daily Energy Expenditure (TDEE)

TDEE is the amount of calories we need on a daily basis to fuel all the functions and activity of the body. Knowing how many calories we need a day can give us a starting point if calorie restriction is being used as part of weight management. In order to offset the starvation response any restriction should not exceed 250 calories.

See Appendix Part 2 ‘The Harris-Benedict Formula’

Energy and Metabolism

The components of energy expenditure are as follows:

  • Basal Metabolic Rate (BMR) 
  • Thermal Effect of Food (TEF)   
  • Thermal Effect of Activity (TEA)  

Each of these components must be taken into account when considering energy balance.

Basal Metabolic Rate (BMR):

We have identified that if the energy deficit is too great, this will cause a lowering of the BMR due to a fall in leptin levels and a reduction in muscle mass or fat free mass (FFM). To minimise this effect, any intervention must therefore, incorporate a more modest energy deficit. 

Thermal Effect of Food (TEF):

The thermal effect of food refers to the amount of energy expended by the body through the ingestion, digestion, absorption, utilisation and storage of food. The TEF accounts for between 6-10% of daily energy expenditure for men and between 6-7% for women (Poehlman, 1989). 

  • a very high fat diet, may promote an increase in body fat for the simple reason that more energy is ingested (Stubbs et al, 1995).  
  • high intakes of heavily refined carbohydrates, which are rapidly absorbed and produce elevated levels of insulin, should be avoided. Increased levels of insulin suppress the release and burning of stored body fat (Giovannucci, 1995; McKeown-Eyssen, 1994).

Thermal Effect of Activity (TEA): 

The thermal effect of activity covers planned and unplanned levels of physical activity. Since research clearly indicates that low levels of activity are heavily implicated in the development of obesity, it follows that increasing levels of activity must play a major role in reversing this process. TEA is the most variable component of energy expenditure, and accounts for approximately 20% – 40% of total energy expenditure. 

Genes

As well as the environmental factors of dietary intake and activity levels, genetic influences clearly play a role. Genetic factors form part of the increasing epidemic of obesity, but it can not be seen to be the sole cause since the advance of the condition has occurred too quickly to be traced back to the gene pool alone. An individual’s genetic make up may predispose them to obesity, but the environmental factors of over-feeding and reduced activity also contribute to the extent of the eventual problem. In an environment conducive to producing obesity, people genetically prone to obesity will gain weight (Bouchard, 1997).

 

Creating an Energy Deficit

In order to lose body fat, a negative energy balance has to be established. Research concludes that if the energy deficit is too great, the body fat is more likely to return, possibly at an even higher rate. A priority for an effective weight management programme is to lose body fat, whilst retaining as much FFM as possible thereby minimising the fall in metabolic rate (US Dept of Agriculture, 1995).  To achieve this, a weight loss of ½ – 1lb per week (ideally from body fat) is recommended. 

Creating an energy deficit
 Create a 500 kcal deficit per day 
500 kcal deficit seven days a week 
= 3500 kcal,
= slightly less than 1lb (0.45kg) 

Available methods to achieve negative energy balance:

  • diet restriction alone: Reduce dietary intake by 500 kcal per day
  • exercise intervention alone: Increase TEA by 500 kcal per day through planned exercise
  • exercise and dietary restriction combined: Increase TEA by 250 kcal and reduce dietary intake by 250 kcal

Each of these methods can achieve a negative energy balance necessary for the desired goal. However, the figures are approximate and the rate of fat loss will vary slightly from week-to-week and between different individuals.

  • out of the above-mentioned interventions, the combination of exercise coupled with a modest dietary restriction has been proven from numerous studies to be the most effective method for achieving the desired negative energy balance, when compared with exercise and diet alone (Miller, 1991; Rachette et al, 1995; Wilmore, 1996). 
  • exercise increases the long term success of weight management programmes in relation to the maintenance of fat loss, as opposed to diet restriction alone (Brownell et al, 1986; Pavlou et al, 1989).
  • exercise and dietary restraint combined, has been shown to stimulate fat loss whilst minimising the loss of FFM and subsequent fall in metabolic rate (Ross, Pedwell, Rissanen, 1995).

