Commonly Consumed Foods In Mauritius Biology Essay

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Satiety is defined as the physiological and psychological of fullness usually experienced after eating or drinking. It therefore contributes to the termination of a meal. Before eating, the animal body is subjected to a sensation of hunger which drives the individual to seek for food. After the beginning of food consumption, the feeling of hunger is replaced by a sense of fullness which is often related to the action of stomach filling.

Satiety is governed by numerous physiological responses. The feeding behaviour involves firstly a pre absorptive and post absorptive humoral mechanism followed by neuronal mechanisms. Factors such as nutrients availability, metabolic processes and gastric contractions bring about hunger signals. The latter are then inhibited on the onset of eating and satiety signals are activated (Tomé D et al, 2009). Satiety signals are activated by psychological factors, chemical senses such as taste and small and through mechanical factors of swallowing and gastric distension. Their main role is to prevent excess eating. The long-term satiety effect is brought about by the gastrointestinal system and the central nervous system.

Moreover, behavioural as well as environmental conditions also affect satiety. These comprise emotional factors, food availability, and time of the day or food characteristics such as colour, texture, taste or smell. The water, fibre and macronutrient content of the foods consumed can all influence satiety. They add weight to the food which promotes a feeling of fullness.

In an attempt to determine which foods cause fullness an Australian scientist, Dr Susanna Holt and her co-workers of the University of Sydney in 1995 developed a satiety rating scale known as the satiety index. The satiety index is a measure employed to rank different foods on their ability to satisfy hunger. Thirty-eight unrelated foods were administered to subjects groups comprising 11- 13 volunteers and their degrees of hunger were monitored at regular intervals of 15 minutes for two hours. It must be noted that degree of satiety depends on numerous factors such as the size and portion of the food.

The more fulfilling a food is, the more it serves as a nibbling deterrent. Following this experiment, a satiety index of 100 was established for white bread which is, in fact, used as the baseline for ranking other foods. In addition it was discovered that the most satisfying food was potatoes while the least satisfying one croissant. In Mauritius, carbohydrate-rich foods are among the most consumed diet of the local people with white rice and white bread being the staple foods of the most Mauritians. Commonly consumed local diets are usually fast-foods, which do not necessarily conform to recommended healthy eating patterns. The quality as well as the quantity of foods consumed must be taken into consideration.

Justification

Obesity is an international health issue and it touches nearly 477,000 Mauritians. The leader cause of obesity is improper eating habits whereby unhealthy foods are eaten the more frequently and in inappropriate amount. Choosing foods based on satiety index may help with weight management. Late activation of satiety signals or overeating beyond sensation of fullness often leads to obesity. The satiety index of the local foods could be an effective means in planning diets which will favour weight gain or weight loss. Hence, it could be suggested as a preventing device in the treatment of overweight or obesity.

Aim

The aim of this study is to produce a validated satiety index for commonly consumed foods in Mauritius

Objectives

Investigate the general eating habits of the local population and measure BMI of volunteers.

Identify the common foods amongst young adults

Set up a satiety index for the mostly consumed foods.

Compare the different foods according to their respective satiety indices.

Chapter 1 : Literature review

Satiety

Satiety may be defined as the fulfilling sensation which is felt and which last after eating. It also inhibits further energy intake, in the form of food or drinks, by individuals until the next feeling of hunger (Benelam B, 2009). Satiation is the term used to designate the process which leads to the cessation of eating (Bellisle et al, 2012). Both satiety and satiation play significant roles in the appetite regulation and weight control. Satiety exerts an effect on the period of time between eating occasions and determines the amount of energy which will be consumed on the following eating occasion. Contrarily, satiation deals with quantity of food eaten on each occasion (Bellisle et al, 2012).

Satiety is governed by numerous physiological responses termed the satiety signals. A concept of a satiety cascade has been established by Blundell and his colleagues in 1987 to classify the physiological satiety signals which occur as a result of food consumption. These are divided into different stages:

sensory

cognitive

post-ingestive

and post-absorptive.

http://www.emeraldinsight.com/content_images/fig/0170940601002.png

Figure 1 describes the satiety cascade (Benelam B, Satiation, satiety and their effects on eating behaviour, British Nutrition Foundation, London, 2009).

