Effect of glycemic index/load of a meal on subsequent food intake - Dissertation Example

Effect of Glycemic Index/Load of a Meal on Subsequent Food Intake Supervisor’s Laboratory/Library In the final version will provide a summary of the principal findings concerning the effect of glycemic index/load of a meal on subsequent food intake. Introduction Terms of reference The theory behind glycemic index is simply to minimise insulin related problems by identifying and avoiding foods that have the greatest effect on blood glucose levels. A number of studies have been done on the effects of glycemic index/load on obesity, satiety and food intake. However, there is a lot of controversy as some findings differ. Diabetes Mellitus is one of the main underlying causes of death worldwide. According to Newnham and Ryan (2002) it has been projected that the number of people with diabetes will increase by 78 per cent, from 124 million in 1997 to 221 million in 2010. This figure is significant by any measure, with countries like India, China and USA topping the list. Aim of Study The aim of this study is to determine the effect of glycemic index of a meal on subsequent food intake. The null hypothesis is that the glycemic or index load of a meal has no effect on subsequent food intake. The study is significant since it will provide updated and more beneficial and accurate information on the optimal diet that will help reduce significantly, the deaths associated with diabetes mellitus as well as other health problems like cardiovascular disease and obesity. Literature Review Glycemic Index and Glycemic Load The glycemic index (GI) was developed by researchers from the University of Toronto approximately 30 years ago (Campbell, n.d.). It is used primarily by diabetics, as a tool to control their blood glucose levels. The GI is a ranking of foods that contain carbohydrates based on their potential to raise blood sugar levels. Carbohydrates with GI values of greater than 70 are said to be high GI foods and those less than or equal to 55 are said to be low GI foods. High GI carbohydrates tend to cause a quick rise in blood glucose levels and in most case a quick rise in insulin levels while low GI foods are slowly absorbed and so cause slow increases in blood glucose and insulin levels. According to Foster-Powell et al (2002) reliable tables of glycemic index and glycemic load (GL) can be very useful in improving the quality of research studies that examine the relationship between GI, GL and health. The GI has proven to be very useful in bringing new insights into the relationship between physiologic effects of foods rich in carbohydrate and health. Foster-Powell et al also states that food with a high glycemic load (GI x Dietary carbohydrate content) is independently associated with an increased risk of type 2 diabetes, cardiovascular disease and certain cancers. Effects of High and Low Glycemic Index on Appetite Leatherwood and Pollet (1988) examined the effects of GI on subsequent food intake (appetite) found that there were lower levels of blood glucose and a slow return of hunger after meals with bean puree which is low in GI starch when compared with meals that included potato which is a high GI starch. Holt et al (1992) also showed that there was an inverse relationship between satiety score and glycemic and insulinemic responses to various breakfast cereals. According to Ludwig (2000) all but one of at least 16 prior studies done showed that after low GI foods were consumed there was increased satiety, a delay in the return of hunger or a reduction in ad libitum food intake. Ludwig et al (qtd. in Ludwig (2000) explored the physiologic events that might relate GI to ones appetite by comparing the effects of three isocaloric test meals with different levels of GI during separate 24 hour admissions. One of the three meals had a low GI, the second a medium GI, and the third a high GI. The low GI meal consisted of vegetable omelette and fruit, the medium GI meal of “steel-cut” oatmeal which slows digestion rate, and the high GI meal of instant oatmeal. These meals were administered to individuals including persons who were obese but otherwise healthy. In administering the tests breakfast they found that the area under the blood glucose curve differed among the low, medium and high GI meals as they expected. It was found that the rapid absorption of glucose from the high GI meal resulted in relatively high insulin and low glucagon concentrations. These are abnormal changes which were expected to promote uptake of glucose in muscle, liver and fat tissue, restrain hepatic release of glucose and inhibit lipolysis.