THE ADVANTAGES OF A HIGH-PROTEIN DIET.

WHAT ARE THE FEATURES OF A GOOD DIET FOR WEIGHT LOSS?

A good diet does ALL of the following:

It gives an energy deficit; less calories must be consumed than are required to meet both the basal metabolic requirements (the energy cost of running the body) and the energy cost of daily activity.

In other words, it provides less calories than you are burning each day, so you draw on your fat reserves to make up the difference.

It preserves full functionality of physiological and biochemical systems and compensates for adaptations to the low energy intake which otherwise would reduce or prevent loss of weight.

Normally, when you consume less calories than you need, your metabolic rate falls, and you burn fewer calories. This is a normal response built into humans (and other animals) to help them get through times of famine (not a problem now-a-days), but is not helpful for weight loss. The good diet prevents your metabolic rate from falling.

It favours loss of weight predominantly from fat tissue and permits no greater loss of lean body mass than is physiologically acceptable.

Fat is what you need to lose, but some bad diets actually cause you to lose muscle and organ tissues, which you may never get back! This weakens you, and if you are a yo-yo dieter on bad diets, you will get weaker with every cycle, because you are losing muscle!

It must prevent occurrence of deficiencies, whether clinical or sub-clinical.

Many bad diets do not allow for enough essential fatty acids, potassium or other essential nutrients, and may cause serious side effects.

Diet programmes which do not meet all these requirements are potentially hazardous and may not only cause adverse effects, but may result in irreparable harm in either short or long term.

High protein weight loss diets, appropriately supplemented with vitamins, minerals and essential fatty acids, have proven the safest and most effective types of diet in weight loss.

WHY DO I NEED PROTEIN?

THE FIRST REASON WHY YOU NEED PROTEIN IS TO MAKE SURE THAT YOU DO NOT LOSE VALUABLE BODY PROTEIN FROM YOUR MUSCLES AND ORGANS, SINCE YOU MAY NEVER BE ABLE TO REPLACE IT AND IT COULD DAMAGE YOU!

Research performed and published over the last 20 years indicates that high protein weight loss diets offer substantial advantages over isocaloric diets with lower amounts of protein and are completely safe, whereas low calorie diets with insufficient protein may cause considerable damage, some of which may be permanent. A normal guideline is a minimum of 1.5 g protein per kg of ideal body weight per day, with a maximum of about 2.5 g protein per kg ideal body weight per day.

The major criticism levied at low calorie diets of any type is that protein can be lost from vital tissues, and from this point of view alone, a demonstrated high protein intake serves as a counter statement. However, from the purely physicochemical point of view, it offers advantages to bias the equilibrium between "protein in" and "protein out" strongly in favour of intake, thus ensuring an adequate amount of available amino-acids.

The term nitrogen balance is, in effect, synonymous with protein balance, and ensuring that the body is in nitrogen balance (or equilibrium) is an important consideration when low calorie diets are given for more than a few days.

A negative nitrogen balance implies that body (structural) protein is being lost, and would therefore support the criticism of low calorie diets often heard, namely that they cause loss of lean body mass, possibly from vital organs. In this respect, however, it must be noted that since a portion of the weight loss consists of fat free mass that in turn contains a small amount of protein, a minor reduction of total body protein could be expected to be a consequence of any weight loss regime in which no steps were taken to facilitate the efficient recycling of the high quality protein released from the cytoplasm of adipose tissue cells.

Bistrian et al. (1981) showed that a diet of about 440 kilocalories per day providing 0.8 grams protein per kg ideal body weight per day was not capable of maintaining nitrogen balance. The baseline diet used by these investigators, which provided 1.5 grams of protein per kg ideal body weight did maintain nitrogen equilibrium.

Vasquez et al. (1985), in a rather complex study with obese volunteers, showed that nitrogen balance was positive on a 500 kilocalorie per day diet composed solely of protein (125 grams per day) given for one week, but was negative in the same volunteers when protein intake was reduced to 50 grams per day and the difference was made up with carbohydrate.