The primary factors affecting food intake are sensory mechanisms. These include the food colour and smell which provoke physiological events before the food is ingested. In addition, the texture, taste and temperature affect palatability of the particular food. Normally, a meal last longer if the food is more palatable (Anon, 2007). The second stage of the cascade includes cognitive phase which is based on learned and previous experience with the ingested food. Post-ingestive stage is initiated as food reaches the stomach. Stimulation of stomach filling and distension transmits signals to the brain to start satiation. As digestion proceeds, promotion of satiety and satiation is favoured by the release of hormones in the gut and by chemo and mechanoreceptors (Bellisle et al, 2012). In the final phase of the satiety cascade, the post-absorptive phase, the production of nutrients triggers satiety and satiation (Blundell et al, 1987).

1.1. Physiological mechanisms of satiety

The appetite control signals can be denoted as either episodic or tonic (Halford & Blundell 2010). Episodic signals are those which occur at several eating occasions or episodes. They are mostly inhibitory and activation of these signals varies with respect to the eating behaviour. They are related to satiety signals. On the other hand, tonic signals are initiated in storage tissues such as the adipose tissues and they have an effect on the expression of appetite.

1.2 Episodic signals

Hormones known as gut hormones are secreted in the gut in parallel to food consumption. These hormones release stimulate specific areas of the brain which in turn, bring about satiety. Such signals are termed episodic signals. They are short-term signals named the satiety factors (Korner & Liebel, 2003).

Some examples of the gut hormones which exhibit these short-term signals include:

Cholecystokinin ( CCK)

Glucagon-like peptide 1 (GLP-1)

Peptide YY3-36 (PYY)

Pancreatic polypeptide( PP)

Amylin

Ghrelin

1.2.1. Cholecystokinin (CCK)

Cholecystokinin (CCK) is a neuro peptide which is secreted by the endocrine L cells in the proximal small intestine in the presence of nutrients especially after fat or protein-rich meals (Wren& Bloom, 2007). Release of cholecystokinin stimulates activation of CCK-A type receptors of the stomach pylorus. This leads to satiation; also, it determines meal size and inhibits hunger (Woods et al, 1998). Its satiating actions were first demonstrated in 1973 by Gibbs and his co-workers. CCK was administered to rats and a decrease in meal size was observed in the eating pattern of these animals. This was later established in human beings at low CCK doses (Muurahainen et al, 1988) while at high doses a feeling of nausea can arise. It must also be noted that reduction in meal size occurs in accordance to stomach expansion by food (Lieverse et al, 1995). Extraneous CCK release and resulting satiety sensation is caused by long fatty acids chain, C 12 or above. In humans, this effect can be prevented by the CCK-A receptor antagonist, loxiglumid (Lieverse et al, 1994). In addition, CCK plays also a role in retarding gastric emptying and secretion of pancreatic enzymes thereby coordinating digestion (Liddle et al, 1985).

1.1.1.3. Glucagon-like peptide 1 (GLP-1)

Glucagon-like peptide1 (GLP-1) is a product of the pre proglucagon gene. This gene is expressed in the pancreas, brain and intestine, to produce glucagon and GLP-1 respectively (Murphy & Bloom, 2004). GLP-1 is secreted into the blood in response to nutrients (Le Quellec et al. 1992; Herrmann et al. 1995). From investigations of exogenous GLP-1 administration in humans, GLP-1 was found to decrease food intake and feeling of hunger but to stimulate fullness sensation (enhanced satiety) in standard weight, obese and diabetic participants (Flint et al. 1998, 2000a; Näslund et al. 1998, 1999a; Gutzwiller et al. 1999a, 1999b; Toft-Nielsen et al. 1999). Moreover, GLP-1 exerts its effect on satiety by activating GLP-1 receptors found in the brain (Yamamoto et al, 2003). Also, GLP-1 is like capable of acting as a biomarker for satiety (De Graaf et al. 2004) and its level has been shown to increase in the next two hours after mealtime (Orskov & Holst 1987).