( Lipolysis is the breakdown of lipids. It is the hydrolysis of triglycerides into free fatty acids, followed by further degradation into acetyl units, by beta oxidation). Consequently, access to the two major metabolic fuels was effectively impaired in the postabsorptive period, as shown by a “reactive hypoglycemia” (difference in glucose nadir of -0.5 mmol/L, p = 0.02) and lower free fatty acid concentrations 3 to 5 hours after the high GI meals in comparison with the low GI meals. The individuals that were subjected to these tests also consumed a lot more energy after the high GI (5.8 MJ) compared with the medium GI (3.8 MJ, P < 0.05) or the low GI (3.2 MJ, P = 0.01) test lunches. Ludwig (200) concluded that a growing body of theoretical and experimental work suggests that diets designed to lower the insulin response to ingested carbohydrate (e.g. low GI) may improve access to stored metabolic fuels, decrease hunger (and therefore subsequent food intake) and promote weight loss. Such a diet would contain abundant quantities of vegetables, fruits and legumes, moderate amount of protein and healthful fats, decreased intake of refined grain products, potato and concentrated sugars. Alfenas and Mattes (2005) found results to support their view that high GI diets enhance appetite and promote positive energy balance. Their study involved the consumption of foods with low GIs and foods with high GIs over an 8 day period. Glucose and insulin concentrations were determine both before and after the subjects were treated. Alfenas and Mattes (2005) found that the differences in the glycemic response of foods tested in isolation under fixed time are not preserved under conditions of chronic ad libitum consumption of mixed meals. This seems to indicate that the environment and the restrictions in place may affect glycemic response and not just the foods themselves. However, at ones own pleasure would be better represented by everyone each subject eating what he or she thinks is best. Additionally, only one food was low GI, while three foods were used for the high GI meal. The fact that the high GI meal had three different foods might have been a factor as it has been found that when some high GI foods were eaten with low GI foods they did not appear to raise the blood glucose level as much (Jenkins 1981). The Importance of the Classification of Foods Based on their Glycemic Index Levels Jenkins et al (Glycemic index of foods: a physiological basis for carbohydrate exchange, 1981), however, found that there was no relationship between glycemic index and dietary fibre or sugar content. Jenkins et al (1981) indicated that this may have been due to the fact that many of the high fibre foods were wheat products and wheat has little effect on blood glucose. No major difference was found between the high fibre wholemeal bread, spaghetti and brown rice and their low fibre white counterparts. Legumes when compared with cereals raised the glucose level in the blood. The average glycemic index for cooked whole grains, breads, spaghetti and porridge was 59% in comparison with legumes -31% with p < 0.001. The dietary fibres guar and tragacanth which are found in leguminous plants have been known to flatten the rise in the levels of glucose in the blood after 50g glucose more significantly than other forms of dietary fibre and fibre analogues. Jenkins et al (1981) found that sugar content was not related to blood glucose response, even though absorption may have been more rapid. This they presume was due to the very low increase of 20% produced by fructose which reflected in the response to sucrose. Jenkins et al (1981) found that fat and protein, with p values of 0.01 and 0.001 respectively, showed a major negative correlation with the glycemic index. According to E. J. Thomas (qtd. in Jenkins et al) fat has been found to delay gastric emptying. Fajans et al (qtd. in Jenkins et al 1981) indicated that protein stimulates insulin secretion. It is not known however, what is responsible for this negative correlation. Jenkins found that the action of fat may not be that simple based on the similarity noticed between the blood glucose response to whole and skimmed milk. In addition, they could not readily explain the action of protein because the addition of cottage cheese to wholemeal bread had minimal effects on response in the glucose levels in the blood. According to Crapo et al (qtd. in Jenkins et al 1981, p.365) a comparison of glucose, potato bread, rice and corn indicated that the nature of the starch may be of high importance as a means to determine the glucose and insulin response and may have part of the explanation for the differences identified between cereals and legumes. Differences in the nature of the food or the way it is prepared may also have a significant influence on the glycemic response. Jenkins et al (1981) indicated the results of their tests were similar to those of Schauberger et al (1977) for the items that were common to both studies. These items were glucose, sucrose, fructose, bread, porridge, rice, potato, orange, apple, dried pea with the correlation coefficient (r) and p values of r = 0.823 and p < 0.001 respectively. The greatest similarities were found in the sugars for which there are no differences in composition or preparation.. According to Jenkins et al (1981) the dose response curves for glucose, bread and lentils demonstrated that when more than 50g carbohydrates were taken from any source, the rise in the glycemic index was less than expected. Jenkins et al (1981) concluded that the relative differences between the three carbohydrate sources was accentuated and thus indicated that small increases in meal size would not invalidate tables based on 50g carbohydrate portions. They expressed the belief that classification of food based on their effects on glucose levels in the blood is useful due to the differences in response