Comparable results were reported by Oi et al. (1987), who conducted balance studies in obese subjects given 1100 kilocalories per day with progessively diminishing protein intakes. They found that there was a clear relationship between protein intake and nitrogen balance, and calculated that the mean requirement for nitrogen equilibrium was 1.26 grams protein per kg body weight per day.

As demonstrated by Rabast et al. (1979), the effect can be quite dramatic; these investigators gave two comparable groups of obese subjects isocaloric diets (1000 kilocalories per day), one of which was low carbohydrate (25 g per day) and high in fat, the other high carbohydrate (170 g per day) and low fat. Both contained 46 g protein per day. Over a 50 day period, weight loss was 14.0 kg in the group given the low carbohydrate diet, but only 9.8 kg in the group receiving the high carbohydrate diet. Though in this case protein content was the same in both diets, the overall thermogenic effect was clearly lower with the high carbohydrate diet, which in view of the known poor thermogenic effect of carbohydrate was predictable.

ANABOLIC EFFECTS OF A HIGH PROTEIN DIET:

The amino-acid arginine stimulates release of growth hormone.

Dietary protein directly stimulatesrelease of somatomedins.

Growth hormone and the somatomedins are potent anabolic agents;
They stimulate amino-acid uptake into protein.

Phenylalanine and tyrosine act as precursors for noradrenaline, which
also has anabolic effects on muscle.

Tryptophan, like some of the drugs used to treat obesity, increases the availability of serotonin in the central nervous system (Nathan and Rolland, 1987), and this is possibly the single most important factor in controlling dietary intake in human beings. However, tyrosine and phenylalanine are catecholamine precursors; they therefore increase the availability of both dopamine and noradrenaline in the central nervous system. This is analogous to the effect of tryptophan on serotonin, and likewise, their action is similar to that of the classical anorectic drugs such as dexamphetamine. They therefore serve to suppress hunger, by increasing noradrenaline levels in the hunger centre. In this respect, they may parallel a postulated effect of ketosis.

In practical terms, tyrosine and phenylalanine probably make little contribution to control of appetite in man; at the time hunger is experienced, blood levels of free amino-acids tend to be low, and thus the transfer of these amino-acids into the central nervous system is at low ebb. They may, however, reinforce the effects of tryptophan at meal-times. It should be noted that many "serotoninergic" drugs have anti-depressive or mood-elevating properties, and the observed effects of high protein diets on mood would hereby be explained. Histidine, glutamic acid and aspartic acid may also play a role, but it has not yet been clarified.

The relationship between post-prandial levels of free amino-acids in the blood and the central nervous system levels of the neurotransmitters for which they are precursors is very complex, and studies in man and animals have given conflicting, sometimes inexplicable, results. However, it is very clear (Wurtman, 1987) that brain serotonin synthesis is coupled to food-induced changes in plasma composition, and catecholamine synthesis is thought to show the same relationship. What is known with certainty is that plasma levels of free amino-acids increase several fold after a protein-rich meal (though not all amino-acids increase to the same level; a possible expression of preferential peripheral utilization), and that insulin secretion (for example after a meal rich in carbohydrate) decreases levels of all amino-acids with the possible exception of tryptophan! It is also clear that increased brain serotonin levels resulting from greater availability of tryptophan (or, for that matter, from drug treatment!) suppress cravings for carbohydrate.

Tryptophan, like some of the drugs used to treat obesity, increases the availability of serotonin in the central nervous system (Nathan and Rolland, 1987), and this is possibly the single most important factor in controlling dietary intake in human beings. However, tyrosine and phenylalanine are catecholamine precursors; they therefore increase the availability of both dopamine and noradrenaline in the central nervous system. This is analogous to the effect of tryptophan on serotonin, and likewise, their action is similar to that of the classical anorectic drugs such as dexamphetamine. They therefore serve to suppress hunger, by increasing noradrenaline levels in the hunger centre. In this respect, they may parallel a postulated effect of ketosis.