1.2.2 Peptide YY3-36 (PYY)

Peptide YY3-36 is a 36 amino acid truncated peptide which is manufactured in the L cells of the ileum, colon and rectum. It is secreted into the bloodstream with respect to the amount energy intake and its level remains high for six hours (Adrien et al, 1985). Release of PYY occurs before nutrients reached the distal small and large intestines. Thus, initiation of PYY secretion occurs via vagus nerves (Fu-Cheng et al. 1997). PYY experimentation with rodents and humans decreases food intake (Batterham et al, 2002; 2003). In the study assessing administration of PPY on thin and obese people by Batterham and colleagues, both exhibit reduced food intake by approximate 30 %. In addition, fasting as well as post-prandial PYY concentrations was higher in lean than in obese subjects in spite of the latter consuming more energy. This may account for development of obesity though this has not yet been proven. Furthermore, PYY hinders gastric emptying and decreases gastric acid release which causes the mechanism of "ileal brake" in the superior digestive tract. This mechanism controls the transport of nutrients from stomach to the intestines ensuring efficient digestion (Näslund et al. 1999)

1.2.3 Pancreatic polypeptide (PP)

Pancreatic polypeptide is produced in the pancreas and in lesser quantities in the large intestine and the rectum (Adrian et al, 1976). It is secreted into the bloodstream accordingly with level of energy intake (Track et al, 1976). Studies have demonstrated that upon PP intake two hours pre- prandial, it decreases food consumption and energy intake by 22 % in humans (Batterham et al, 2003b). Prader-Willi Syndrome is a genetic state which is related to excessive eating and obesity. Suppression of pre and post prandial levels has been observed in Prader- willi syndrome patients (Bemtson et al, 1993). Thus a distorted in PP response may contribute to expression of this genetic disorder.

1.2.4 Amylin

Recently much emphasis has been put on this pancreatic hormone, amylin. These current researches suggest that amylin has a potential consequence on food intake as well as body weight (Reda et al, 2002). Rats have been the subjects of these studies and it peripheral administration of amylin in those animals, causes decrease in both food intake and meal size, hence, affecting body weight and mass ( Rushing et al, 2001). In humans, pramlintide, an amylin analogue hormone,given to amylin-deficit diabetic patients, modified body weight in insulin-dependent obese diabetics and obese non-diabetics (Hollander et al., 2003; 2004; Riddle et al., 2007; Aaron et al, 2007). In skinny healthy participants, decrease in meal intake, size and length was noted (Chapman et al, 2007).

1.2.5 Ghrelin

Ghrelin is a peptide hormone manufactured in the gut as plasma ghrelin. Its level is highest in the stomach and in the small intestine. Ghrelin has been shown to increase food consumption and appetite (Tschöp et al. 2000; Wren et al. 2001). In contrast to the previous mentioned hormones, ghrelin stimulate eating, that is, it inhibits satiety feeling. A rise in ghrelin concentration has been noted before meals. This suggests that it can promote eating initiation in humans (Cummings et al, 2001). Interestingly, ghrelin has also been found to regulate long-term energy stability. In obese individuals, its level is relatively low (Tschöp et al. 2001) while in skinnier persons it is higher, it can also be much higher in those persons whose energy intake is limiting (Tolle et al, 2003). Thus, ghrelin acts both as an epidosonic and tonic satiety signal. Generally, ghrelin causes meal initiation but factors such as fat mass may reduce its level. In addition, occurrence of weight loss, for instance, following a diet period, can cause uncontrollable ghrelin level rise leading to stimulation of hunger. Ghrelin blockage may therefore acts as a very effective anti-obesity cure (Anon, 2007).

