Lower GI diets found to boost levels of appetite-sating hormone

There are a number of ways of tackling excess weight, one of which is to eat less. What is important here is that food intake is cut without inducing much in the way of hunger. Why? Because for most of us, hunger is not something we will wilfully put up with in the long term. It is a major reason why individuals default from dietary change, and also a major reason why, generally speaking, diets don’t work.

At first glance the idea of eating less without being more hungry does not make sense. But it does when one considers the fact that different foods satisfy the appetite to different extents. One factor which appears to play a part here is the speed and extent to which a food releases sugar into the bloodstream (the food’s ‘glycaemic index’). There is plenty of evidence which shows that lower GI foods are, calorie for calorie, more satisfying than higher GI ones [1]. I wrote about this only last month here.

This blog was about a study which found that a diet lower in carbohydrate and higher in fat was found to be more satisfying than a higher carb, lower-fat one. In this blog it was mentioned that lower GI foods have a more blood sugar stabilising effect than higher ones. This is good because they will help to prevent episodes of lower blood sugar (hypoglycaemia) that can stimulate hunger and food cravings. I also mentioned that the higher fat content of the more satisfying diet might have helped here too, in that it stimulates the hormone cholecystokinin, which promotes feelings of satisfaction and fullness.

I was interested to read recently about study published this month in the European Journal of Clinical Nutrition which tested the biochemical impact of high and low GI diets [2]. Biochemical parameters checked were levels of glucose, insulin, cholecystokinin and ghrelin (ghrelin is a hormone that stimulates appetite).

The lower GI diet led to a lower levels of sugar and insulin, perhaps not surprisingly. What would have been more useful, here, is for sugar levels to be checked for any episodes of subnormal sugar levels. A study which took this approach found that the extent of low sugar levels tallied with hunger levels [3].

This study found no difference in ghrelin levels after the two diets. However, it did find that over a 7-hour period after eating, cholecystokinin levels were higher after the lower GI food. This hormone, remember, help promote feelings of satisfaction and fullness. Traditionally, it is thought to be secreted in response to fat. However, fat levels were the same in the two test diets. Here, it seems, we have a new mechanism which helps to explain the observation that lower GI foods are more sating than higher ones.

References:

1. Roberts SB. High-glycemic index foods, hunger, and obesity: is there a connection? Nutrition Review 2000 58:163-169

2. Reynolds RC, et al. Effect of the glycemic index of carbohydrates on day-long (10 h) profiles of plasma glucose, insulin, cholecystokinin and ghrelin. European Journal of Clinical Nutrition 2009;63:872″878

3. Arumugam V, et al. A high-glycemic meal pattern elicited increased subjective appetite sensations in overweight and obese women. Appetite 2008;50(2-3):215-22

4 Responses to Lower GI diets found to boost levels of appetite-sating hormone

  1. Antje 10 July 2009 at 8:12 am #

    Dr. Briffa,

    the amount of fat being in equal in the two diets means maybe it is the ratio carbs/fats rather than fat as such that causes cck secretion. Pardon my english, i am Dutch.

    Thanks for your very interesting posts.I follow them closely.

  2. Dr John Briffa 10 July 2009 at 8:30 am #

    Antje

    Yes, that’s right. Or it might be down to something to do with the extent of sugar release (GI) of the carbs. Or both. Or perhaps some other factor(s).

    The most important thing, though, is that lower GI foods are generally more sating than higher GI ones. Protein is generally sating too, by the way.

  3. Trinkwasser 12 July 2009 at 9:14 pm #

    Fascinating! Give it another decade or two and we might have a better idea of how all this works. At the moment we seem to be discovering new factors (leptin, ghrelin, incretins, anandamide etc) faster than we’re working out what they do

  4. Christopher Palmer 6 November 2012 at 3:59 pm #

    A consequence of deliberately altering my dietary balance away from carbs and towards fat is that I do often feel fuller for longer. On occasions I noticed a slight sense of my guts still being distended even after a nights sleep. This sensations led me to wonder if gastric emptying was being modulated in any way, not so much in relation to the mere presence of contents following a meal, but more in relation to the call for metabolites to be passed across the gastrointestinal divide.

    From an engineering point of view, providing it could be established that fats in the guts have a capacity to coat the fellow constituents of chyme (carbs and proteins), then the way to gain mastery over modulation would be via this property of fat to coat everything it has contact with. Basically, providing the premises are correct, then if something has control over the amount of emulsifying factor (bile) that is supplied for digestion then digestion itself may be modulated because the presence of fats in chyme may impede the ability of other digestive factors to act upon carbs and proteins. Potentially, if the supply of bile is modulated so too is the rate of digestion itself, but it remains an untamed thought.
    However lessons from the notion of GI/GL do lend some clues.

    The GI/GL for a food can be a function of several factors. The nature (complexity) of the carbohydrate being one, the presence of ‘starches’, (fibre) that resist digestion being another, whether process such as mashing or cooking has been applied, and the presence of fat. The proponents behind GI/GL acknowledge the presence of fat lowers the glycemic result. Potato crisps have lower indices than boiled potato. Dr Robert C Atkins seems to have spotted these indications but seems not to have explored them to their logical extremities. It is generally acknowledged fats are digested more slowly, but lessons from GI/GL indicate fats also slow the digestion of carbs.

    Although still very much an untamed thought I think gastric or digestive modulation has the look of something that has received less attention than it deserves. It is clear that unregulated and elevated levels of insulin and ghrelin may play a part in overeating. It is clear that equipping a creature with the means to sequester energy as fat reserves makes no sense unless the creature can draw down upon those reserves periodically. And Atkins appears to be correct when he indicated that glucosis in extremis describes the process of sequestering fat, and that lipolysis/ketosis is the metabolic pathway by which metabolism draws down sequestered fat. Hormonal balances that result from the macronutrient balance of a diet must be important. Nature doesn’t seem to have equipped us to run perpetually on glucosis, or hyperglucosis. Being overweight is really the outward expression of chronic hyperglucosis.

    When I began ‘surfing’ I was hopeful of finding some clear directions. Whatever would modulate bile supply would modulate digestion, and in turn that process could engender a more balanced metabolism. I noted that cholecystokinin (CCK) got a mention, but to my untrained eye discussion seemed inconclusive and sometimes contradictory. After more time ‘surfing’ I stumbled across ‘oleoylethanolamine’ (OEA), which is also credited with signaling satiety and suppression of appetite.

    The idea that fats might modulate the rate of digestion and gastric emptying and that signaling pathways may stem from receipt and passage of fats to the GI tract seems to me to be systemically strong and it provokes interest, that if correct, as to which fatty acids would be the stimulus for feedback. Would it be all fatty acids or would chain length matter? Would short-chain, medium-chain, or long-chain be treated the same in this potential reporting pathway?

    I wondered, Dr Briffa, if you have had opportunity to look at oleoylethanolamine (OEA) in relation to modulation of appetite.

Leave a Reply to Christopher Palmer Click here to cancel reply.