which exists. The Effects of High and Low Glycemic Index Foods Ludwig et al (1999) found that after eating foods with high glycemic index, the rapid absorption of glucose which results induces a sequence of hormonal and metabolic changes that promote excessive intake of food in overweight persons. Ludwig et al’s (1999) study involved twelve obese teenage boys who were evaluated on three separate occasions using a crossover study protocol. They were administered test meals that had a high GI, a medium GI and a low GI. Voluntary energy intake after the high GI meal consisting of 5.8 MJ was 53% greater than after the medium GI meal of 3.8 MJ and 81% greater than after the low GI meal of 3.2 MJ. Additionally, when the low GI meal was compared with the high GI meal, the high GI meal led to higher serum levels; lower plasma glucagon levels; lower postabsorptive plasma glucose and serum fatty acid levels, as well as an elevation in plasma epinephrine. Ludwig et al (1999) found that the area under the glycemic response curve for each of the different test meals caused 53% of the variance in the intake of food within subjects. Anderson and Woodend (2008) examined the relationships between glycemic carbohydrate and the effect it has on satiety and the intake of food in the short term. The results reveal that both high and low glycemic carbohydrates do have an impact on satiety. However, it was found that their effects take place at different time periods after their consumption. High glycemic carbohydrates were found to found to be associated with the reduction in the need for food and therefore appetite within a one hour period (short term), while the satiating effects of lower-glycemic carbohydrates appear to be delayed for between two and three hours. No evidence was found to suggest that either an acute of sustained increase in the level of glucose in the blood is the primary determinant of the effects of food intake on satiety. However, it was found that other pre-absorptive as well as post-absorptive signals for satiety exists and may have been a determining factor. Anderson and Woodend (2008) conceded that further studies are required to separate the role of glycemic carbohydrates and the way they operate in determining satiety. Burton-Freeman and Keim (2008) notes the controversy surrounding the usefulness of a low GI diet to control appetite and food intake. They add that both psychological and behavioural influence complicates the issue. Burton Freeman and Keim (2008) investigated the satiety and glycemic response to high GI and low GI meals in overweight women, some of whom were unrestrained and some restrained. In a randomised crossover study subjective satiety, glucose, insulin, cholecystokinin (CCK), triacylglyceride (TG) and free fatty acids (FFAs) were measure at intervals of 8 hours after the treatment was administered. Test meals were matched for the most part but differed in terms of carbohydrate source: refined grain being part of the low GI diet versus whole grain being part of the high GI diet. The high GI meal resulted in greater satiety, suppressing hunger and therefore the desire to eat when compared with the low GI meal (p < 0.01). Plasma CCK level were found to be significantly higher after the high GI mean compared with the low GI meal (p < 0.001). Plasma glucose, insulin and TG were higher while FFAs were found to be lower after the high GI meal compared with the low GI meal (p < 0.0001). Neither CCK (p = 0.14) nor subjective satiety were significantly influenced (p > 0.4) significantly by the dietary restraint. However, there was an apparent inhibition of restraint and disinhibition on CCK. It was found that CCK was blunted in the restrained subjects with higher disinhibition scores than unrestrained subjects of restrained subjects with lower disinhibition scores (p , 0.05). A problem with these studies is that it aside from the fact that most of them focus on obesity they do not indicate anything about genes. Diabetes appears to be hereditary and controls need to be put in place for factors like these to ensure that they do not influence the results. These controls may include having several groups of different races as subjects. Another problem is that individuals have high metabolic levels and even though they eat a variety of foods they never become fat or seem to suffer from diabetes mellitus. There appears to be some contravening factors that have allowed for these. It is therefore important that tests be varied to account for these factors. Additionally, most of the studies done appeared to be either all males or all females which suggests bias. We are also not informed of the race of the subjects which can help to determine if this has an impact on the controversy surrounding different finding. Furthermore, age may be a factor and so different racial groups of different ages may indicate what additional research needs to be done. Effects of Glycemic Load and Subsequent Meal Intake on Children of Preschool Age LaCombe and Ganji (2008) sought to determine the effects of two breakfast meals that differed in terms of Glycemic Load (GL) on preschool children ranging from ages 4 to 6. The aim of the study was to find out whether differing levels of GL impacted on hunger, satiety and subsequent food