Recently, a paper by Kokkinos et al. (1) was published on an experiment finding different postprandial Peptide YY and Glucagon-Like Peptide-1 concentration responses with varying eating speed. This immediately prompted such media headlines as: “Eating Slowly May Help Weight Control,” “Cut Calories by Eating Slowly,” “Eating Slowly Can Help with Weight Loss,” and “Eating Quickly is Associated With Overeating, Study Indicates.”
Bold extrapolations if you actually read the study.
A look at the paper and an understanding of previous literature made this an easy next choice for a blog topic. Note that this is an incomplete literature review but enough to get the idea that the issue is more complex than media reports will suggest.
First, our journey through the body of research takes us back to 1975, where Gaul et al. (2) examined the assumption “that overweight individuals eat faster and take fewer bites (cf. Stuart & Davis, 1972)” as well as (Ferster, 1962). The study involved subjective (visual) determinations of age and obesity who ate at an establishment that served hamburgers, french fries, and soda. Frequency bites and sips were taken for 5 minutes, as well as number of chews per bite, and time spent chewing. They found that subjects labeled obese took more bites (av. 16.94) compared to nonobese (av. 12.66), chewed fewer times per bite (9.24 vs 18.60), and spent less time chewing (104.26 sec vs 157.54 sec). They noted differences in chewing rate may influence satiety because of the role of texture. It appears that “bite counting” was a guideline to attempt to try to reduce total food consumption, interestingly, but was not supported by research at the time. Certainly this study with limited food choices and contexts is not evidence that faster eating caused the obesity.
Marston et al. (3) in then replicated the study in children with a few changes and published the results in 1977. They found again that obese subjects took more bites in a 3 minutes period (av. 6.85 vs 5.33), and larger mouthfuls. Possibly of importance, obese subjects had less than half of the frequencies of hesitation, toying, putting utensils down, etc. They had found the same results in children (1976) as well.
There were also a number of other similar studies to these, characterizing an “obese eating style.” With a weak consensus on important control variables, however, and yet other studies showing that rate changes occur while eating, not accounted for in the initial research.
In 1980, Kaplan (4) used one food item and examined rate differences during eating in obese and lean subjects. This time, no significant differences were between the groups for meal size, meal duration, total bites, bites per sandwich quarter, bites per minute, calories per minute, calories in the first 3 minutes, and calories in the first 5 minutes. There was actually a trend that the nonobese consumed a greater amount of their meal during the first half of the measured time. No differences were found on satiety or taste ratings.
In another experiment, the rate of consumption was changed. The author notes previous research with liquid calories in which subjects tend to consume more when speed of consumption is increased. This suggests that regulatory satiety mechanisms may not adequately monitor food when it is consumed too quickly. Also, a study by Shaw (1973) found that depending on the type of food or or how it was presented (e.g. size of cup) effects rate of ingestion. So the second study used a common food (sandwich) and adjusted rate of consumption based on each individual’s normal rate. The results confirmed what the first experiment found: no differences between obese and nonobese in meal size, meal duration, total bites, bites per sandwich quarter, bites per minute, calories per minute, calories in first 3 minutes, and calories in first 5 minutes. The obese, however, consumed a smaller portion of the total meal in the first half of the meal, and increased speed during the latter half to match the average of the nonobese at the end. There was also a trend for consumption of more calories when food was consumed quickly versus slowly, though low subject numbers limit the statistical power. Subjective ratings of fullness was not different between the groups.
Several studies (by Mahoney; Dodd, Birkey and Stalling; Hill and McCutcheon; Adams et al.) noted in the text support the findings of no differences in meal duration in obese versus nonobese subjects. While I won’t go into those in detail, the point is that there is no conclusive answer from the group of pioneering studies.
Fast forward to the new study.
The authors (1) summarize our understanding of appetite control mechanisms; a postprandial reduction in ghrelin, and increase in peptide YY (PYY) and glucagon-like peptide (GLP)-1, all which signal mainly the hypothalamus to regulate satiety. GLP-1 is also an incretin (effects insulin release). These three peptides were measured in this study in response to identical meals at 2 different occasions in a cross-over fashion consuming them slow or quickly. The meal consisted of 300 ml of ice cream (675 kcal, 59% fat, 33% CHO, 8% protein). In the group consuming it slowly, the ice cream was divided into 7 equal portions and consumed every 5 minutes until gone (within 30 minutes), and in the group consuming it fast, it was divided into 2 portions and consumed 5 minutes apart (supposedly in about 5 minutes). Beside the blood markers, VASs (visual analog scales) were used to assess subjective hunger and fullness during the meal and at 30 minute intervals after the meal for 3.5 hours.
A trend was found for a higher fullness but not hunger VAS rating after the 30 minute meal compared to the 5 minute meal. Fullness and hunger VAS ratings increased and decreased, respectively, postprandially without statistical significance between the groups. In my (very humble) opinion, these results are next to useless with the subject number (17), because of subjective variability.