1.3 Tonic signals

Appetite is also regulated by long-term storage of energy by the body organism (Caballerro B et al, 2005). Tonic satiety signals detect the levels of fats and transmit it to the brain so as to regulate the body weight by monitoring energy intake and expense (Benelam B, 2009).

Leptin

Leptin is the hormone involved in the regulation of storage of fats. It is produced in adipose tissues by ob gene (Zhang et al, 1994). Leptin circulates in the bloodstream and signals elevated fat supplies to the brain via specific receptors in the hypothalamus (Margetic et al, 2002). Rise in leptin causes reduced hunger which in turn decreases food intake. In experiments performed on obese animals it was found that leptin injections cause body weight and fat loss (Forbes et al, 2001). Simultaneous administration of leptin and low levels of CCK reduce food intake (Barrachina et al, 1997). Mutation in the ob gene produces a deficit in leptin which lead to severe obesity in humans (Montague et al, 1997). This can be counteracted by injecting exogenous leptin (Farooqi et al. 1999; Licinio et al. 2004). However, the prevalence of obesity in altered ob gene is relatively low. Most obese persons have a high level of effective circulating leptin and exogenous leptin injection has little effect on their weight. This implies that obesity is mainly associated with leptin resistance instead of leptin shortage (Fogteloo et al, 2003). Some evidence suggests that this can be due to firstly, an improper transport across the blood-brain barrier (Kastin &Pan 2000) or secondly from the resistance of neurones to the leptin hormone (Sahu 2002).Application of leptin as a biomarker of satiety can therefore be recommended in the longer run but it will not be effective on individuals suffering from high leptin plasma concentration.

1.4 Stimulation of satiety signals in the brain

Satiety signals, tonic as well as epidosic, are activitated directly or indirectly via receptors found in the brain. The central region of the brain which has been found to be involved in appetite control is the hypothalamus (Morgane & Jacobs, 1969). Approximately 20 neurotransmitters and neuromodulators transmit signals to different areas of the hypothalamus or the remaining brain regions. Appetite signals are integrated in the hypothalamus to bring about energy intake or expenditure. The lateral hypothalamus consists of a network system which encourages eating. However, eating is stopped when signal passes through another network system linked to the ventromedial nucleus of the hypothalamus (Kent et al, 1994). It is believed that the ventromedial region causes meal termination via the stimulation of another hypothalamus region, the paraventicular nucleus. Impaired paraventricular nucleus leads to obesity (Leibowitz, 1992). Moreover, numerous neurotransmitters are related to hunger such as neuropeptide Y and serotonin which stimulate and inhibit carbohydrate intake respectively (Kishi &Elmquist, 2005). Similarly fat intake is increased and suppressed by galanin and enteristatin (Lin et al, 1998).

1.5 Satiety and stomach mechanism

According to Read in 1990, gastric stimuli or mere presence of food in the gastro-intestinal tract leads to the secretion of chemicals which play a role in appetite control. Most of these chemicals are peptide neurotransmitters and it has been observed that if administered peripherally, they can provoke modifications in normal food intake (Smith & Gibbs, 1995).

During eating, when food bolus reaches the stomach, a rise in gastric volume is initiated via nerve communication to the central nervous system (Ritter 2004). Satiation is brought about by gastric distension and this occurs independently of the type of nutrients present in the bolus (Philips & Powley 2000).

1.6 Food composition and satiety

Satiety is affected by the food and drinks individuals consume. Foods comprise many nutrients such as carbohydrates, fats, proteins, fibres. Diverse nutritional component of a meal has a different effect on satiety and can affect the ensuing energy intake.