intake. The subjects consumed low and high GL breakfast meals according to a randomised crossover design. This was followed by them eating anything that they wanted to for lunch, four hours after the treatment. The tests were repeated two times on non-consecutive days. LaCombe and Ganji (2008) discovered that children in the high GL group when compared with those in the low GL group were hungrier before prior to lunch with p < 0.03. However, it was observed that there was no significant difference in the amount of food and energy consumed during lunch. LaCombe and Ganji (2008) concluded that the decreased hunger in children in the low GL group may have been caused by the higher protein and fat content of the low GL breakfast. Furthermore, they suggested that diets low in GL should become part of a healthy diet for preschool children. We are not sure if what the children had before breakfast influenced the amount that they ate. How was full defined? A child may have a feeling of fullness if he/she is not happy with the food. Materials and method According to Babbie (2004, p. 44) Scientists begins with a theory from which testable hypotheses are derived. In order to test a hypothesis all variables should be specified. The proposed project is for dietary intervention in which subjects will consume: a) High GI meal b) Low GI meal – isocaloric/isonitrogenous. A diet history record will be used to assess food intake for 8 hours following a) and b) above. Rating to hunger will be assessed using a visual analogue scale Subjects will act as their own control Resources to be used are high and low GI breakfast foods The project will take place in a food preparation lab at the university Paired data will be analysed to assess whether high/low GI of breakfast significantly affects subsequent food intake. Results The results will be analysed using repeated measures analysis of variance using one of the several data analysis packages available. Significant differences among treatment means will be analysed by pair-wise t tests for appropriate comparisons. The level that will be used to determine statistical significance is p < 0.05. The diagram below shows results from an analogue hunger rating scale. Copied from Ludwig et al (1999) The above diagram represents hunger ratings on 10 cm analogue scale that will be used in this study. Conclusion/Discussion The results of this study should support research already carried out by Alfenas and Mattes (2005). They found that ad libitum ingestion of only empirically documented low and high GI foods does not result in any significant differences of appetite or energy or macronutrient intake on any assessment day or overall. References Alfenas, R.C.G. and Mattes, R.D. (2005). Influence of Glycemic Index/Load on Glycemic Response, Appetite, and Food Intake in Healthy Humans. Diabetes Care. 28(9). p. 2123-2129 Anderson, G.H and Woodend, D. (2008) Effect of Glycemic Carbohydrate on Short-term satiety and Food Intake. Nutritional Reviews: 16(5). Babbie, E. (2004). The Practice of Social Research. 10th ed. USA: Thomson-Wadsworth Burton-Freeman, B.M. and Keim, N.L. (2008). Glycemic index, cholecystokinin, satiety and disinhibition: is there an unappreciated paradox for overweight women? International Journal of Obesity. 2008 32. p. 1647-1654 Campbell, B. (n.d.) Glycemic Load vs. Glycemic Index. Retrieved: www.ncsa-lift.org. 18th Apr 2011 Foster-Powell, K., Holt, S.H.A and Brand-Miller, J.C. (2002). International table of glycemic index and glycemic values: 2002. American Journal of Clinical Nutrition: 76(1). p. 5-56. Jenkins, D.J.A., Thomas, D.M., Wolever, M.S., Rodney, H.T., Barker, H., Fielden, H., Baldwin, J. M., Bowling, A.C. Newman, H.C., Jenkins, A. L. and Geoff, D.V. (1981).Glycemic index of foods: a physiological basis for carbohydrate exchange. The American Journal of Clinical Nutrition. 34(March 1981). p. 362-366. LaCombe, A and Ganji, V. (2010). Influence of two breakfast meals differing in glycemic load on satiety, hunger, and energy intake in preschool children. Nutrition Journal 2010 9:53. Ludwig, D.S. (2000). Dietary Glycemic Index and Obesity. The Journal of Nutrition: p.280-283 Ludwig, D.S., Majzoub, J.A., Al-Zahrani, A., Dallal, G.E., Blanco, I and Roberts, S.B. (1999). High Glycemic Index Foods, Overeating, and Obesity. Pediatrics: 103(3). Retrieved: http://www.pediatrics.org/cgi/content/full/103/3/e26. Last accessed 6th Apr 2011 Appendices Gantt chart Research Process TIME PERIOD April May June July Aug Sept Oct Nov Dec Jan Feb Mar Apr May Research Proposal   Literature Review     Contacting Posssible subjects       Prepare lists of subjects     Select Subjects     Administering Treatments       Analyse Results       Prepare First Draft of Report       Prepare Second Draft     Prepare Final Draft     Type Set Report       Print     Risk Assessment 1. Subsequent medical problems may arise for various reasons 2. Some subjects may be allergic to some of the foods included as treatments. 3. Subjects if not monitored properly try to do things so as to alter the results of tests that will make them eligible for being a subject. 4. Important that information on subjects be kept confidential. This is one of the ethical guidelines to be adhered to in doing any form of research Read More