Effective Dietary Interventions

If exercise interventions are most effective when correctly designed, implemented and evaluated, then the same must be true for any dietary interventions. The weight loss diet should contribute towards the desired energy deficit, whilst also providing sufficient nutrients required for health and normal functioning. Factors to consider include:

  • frequency of meals
  • insulin 
  • macronutrient balance
  • biochemical individuality

Frequency of meals:

Advice to eat little and often is freely given so is there any rationale behind such advice? The answer is yes. Although the TEF over 24 hours is the same for several smaller meals totalling 1500 kcal as for one single meal totalling 1500 kcal, the physiological effects on the metabolism do differ. One study consisted of feeding two trial groups a total of 800 kcal per day. The first group had one meal per day, whilst the second consumed their 800 kcal from several smaller feeds. The group which consumed one meal a day experienced more hunger and a greater loss of FFM (Garrow, 1981). Both of these effects are detrimental to long term weight management. These results show that in order to minimise the loss of FFM and to avoid the subsequent fall in metabolism, regular meals throughout the day seems the most appropriate approach. A minimum of 3 meals a day is advised.

Large meals often contain too much energy to be metabolised at one time. Since carbohydrate and protein in large amounts both suppress the oxidation of dietary fat, larger meals increase the probability of energy being stored as fat, unless the macronutrients are in a favourable balance. 

Blood Glucose and Insulin:

Insulin plays a significant role in the storage of energy, and is a major contributing factor towards obesity. The following graph helps to illustrate the hormonal response in relation to high or low blood glucose levels:

Insulin drives glucose in the blood into the cells of the body for use. It primarily sends glucose to the muscles and liver where it is stored as glycogen. Glycogen is a large complex chain of glucose molecules and is better for storage. Glucose will be driven to other cells throughout the body. It will also send glucose into the adipose tissues. Higher insulin levels mean more glucose converted and stored in adipose tissue. It is important when striving to manage weight and body fat stores that insulin levels are kept reasonably constant. High glycaemic index foods and refined carbohydrates tend to cause insulin levels to ‘spike’ in an attempt to control rocketing blood glucose levels. This will favour fat storage and suppress the burning of fat as a fuel. Spiking often results in a subsequent crash in blood glucose, which creates tiredness and hunger and may lead to overeating. 

A high carbohydrate diet cannot be said to be the only cause of insulin resistance, but it can compound the problem. Insulin resistance is closely linked with becoming over fat through an excessive intake of energy, be it from carbohydrate, protein, fat or more commonly from a combination of all three. A high fat diet is just as likely to promote insulin resistance since its high energy density can lead to overfeeding and the development of obesity.

It is important to realise that insulin resistance is not just associated with increased body fat, but also with low levels of activity. Regular moderate intensity aerobic exercise incorporating large muscle groups has been shown to reduce insulin resistance by increasing insulin sensitivity particularly within the muscle tissue (Eriksson, 1999).

Macronutrient balance:

Macronutrient balance means that the intake of each macronutrient is equal to its oxidation or use as fuel. Simply put this means that we have to be able to metabolise the food we eat by utilising it as energy or heat. Any macronutrient, which is ingested in excess of our ability to oxidise it, will be stored as energy most commonly as fat within the adipose tissue. The key here is to understand the hierarchy or preference, which exists with regards to the oxidation of each of these nutrients. The order is as follows:

  • alcohol
  • protein
  • carbohydrate
  • fat

Research has shown that intakes of carbohydrate, protein and alcohol are met by corresponding increases in their rates of oxidation and that under normal circumstances they are not easily converted to fat (Swinburn and Ravussin, 1993). However, an increase in dietary fat is not matched by an increase in the rate of its oxidation (Abbot et al, 1998). Protein, carbohydrate and alcohol will suppress the burning of dietary fat. It has been suggested that many people who gain weight on high carbohydrate diets do so due to a failure to oxidise the fat in their diet, causing them to store it instead (Jebb et al, 1996). 

Biochemical individuality: 

Whilst we share many similarities, we are each an individual biological entity in our own right, shaped by our genetic makeup and our environment. Our function is related to our structure. This is reflected from the whole body right down to the individual organs. For example, the size and shape of individual stomachs differ widely and in return exert an influence on our ability to digest and handle protein.

In dietary terms, what suits one person may not suit another.  Hence there are those who may thrive on large amounts of dietary carbohydrate, whilst others may thrive on a high protein, ketogenic diet. Yet others favour less heavy carbohydrates in favour of more protein and large amounts of nutrient dense raw vegetables, nuts and seeds, such as our Palaeolithic ancestors would have eaten. In the words of the Roman philosopher “One man’s food is another man’s poison” (Lucretious, 200 BC). 