In practical terms, tyrosine and phenylalanine probably make little contribution to control of appetite in man; at the time hunger is experienced, blood levels of free amino-acids tend to be low, and thus the transfer of these amino-acids into the central nervous system is at low ebb. They may, however, reinforce the effects of tryptophan at meal-times. It should be noted that many "serotoninergic" drugs have anti-depressive or mood-elevating properties, and the observed effects of high protein diets on mood would hereby be explained. Histidine, glutamic acid and aspartic acid may also play a role, but it has not yet been clarified.

The relationship between post-prandial levels of free amino-acids in the blood and the central nervous system levels of the neurotransmitters for which they are precursors is very complex, and studies in man and animals have given conflicting, sometimes inexplicable, results. However, it is very clear (Wurtman, 1987) that brain serotonin synthesis is coupled to food-induced changes in plasma composition, and catecholamine synthesis is thought to show the same relationship. What is known with certainty is that plasma levels of free amino-acids increase several fold after a protein-rich meal (though not all amino-acids increase to the same level; a possible expression of preferential peripheral utilization), and that insulin secretion (for example after a meal rich in carbohydrate) decreases levels of all amino-acids with the possible exception of tryptophan! It is also clear that increased brain serotonin levels resulting from greater availability of tryptophan (or, for that matter, from drug treatment!) suppress cravings for carbohydrate.

Other known facts are that different proteins have different effects on brain serotonin levels; lactalbumen, rich in tryptophan, gives a better response than proteins with a more balanced amino-acid composition, and interestingly, low quality proteins such as gelatine supplemented with tryptophan also give good responses. This latter fact is readily explained; all the so-called "large neutral amino acids" have to compete for the same transport mechanism into the brain, so that in the presence of tyrosine, histidine or phenylalanine, tryptophan transport can actually be reduced.

Thus if tryptophan is the most prominent amino-acid in the mixture produced by digestion, it will readily pass into the brain.

In this respect, a recent study by Anderson et al. (1990) revealed that dieting reduces plasma tryptophan levels in women and has an effect on brain 5-HT function. These effects were not seen in men.

To summarize in simpler terms, the quality and quantity of protein consumed can affect certain functional centres in the brain, and many of the observed effects of high protein diets, such as lack of hunger (or better, feeling of satiety) and elevation of mood could be explained by conversion of tryptophan to serotonin in the brain.

The sleepiness that may occur after a large meal may also, in part, be explained by this mechanism, though in this case diversion of blood flow to the gastro-intestinal tract (to assist in digestion) and away from the brain is probably the most important factor. However, tryptophan is only part of the story, and the full explanation almost certainly involves the other amino-acid precursors of neurotransmitters in a complex and interrelated fashion.

Stated at the most superficial level, composition of the diet itself regulates satiety, hunger and cravings; the high protein, low carbohydrate diet has physiological actions that are compatible with weight reduction programmes and it facilitates adherence to such programmes!

THE BODY WILL RUN WHEN THE BLOOD IS FULL OF KETONE BODIES, BUT THIS IS BASICALLY A BIOCHEMICAL TRICK AND NOT VERY SOPHISTICATED. IT ALSO INVOLVES A RISK OF SIDE EFFECTS, SUCH AS ACIDOSIS (THE BODY FLUIDS BECOME MORE ACID, WHICH CAN CAUSE PROBLEMS), SIGNIFICANT EUPHORIA (ALMOST LIKE BEING DRUNK), MOOD CHANGES IN SUSCEPTIBLE INDIVIDUALS, AND INCREASED URIC ACID LEVELS (WHICH MAY RESULT IN GOUT OR KIDNEY STONES). IT ALSO MAKES THE BREATH SMELL BAD!