1.6.1 Fibre

Dietary fibre is undigested plant material. It consists of the soluble (fruits, oats) and insoluble fibres (wheat bran) and as their names suggest, the soluble portion dissolves in water and is absorbed in the colon while the insoluble part is removed by egestion. Physiological features of a fibre type determine its effect on satiety. Different experiments were carried out to assess impact of dietary fibre on satiety. In one of them, Burley and co-workers in 1987, observed a higher degree of fullness in subjects who consume a high-fibre breakfast. In another one, no effect on energy intake was identified (Slavin and Green, 2007)

1.6.2 Protein

Most investigation on effects of proteins on satiety has concluded that high levels of protein have a greater impact on satiety compared to equitable energy content of fats or carbohydrates. Halton and Hu in 2004 studied the effect of high-protein diets on weight loss. 7 out of the 15 studies recognised a major weight loss following dieting period. It has been discovered that high-protein diets which are at the same time, very low in carbohydrates, inhibit food intake by inducing a phenomenon known as ketosis. Ketosis is a condition whereby the body glycogen stores are depleted due to a severe carbohydrate restriction

(Astrup Arne, 2005). In an attempt to distinguish effect of high-protein, low carbohydrate (LC) ketogenic and high-protein, medium-carbohydrate(MC) non-ketogenic diets on satiety and weight loss, Johnstone et al in 2008 found that the ketogenic one suppresses hunger and food intake. In addition, more significant weight loss occurred on the LC ketogenic diet.

1.6.3 Carbohydrates

Carbohydrates are a large group of macronutrient which consists of monosaccharide, disaccharides, oligosaccharides and starches. Different forms of carbohydrates exert different effect on satiety. Glucose provides energy and its level is closely monitored and detected in the body (Marty et al, 2007). Satiety regulation is directly affected by glucose concentration along with hormonal signals. In an experiment performed by Anderson & Woodend in 2003 it was found that 50g or more sucrose rise satiety and lower energy intake. Its lowest detection limit to promote satiety was an amount of 25g. Glucose and fructose have different effects on satiety since they are absorbed and metabolised differently. Glucose causes insulin level rise while fructose has been found to be associated leptin levels fall (Teff et al, 2004). Most studies on carbohydrates and satiety has dealt with glycaemic index (GI) and glycaemic load (GL). GI is the capacity of a carbohydrate-rich food to raise blood glucose level with white bread as reference. Aston and colleagues in 2008 detect no difference on satiety between high GI and low GI states. With respect to Holt's study carbohydrate rich-foods

1.6.4 Fats

Dietary fats s retards gastric emptying which in turn promote secretion of satiating hormones as well as it prevents secretion of ghrelin (Little et al, 2007). It has been observed that fat impacts satiety in the same way as other macronutrients do when energy density is monitored (Blundell et al, 1993). Although another school of thought suggests that its effect is weaker. In Holt's study, fatty foods were found to be less satisfying than the other macronutrients (Holt et al, 1994).Still, it must be noted that when energy density is not controlled that is, in free-living individuals, fat -rich foods have higher density than carbohydrate or protein-rich foods. In addition, high-fat foods 'palatabililty influences people's consumption. The fatty acids chain lengths influence the way the are metabolised in the body and the unsaturation level of monounsaturated fatty acids (MUFA ) and polyunsaturated fatty acids (PUFA) also affect satiety on extreme diets (French et al, 2000).

Additional factors affecting satiety

In addition to the internal regulatory mechanism controlling appetite there are other external, independent, factors which influence a person's desire to eat. These may act on internal signals and appropriate actions may occur which can affect satiety.

1.7.1 Palatability

Palatability is the degree of acceptance of a food to a person's palate taste. Palatability of a food can be increased by fat addition and by rising meal portion and duration (Yeomans 1998). The most palatable foods tend to be the least satiating and vice versa if composition is not controlled (Drewnowski 1998). This has been confirmed in Holt's experiment, palatability correlated negatively with satiety score. There exists a correlation between palatability and energy density. The lowest energy dense foods are the least palatable and vice versa (Drenowski 1998). This can be refuted as alteration of taste and appearance of food can produce different satiety responses.

1.7.2 Variety

Studies have demonstrated that the wider choices a person has, the more that person will eat (Rolls 1984). Sensory-specific satiety (SSS) describes that a person desire to eat and taste a new food is higher than the will to eat an already tasted food (Hetherington et al, 1989). It has been suggested by Rolls and McDermott in 1991 that age also affect SSS. It was found that youngsters' response was more apparent and the response is reduced with increasing age.