So what are the options? 

Carbohydrate Diet                

Best suited for Ectomorphs & some Mesomorphs                                  

The research:

High carbohydrate, low fat diets still constitute the mainstream approach. Research tells us they can be effective:

  • diets consisting of unrefined low glycaemic index carbohydrates alongside sufficient levels of monounsaturated fat have been shown to produce prolonged satiety (the state of being satisfactorily full). Therefore, they provide an effective method for reducing calorie intake and achieving long-term weight control (Ball et al, 2003)
  • maintaining a carbohydrate based diet, but substituting saturated fat for greater amounts of monounsaturated, has been implicated with a reduced risk of CHD in overweight insulin resistant individuals (Connor and Connor, 1997)      

The aims:

  • create favourable fuel mix  
  • create energy deficit
  • prescribe an appropriate exercise programme
  • minimise insulin levels
  • provide wide spectrum of nutrients 
  • provide ample dietary fibre

The guidelines:

  • cut out processed foods to reduce trans fats
  • reduce refined  high glycaemic index carbohydrates 
  • moderate saturated fat intake (minimise competition for fuel)
  • include  monounsaturated fat (helps maintain HDL cholesterol) 
  • include oily fish or flax oil for omega 3 fatty acids
  • maintain a ratio of 2:1 or 1:1 of omega 6 to omega 3 fatty acids
  • include plenty of fresh fruit and vegetables
  • include plenty of unrefined low to moderate glycaemic carbohydrates such as wholemeal bread and pasta

Ketogenic Diet

Best suited for Endomorphs & some Mesomorphs

The principle:  

A high fat, moderate protein, low carbohydrate diet permits a much higher intake of fat & protein than a more standard diet. When carbohydrate is removed from the diet causing a dramatic shortage of available glucose, the body is forced to undergo metabolic changes. The body responds by releasing more fatty acids from its reserves within the adipose tissue. These fatty acids circulate to the liver where they are converted into smaller fragments and released back into circulation. These fragments are called keto acids or ketone bodies, and can be easily utilised by tissue as fuel. The individual is said to be in a ketogenic state.

The classical Ketogenic Diet requires the following ratio of macronutrients:

Fat:                  80%

Protein:           14%

CHO:               6%

The research: 

  • higher protein diets with reduced carbohydrate intake appear to improve blood lipid profiles in some individuals. (Wolfe, 1995)
  • replacing carbohydrate with protein from meat, poultry, and dairy foods, produced beneficial metabolic effects and no detectable effects on markers of bone turnover or calcium secretion (Farnsworth et al, 2003)
  • researchers found that low carbohydrate diets appeared to be effective for short-term weight loss in overweight adolescents, and did not harm the lipid profiles (Sondike et al, 2003). Caution with such diets was still advised

The risk factors:

  • possible kidney damage
  • possible risk of osteoporosis. The ketone bodies cause the kidneys to become more acidic, forcing the body to respond by releasing more calcium from the bones in order to act as a chemical buffer to control acid levels
  • lack of unrefined carbohydrate can lead to micronutrient and dietary fibre deficiency

The conclusion:

Whilst some individuals may thrive on these ketogenic diets, they are by no means suitable for everyone, and are associated with some inherent risk factors.

These diets are very extreme and restrictive, but may well suit a proportion of individuals, providing improvements in fat loss, insulin resistance and blood lipid profiles. However, they may equally be less suited to others, especially people with a history of kidney function problems. The ability to handle these diets may be down to biochemical individuality and genetics. 

The Palaeolithic Diet

Best suited for mesomorphs & Endomorphs

The concept:

The concept of the diet is well researched, and brings many scientific disciplines together. The basic argument centres on the fact that 99.9% of our genes were formed 10,000 years ago by the beginning of the Neolithic or agricultural era.  This indicates we are better suited to the Palaeolithic or Stone Age diet, since this is what we evolved with. Only after the beginnings of an agricultural era did we extend the variety and percentages of carbohydrates within the human diet. The Neolithic diet came about as the result of the diminishing availability of wild game in relation to an expanding population, not out of an increased need for carbohydrate. 