For PYY and GLP-1 over the 3.5 hours, the AUCs were greater after the slowly eaten meal compared to the fast meal. PYY and GLP-1 concentrations tended to be higher at some timepoints in the slowly eaten meal group. The ghrelin AUC differences were non significant but there was a trend for lower ghrelin at 120 minutes for the slowly eaten meal group. Insulin and glucose did not differ significantly between the groups in concentrations or AUC at any timepoints.
PYY and GLP-1 are produced in the GI tract in response to food intake, acting in parts of the brain thought to regulate satiety, and are exaggerated in patients with gastric bypass surgery so perhaps they are important in the appetite and glycemic control successes.
An important limitation to the study, is that as noted before, only 17 subjects were included in the study. The authors note that both normal-weight and overweight subjects were included. Excess weight can alter resting concentrations of PYY, GLP-1, and ghrelin, but the authors maintain this did not change results with a separate analysis of subjects below and above a BMI of 25.
The PYY and GLP-1 differences are the only notable results, in my opinion, but much more research is needed to replicate this with more subjects, with different foods, and to elucidate if the small differences in hormone concentrations actually are enough to influence appetite (this study found no significant difference in subjective measures), in the short and long term.
The paper as a whole reads in favor of eating slow, and the authors cited several observational studies in that show a correlation between eating speed and obesity. But they seemingly completely ignore previously discussed interventional research that complicates the big picture. These are the following that they cite:
Two observational studies showing a correlation between eating speed in children and obesity based on questionnaires (!) [here] and [here] and one that found differently [here]. A larger cross sectional survey found associations with eating speed and eating until full and obesity risk [here]. They do cite one better controlled study using donuts showing a relationship between eating speed and obesity, however in the context of what has been discussed previously this is an anomalous find.
However, these types of studies are starting points in research, and interventional studies must follow up with consistent support. Clearly it is not so simple.
Let’s go back and look at a couple of the more recent controlled interventional studies. Martin et al. (5) in 2007 published results of a study using both men and women that tested consumption of three different test meal patterns: normal eating rate, a reduced rate (50% reduction of normal), and a combined meal (normal at first, 50% reduction during the latter half of the meal). They found that a reduction in eating rate reduced food intake in men, but not women, and appetite ratings were decreased most in the combined meal pattern. This suggests there are additional variables to consider such as gender.
Then a year later, Andrade et. al (6) found that taking small bites, pausing between bites, and chewing thoroughly in women reduced total food intake and resulted in higher feelings of satiation, though further research clearly needs to be done to elucidate the differences in which each recommendation influenced the results most.
Other studies to consider
Instead of detail out every paper, I will highlight some of the things not yet fully understood.
Food preferences/palatability may outweigh factors such as rate of consumption on total consumption (consider the cited donut study).
Sensory perception may influence intake rate, possibly explaining some of the differences in study results with different foods.
One study found that when instructed to pause between bites, subjects eating slower actually consumed more food.
There may be an acute association between eating rate and weight control, but this study found that after a number of weeks, the association was lost, and weight loss was no different between those who ate faster and slower.
Water consumption on appetite is still complicated, even more so because this study found that water in a food influenced food consumption but not served with food.
The form of food may influence appetite. Chewing may trigger satiety signals that liquid foods do not.
And so on.
The point of this long rambling is that the issue is still far from conclusively answered. For a true understanding of the complexity of potential variables that confound each study’s results, I recommend reading through some of the most recent papers (e.g. 5, 6). At this point, there is no clear evidence to suggest that eating slower will help you maintain or lose weight more easily.
Media reporting almost ALWAYS ignores the body of evidence in favor or misinterpreting the real value of a new publication to our knowledgebase. Always consult the study methodology and search for existing literature on the topic for an accurate understanding.
1. Kokkinos A, le Roux CW, Alexiadou K, Tentolouris N, Vincent RP, Kyriaki D, Perrea D, Ghatei MA, Bloom SR, & Katsilambros N (2009). Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY and Glucagon-Like Peptide-1. The Journal of clinical endocrinology and metabolism PMID: 19875483
2. Gaul, D., Craighead, E., & Mahoney, M. (1975). Relationship between eating rates and obesity. Journal of Consulting and Clinical Psychology, 43 (2), 123-125 DOI: 10.1037/h0076522
3. Marston AR, London P, Cohen N, & Cooper LM (1977). In vivo observation of the eating behavior of obese and nonobese subjects. Journal of consulting and clinical psychology, 45 (2), 335-6 PMID: 850018
4. Kaplan DL (1980). Eating style of obese and nonobese males. Psychosomatic medicine, 42 (6), 529-38 PMID: 7465738
5. Martin CK, Anton SD, Walden H, Arnett C, Greenway FL, & Williamson DA (2007). Slower eating rate reduces the food intake of men, but not women: implications for behavioral weight control. Behaviour research and therapy, 45 (10), 2349-59 PMID: 17517367
6. Andrade AM, Greene GW, & Melanson KJ (2008). Eating slowly led to decreases in energy intake within meals in healthy women. Journal of the American Dietetic Association, 108 (7), 1186-91 PMID: 18589027