1.7.3 Portion size

Food servings have increased for the past few decades in the US and products are sold at relatively larger portions than before. No change in portion size was noted in the UK .According to Food Standard Agency (FSA) 2008; standard portion sizes have stayed invariable. It seems that when food is available in larger portion, most individuals except children below four years old, will tend to consume more food thereby increasing energy intake (Ello-Martin et al, 2005). Yet, in some studies no difference in appetite ratings were observed between smaller and larger food servings (Rolls et al, 2002, 2004a-b).In addition, long period experiments carried out on 2days, 11 days and 2 months, showed that subjects continued to eat larger food portions without reducing energy intake to compensate the extra energy already consumed (Rolls et al, 2006, 2007, Jeffrey et al, 2007). Presence of food acts as a stimulus that promotes consumption and this stimulation can be stronger than the physiological satiety signals which inhibit intake.

1.7.4 Physical activity

Numerous studies have investigated the relationship between physical activity and hunger ratings. Physical activities usually raise lean body mass and energy expenditure. Intense physical activities seem to exert a negative effect on hunger thus suppressing it for short periods (Thompson et al. 1988; Kissileff et al. 1990; King et al. 1994, 1996; Westerterp- Plantenga et al. 1997).This hunger-inhibition phenomenon is termed the physical-activity induced anorexia. This is not observed in low or moderate intensity physical activity and may be caused by the transport of blood away from the gut towards the muscles (Blundell et al, 2003). Physical-activity induced energy deficit studied on lean men and women over a few weeks showed that these participants can stand this energy deficiency without the need to compensate with ensuing energy intake. Reduction in physical activity leads to a smaller energy expense than with active routine. This results in increase appetite and energy intake, which is also directly proportional to weight gain (Stubbs et al, 2004).

1.7.5 Distractions such as television (TV) viewing

Experiments performed by Bellissimo and team in 2007 on young children noted an increase in energy intake in children who ate while watching TV than those who were undistracted. In addition, it is also observed that subsequent snack consumption is higher in the former group (Higgs et al, 2009). It has been postulated that memory of a previous meal decreases following food consumption. Television viewing has been suggested to disrupt the memory of the earlier meal in those subjects which in turn consume more. In fact, the existing correlation between obesity and time taken in television watching may be due to the increase food and drink intake while viewing TV (Cleland et al, 2008).

Moreover, it has also been noted that energy intake is affected that number of people present and eating simultaneously. Generally mealtime is longer when there is social interaction and hence increases energy intake (De Castro 1994).

Satiety and weight control

To date, there are approximately 477,000 obese Mauritians and this number is likely to increase at a rapid rate. This suggests that in most cases, the factor that influences obesity is not related to genetic makeup of an individual but rather is an environmental factor (Blundell et al, 2009). Yet, some individuals seem to have higher risk of developing obesity than others. Development of satiety and satiation is a key feature to be considered during weight control.

Obesity, satiety and genetics

Genetic changes can influence prevalence of obesity. In exceptional cases, obesity may arise due to a single mutation in a gene. This genetic difference can disrupt satiety and satiation signalling pathways (O'Rahilly & Farooqi 2008). As an instance, a mutation occurring in the leptin gene can lead to irregular over-eating and obesity in early childhood. This issue can be overcome through administration of leptin (Gibson et al. 2004). This type of gene mutation represents a very small percentage of the human obesity cases though a person's genetic profile may contribute up to 75 % of their BMI variation showing that genetics can impact on an individual's risk of obesity (Farooqi & O'Rahilly 2007).