Key facts:

  • early man consumed approximately 30% protein; which would vary according to season and geographic location. The protein would have come from wild game meat such as deer, bison and antelope (Eaton and Konner, 1983) 
  • wild game would have had a more ideal ratio of 1:1 up to possibly 1:4 omega 6 to omega 3 fatty acids
  • game meat had a greater percentage of monounsaturated fat, and less saturated fat
  • most of early human carbohydrate came from quantities of fruit, wild vegetables, roots, legumes and nuts. These would have been high in soluble fibre and micronutrients, and much lower in anti-nutrients such as phytic acid which adversely affects mineral absorption 
  • the diet helps to control insulin levels 
  • the hunter gatherer life style was very physically active, an important component relating to this diet

The basis of the diet is a return to the foods that would have been available to us in a Stone Age setting, whilst avoiding the modern mass agricultural foods available today that would not likely have been present.

Avoid the following Neolithic foods
all grains i.e. wheat, rye, barley, oats etc.
all grain products i.e. bread and pasta
all processed food
milk and dairy products
all pulses i.e. beans of any kind, including string beans, peas, cashews potatoes and sweet potatoes
sugar 
 
 Include the following Palaeolithic foods 
a variety of organic meat, poultry
organic organ meats i.e. liver and kidneys
organic free range eggs
plenty of fruits (strawberries, raspberries, blueberries etc)
plenty of root vegetables (carrots, turnips, parsnips, swedes, radishes etc.
plenty of broad green leafed vegetables (lettuce and spinach leaves, kale etc)
bulbs (onions, garlic) 
seeds (sunflower seeds, pine seeds, flax seeds, sesame seeds, prickly pear seeds etc)
a variety of nuts  

A balanced view:

Many debates continue within the field of nutrition, and the benefits of the Palaeolithic diet are no exception. This diet may not be the solution for everyone; yet again others may thrive on it. Critics argue that it is restrictive and some may find it hard to adhere to. Others express concern that the lack of dairy produce may promote poor calcium intake, although dark green leafed vegetables are themselves a good source of calcium and magnesium.

Nutritionists agree that the Palaeolithic diet does have some favourable points. The exclusion of processed food has to be an improvement for everyone, reducing both sugar and the heavily refined carbohydrates within the diet. Most sides in nutrition recognise the importance of increased fruit and vegetables in the diet, which provide soluble fibre, micronutrients, antioxidants and phytochemicals. A more favourable lipid content is also beneficial, with a dramatic reduction in trans fatty acids, and an improved ratio of omega 3 to omega 6 essential fats. 

Concerns still exist within some quarters over the increased intake of saturated fat. 

Although a large percentage of fat within meat is in fact monounsaturated, which we know to be good, the amount of saturated fat within domesticated livestock is higher than within the original Palaeolithic wild game. 

Anorexia and Bulimia Nervosa

Occasionally in dealing with weight management clients may present with significant eating disorders like anorexia or bulimia. These are difficult issues to deal with for anyone. It should be recognised that while the outward symptoms are not eating enough food or vomiting food after meals, the root cause of the problems are psychological in nature. Sufferers are often in denial about the problem so nutritional advice does not normally have much influence. Appropriate professional help should be sought if or when dealing with individuals suspected of suffering from one of these mentally challenging conditions.

The following tables list the signs and symptoms associated with anorexia nervosa and bulimia nervosa:

Eating Disorders Association

www.edauk.com

Telephone helpline: 0845 634 1414

References 

Acheson K, J., Schutz Y, Bessard, T, Ananthraman K, Flatt J. P., Jequier E. (1988). Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. 48:240-7.

Bouchard, C., et al, (1997). Human variation in body mass: evidence for role of genes. Nutr. Rev 55:S21. 

Brownell, K., and Rodin., (1994). Medical, metabolic, and psychological effects of weight cycling. Archives of Internal Medicine. 154: 1325-30. 

Garrow, J., S., Webster, J., D., (1989). Effects of weight and metabolic rate of obese women of a 3.4 MJ (800 kcal) diet. Lancet I: 1429-1431. 

Helmrich, S, P,. Ragland, D, R,. Leung, R, W,. Paffenbarger, R, S,. (1991). Physical activity and reduced occurance of non-insulin-dependant diabetes mellitus. New England Journal of Medicine 325: 147-152.

Malina, R., and Bouchard, C. (1991). Growth, maturation, and physical activity. Champaign, IL:: Human Kinetics. 