Ketone bodies are normal products of lipid metabolism, though generally not present in great amounts. They result from the breakdown of acetoacetyl-coenzyme A, itself derived from acetyl-coenzyme A. Under normal circumstances, most of this latter substance is oxidized directly in the liver, or used to build up fats, but when the body is in negative energy balance, using fats rather than storing them, the flow is in the reverse direction, and acetyl-coenzyme A is being produced from fatty acids rather than the reverse. There is a link between liver content of glycogen (the way in which carbohydrate is stored) and the production of ketone bodies, again very complicated, but in essence it means that when the liver has enough glycogen (from a high carbohydrate intake!), acetyl-coenzyme A is reconverted into fatty acids rather than into the acetoacetyl compound which ends up as ketone bodies. Thus to generate the ketosis, carbohydrate intake must be kept low.

In the absence of glucose, brain and many other tissues adapt readily to use of ketone bodies as a source of energy. Thus the fat or normal person, deprived of food, switches over to being a "ketone burner".

This can help "push" the metabolism into the protein-sparing mode, but the same effect can be obtained with a non-ketogenic protein diet, without the risk of side effects. Using ketosis as a tool to lose weight is something that should only be done under medical supervision.

The hunger-suppressing effect of ketosis (as distinct from the satiety-inducing effect of protein) was strongly commented by Duncan et al. (1962), and has subsequently been investigated by Blackburn and his colleagues (see, for example, Lindner & Blackburn, 1976). It is generally accepted (Jones, 1979, 1981) that induction of ketosis creates a mental state of mild euphoria, and suppresses hunger.

Mood changes have been conclusively demonstrated in ketotic patients undergoing therapy with low calorie diets (Jones, unpublished observations). The mechanism involved is not clearly understood, but the moderate elevation of ketone bodies in the blood appears to have a range of behavioural properties, unrelated to the Calorie content per se.

Wadden et al., (1985), for example, compared groups of patients on isocaloric PSMF and non-ketogenic formula diets. They found that patients on the PSMF had significantly less hunger, and were also much less pre-occupied with food (a behavioural parameter that is not necessarily closely related to hunger sensations). Davies et al. (1989) found that hunger scores increased as the Calorie content of a Very Low Calorie Diet was increased.

Silverstone et al. (1966) could not find a direct relationship between levels of ketone bodies and hunger, and this has been the experience of other investigators (Baird et al., 1974; Howard, 1981). Other groups (Apfelbaum et al., 1967, 1981) claim that the suppression of hunger increases as the ketosis becomes more severe, and strive to induce moderate to severe ketosis in their studies.

The general consensus leans to the argument, that while suppression of hunger (and other mood-related effects) may be triggered by ketosis, equivalent results can be obtained by ensuring that protein intake is sufficiently high, and that this is a much more "natural" way to help dieters cope with their low calorie diet.

ENOUGH PROTEIN TO ENSURE THAT ALL THE BENEFITS OF A HIGH PROTEIN INTAKE ARE OBTAINED, ENOUGH CARBOHYDRATE TO PREVENT KETOSIS, AND ENOUGH FAT (OF THE RIGHT TYPE) TO MAKE SURE THAT ESSENTIAL FATTY ACID DEFICIENCY DOES NOT OCCUR!

It has been argued that the PSMF, devoid or almost completely devoid of carbohydrate, is the most effective dietary approach to the treatment of obesity, because it gives rise to the greatest degree of ketosis, but this argument lacks experimental verification. While it is clear that ketosis has some interesting effects, it does not necessarily help weight loss and can be risky. In fact, some studies have indicated that the presence of a moderate amount of available carbohydrate can improve rates of weight loss, increase the protein-sparing effects (through reduction of gluconeogenesis) and partially offset some metabolic consequences of the lack of dietary carbohydrate, such as the increase in blood uric acid levels (Vasquez et al., 1995). Such research has also indicated that with regard to protein sparing on low calorie diets, the effects of protein and carbohydrate are independent but additive. Thus there are advantages to the use of high protein diets which are not ketogenic.

The inclusion of moderate amounts of fat in the high protein diet optimizes body fat composition, and Flatt (1995) has shown that lipogenesis in humans significantly increases when the fat content of a diet falls below 10% of calories.