Satiety physiological difference in obese individuals

Differences in physiological responses can lead to obesity. Gastric distension is involved in satiety mechanism. Some researchers have discovered that obese subjects have higher gastric capacities than thin or normal-weight individuals. Therefore, higher energy intake occurs before gastric distension process starts (Geliebter 1988; Kim et al. 2001). In addition, differences in satiety signalling have been noted in obese people. The hormone ghrelin stimulates hunger but is inhibited following energy intake. In lean subjects, there are a significant higher ghrelin concentrations and post-prandial ghrelin suppression. The latter is not observed in obese and this may be because maximum ghrelin suppression already occurs due to surplus fat storage (English et al, 2002). Lower levels GLP-1 and PYY hormones have also been noted in obese.

Behavioural differences to satiety

Eating behaviours also affect satiety responses. For instance, some studies revealed an association between the speed of eating and bodyweight (.Barkeling et al. 1992; Sasaki et al. 2003; Otsuka et al. 2006; Maruyama et al. 2008). One such study carried out by Laessle and team in 2007 showed that obese persons ate at a more rapid rate and swallow bigger spoonfuls than thin ones. Hence, they had generally a greater energy intake. Eating rate promotes excess food intake before internal satiation signals can be stimulated leading to a positive association between energy balance and weight increase.

Moreover, consumption of high fatty foods is a major factor for obesity. Blundell and co-workers in 2005 observed that obese subjects who had a preference for diets rich in fats had a weaker response to satiety. Their dietary habits contribute to greater weight gain. Also, they respond positively to palatable foods and suffer more from hunger cravings. Besides, this receptiveness of obese to palatable foods has been considered as the chief factor which accounts for differences between lean and obese persons. These behavioural features predispose individuals to excessive gain weight.

In an experiment performed by Carnell and Wardle in 2008 in subjects having ages between 3 year old and 11 year old, it was discovered that subjects having greater BMI, respond negatively to satiety and had higher external food cues.

Chapter 2: Methodology

2.1 Project design

In line with the objectives formulated in this study, a population- based survey was carried out to investigate the dietary habits and consumption pattern of the Mauritian population.

A satiety protocol was devised to assess the satiety responses of young university adults to 7 common foods consumed by the Mauritian population.

2.2 Questionnaire design

The questionnaire consists of a primary section detailing the demographic information of the respondents. Information such as age, height, weight, education level attained was gathered. Medical history of diseased participants was also recorded

The second section assessed the dietary habits of the participants. This includes basic questions such as balanced diet knowledge, nutritional knowledge and food preferences. In an attempt to investigate personal awareness about unhealthy diets, respondents gave a self- assessment rating of their diet with respect to their effect on health. Respondents were then asked to denote their eating frequency of particular listed local foods over a month. No quantitative information was collected.

The questionnaire was further divided into the sections A, B and C. In this study, only the Section A was taken into consideration. Section A covered eating behaviours of the subjects. Duration of main meals and snack was noted. Participants were lastly asked to choose from a list of ready-made answers which best represent their feeding behaviours.

2.3 Subject criteria

The population based survey conducted was purely on a voluntary basis. People were not remunerated for participation in the study. Anonymity of respondents was respected. Subjects were recruited from a randomly Mauritian population. A total of 250 individuals comprising of 124 males and 126 females took part in the study. The participants were between the age of 12 and 60 years old. The survey was carried between November 2012 and January 2013. Assistance was provided to subjects through the explanation and translation of the questions in 'Creole' whenever they had difficulties in understanding a particular question.

2.4 Satiety Protocol

Using satiety index of Holt as a model, 8 different foods were chosen for examination. These include:

White bread

Dholl puri

Dholl puri and vegetable fillings

Farata

Farata and vegetable fillings

Fried noodles

Fried rice

White bread was chosen as a baseline value, as per Holt's study.

These foods were chosen based on the Mauritians' food preferences and their relative availability.

10 healthy young adult participants (40 % males and 60%females) were recruited on a purely voluntary basis and were remunerated to take part in the study.

Table 1 shows subjects characteristics for each test food.