Seidell J, C., Hautvast J, G., Deurenberg P. (1989) Overweight: fat distribution and health risks. Epidemiological observations. A review. Infusiontherapie. 16:276-81

Stubbs R. J., Harbron C. G., Murgatroyd P. R., Prentice A. M.,. (1995) Convert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. American Journal of Clinical Nutrition. 62:316-329.

Woods, S. C., Seeley, R. J., Porte, D., and Schwartz, M. W. (1998) Signals that regulate food intake and energy homeostasis. Science. 280:1378-1383.    

Abbott WGH, Howard B, Christian L, et al. (1988). Short-term energy balance: relationship with protein, carbohydrate, and fat balances. Am J Physiol; 255:E332-7.  

Ball, S.D., Keller, K. R., Moyer-Miller, L. J., et al (2003). Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. Pediatrics 111(3): 488-494. 

Conner, W. E., Conner, S. L., (1997). Should a low fat, high carbohydrate diet be recommended for everyone? The case for a low fat, high carbohydrate diet. New England Journal of Medicine 337:562-563. 

Eaton, S. B., Konner, m., (1983). Palaeolithic nutrition: a consideration of its nature and current implications. New England Journal of Medicine, 312:283-289.

Eriksson, J.,G., (1999). Exercise and the treatment of type II Diabetes Mellitus. An update. Sports Medicine, 27(6):318-391. 

Farnsworth, E., Luscombe, M. D., Noakes, M., Wittert, G., Argyiou, E., Clifton, P. M., (2003). Effect of high protein, energy restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulemic men and women. Am.J. Clin. Nutr, 78(1):31-39. 

Giovannucci E. (1995). Insulin and colon cancer. Cancer Causes and Control 6:164-179.

Jebb SA, Prentice AM, Goldburg GR, Murgatroyed PR, Black AE, Coward WA. (1996). Changes in macronutrient balance during over-and underfeeding assessed by 13-d continuous whole-body calorimetry. Am J Clin Nutr; 64:259-66. 

McKeown-Eyssen G. (1994). Epidemiology of colorectal cancer revisited are serum triglycerides and / or plasma glucose associated with risk. Cancer Epidemiology Biomarkers and Prevention 3:687 – 695.

Miller, W.C., Diet composition, energy intake, and nutritional status in relation to obesity in men and women. Med. Sci. Sports Exercise, 234:280. 

Milton, K., (1993). Diet and primitive evolution. Scientific America, 269:86-93.

Pavlou, K.,N., (1989). Exercise as an adjustment to weight loss and maintenance in moderately obese subjects. Am. J. Clin. Nutr. 49:1115.  

Poehlman, E.T., (1989). A review: exercise and its influence on resting energy metabolism in man. Med. Sci. Sport. Exerc. 21:515-525.

Rachette, S. B., et al, (1995). Effects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women. Am. J. Clin. Nutr. 61:486. 

Robinson, J.I., Hoeer, S.L., Petersmarck, K.A., Anderson,J.V., (1995). Redefining success in obesity intervention: the new paradigm. Am. J. Diet. Assoc. 4;422-423. J. Am. Diet. Assoc, 96:342. 

Ross, R., Pedwell, H., Rissanen, J., (1995). Effects of energy restriction and exercise on skeletal muscle and adipose tissue in women as measured by magnetic resonance imaging. Am. J. Clin. Nutr. 61:1179-1185. 

Sondike, S. B., Copperman, N., Jacobson, M. S., (2003). Low carbohydrate diet helps overweight adolescents lose weight safely. The Journal of Pediatrics, 142(3):253-258. 

Staten, M., A., (1991). The effect of exercise on food intake in men and women. Am. J. Clin Nutr. 53:27. 

Swimburn B, Ravussin E. (1993). Energy balance or fat balance? Am J Clin Nutr; 57 (suppl): 766S – 71S.  

U.S. Department of Agriculture, U.S. Department of Health and Human Services. (1995). Nutrition and your health: dietary guidelines for Americans. 4th ed. Home and Garden Bulletin No. 232. Hayattville, Md.; U.S. Government Printing Office. 

Wilmore, J. H., (1996). Increasing physical activity: alterations in body mass and composition. Am.J. Clin. Nutr. 63:S456

Wolfe, B. M., (1995). Potential role of raising dietary protein intake for reducing risk of atherosclerosis. Clin. Invest Med, 15(S G) 127G-131G. 

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