Thus quite apart from the very real risk of essential fatty acid (EFA) deficiency, the use of very low fat diets increases body fat content, and in the presence of protein and absence of sufficient carbohydrate can create a complex metabolic chain where protein is converted to carbohydrate via gluconeogenesis, and the carbohydrate in turn is converted to fat by lipogenesis, with an ultimate reduction in protein sparing.

The presence of fat in the diet, and in particular EFAs, has also been related to increases in rates of weight loss. The fact that patients on low calorie diets are at greater risk of EFA deficiency than the general population is well known, is in itself sufficient justification for assuring adequate EFA intake, but EFAs do more than prevent skin problems, gall bladder problems or a rise in cholesterol; they actually contribute to fitness and weight loss. EFAs of the omega-6 and omega-3 families have been shown to increase thermogenesis. It is not known whether this is an intrinsic consequence of their mechanisms of action (as precursors for eicosanoids and as membrane constituents), or whether it merely represents the rectification of a pre-existent but unsuspected EFA deficiency. Goubern et al. (1990), for example, showed that brown adipose tissue cells recovered from EFA-deficient rats responded poorly to noradrenaline (norepinephrine; the hormone which stimulates thermogenesis), but that addition of linoleic acid (omega-6 EFA) and the saturated fatty acid, palmitic acid, to the medium normalized the response.

Alam et al. (1995) also presented evidence that cyclic adenosine monophosphate (cAMP) production can be impaired in EFA deficiency, which would manifest as decreased sensitivity to catecholamines, with subsequent reduced thermogenesis.

Clandinin et al. (1992) similarly showed that linoleic acid increased the binding of insulin to adipose tissue cells (and thus inproved their metabolic responses).

These researchers also reported that omega-3 EFAs increased the responsiveness of muscles to insulin, and significantly increased the rate of glucose uptake by the muscle. Takada et al. (1994) showed that a dietary intake of gammalinolenic acid increased the ability of the liver to oxidize fats.

At an empirical level, Bucci (1994) cites studies which have shown that supplementation with long chain omega-3 EFAs (from fish oil) improves aerobic metabolism, while some research groups (Cunnane et al., 1986; Jones and Schoeller, 1988) have shown that increases in EFA intake improve rates of weight loss by a presumed thermogenic mechanism and also improve the efficiency of energy-generating metabolic processes in the body.

A significant daily intake of protein, ideally 1.5 g per kg ideal body weight per day; at least 60 - 70 g must be of excellent biological value, but once an adequate intake of essential amino acids has been assured, the remainder may be of lesser biological value. All protein should be of high digestibility.

A moderate intake of carbohydrate, sufficient to completely prevent ketosis (about 1.5 g per kg ideal body weight per day appears satisfactory). Compositionally, this should include simple sugars and complex carbohydrates, including some dietary fibre. The presence of simple sugars may be important for optimal absorption.

A moderate intake of fat rich in EFAs but free from "trans" fatty acids; at least 10% of energy, but probably less than 24%, provided compositional requirements are met.

Additionally, and hardly requiring comment, the daily intake of vitamins and minerals must be assured.

One further point justifies the presence of small amounts of available carbohydrate in products intended for use in the PSMF. The absorption of amino acids resulting from the digestive breakdown of protein in the lumen of the intestine is an active process, utilizing significant amounts of energy.

Ideally, the cells of the intestinal wall oxidise glucose as an energy source, though as with cells of other tissues, they can utilize ketone bodies, amino acids and free fatty acids. The liver and kidney are the only gluconeogenetic organs in the body, and during profound carbohydrate restriction, the role of the kidney gradually increases. In other words, gluconeogenesis does not occur in the cells of the intestinal wall whose function is to actively transport amino acids resulting from protein digestion, therefore glucose availability in these cells is reduced. Presence of small amounts of simple sugars in the mixture presented for absorption may help offset this reduced availability of the preferred substrate and improve the efficiency of amino acid absorption.

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