Foods

Subjects(n)

Female(n)

Male(n)

Age ( years)

BMI (Kg)

White bread

10

6

4

21

19.7+4.16

Dholl puri

10

6

4

21.2+0.42

20.8+2.96

Dholl puri + vegetable fillings

10

6

4

20.9+0.73

20.7+3.30

Farata

10

6

4

21.1+0.32

23.1+5.71

Farata+ vegetable fillings

10

6

4

21+0.82

21+3.98

Fried noodles

10

6

4

21.2+0.42

22.7+3.6

Fried rice

10

6

4

21.1+0.32

21.6+5.68

Height and weight of participants were taken and BMI calculated from the data collected.

The volunteers were required not to eat anything other than the test material during the

testing session which lasted for two hours. Isoenergetic 1000KJ or 240 Kcal servings for the foods listed above were provided to the participants. This was served with 220ml cups of water to aid with ingestion.

Subjects were provided a different food each day in a randomised order to avoid any influence of effect of order of presentation. They were asked to eat the food and drink the water at a comfortable rate but were asked to try to finish the meal within 10 minutes. The time taken to complete the meal was then recorded.

Immediately following the meal, participants were asked to answer these two questions:

How difficult was the food to eat (ranging from very easy to very difficult)?

Very Easy Easy Neutral Difficult Very difficult

The palatability of the food- ranging from dislike very much to like very much.

Dislike very much Dislike Neutral Like Like very

much

At regular intervals of 30 minutes over the two hours testing session, subjects were asked to rate their feelings 'appetite for a meal', 'satiety' and 'fullness" by means of a visual analogue scale rating:

Each 30 minutes after meal initiation.

Very hungry Hungry A little hungry No Somewhat Satisfied Very Full

Particular Satisfied

Feeling

Forms were be filled out independently and without sharing of information. A scoring method was used in addition to the visual analogue scale. Integer values from one to seven, in the form of a table(2), were provided for each self assessment of hunger/satiety level, one being very hungry, and seven being very full.

Table 2 shows the satiety score attributed to each degree of hunger or fullness.

Degree of hunger

Ratings ( 1-7)

very hungry

1

hungry

2

a little hungry

3

no particular feeling

4

somewhat satisfied

5

satisfied

6

very full

7

Satiety index for each test food was estimated by determining the area under the curve (AUC) using the trapezoidal method (x-axis- testing duration (30,60mins etc) and y-axis satiety score).

Satiety index was then calculated as per Holt's study:

Area under the 2hour satiety curve of particular test food x 100

Group average area under the 120 min satiety curve of white bread

Chapter 3: Results and Analyses

3.1 Demographic information

Of the 250 participants 124 were female and 126 were males. All participants have a level of schooling. In both males and females, the highest proportion contained those who had tertiary level education. The proportion of male respondents (25.4%) in the age group 12-20 was higher than the proportion of females (20.2%) in the same age group. Over 50 and 54% of the males and females respectively sample were in the 21-30 age groups while the proportions of males and females over 30 years old were 24.6 % and 25.8% respectively.

Table 3 shows the distribution of participants by gender, age and education level.

 

Males

Females

 

n

%

n

%

Age in years

 

 

 

 

12 to 20

32

25.39683

25

20.16129

21 to 30

63

50

67

54.03226

31 to 40

9

7.142857

10

8.064516

41 to 50

13

10.31746

10

8.064516

51 to 60

9

7.142857

12

9.677419

Education

 

 

 

 

Primary school

5

3.968254

6

4.83871

Secondary school

20

15.87302

21

16.93548

Completed O level

13

10.31746

11

8.870968

Completed A Level

43

34.12698

39

31.45161

Tertiary education

45

35.71429

47

37.90323

The males have a mean BMI of 23.8 + 3.89 Kg while the females have a mean BMI value of 23.1 + 3.8 Kg. A Spearman's correlation was run and it confirms that there is a very weak, positive correlation, rs= 0.085 and p value=0.182 between the two variables.

Figure 5 describes the BMI between males and females

The mean BMI among the different age groups vary with

Chapter 6: References

Tomé D et al, protein, amino acids, vagus nerve signaling and the brain, Clininal J nutrition, 2009.

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